IntensiveEENT/Ophthalmologic Emergencies 397-428 Marc Dorfman, MD, FACEP, MACP GI Emergencies...

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2013 SyllabusVolume 2

ILLINOIS COLLEGE OF EMERGENCY PHYSICIANS3000 Woodcreek Drive, Suite 200 Downers Grove, IL 60515

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Release date: August 13, 2013 Expiration date: August 12, 2014

Recent Date of Review: Not Applicable Recent Update: Not Applicable

Disclaimer and Conflict of Interest: This product is being made available by the Illinois College of Emergency Physicians for educational purposes only. The material is not intended to represent the only, nor necessarily the best methods or procedures appropriate for the medical situations, but rather is intended to present an approach, statement or opinion of the authors or presenters which may be helpful or of interest to the participants. This product is not sponsored by or affiliated with the American Board of Emergency Medicine, or the American Board of Osteopathic Emergency Medicine.

The Illinois College of Emergency Physicians has indicated, in accordance with the Accreditation Council of Continuing Medical Education (ACCME) Standards and the policy of the American College of Emergency Physicians, that all individuals with control over CME content (including but not limited to staff, planners, reviewers, and faculty) must disclose whether or not they have any relevant financial relationship(s) to learner prior to the start of the activity. (Refer to the CME Section on the Syllabus Flash Drive for complete listing)

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TABLE OF CONTENTS – VOLUME 2

Pages Trauma Topics

Head Injury/C-spine/Spinal Cord Trauma 3-34 Scott Heinrich, MD, FACEP Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma 35-78 Michael Schindlbeck, MD, FACEP Hand and Wrist Injuries 79-100 Scott C. Sherman, MD Upper and Lower Extremity Trauma 101-148 Wesley Eilbert, MD, FACEP Urology/GU Trauma 149-168 Dr. Eilbert Stroke and Seizures 169-194 E. Bradshaw Bunney, MD, FACEP Psychiatric Emergencies 195-218 Dr. Bunney

Miscellaneous Topics Pulmonary Emergencies 221-246 Matthew Jordan, MD, FACEP Environmental Emergencies 247-298 Jay Sharp, MD, FACEP, FAWM Gynecological and Obstetrical Emergencies 299-396 Collette Wyte, MD, FACEP

EENT/Ophthalmologic Emergencies 397-428 Marc Dorfman, MD, FACEP, MACP GI Emergencies 429-488 Brian Donahue, MD, FACEP Infectious Disease 489-516 Joseph Peters, DO, RDMS, FACEP, FACOEP, FACOI

Course Faculty and Planners

James Ahn, MD Emergency Medicine Board Review Intensive Course Committee; Assistant Professor

of Clinical Medicine, Section of Emergency Medicine, University of Chicago Amy Archer Uyenishi, MD, FACEP Attending Physician, Department of Emergency Medicine, Advocate Lutheran General Hospital, Park Ridge; Clinical Assistant Professor, University of Illinois at Chicago Kate Blackwelder Communications Manager, Illinois College of Emergency Physicians, Downers Grove Christine Babcock, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Assistant Professor of Clinical Medicine, Residency Program Director, Section of Emergency Medicine, University of Chicago E. Bradshaw Bunney, MD, FACEP Associate Professor and Residency Director, Department of Emergency Medicine, University of Illinois at Chicago Joseph Colla, MD, RDMS Clinical Associate Professor and Ultrasound Fellowship Director, Department of Emergency Medicine, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago Nicole Colucci, DO, FAAP

Attending Physician, Presence Resurrection Medical Center, Chicago; Attending Physician, Loyola University Medical Center, Maywood Brian Donahue, MD, FACEP Clinical Assistant Professor, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, Presence Resurrection Medical Center, Chicago Marc Dorfman, MD, FACEP, MACP Residency Director, Emergency Medicine Residency, Presence Resurrection Medical Center; Assistant Clinical Professor, University of Illinois at Chicago

Wesley Eilbert, MD, FACEP Clinical Associate Professor, Department of Emergency Medicine, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago Carl Ferraro, MD, FACEP Education Director, Department of Emergency Medicine, Mercy Hospital and Medical Center, Chicago; Clinical Associate Professor, University of Illinois at Chicago

Lora Finucane Educational Programs and Meetings Manager, Illinois College of Emergency Physicians, Downers Grove Shannon Finucane CME and Marketing Coordinator, Illinois College of Emergency Physicians, Downers Grove John W. Hafner, Jr., MD, MPH, FACEP Clinical Associate Professor of Surgery, University of Illinois College of Medicine at Peoria; Attending Physician, Department of Emergency Medicine, OSF Saint Francis Medical Center, Peoria

Scott Heinrich, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Attending Physician, Department of Emergency Medicine, Mercy Hospital and Medical Center; Clinical Assistant Professor and Associate Residency Director, Department of Emergency Medicine, University of Illinois at Chicago Linda Herman, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Clinical Assistant Professor, University of Illinois at Chicago; Attending Physician and Core Faculty, Presence Resurrection Medical Center; Attending Physician, Presence Our Lady of the Resurrection Medical Center, Chicago Matthew Jordan, MD, FACEP Clinical Assistant Professor, University of Illinois College of Medicine; Department of Emergency Medicine, Presence Resurrection Medical Center, Chicago. Samuel Hiu-Fung Lam, MD, RDMS, FACEP Emergency Medicine Board Review Intensive Course Committee; Attending Physician, Department of Emergency Medicine, Assistant Emergency Ultrasound Director, Advocate Christ Medical Center, Oak Lawn

Abhishek Katiyar, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician and Medical Toxicologist, Department of Emergency Medicine, Advocate Christ Medical Center, Oak Lawn John Martini, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Clinical Assistant Professor, University of Illinois at Chicago; Associate Medical Director, Presence Our Lady of the Resurrection Medical Center, Chicago Alisa McQueen, MD, FAAP, FACEP Assistant Professor of Pediatrics, Program Director, Fellowship in Pediatric Emergency Medicine, The University of Chicago, Chicago, IL Joseph Ogarek, MD, FACEP Attending Physician, Department of Emergency Medicine, Advocate Lutheran General Hospital, Park Ridge Laura Oh, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician,

Department of Emergency Medicine, Loyola University Medical Center, Maywood Jon Olsen, MD, FACEP Assistant Professor of Clinical Medicine, Section of Emergency Medicine, University of Illinois at Chicago; Program Director and Director of Clinical Operations, Department of Emergency Medicine, Advocate Lutheran General Hospital, Park Ridge Joseph Peters, DO, RDMS, FACEP, FACOEP, FACOI Clinical Assistant Professor of Surgery, University of Illinois College of Medicine at Peoria; Attending Physician, Department of Emergency Medicine, OSF Saint Francis Medical Center, Peoria John T. Piotrowski, MD, FACEP Associate Medical Director and Vice Chairman, Department of Emergency Medicine, Advocate Condell Medical Center; Assistant Clinical Professor of Emergency Medicine, University of Illinois; Physician Champion of the Advocate Condell Stroke Center of Excellence; Lecturer, Rosalind Franklin Medical School, Chicago

Henry Pitzele, MD, FACEP Chair, Emergency Medicine Board Review Intensive Course Committee; Director,

Section of Emergency Medicine, Jesse Brown VA Medical Center, Chicago; Clinical Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago

Robert P. Rifenburg, DO, RDMS, FACEP Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago; Fellowship Director, Emergency Ultrasonography, Presence Resurrection Medical Center, Emergency Medicine Residency Program, Chicago T.J. Rittenberry, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Associate Residency

Director, Associate Professor of Clinical Emergency Medicine, University of Illinois at Chicago; Director, Emergency Medical Education, Advocate Illinois Masonic Medical

Center, Chicago Rachel Rubin, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician,

Northwestern Lake Forest Hospital, Lake Forest Michael Schindlbeck, MD, FACEP Assistant Professor of Emergency Medicine, Rush Medical College; Assistant Program Director, Department of Emergency Medicine, John H. Stroger Jr. Hospital of Cook County, Chicago Meeta Shah, MD Emergency Medicine Board Review Intensive Course Committee; Attending Physician,

Rush University Medical Center; Attending Physician, Section of Emergency Medicine, Jesse Brown VA Medical Center, Chicago Jay Sharp, MD, FACEP, FAWM Emergency Medicine Board Review Intensive Course Committee; Core Faculty,

Emergency Medicine Residency, Presence Resurrection Medical Center; Attending Physician, Presence Resurrection Medical Center Scott C. Sherman, MD Assistant Residency Director, Associate Professor of Emergency Medicine, Rush Medical College; Attending Physician, Department of Emergency Medicine, John H. Stroger Jr. Hospital of Cook County, Chicago William Sullivan, DO, JD, FACEP Attending Physician, St. Margaret's Hospital, Spring Valley; Attending Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago; Clinical Instructor, Department of Emergency Medicine, Midwestern University, Downers Grove; Clinical Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago

Midori Takeyasu, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Associate Clinical Professor of Emergency Medicine, University of Illinois College of Medicine; Attending Physician, Presence Resurrection Medical Center and Presence Our Lady of the Resurrection Medical Center; Director, Emergency Medical Services, Presence Our Lady of the Resurrection Medical Center; Residency Coordinator, Presence Resurrection Medical Center and John H. Stroger Jr. Hospital of Cook County, Chicago

Trevonne M. Thompson, MD, FACEP, FACMT

Attending Physician, Department of Emergency Medicine, and Associate Director, Division of Medical Toxicology, Department of Emergency Medicine, University of Illinois at Chicago; Consultant, Illinois Poison Center, Chicago Carissa Tyo, MD Assistant Professor, Department of Emergency Medicine and Internal Medicine, University of Illinois Hospital and Health Sciences System, Chicago Matthew Valente, MD, FACEP Emergency Medicine Board Review Intensive Course Committee; Attending Physician, St. Francis Hospital, Evanston; Teaching Faculty, Emergency Medicine Residency, Presence Resurrection Medical Center, Chicago; Clinical Assistant Professor, University of Illinois at Chicago Edward Ward, MD, MPH, FACEP Emergency Medicine Board Review Intensive Course Committee; President, Illinois

College of Emergency Physicians, Downers Grove; Medical Director, Department of Emergency Medicine, Rush University Medical Center; Assistant Professor, Rush University, Chicago Deborah E. Weber, MD, FACEP Emeritus Faculty, Department of Emergency Medicine, Advocate Lutheran General

Hospital, Park Ridge; Author of “Questions for Board Preparation in Emergency Medicine (Editions I, II & Slide Review)”, Author of “EM4LIFE – Emergency Medicine LLSA Article Review and CME Program (Editions 2004-2011)”, Author of “EM4LIFE – Emergency Medicine LLSA Article Review Pearls - 2012”, Co-author of “Preparing for the Oral Board Exam in Emergency (Editions IV, V, VI and VII)” and Managing Editor of “Preparing for the Written Board Exam in Emergency Medicine (Editions I, II, and III)”; consulting contributor to all chapters of “Preparing for the Written Board Exam in Emergency Medicine”, 5th Edition; consulting contributor to “Preparing for the Oral Board Exam in Emergency Medicine”, 9th Edition, Riverwoods

Nicole White, MD, MA Fellowship, Emergency Ultrasonography, Presence Resurrection Medical Center, Emergency Medicine Residency Program, Chicago Collette Wyte, MD, FACEP Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Oakland University William Beaumont School of Medicine, Royal Oak, Michigan

COURSE FACULTY AND PLANNER DISCLOSURE

In accordance with the ACCME Standards for Commercial Support and policy of the American College of Emergency Physicians, all individuals with control over CME content (including but not limited to staff, planners, reviewers, and faculty) must disclose whether or not they have any relevant financial relationship(s) to learners prior to the start of the activity. These individuals have indicated, that they have a relationship which, in the context of their involvement in the CME activity, could be perceived by some as a real or apparent conflict of interest (e.g., ownership of stock, grants, honoraria, or consulting fees), but these individuals do not consider that it will influence the CME activity.

Faculty Name /Credentials Company Name Nature

E. Bradshaw Bunney, MD, FACEP Genentech Consultant

William Sullivan, DO, JD, FACEP Law Office of William Sullivan Owner

All remaining individuals with control over CME content have no significant financial interests or relationships to disclose.

James Ahn, MD Amy Archer Uyenishi, MD, FACEP Christine Babcock, MD, FACEP Kate Blackwelder Joseph Colla, MD, RDMS Nicole Colucci, DO, FAAP Brian Donahue, MD, FACEP Marc Dorfman, MD, FACEP, MACP Wesley Eilbert, MD, FACEP Carl Ferraro, MD, FACEP Lora Finucane Shannon Finucane John W. Hafner, Jr., MD, MPH, FACEP Scott Heinrich, MD, FACEP Linda Herman, MD, FACEP Matthew Jordan, MD, FACEP Abhishek Katiyar, MD Samuel Lam, MD, RDMS, FACEP John Martini, MD, FACEP Alisa McQueen, MD, FAAP, FACEP Joseph Ogarek, MD, FACEP Laura Oh, MD

Jon Olsen, MD, FACEP Joseph Peters, DO, RDMS, FACEP, FACOEP, FACOI John T. Piotrowski, MD, FACEP Henry Pitzele, MD, FACEP Robert P. Rifenburg, DO, RDMS, FACEP T.J. Rittenberry, MD, FACEP Rachel Rubin, MD Michael Schindlbeck, MD, FACEP Meeta Shah, MD Jay Sharp, MD, FACEP, FAWM Scott C. Sherman, MD Midori Takeyasu, MD, FACEP Trevonne M. Thompson, MD, FACEP, FACMT Carissa Tyo, MD Matthew Valente, MD, FACEP Edward Ward, MD, MPH, FACEP Deborah E. Weber, MD, FACEP Nicole White, MD, MA Collette Wyte, MD, FACEP

Intensive



TraumaTopics

Page 1

Head Injury/C-Spine/ Spinal Cord Trauma

Scott Heinrich, MD, FACEP

Emergency Medicine Board Review Intensive Course Committee; Attending Physician, Department of Emergency Medicine, Mercy Hospital and Medical Center; Assistant

Professor and Associate Residency Director, Department of Emergency Medicine University of Illinois at Chicago

Page 3

Page 4

Notes

Head Injury/C-Spine/Spinal Cord Trauma

HEAD INJURY/C-SPINE/SPINAL CORD TRAUMA

I. HEAD TRAUMA

A. Anatomy:

1. Skull - rigid brain case protecting neural structures:

a. Frontal, ethmoid, sphenoid, parietal (2), temporal (2),

occipital bones.

b. Bones of skull have inner and outer tables with cancellous

bone between.

c. Irregularity of floor or cranial vault increases problems with

brain contusion.

2. Scalp (five layers) - pneumonic – S-C-A-L-P:

a. Skin, subCutaneous, galea Aponeurotica, Loose areolar and

Periosteum.

b. Vascular with vessels between the dermis and galea.

c. Lacerations of scalp may cause significant or even fatal

hemorrhages, especially in children.

d. Hematoma of the scalp occurs between galea and

periosteum (subgaleal) or beneath the periosteum

(subperiosteal).

e. The sharp cutoff of a subperiosteal hemorrhage at a suture

line may be mistaken for a fracture on palpation.

3. Meninges (intracranial hemorrhages are named in relation to

these layers):

a. Dura mater - tough outer covering, adheres to bone, folds

compartmentalizes the brain.

i. Midline falx cerebri – separates brain into 2 cerebral

hemispheres.

ii. Tentorium cerebelli – separates cerebellum & brainstem

from cerebrum.

iii. Falx cerebelli – separates cerebellum hemispheres.

iv. Dural layers also separate to form dural sinuses.

b. Arachnoid - thin, filmy, veil-like membrane.

c. Pia mater - thin membrane adherent to brain surface.

4. CSF:

a. Production by choroid plexus in lateral, third and fourth

ventricles.

b. Function:

i. Protection during trauma.

ii. Fluid pathway for delivery of substances to the brain and

spinal column.

iii. pH influences respiratory drive and cerebral blood flow.

c. Pressure – 5-15 mmHg in ventricles.

5. Brain:

a. Weighs 1400 g.

Page 5

Notes


b. Occupies 80% cranial cavity.

c. Divisions – cerebrum, cerebellum, brainstem.

6. Blood.

B. Cerebral hemodynamics:

1. Blood brain barrier (BBB) – maintains microenvironment.

2. Cerebral blood flow (CBF):

a. 15% of cardiac output.

b. Maintained by altering diameter of cerebral vessels.

c. HTN, alkalosis, hypocarbia – vasoconstriction.

d. Hypotension, acidosis, hypercarbia, hypoxia – vasodilatation.

e. Injured vessels lose responsiveness.

f. Constant at mean arterial pressure of 50-150 mmHg.

g. CBF increases linearly as MAP increases above 150 mmHg.

3. Cerebral Perfusion Pressure (CPP) - Pressure gradient across the

brain:

a. Estimated by MAP – ICP (intracranial pressure) = CPP.

b. CBF depends on CPP, CBF remains constant when CPP is

50-160mm Hg.

c. Autoregulation is lost when CPP < 40 mmHg.

C. Pathophysiology:

1. Primary brain damage:

a. Mechanical, irreversible damage occurs at time of trauma –

lacerations, hemorrhages, etc.

b. Produces injury at the cellular level.

2. Secondary brain damage – intracellular and extracellular:

a. Pathological processes arise as a direct result of trauma.

b. Damage to nerve axons is followed by chromatolysis.

c. Followed by either dissolution of cell or subsequent recovery.

3. ICP closed box model - intracranial pressure (ICP) is a function

of the volume of these three components and any space

occupying lesion.

a. Increased ICP > 15 mmHg.

b. 1st compensatory mechanism – displace CSF to spinal

column:

i. Can accommodate 50 to 100 ml lesion – after that small

increases in volume produce large increases in ICP as can

be seen by the diagram below.

ii. CSF production not increased in trauma unless a space

occupying lesion obstructing CSF flow; usually not a

major contributing factor.

Page 6

Notes


Pressure-Volume Curve

c. Blood - autoregulated:

i. As ICP increases, CPP decreases, autoregulation is lost.

d. Brain parenchyma - types of brain swelling:

i. Congestive brain swelling – caused by increased blood

volume.

ii. Cerebral edema – increase in brain volume:

Vasogenic edema – altered permeability of blood-

brain barrier.

Cytotoxic edema – disables Na-ATP pump, allows

sodium and water to accumulate intracellularly.

iii. Increase in aldosterone and vasopressin secretion, causing

overall water retention.

D. Herniation syndromes:

1. Subfalcine herniation:

a. Cingulate gyrus on medial part of frontal lobe is displaced

medially under free end of the falx.

b. Can compromise blood flow through anterior cerebral artery

complexes.

c. Does not usually cause brainstem effects seen in other

herniation syndromes.

2. Central transtentorial herniation:

a. Increased volume or pressure in the supratentorial

compartment (usually frontal or occipital areas) causing

bilateral or central pressure exerted on brain above.

b. Results in brainstem ischemia or hemorrhage from

compression and shear of perforating arteries from basilar

artery (Duret hemorrhages).

c. May be the etiology of the Cushing response (i.e., arterial

hypertension, bradycardia and respiratory irregularities seen

with increasing ICP).

d. Decreased LOC.

e. Motor – bilateral weakness, increased tone, bilateral

Babinski’s.

f. Pupils – pinpoint, loss of light reflex.

g. Respiratory – yawns and signs sustained

hyperventilation slow and irregular breaths apnea.

h. Posturing – decorticate decerebrate.

Page 7

Notes


3. Uncal herniation (transtentorial):

a. Due to increasing volume in the temporal lobe or middle

cranial fossa.

b. Uncus of temporal lobe herniates across incisura of the

tentorium cerebelli and impacts against midbrain.

c. Ipsilateral CN III compressed by the shift resulting in

ipsilateral pupillary dilatation - aniscoria, ptosis, impaired

EOM, sluggish pupil, finally nonreactivity.

d. Contralateral Babinski develops early.

e. Weakness is usually contralateral.

f. 25% have ipsilateral weakness due to compression of the

contralateral cerebral peduncle against the opposite tentorium

(Kernohan's notch phenomena) – gives false localizing

signs.

g. Impaired consciousness is NOT a reliable early sign but

continued herniation results in agitation and restlessness

lethargy coma.

h. As herniation continues, contralateral pupil may dilate in the

preterminal stage.

i. Develop decerebrate posturing.

j. Respiratory – normal hyperventilation ataxic breathing

apnea.

k. Cardiac – large fluctuations of blood pressure and cardiac

conduction hypotension, pulselessness, death.

4. Cerebellotonsillar or posterior fossa herniation:

a. When supratentorial compression continues unchecked, or

when an expanding mass is situated in the posterior fossa or

large central vertex mass.

b. Cerebellar tonsils prolapse through the foramen magnum.

c. Compression of the medulla and respiratory arrest (rapidly

fatal).

d. Pupils – pinpoint.

e. Motor – flaccid quadriplegia.

5. Upward transtentorial:

a. Caused by upward expanding posterior fossa lesion.

b. LOC declines rapidly.

c. Pupils – pinpoint.

d. Downward conjugate gaze.

E. Assessment:

1. History.

2. Mechanism of injury.

3. Loss of consciousness.

4. ETOH or drugs.

5. Complaints before the trauma.

6. Assessment and treatment on the scene.

Page 8

Notes


7. Posttraumatic seizures.

8. Past medical history:

a. Comorbid conditions – coagulopathy.

b. Medications – anticoagulants.

9. Return to normal mental status now.

10. Vital signs:

a. Cushing response - hypertension, bradycardia and respiratory

irregularities.

b. Hypotension from head injury occurs only as a preterminal

event (brainstem regulatory collapse) or from intracranial

bleeding into an expandable skull of a young child. Look for

associated visceral injuries.

11. Neurologic exam:

a. Assess level of consciousness - single most important factor

i. AVPU – alert, awake to verbal stimuli, responds to

painful stimuli, unresponsive.

ii. Glasgow Coma Scale:

Proposed by Teasdale and Jennett in 1974 as a means

of providing uniformity for all examiners.

3 criteria:

Eye Opening Verbal Stimuli Motor Response

Spontaneously 4 Oriented, converses 5 Obeys verbal commands 6

To verbal 3 Disoriented, converse 4 Localizes pain 5

To pain 2 Inappropriate words 3 Flexion withdrawal 4

None 1 Incomprehensible 2 Abnormal flexion 3

No response 1 Extension 2

No Response 1

Good for rapid serial exams – not a substitute for a

careful neuro exam.

Falsely lowered due to hypoxia, hypotension,

intoxication, intubation, non-English speaking, etc.

Risk severity:

•• < 8 for at least 6 hours severe injury.

•• 9 – 13 moderate head injury.

•• 14 – 15 mild head injury.

b. Examine pupils - note size, shape, and reactivity:

i. Unilateral fixed, dilated pupil:

With normal mental status, R/O drops, surgery or

congenital.

Abnormal mental status, R/O increasing ICP and

uncal herniation. ii. Pinpoint pupils:

Pontine lesion.

Narcotics.

iii. Pupils fixed and dilated bilaterally:

Page 9

Notes


Hypoxia/anoxia or hypotension.

Atropine/cycloplegics.

Brain death.

Hypothermia.

Herniation syndromes.

c. Check extra-ocular movements (EOM) for weakness:

i. Spontaneous eye opening suggests intact reticular

activating system.

ii. Reflexes – test the brainstem:

Oculocephalic (Doll's eyes) –(must r/o C-spine injury

first):

•• Turn patient’s head to stimulate vestibular

apparatus - movement of eyes in opposite

direction intact brainstem.

•• Eyes turn same direction as head damaged.

Oculovestibular (caloric response) (Safe to test w/ C-

spine injury):

•• Need intact tympanic membrane.

•• Cold water placed in ear canal results in

movement of endolymph in semicircular canals.

•• Interpreted by pons as movement of head in

opposite direction – eyes deviated toward the

ear and nystagmus away normal.

•• Comatose – no nystagmus, just turn eyes

toward cold water intact brainstem.

These tests assess integrity of cranial nerves III, VI.

Plus nuclei in the midbrain and pons.

d. Assess cranial nerves II through XII.

e. Check movement and power of each extremity. Also

examine sensation DTR’s and Babinski sign.

f. Rectal sphincter tone, voluntary contraction and sensation.

g. Posturing:

i. Decorticate – flexion of upper and extensions of lower

ext, lesion of the midbrain.

ii. Decerebrate – extension of both upper and lower

extremities – lesion more caudally, worse prognosis.

F. Diagnostic evaluation:

1. Skull films have little to no use clinically.

2. CT- initial imaging modality of choice:

a. Availability, speed, readily detect osseous injury, foreign

body and intracranial hemorrhage.

b. ACEP 2008 Guidelines for CT imaging:

i. Level A – CT recommended if has loss of consciousness

or posttraumatic amnesia with 1 or more of the following:

Headache.

Page 10

Notes


Physical evidence of trauma above the clavicle.

Vomiting.

Age > 60 years.

Posttraumatic seizure.

Drug or alcohol intoxication.

GCS score < 15.

Deficits in short-term memory.

Focal neurologic deficits.

Coagulopathy.

ii. Level B – CT considered if no loss of consciousness or

posttraumatic amnesia and 1 of more of the following is

present:

Focal neurologic deficit.

GCS score < 15.

Vomiting.

Coagulapathy.

Severe headache.

Dangerous mechanism of injury – ejection from a

motor vehicle, a fall from height of > 3 feet or 5 steps.

> 65 years of age.

Physical signs of a basilar skull fracture.

3. MRI - when patient’s symptoms not explained by CT.

a. Better at detecting nonhemorrhagic contusions, brainstem

injuries and SAH.

G. Risk stratification of TBI:

1. < 8 for at least 6 hours severe injury.

2. 9 – 13 moderate head injury.

3. 14 – 15 mild head injury.

H. Lesions following head injury:

1. Concussion: a. Transient loss of neurological function resulting in loss of

consciousness.

b. Amnesia for events before injury (retrograde) and after injury

(anterograde) may be present.

c. No significant gross anatomic, microscopic or radiographic

damage demonstrable.

d. Adults - headache, confusion, amnesia.

e. Peds – confusion, restlessness, lethargy, irritability.

f. Admit if:

i. Unconscious for prolonged period.

ii. Unstable home environment.

g. Worrisome sports injury, development of several scoring

systems; none accepted as the sole system to use.

Page 11

Notes


i. Recommendation for return to sports:

Must wait 1 week after becoming asymptomatic.

Must wait 1 month if period of LOC or prolonged

posttraumatic amnesia.

h. Second impact syndrome - sustain second concussion before

complete resolution of symptoms from first concussion,

experiences rapid, usually fatal, neurologic decline.

i. Postconcussive syndrome – headache, sensory sensitivity,

memory or concentration difficulties, irritability, sleep

disturbances, or depression which persist for days to months

after a concussion.

2. Cerebral contusion: a. Bruises on surface of brain after direct local trauma or

sudden acceleration / deceleration injuries.

b. Coup lesions occur at the site of impact. More common

contrecoup lesions occur opposite the site of impact.

c. Contusions occur most frequently at the frontal and

temporal polar regions, as well as over the irregular basal

areas.

d. Neurologic deficits reflect location of the contusion.

e. Can be ischemia of underlying brain tissue due to

compression by blood.

f. Cerebral edema with increasing ICP likely reaching

maximum at 48 to 72 hours.

g. Work-up includes CT and admission for observation.

h. Patient is at risk for seizures so anticonvulsant prophylaxis

indicated.

3. Subdural hematoma (SDH):

a. Bleeding in the potential space between the dura and brain.

b. From tearing of a cortical bridging vein to sagittal sinus

with sudden acceleration/deceleration injuries.

c. Blood spreads paralleling both brain surface and inner table

of skull characteristic crescent-shaped appearance on CT.

d. Often associated with significant underlying brain injury.

e. Most common in alcoholics and elderly w/ atrophy.

f. Classification:

i. Acute subdural hematoma - discovered within the first

24 hours of injury. Fresh clotted, high density blood on

CT.

Have mental status changes and/or neurologic deficit.

Mortality - 25% to 60%.

Good functional recovery occurs 25% to 35% of cases

Surgical treatment: > 10 mm in size or > 5mm

midline shift.

ii. Subacute SDH - symptomatic between 24 hours to 14

days post injury. These have improved prognosis.

Appears iso-dense on CT scan.

Most require surgery.

Page 12

Notes


iii. Chronic SDH- symptomatic greater than 2 weeks post

injury.

Hypo-dense or isodense on CT.

Current theory - continued small hemorrhages within

the capsule lead to a gradual increase in size over

time.

If symptomatic – need surgery.

Present with subtle symptoms: H/A, dementia,

lethargy, or stroke-like symptoms of focal weakness.

4. Subdural hygroma: a. Collection of clear, xanthochromic blood-tinged fluid in the

dural space.

b. Pathogenesis not clear.

c. Sx – headache, nausea, vomiting, decreased LOC, focal

motor deficits.

d. Treatment – if asymptomatic observation, symptomatic

surgery.

5. Epidural hematoma:

a. Bleeding between inner table of skull and dura.

b. Rare in elderly and children under 2 y.o.

c. Due to laceration of meningeal vessel (artery or vein) or

dural sinus.

d. Most common site (70%) is the lateral aspect of the cerebral

hemisphere with tears of the middle meningeal artery or vein

due to fracture of the temporal bone.

e. Occurs in frontal pole, temporal fossa, and posterior fossa

(10% each).

f. Bleeding strips the tightly adherent dura from the bone,

yielding a bi-convex appearance on CT.

g. Classical presentation - patient is stunned or knocked

unconscious by a blow to the head, recovers (lucid interval),

then develops a progressive contralateral hemiparesis and

lapses into unconsciousness as the clot expands.

h. Incidence - 1% - 2% of head injured patients presenting to

ED.

i. Mortality rate - 6% to 27%.

j. Treatment - surgical evacuation:

i. > 30 cm in volume.

ii. Comatose w/ anisocoia – the sooner the better.

iii. Pediatric patients.

6. Intracerebral hemorrhage:

a. Bleeding into the brain parenchyma from small blood vessel

injury.

b. Most common frontal and temporal lobe (85%).

c. Reactive brain swelling as with contusions at 48 to 72 hours.

d. May require surgical evacuation for control of ICP.

e. Mortality rate - 55%.

f. Presentation - altered level of consciousness and focal deficits

Page 13

Notes


depending on size and location of hematoma.

7. Traumatic subarachnoid hemorrhage:

a. Trauma is the most common cause of blood in the

subarachnoid space and CSF.

b. Sx -headache, neck stiffness, photophobia.

c. Vasospasm occurs 48 hours to 2 weeks post injury.

d. Treat calcium channel blockers (nimodipine and nicardipine).

e. No CT angio needed. Admit for observation.

8. Diffuse axonal injury: a. Caused by mechanical shear force.

b. Damaged axons become edematous and separate from each

other.

c. Macroscopic appearance may be normal or show small

hemorrhages usually located near third ventricle, within the

white matter of the corpus callosum, internal capsule of the

brainstem, better seen with MRI.

d. Management is directed at controlling ICP and supportive.

e. Clinically, all patients present in coma, and duration of

coma indicates severity of injury.

i. Mild – coma 6 – 24 hours, 15% mortality, recover and

have mild or no disabilities.

ii. Moderate – coma > 24 hours, 25% mortality, awake and

have persistent moderate to severe cognitive deficits.

iii. Severe – coma > 24 hours, persistent brainstem and

autonomic dysfunction, mortality high, few in persistent

vegetative state.

9. Penetrating head injuries: a. Nonprojectile:

i. Less likely to penetrate calvarium.

ii. Damage usually restricted to path of travel.

b. Projectile:

i. More extensive damage.

ii. High pressure in immediate vicinity causes more

extensive tissue damage.

iii. Civilian bullets are not jacketed and cause more

fragmentation and more damage.

iv. Military bullets are jacketed and do not fragment so less

damage.

I. Skull fractures:

1. Significance:

a. Presence of skull fracture in a conscious patient increases risk

of intracranial hemorrhage 400 times.

b. Clinically significant if:

i. Result in intracranial air and pass through an air-filled

space (sinus).

ii. Associated with an overlying scalp laceration (open).

Page 14

Notes


iii. Depressed skull fx below the inner table.

iv. Overlie a major dural venous sinus or middle meningeal

artery.

2. Linear fractures do not have displacement of bone edges.

a. May have damaged meningeal vessels with resulting epidural

hematoma.

b. If no intracranial hematoma is present, no specific ED

treatment is required.

c. Children with linear fractures should have repeat

skull X-rays in 6 months to rule out a leptomeningeal cyst or

growing fracture.

3. Basilar skull fracture:

a. Fracture through one or more of the bones of the skull base -

sphenoid, ethmoid, temporal or occipital bones.

b. Usually clinical diagnosis based on signs such as raccoon

eyes (periorbital ecchymosis), Battle sign (mastoid

ecchymosis), hemotympanum, otorrhea, or rhinorrhea.

c. Can injure CN III, IV, and V.

d. Fx of sphenoid can cause carotid pseudoaneurysms or carotid

venous fistulae.

e. Rarely demonstrable on plain X-ray.

f. Routine CT with bone windows may or may not show

fracture line – can increase yield with posterior fossa views

and thin cuts < 5mm.

g. All require admission until cessation of CSF leak – usually 1

week.

h. Increased risk of meningitis. Use of prophylactic antibiotics

is controversial – usually not given in 1st wk.

4. Depressed skull fractures - bone piece below the plane of the

skull.

a. Greater than the full thickness of the skull require surgical

treatment whether open or closed.

b. Greater incidence of underlying brain injury.

5. Open fractures violate skin, nasal sinuses, and/or middle ear.

a. Requires hospital admission for observation, possible

antibiotic coverage / may need debridement.

6. Closed fractures do not violate dura, skin, or sinus.

7. Sutural diastasis – traumatic disruption of a cranial

suture - coronal or lambdoid sutures.

8. Comminuted skull fracture – multiple linear fractures radiate

from impact site.

J. Management of severe head trauma:

1. AVOID HYPOTENSION - Strive to maintain systolic BP of at

least 90 mm Hg.

a. Avoid other secondary insults such as hypoxia, hyperthermia,

seizures or electrolyte imbalances.

Page 15

Notes


2. Elevated intracranial pressure:

a. Normal ICP in adults is < 15-20 mm Hg.

b. CT cannot estimate or predict ICP.

c. Fatal if uncontrolled > 25-30 mm Hg.

3. Hyperventilation:

a. Fastest means of decreasing ICP.

b. PCO2 should be reduced to 30-35 torr.

c. Onset of action <30 sec, peak effect 8 min.

d. Should not be continued over 24 hours.

e. Hyperventilation causes cerebral vasoconstriction decreasing

intracranial blood volume. May cause focal areas of ischemia.

4. Osmotic agents:

a. Mannitol 20% solution:

i. 0.25 - 1 gm/kg IVPB.

ii. Results in decrease in brain volume – draws out tissue

water.

iii. Onset - minutes, peak 60 minutes, duration 6 – 8 hours

iv. Side effects – renal failure in large amt, paradoxical

intracranial hemorrhage, hypotension.

v. Neuroprotective properties – blood volume expander

reduces blood viscosity, free radical scavenger.

vi. No evidence that fluid restriction is beneficial. Patients

should be kept normovolemic. Avoid over-hydration.

b. Hypertonic saline:

i. Originally encouraging data; largest study done in

Washington was discontinued.

ii. Side effects – renal failure, central pontine myelinolysis,

rebound ICP elevation.

5. Steroids of no benefit – high dose methylprednisolone

detrimental.

6. Decompression:

a. Burr holes – for herniation not responding to other methods.

b. Surgical decompression – no focal lesion, but massive edema.

c. External ventricular drain EVD (ventriculostomy):

i. In rare circumstances, a neurosurgeon may place a

bedside or emergency department EVD for drainage of

CSF.

ii. Controversial, but works immediately.

iii. It is recommended by the Brain Trauma Foundation.

7. Seizure prophylaxis – indications :

a. Depressed skull fracture.

b. Paralyzed and intubated patient.

c. Seizure at time of injury or ED presentation.

d. GCS<8.

e. Acute subdural or epidural hematoma.

f. Acute ICH.

g. Prior history of seizures.

h. Penetrating brain injury.

Page 16

Notes


8. Barbituate coma – Pentobarbital is drug of choice:

a. Reduce cerebral metabolic demands.

b. Affects vascular tone.

c. Inhibits free radical-mediated cell membrane lipid

peroxidation.

d. Used when other methods to reduce ICP unsuccessful.

e. Causes hypotension in up to ¼ of patients that receive it.

9. Antibiotics:

a. Indicated – open skull fx, penetrating head injury, openly

contaminated head injuries.

b. Not indicated – presence of otorrhea or rhinorrhea.

10. Factor VII:

a. Indicated for bleeding in the face of coagulopathy.

b. Faster and cheaper than giving multiple drug products.

c. Increased incidence of DVT.

K. Classification:

1. MINOR head injury (GSC 14-15):

a. Low risk, don’t necessarily need a CT scan, possibly just a 4-

hour period of observation.

b. Disposition – Consider admission if:

i. Possible abuse.

ii. Persistent or progressive symptoms.

iii. Inadequate home situation.

iv. Intoxication or ingestion.

v. Anticoagulation – recent articles state may be ok to

discharge with close phone follow-up.

2. Moderate traumatic brain injury:

a. GCS of 9 – 14.

b. All should receive CT scan.

c. All should be admitted for observation regardless of CT scan.

3. Severe traumatic brain injury:

a. GCS of < 8.

b. All should receive CT scan.

c. All should be admitted

L. Complications after head injury:

1. Seizures:

a. Common in children.

b. Acute – within 24 hours following injury, transient, not

repeated.

c. Subacute - 24 –48 hours following injury.

d. Etiology: increasing cerebral edema, small hemorrhages,

penetrating injuries.

2. Central nervous system infections:

a. Meningitis after basilar skull fractures:

Page 17

Notes


i. Typical signs and sx of meningitis.

ii. Organisms:

Pneumococci – within 3 days of injury, treat w/

Ceftriaxone or ceftoxamine.

Gram negatives - > 3 days after injury – Ceftriaxone

or ceftoxamine plus naficillin and vancomycin.

b. Brain abscess:

i. Infrequent.

ii. From penetrating injuries, depressed skull fx, fx that

crosses paranasal sinuses.

iii. Sx – headache, nausea, vomiting, decrease LOC, focal

neurologic deficit, nuchal rigidity, seizure.

iv. Organisms – S. aureus and gram negatives.

c. Cranial osteomyelitis:

i. Due to penetrating injury.

ii. Sx – redness, swelling, warmth at site.

iii. Diagnosis – 50% seen on plain skull films; others - bone

scan or gallium scan.

iv. Treatment – surgical debridement and antibiotics.

3. Medical:

a. DIC:

i. Develops within hours after injury.

ii. Injured brain activates the extrinsic clotting system.

iii. If stable, develops DIC, repeat the CT scan to find new

hemorrhage.

iv. Treatment – correct neurosurgical condition, treat with

FFP and platelets as indicated.

b. Neurogenic pulmonary edema:

i. Develops minutes to days after injury.

ii. Caused by altered hydrostatic forces and microvascular

permeability.

iii. Treatment – lower ICP.

c. Cardiac dysfunction:

i. Variety of arrhythmias – most common is SVT.

ii. Theory – cause is autonomic nervous system dysfunction

and/or high level of catecholamines.

iii. Treatment goals stop arrhythmia and support cardiac

output.

II. CERVICAL SPINE TRAUMA

A. Immobilization:

1. Indications:

a. Abnormal mental status of uncertain cause.

b. Any trauma victim, especially sports, MVA, falls.

c. Head or facial trauma.

d. Any neurologic deficit.

Page 18

Notes


e. Neck or back pain.

f. Localized tenderness.

g. Unexplained hypotension.

h. Priapism or abdominal breathing.

2. Techniques:

a. Initially at site - spine board and extrication collar.

d. Immobilize head and body.

e. Anchor torso to spine board.

f. Blocks along sides of head.

g. Tape/strap across forehead and collar to board.

h. HARD COLLAR NOT ADEQUATE ALONE!

B. Initial management and assessment:

1. Primary survey:

a. Assure patient airway and ventilatory ability.

i. Recommended method - orotracheal intubation with RSI

and in-line stabilization.

ii. LMA or cricothyrotomy – failed orotracheal intubation,

associated massive facial trauma or RSI contraindicated.

b. Circulation – Check adequacy.

i. Spinal shock – loss of reflexes and sensorimotor function

below level of injury:

Flaccid paralysis with loss of bladder tone and

reflexes.

Temporary physiologic response to trauma that lasts

hours to days.

ii. Neurogenic shock – Occurs w/ complete cord transection

or injury above sympathetic plexus. Rarely due to

temporary spinal cord concussion.

iii. Heart rate normal or bradycardic due to unopposed vagal

tone. Bradycardia responds to atropine

iv. No peripheral signs of vasoconstriction – patient usually

warm and vasodilated.

v. Diagnosis of exclusion – rule out blood loss.

vi. Start treatment with crystalloids.

vii. High cervical lesions, severe hypotension (<70 mm Hg) –

Trendelenburg position, vasopressors, cardiac pacing.

viii. Usually good urine output.

ix. Cessation marked by return of reflexes or

bulbocavernosus reflex.

2. Secondary survey – assess motor and sensory functions

completely.

a. Assess breathing pattern - abdominal breathing indicates

lower cervical injury - low tidal volume breaths.

b. Look for muscle fasciculations.

c. Look for Horner's Syndrome – unilateral facial ptosis, miosis

and anhydrosis - from C7-T2 level.

Page 19

Notes


d. Look for painful dysesthesias.

e. Palpate entire spine and musculature.

f. Test DTRs – localizes and diagnostic.

i. Paralysis with intact DTRs – upper motor neuron (spinal

cord) lesion.

ii. Paralysis with absent DTRs – lower motor neuron (nerve

root) lesion or spinal shock.

g. Baseline assessment of sensation:

i. Light touch-posterior column.

Pain (pin prick) – anterior spinothalamic tract.

Proprioception – posterior column.

ii. Islands of sparing means patient has 50% chance of

functional motor recovery. Must find early to facilitate

treatment. Sacral sparing, normal rectal tone, flexor toe

movement.

C. Spinal cord syndromes:

1. Mechanisms:

a. Primary:

i. Transection of the neural elements.

ii. Compression between the vertebra.

iii. Primary vascular damage – ischemia or compression.

b. Secondary – cascade of events caused by the primary event

causing ischemia to the neurons.

2. Complete spinal cord syndrome – nothing below injury.

a. If persists greater than 24 hours after injury, 99% will not

have functional recovery.

b. Check for persistent perianal sensation, rectal sphincter tone

or slight flexor toe movement - indicates partial lesion with

potential for functional recovery.

c. R/O spinal shock (see above).

d. R/O intra-abdominal, etc., injuries as no sensation in

abdomen.

3. Incomplete spinal cord lesions:

a. Central cord syndrome (most common):

i. Degenerative arthritis of neck w/ forceful hyperextension.

ii. Hypertrophied ligamentum flavum buckles into cord,

contuses central portion.

iii. Affects pyramidal and spinothalamic tracts, in center of

cord.

iv. Upper extremities affected more than lower.

v. Urinary retention invariably found.

vi. Variable prognosis - 50% regain some function.

b. Anterior cord syndrome:

i. Hyperflexion injuries, protrusion of bony fragments or

herniated disc into anterior spinal canal OR by

laceration/thrombosis of anterior spinal artery.

Page 20

Notes


ii. Complete motor paralysis and hypalgesias below level

injury with preservation of position, touch and

vibration (posterior column).

iii. Requires surgery if ventral compression demonstrated.

Need emergent MRI or CT to determine if cord

decompression is indicated.

c. Brown-Sequard syndrome:

i. Functional hemisection of cord.

ii. Penetrating injury or lateral mass fractures of C-spine.

iii. Ipsilateral paralysis, loss of proprioception, touch and

vibration (posterior column) and contralateral loss of

pain and temperature (spinothalamic tract). iv. Prognosis fair to good.

d. Posteroinferior cerebellar artery syndrome - dysphagia,

dysphonia, hiccups, nausea, vomiting, dizziness or vertigo,

cerebellar ataxia.

e. Horner's syndrome:

i. Damage to cervical sympathetic chain.

ii. Ipsilateral ptosis, miosis, anhydrosis.

iii. Due to direct cervico-medullary trauma or vertebral artery

occlusion.

f. Cauda equina syndrome:

i. Perineal or bilateral leg pain.

ii. Bowel or bladder dysfunction.

iii. Perianal anesthesia.

iv. Diminished rectal sphincter tone.

v. Lower extremity weakness.

g. SCIWORA:

i. More common in peds.

ii. Mechanism is unclear.

iii. Brief episode of upper extremity weakness or paresthesias

followed by neurologic deficits hours to days later.

iv. No radiographic evidence.

h. Dejeune onion skin pattern:

i. Analgesia of the face.

ii. Damage to spinal trigeminal tract.

D. Cervical diagnostic evaluation:

1. Indications:

a. Nexus criteria – don’t need if:

i. No midline tenderness.

ii. No focal neurologic deficit.

iii. Normal alertness.

iv. No intoxication.

v. No painful, distracting injury.

vi. Sensitivity 99% and specificity 12.9%.

b. Canadian C-spine Rule:

Page 21

Notes


i. Any high risk factors?

> 65 years of age.

Fall from height > 1 meter.

Axial loading injury.

High-speed motor vehicle crash > 100km/h.

Rollover.

Ejection.

Motorized recreational vehicle.

Bicycle collision.

Presence of paresthesias.

ii. Any low-risk factors that allow safe assessment?

Simple rear-end vehicle crashes.

Sitting position in the ED.

Ambulatory at any time.

Delayed onset of neck pain.

Absence of midline neck tenderness.

iii. Is the patient able to actively rotate his or her neck 45

degrees to the left and right?

2. Cervical spine films:

a. Cross table lateral - all 7 cervical and 1st thoracic vertebrae:

i. Methodically review – ABCs.

ii. Alignment – anterior and posterior contour lines and

spino-laminar line for smooth lordotic curvature.

iii. Bony changes – look for fractures.

iv. Cartilage space assessment –anterior or posterior

widening of the intervertebral space or interspinous space.

b. A-P film:

i. Views lower 5 cervical and upper thoracic vertebrae.

ii. Overlapping articular pillars create wavy margin.

iii. Spinous processes connected with straight line.

iv. Bodies intact and uniform.

v. Tracheal and laryngeal air shadows within midline.

c. Soft tissue:

i. Retropharyngeal – Ant border of C2 to posterior wall of

pharynx - <7mm in adults and children.

ii. Predental space should not exceed 3 mm in adults and 5

mm for children.

iii. At C3-C4 not greater than 5 mm, or ½ the width of the C2

body.

iv. Retrotracheal space – anterior body of C6 to posterior

surface of the trachea - < 22 mm in adults or < 14 mm less

than 15 yo.

d. Obliques:

i. Demonstrate pedicles and facets better.

ii. Laminae should look like overlapping roof shingles.

iii. Laminar fractures seen well.

iv. Assess the patency of the intervertebral foramina.

Page 22

Notes


e. Odontoid view (usually open mouth) – x-ray of atlas and axis.

i. Check for alignment of lateral masses with odontoid.

ii. Patient cannot be rotated or tilted.

iii. Spinous process midline.

iv. Inspect transverse processes for fx.

v. Odontoid fractures – three categories:

Type I involves the distal portion of the dens (tip) –

most stable of the three types.

Type II involves the base of the dens – most common

type, always unstable.

Type III involves the body of C2.

f. Swimmer's (transaxillary) helpful in trying to visualize lower

C-spine.

g. Flexion-extension views:

i. Indicated if concern for ligamentous injury.

ii. Must be awake, cooperative patients, no deficits.

iii. Considered abnormal if > 3.5 mm of horizontal

displacement between the disks, displaced apophyseal

joints, widened disk spaces, loss of greater than 30% of

the disk height, presence of prevertebral hematoma.

iv. Replaced by CT and MRI.

h. Pediatric variations:

i. Pseudosubluxation of C2-C3 – less than 8 years:

Immature muscles – hypermobile spine.

If suspect injury, use posterior cervical line on lateral

film line from anterior cortex of C1 spine to anterior

Page 23

Notes


cortex of C3 spine.

ii. Retropharyngeal space:

Less than 2 years old may normally be widened on

expiration, so use inspiratory films.

iii. Nonfusion of odontoid in kids mimics fracture.

3. CT scan:

a. Indications:

i. High-energy injury mechanism.

ii. High-risk clinical parameter.

iii. Plain films reveal an injury, an area of suspicion, or are

inadequate.

iv. High clinical suspicion of injury, despite normal plain

films.

b. Advantages – patient lies supine, can evaluate injuries already

diagnosed by x-ray, sensitivity is better than x-ray.

c. Disadvantages – cost and radiation.

4. MRI C-spine:

a. Indications:

i. Complete or incomplete neurologic deficits with

radiographic evidence of fracture or subluxation.

ii. Neurologic deficits not explained by plain films or CT –

SCIWORA.

iii. Deterioration of neurologic function.

iv. Suspicion of ligamentous injury following inadequate or

negative flex-ex films.

b. Contraindications – pacemaker, cerebral aneurysm clips,

metallic foreign bodies.

c. CT and x-ray are still superior when evaluating bony

structures.

E. Anatomy of spinal column – spine has two columns:

1. Anterior column:

a. Vertebral bodies.

b. Intervertebral discs.

c. Anterior and posterior longitudinal ligaments.

2. Posterior column:

a. Contains spinal canal.

b. Formed by: pedicles, transverse processes, articulating facets,

laminae, and spinous processes.

c. Held in alignment by: nuchal ligament complex

(supraspinous ligaments, interspinous ligaments, infraspinous

ligaments), capsular ligaments and ligamentum flava.

F. Classification of spinal injuries (based on mechanism):

1. Flexion injuries:

a. Simple wedge fractures - of anterosuperior vertebral body:

Page 24

Notes


i. Stable – rare nervous system damage.

ii. Impaction of vertebrae against subjacent vertebra.

iii. Becomes unstable if multiple or involves > ½ of height.

b. Flexion teardrop fracture:

i. Wedge or chip-shaped fragment of antero-inferior

vertebral body, displaced anteriorly.

ii. Common cause of anterior cord syndrome .

iii. Involves ligamentous injury and may have deficit.

iv. Unstable.

c. Clay-shoveler's fracture:

i. Now due to direct trauma to spinous processes or forced

hyper-flexion.

ii. Oblique fracture of spinous process base (C7, C6, T1).

iii. Stable, no associated deficits.

d. Anterior subluxation:

i. Disruption of ligamentous complexes, starts posteriorly

and proceeds anteriorly.

ii. Potentially unstable.

iii. Widening of interspinous or intervertebral spaces

posteriorly.

iv. High incidence of delayed instability.

Page 25

Notes


e. Bilateral facet dislocation (locked facets):

i. High incidence cord deficit.

ii. All anterior and posterior ligaments disrupted.

iii. Extremely unstable.

iv. See anterior displacement of spine above level of injury

(greater than 2 A-P diameter of lower body).

v. Requires traction or even surgery.

2. Flexion - rotation injuries:

a. Unilateral facet dislocation (locked facet):

i. Stable.

ii. Symptom – torticollis (muscle spasm).

iii. On lateral, see forward displacement of dislocated

segment on vertebra below.

iv. A-P and obliques helpful – lose "shingles on roof".

v. If unilateral facet dislocation occurs at C1-C2, is unstable.

Seen as marked asymmetry between odontoid and lateral

masses of C1 (rotary atlantoaxial dislocation).

vi. Larger facets of lumbar region make this injury rare, but

if one or both articular processes fracture, upper vertebra

swings anterior.

3. Extension injuries:

a. Posterior neural arch fracture of C1:

i. Occiput compresses onto spinous process of axis.

ii. Potentially unstable due to location.

b. Hangman's fracture:

i. Traumatic C2 spondylolysis.

ii. Abrupt deceleration.

Page 26

Notes


iii. Unstable, yet cord damage usually minimal due to width

of neural canal here.

iv. Bilateral fractures of pedicles of C2 (axis) +/- subluxation

of C2 on C3.

v. Associated prevertebral swelling may cause airway

obstruction.

c. Extension teardrop fracture:

i. Large teardrop-shaped fragment off anteroinferior corner

of vertebral body (ligament pulls it off).

ii. Often occurs at C5-C7 in driving accidents.

iii. Unstable.

iv. High association with central cord syndrome.

4. Vertical compression injuries:

a. Burst fracture of vertebral body:

i. Compressive forces from above or below force nuclear

pulposus of disc into vertebral body causes burst

fracture.

ii. Stable as all ligaments intact, although fracture segments

can impinge into neural canal.

iii. Associated with anterior cord syndrome.

b. Jefferson Fracture of Atlas (C1):

i. Rare.

ii. Lateral masses driven laterally.

iii. See widening of predental space on lateral.

iv. Odontoid view differentiates this from fracture of

posterior neural arch of C1.

v. Extremely unstable.

Page 27

Notes


5. Stability:

a. Stable:

i. Simple wedge fracture.

ii. Clay-shoveler’s fracture.

iii. Unilateral facet dislocation.

iv. Burst fracture.

b. Unstable:

i. Flexion teardrop.

ii. Bilateral facet dislocation.

iii. C1C2 dislocation.

iv. Hangman’s fracture.

v. Extension teardrop.

vi. Jefferson fracture.

c. Potentially unstable:

i. Posterior neural arch fracture.

ii. Anterior subluxation.

C. Treatment (fracture, dislocation or deficit):

1. Strict immobilization.

2. Rapid neurosurgical consultation.

3. Surgery:

a. Emergency - Relieving impingement from herniated disks,

foreign bodies, bony fragments, epidural hematoma.

b. Delayed – to stabilize fracture.

4. Steroids – 2013 CNS/AANS Guidelines discourage use

5. Transfer – regional spine center where all specialists are

available.

Page 28

Notes


HEAD INJURY/C-SPINE/SPINAL CORD TRAUMA

PEARLS

1. Cerebral blood flow is maintained at a constant level by autoregulation.

2. Increased intracranial pressure occurs if there is an increase in brain

parenchyma, intracranial blood or CSF.

3. Increased intracranial pressure may result in the Cushing response -

hypertension and bradycardia.

4. Hyperventilation to a pCO2 of 30 - 35 torr is the fastest means of

decreasing ICP but only lasts a short while.

5. There is no evidence that corticosteroids decrease ICP.

6. Uncal herniation symptoms are ipsilateral papillary

dilatation, contralateral Babinski, and contralateral muscle weakness.

7. Central transtentorial herniation symptoms are decreased LOC, bilateral

muscle weakness and Babinski reflexes, sustained hyperventilation,

possibly Cushing’s.

8. Pinpoint pupils and a brain injury is a pontine lesion.

9. A normal Doll’s eye is when the head is turned and the eyes turn in the

opposite direction; that is an intact brainstem.

10. A Glasgow Coma Scale has 3 criteria: eye opening (4), Verbal Stimuli

(5) and motor response (6).

11. Depressed skull fractures greater than the full thickness of the skull

require surgical elevation.

12. Suspect a basilar skull fracture in a patient with raccoon eyes

(periorbital ecchymosis), Battle Sign (mastoid ecchymosis),

hemotympanum or CSF rhinorrhea. The most common area is the

temporal bone with hemotympanum.

13. Epidural hematomas appear at biconvex (lens-shaped) and subdural

hematomas appear as crescent-shaped on CT scans.

14. Epidural hematomas are due to laceration of a meningeal artery (most

commonly the middle meningeal) or a vein.

Page 29

Notes


15. Epidurals are rare in children under 2 years and in the elderly, but

subdurals occur in the very old, the very young and the very intoxicated.

16. Trauma is the most common cause of subarachnoid hemorrhage.

Subarachnoid hemorrhage is the most common finding on a CT scan of

a brain injured patient.

17. Intracerebral hemorrhage most commonly occurs in the frontal and

temporal lobes.

18. Subacute subdural hematomas may not be seen well on a CT scan

because they are isodense.

19. The treatment for most complications of increased ICP such as

neurogenic pulmonary edema and DIC is to lower the ICP.

20. Spinal cord injury may result in spinal shock: hypotension and

bradycardia but warm skin. It is a diagnosis of exclusion.

21. Central cord syndrome results in greater upper extremity weakness than

lower extremity weakness.

22. Brown-Sequard syndrome results in contralateral loss of pain and

temperature and ipsilateral loss of proprioception, light touch and

vibration.

23. Anterior cord syndrome results in motor paralysis and hypalgesia below

the level of the injury with preservation of position, touch and vibration.

24. The biggest difference between NEXUS criteria and the Canadian C-

spine rule is the addition of patients 65 years and older as high risk for

injury, and the ability to move the neck.

25. Adequately done C-spine x-rays miss significant injuries < 1 % of the

time.

26. Bilateral C-spine facet dislocations (locked facets) are extremely

unstable and require traction or surgery to reduce.

27. The Jefferson fracture of C1 is from a vertical compression resulting in

an extremely unstable fracture.

28. Unilateral facet dislocations are stable. They are difficult to diagnose on

x-ray. Be sure to look at the alignment of the transverse processes on

the AP view.

Page 30

Notes


29. High dose methylprednisolone for spinal cord injury is no longer

recommended.

30. Anterior subluxation is unstable due to the disruption of ligaments

which begins posteriorly and moves anteriorly. High propensity of

delayed stability.

Page 31

Notes


REFERENCES

1. American College of Emergency Physicians, Centers for Disease

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Decisionmaking in Adult Mild Traumatic Brain Injury in the Acute

Setting. Ann Emerg Med 2008: 52; 714-748

2. ATLS Manual 8th

edition. “Chapter 6: Head Trauma.” American

College of Surgeons, Copyright 2008.

3. Baron BJ, McSherry KJ, Larson JL, and Scalea TM. Chapter 255: Pine

and Spinal Cord Trauma.” ” Emergency Medicine A Comprehensive

Study Guide7th

edition. Editors: Tintinalli, Stapczynski, Ma, Cline,

Cydulka, and Meckler. McGraw-Hill Copyright 2010, pg. 1709 - 1730.

4. Biros MH, Heegaard WG. “Chapter 38: Head Injury.” Rosen’s

Emergency Medicine Concepts and Clinical Practice 7th

Edition. Ed.:

Marx, Hockberger, and Walls. Elsevier Copyright 2010: 295 - 322.

5. Bracken MB. “ Steroids for acute spinal cord injury.” Cochrane

Database Systematic Review 2002; 3.

6. Brown, CV et al. “Reombinant factor VIIa for the correction of

cagulopathy before emergent craniotomy in blunt trauma patients.”

Journal of Trauma 2010 Feb;68(2): 348-352.

7. Bulger EM et al. “out-of-hospital hypertonic resuscitation follolwing

severe traumatic brain injury: A randomized controlled trial.” JAMA

2010 Oct 6;304:1455.

8. Consortium for Spinal Cord Medicine: Early Acute Management in

Adults with Spinal Cord Injury: A Clinical Practice Guideline for

Healthcare Providers. Washington, DC, Consortium for Spinal Cord

Medicine, 2008.

9. Davis RL, et al: Cranial Computed Tomography Scans in Children

After Minimal Head Injury With Loss of Consciousness: Annals of

Emer Med 1994; 24:640-645

10. Duus BR, et al: The Role of Neuroimaging in the Initial Management

of Patients With Minor Head Injury: Annals of Emer Med 1994;

23:1279 – 1283.

11. Harnan SE, er at: Clinical Decision Rules for Adults With Minor Head

Injury: A Systematic Review. J Trauma 2011, 71: 245-251.

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http://www.expertconsultbook.com/expertconsult/p/linkTo?type=journalArticle&isbn=978-0-323-05472-0&title=Steroids+for+acute+spinal+cord+injury&author=Bracken%C2%A0MB&date=2002&volume=3&issue=&firstPage=CD001046&shortTitle=Cochrane%20Database%20Syst

Notes


12. Hockberger RS, Kaji AH, Newton E. “Chapter 40: Spinal Injuries.”

Rosen’s Emergency Medicine Concepts and Clinical Practice 7th

Edition. Ed.: Marx, Hockberger, and Walls. Elsevier Copyright 2010;

337 – 375.

13. Hoffman JR, et al: Low-Risk Criteria for Cervical-Spine Radiography

in Blunt Trauma: A Prospective Study. Annals of Emergency Medicine

1992; 21:1454 1460.

14. Hoffman JR, et al: Selective Cervical spine Radiography in Bunt

Trauma: Methodology of the National Emergency X-radiography

Utilization Study (NEXUS). Annals of Emergency Medicine 1998;

32(4): 461 - 469.

15. Holmes JF and Akkinepalli R. Computed Tomography Versus Plain

Radiography to Screen for Cervical Spine Injury; A Meta-Analysis.

Journal of Trauma 2005 May; 58:902-905.

16. Jagoda, AS, et al. “Clinical Policy: Neuroimaging and Decisionmaking

in Adult Mild Traumatic Brain Injury in the Acute Setting.” Annals of

Emergency Medicine 2008; December, 52:714-748.

17. Kuppermann N, Holmes JF, Dayan PS, Hoyle JD Jr, Atabaki SM,

Holubkov R, Nadel FM, Monroe D, Stanley RM, Borgialli DA, Badawy

MK, Schunk JE, Quayle KS, Mahajan P, Lichenstein R, Lillis KA,

Tunik MG, Jacobs ES, Callahan JM, Gorelick MH, Glass TF, Lee LK,

Bachman MC, Cooper A, Powell EC, Gerardi MJ, Melville KA,

Muizelaar JP, Wisner DH, Zuspan SJ, Dean JM, Wootton-Gorges SL;

Pediatric Emergency Care Applied Research Network (PECARN).

Lancet 2009 Oct 3;374(9696):1160-70.

18. Looby S and Flanders A. “Spine Trauma.” Radiol Clin N Am

2011;49:129-163.

19. Melanson, SW. Lecture:64 and 128 Slice CTs: What’s Their Role in

Emergency Medicine? ACEP Scientific Assembly October 2007.

20. Meyer S, et al: Evaluation and Significance of Pupillary Light Reflex in

Trauma Patients: Annals of Emer Med 1993; 22:1052-1057

21. Miller EC, et al: Minor Head Trauma: Is Computed Tomography

Always Necessary? Annals of Emer Med 1996; 27:290-294.

22. Morrison LJ, et al. “The Toronto prehospital hypetonic resuscitation-

head injury and multi organ dysfunction trial (TOPHR HIT) methods

and data collection tools.” www.ncbi.nlm.nih.gov/pubmed. Trials. 2009

November;20:10:105.

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http://www.ncbi.nlm.nih.gov/pubmed

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23. Pimental L and Diegelmann L. “Evaluation and Management of Acute

Cervical Spine Trauma.” Emerg Med Clin N Am 2010; 28:719-738.

24. Reinus WR, Zwemer FL: Clinical Prediction of Emergency Computed

Tomography Results: Annals of Emer Med 1994; 23:1271-1278.

25. Rockswold GL, et al. “Hypertonic saline and its effect on ICP, erebral

perfusion pressure, and brain tissue oxygen.” Neurosurgery 2009

December;65(6):1035-1041.

26. Rosenthal M: Mild Traumatic Brain Injury Syndrome: Annals of Emer

Med 1993; 22:1048-1051.

27. Schenarts PJ, et al. Prospective Comparison of Admission Computed

Tomographic Scan and Plain Films of the Upper Cervical Spine in

Trauma Patients with Altered Mental Status. Journal of

Trauma 2001;51(4):663-669.

28. Siesjo BK: Basic Mechanism of Traumatic Brain Damage: Annals of

Emer Med 1993;22:959-969.

29. Stiell IG, et al: Variation in ED Use of CT for Patients With Minor

Head Injury: Annals of Emer Med 1997; 30:14-22.

30. Stiell IG, et al. The Canadian C-spine Rule versus the NEXUS Low-

Risk Criteria in Patients with Trauma. NEJM 2003 December; 349(26):

2510-2518.

31. Stiell IG, et al. The Canadian C-Spine Rule for Radiography in Alert

and Stable Trauma Patients. JAMA 2001;286(15):1841-1848.

32. Wright DW and Merck LH. “Chapter 254: Head Trauma In Adults and

Children.” Emergency Medicine A Comprehensive Study Guide 7th

edition. Editors: Tintinalli, Stapczynski, Ma, Cline, Cydulka, and

Meckler. McGraw-Hill 2010: 1692-1709.

33. “Hypertonic Resuscitation Following Severe Traumatic Brain Injury.”

University of Washington.

http://www.clinicaltrials.gov/ct2/show/NCT00316004?term=Hypertonic

+Resuscitation+Following+Traumatic+Brain+Injury&rank=1

34. Yuan, ZH, et al. “A meta-analysis of the efficacy and safety of

recombinant activated factor VII for patients with acute intracerebral

hemorrhage without hemophilia.” Journal of Clinical Neurology 2010

Jun;17(6):685-693.

08/13

Page 34

Airway/Maxillofacial/ Penetrating Neck/Thoracic/

Abdominal Trauma

Michael Schindlbeck, MD, FACEP

Assistant Professor of Emergency Medicine, Rush Medical College; Assistant Program Director,

Department of Emergency Medicine, John H. Stroger Jr. Hospital of Cook County, Chicago

Page 35

Page 36

Notes

Airway/Maxillofacial/Penetrating Neck/Thoracic/Abdominal Trauma

AIRWAY/MAXILLOFACIAL/PENETRATING NECK/

THORACIC/ABDOMINAL TRAUMA

Airway Management in Trauma

I. INITIAL MANAGEMENT

A. Assess the airway: Common indications for advanced airway

management in trauma:

1. Cardiopulmonary arrest.

2. Advanced hemorrhagic shock.

3. Severe head injury (GCS ≤ 8 = intubate).

4. Significant airway burns.

5. Penetrating face or neck wounds.

6. Flail chest.

7. Pulmonary contusion.

B. Open the airway:

1. Head tilt and chin lift vs. jaw thrust (always suspect potential C-

spine injury).

II. MAINTAINING THE AIRWAY

A. Oral adjunct:

1. Indications: Unconscious patient.

2. Contraindications: Awake patient, intact gag reflex.

3. Size: Central incisors to the angle of mandible.

4. Technique of insertion: 180°, then rotate (adults only) or use

tongue depressor.

B. Nasal adjunct:

1. Indications: Awake patient, intact gag reflex.

2. Contraindications: Coagulopathy, significant midface trauma.

3. Size: Tip of nose to the ear lobe, same diameter as opening of

nares.

4. Technique of insertion: Adequate lubrication, guide posteriorly

along the floor of the nasal cavity into nasopharynx.

Page 37

Notes


III. NASOTRACHEAL INTUBATION

A. Advantages:

1. Can be inserted into an awake patient.

2. Can be placed blindly or with laryngoscopic guidance.

3. Patient cannot bite/occlude the ETT.

4. Requires no/minimal neck movement.

5. Not dependant on ability to adequate open the mouth.

B. Disadvantages:

1. Requires spontaneously breathing patient.

2. Blind insertion is heavily operator dependant.

C. Contraindications:

1. Apneic patient.

2. Pediatric patient.

3. Significant midface trauma.

4. Basilar skull fracture.

5. Coagulopathy (relative).

D. Technique:

1. Local anesthesia (e.g., benzocaine spray, lidocaine neb).

2. Topical vasoconstriction (e.g., phenylephrine, oxymetazoline).

3. Adequate lubrication (e.g., lidocaine jelly, Surgilube).

4. Gently insert size 7-7.5 ETT posteriorly into nasopharynx.

5. Listen carefully for exhalation/ check for tube condensation.

6. Advance tube during inhalation (vocal cords maximally open).

7. Confirm placement (optimal depth 26-28 cm):

a. Inability to vocalize.

b. Air movement through tube.

c. Bilateral thoracic breath sounds.

d. End tidal CO2.

e. Chest X-ray.

E. Complications:

1. Airway trauma.

2. Epistaxis with secondary vomiting and aspiration.

3. Malposition.

4. Sinusitis.

Page 38

Notes


IV. OROTRACHEAL INTUBATION: TECHNIQUE OF CHOICE

A. Advantages:

1. Can be inserted in apneic patient.

2. Direct visualization precludes malpositioning.

3. Fewer infectious complications.

B. Disadvantages:

1. Increased patient discomfort.

2. Requires patient capacity to widely open mouth.

3. Increased potential for inadvertent C-spine movement.

C. Contraindications:

1. No absolute contraindications.

D. Technique:

1. Laryngoscope selection (essentially a matter of preference):

a. Miller blade:

i. Directly lifts epiglottis.

ii. More difficult to move tongue.

b. Macintosh blade:

i. Indirectly lifts epiglottis.

ii. Designed to sweep tongue.

2. Patient positioning:

a. “Sniffing” if possible (if absolutely no concern for C-spine

injury).

b. C-spine immobilization, not traction.

3. Sellick’s maneuver (cricoid pressure):

a. Attempt to minimize aspiration.

b. Start when induction agent given.

c. Release only after cuff inflated and endotracheal placement

confirmed.

4. Confirm placement:

a. Visualize tube pass through cords.

b. End-tidal CO2 after 6 bag breaths.

c. Bilateral thoracic breath sounds upon auscultation.

d. Tube condensation.

e. Chest X-ray.

E. Complications:

1. Airway trauma.

Page 39

Notes


2. Malposition (esophagus, right mainstem bronchus).

3. Cervical cord injury secondary to movement of an unstable

fracture.

V. RAPID SEQUENCE INTUBATION IN TRAUMA

A. Induction agents:

1. Etomidate (0.3mg/kg):

a. Minimal effect on hemodynamics.

b. May lowers seizure threshold in patients with focal seizures.

c. Transiently suppresses cortisol production.

2. Thiopental (3mg/kg):

a. Marked cardiovascular depressant.

b. Transiently suppresses seizure potential.

c. May lower ICP via decreasing cerebral perfusion.

3. Ketamine (2 mg/kg):

a. Minimal cardiovascular effect.

b. Increases ICP and IOP.

c. Give with atropine to minimize secretions.

d. Give with midazolam in adults to block emergence reactions.

B. Paralytic:

1. Succinylcholine (1.0-1.5 mg/kg adults, 1.5-2.0 mg/kg peds):

a. Rapid onset and short duration.

b. Depolarizing agent; contraindicated in acute crush injuries,

subacute burns and spinal cord injury.

c. Coadminister atropine in children to block excessive

bradycardia.

2. Rocuronium (0.6-1.2 mg/kg):

a. Non-depolarizing agent.

b. Rapid onset - duration of onset roughly 30-45 minutes.

c. Reversing agents in development.

C. Increased ICP/ head trauma precautions:

1. Lidocaine (1.5 mg/kg).

2. Defasciculating agent (Non-depolarizing agent at 1/10th

the RSI

dose)

Fentanyl (3 mcg/kg)

Page 40

Notes


VI. SURGICAL CRICOTHYROTOMY

A. Indications:

1. Inability to intubate orally (can’t intubate, can’t ventilate):

a. Glottic edema.

b. Laryngospasm.

c. Severe oropharyngeal hemorrhage/secretions.

d. Foreign body obstruction.

e. Masseter spasm/ clenched teeth.

B. Contraindications:

1. Laryngeal pathology.

2. Pediatric patient (<8 years old).

3. Tracheal transaction w/ retraction.

C. Technique:

1. Identify anatomic landmarks (cricothyroid membrane between

thyroid and cricoid cartilages).

2. Antiseptic skin preparation.

3. 1-2 cm transverse skin incision via #11 blade (longitudinal

ONLY if laryngeal pathology or significant edema precludes

anatomical landmarking).

4. Tracheal hook to stabilize thyroid cartilage.

5. Dilation with hemostat or trousseau dilator.

6. Insert tube (#4 or smaller Shiley/ 6.0 or smaller ETT).

7. Secure tube.

8. Connect to ventilator/Ambu bag.

9. Confirm placement.

D. Complications:

1. Malposition:

a. Subcutaneous cervical soft tissues.

Special Situations

Low BP Head Injury Peds

Drugs Etomidate 20 mg

Sux 100 mg

Lido 100 mg

Pavulon 1 mg

Thiopental 200 mg

Fentanyl 200 mcg

Sux 100 mg

Give atropine with

Sux

Other Works for

everyone

Watch the BP, lowers

seizure potential

Age/4 + 4 = ET tube

size

Page 41

Notes


b. Esophagus.

2. Significant hemorrhage (usually secondary to lateral incision):

a. Anterior jugular veins.

b. Thyroid vessels.

3. Wound infection.

4. Laryngeal injury:

a. Fracture from oversized tube.

b. Delayed subglottic stenosis.

c. Vocal cord palsy.

VII. NEEDLE CRICOTHYROTOMY

A. Indications:

1. Same as outlined for surgical cricothyrotomy.

2. Pediatric patient (<8 years old).

B. Contraindications:

1. Same as outlined for surgical cricothyrotomy.

2. Adult patient.

C. Technique:

1. Identify anatomic landmarks (cricothyroid membrane between

thyroid and cricoid cartilages).

2. Antiseptic skin preparation.

3. 14 gauge over-needle catheter attached to 5 ml syringe.

4. Advance at 45° angle caudally until air is aspirated.

5. Advance catheter and remove needle.

6. Connect to oxygen source:

a. 3.0 ETT adapter and Ambu bag/ventilator.

b. Direct connection of high-flow oxygen tubing with Y

connector or in-line side port.

c. Cycle ventilation (inspiration 1 second: expiration 4 seconds).

7. Confirm placement.

8. Carefully secure catheter without kinking.

9. Convert to formal tracheostomy ASAP.

D. Complications:

1. Subcutaneous emphysema.

2. Pulmonary barotrauma (pneumomediastinum, pneumothorax).

VIII. ALTERNATIVE AIRWAY TECHNIQUES

A. Laryngeal mask airway:

Page 42

Notes


1. Indications:

a. Failed intubation and inadequate BVM ventilation.

2. Pros:

a. Easy/blind insertion.

b. Temporizing measure.

c. May facilitate secondary ETT placement.

3. Cons:

a. Does not secure/protect airway.

B. Fiberoptic intubation:

1. Indications:

a. Patients with significant maxillofacial and penetrating neck

trauma.

b. Patients with severely limited neck mobility or mouth

opening.

c. Patients with prior history of difficult intubation.

2. Pros:

a. Allows direct visualization of airway and possible airway

injury.

b. Facilitates guided placement of ET tube.

c. Provides a definitive/secure airway.

3. Cons:

a. Requires times to call anesthesia/obtain bronchoscope.

b. Adequate visualization depends upon suctioning all

blood/secretions.

C. Combitube:

1. Indications:

a. Failed intubation and inadequate BVM ventilation.

2. Pros:

a. Easy/blind insertion.

b. Temporizing measure.

c. May permit OG tube placement and gastric decompression.

3. Cons:

a. Does not secure/protect the airway.

b. Secondary vomiting may cause esophageal rupture.

c. Contraindicated in patients with caustic ingestions.

D. Wire-guided retrograde intubation:

1. Indications:

a. Severe orofacial trauma with significant airway distortion.

2. Pros:

a. Doesn’t require neck movement.

b. Provides a definitive/secure airway.

3. Cons:

Page 43

Notes


a. Requires ability to externally landmark significant neck

anatomy.

b. Requires the right kit and operator experience.

IX. INHALATION INJURIES

A. Types of inhalation injury:

1. Supraglottic injuries:

a. Thermal mediated tissue destruction.

b. Significant upper airway edema (minutes).

c. Rapid onset post exposure.

2. Infraglottic injury:

a. Chemical mediated tissue injury.

b. Tracheobronchiolitis +/- secondary ARDS.

c. Delayed presentation (hours-days).

3. Toxic gas poisoning:

a. Impaired tissue oxygenation.

b. Inhibited cellular respiration.

B. Indication for airway management:

1. Historical:

a. Closed space.

b. Respiratory distress/arrest.

2. Clinical:

a. Facial burns/singing.

b. Soot in/around nose and/or mouth.

c. Carbonaceous sputum.

d. Oropharyngeal edema.

e. Voice changes.

f. Stridor.

g. Rales/wheezing.

C. Additional considerations:

1. Carbon monoxide:

a. Incomplete combustion of fossil fuels.

b. 280-fold higher affinity for hemoglobin than O2.

c. Pulse oximetry not helpful (misreads carboxyhemoglobin as

oxyhemoglobin).

d. “Cherry red” blood on sampling.

e. Carboxyhemoglobin levels on ABG or VBG:

i. 0-15% - asymptomatic.

ii. 15-50% - progressive neurologic dysfunction.

iii. >50% - lethal.

2. Cyanide toxicity:

a. Combustion of plastics and solvents.

Page 44

Notes


b. Metabolic acidosis with high lactate with normal PaO2.

c. “Poor man’s test” - increased venous O2 saturation.

d. If concurrent CO poisoning suspected, then avoid oxidizing

agents from CN- antidote kit. Treat with only IV sodium

thiosulfate or IV hydroxycobalamin.

D. Management:

1. Supplemental 100% oxygen.

2. Early intubation (permissive hypercapnia/low airway pressures).

3. Ensure adequate chest wall mechanics (escharotomy).

4. Early bronchoscopy to determine severity of injury.

5. Specific antidotes as indicated.

MAXILLOFACIAL TRAUMA

I. GENERAL PRINCIPLES

A. Rarely the direct cause of death; other injuries take precedence.

1. Exceptions:

a. Airway occlusion.

b. Distal carotid artery injury.

B. Definitive treatment can be delayed for several days.

1. Initial tetanus and antibiotic prophylaxis as appropriate.

2. Allow time for soft tissue swelling to resolve.

3. Conclusive CT imaging completed.

4. Goal is to restore normal function and then address cosmetics.

II. INITIAL MANAGEMENT

A. Airway management:

1. Alleviate obstruction:

a. Aspiration (blood, saliva, teeth, vomit, etc.).

b. Inability to control tongue (pull tongue forward with towel

clip or suture).

c. Extensive edema of the soft palate.

2. Indications for ETT same as previously described.

3. Follow standard C-spine precautions.

B. Hemorrhage control:

1. Local direct pressure.

2. Sterile packing.

Page 45

Notes


3. Avoid blind clamping.

III. DIAGNOSIS

A. History and physical:

1. Mechanism (always consider abuse).

2. Dental malocclusion.

3. Facial paresthesias.

4. Visual symptoms:

a. Monocular diploplia – lens dislocation.

b. Binocular diploplia – extraocular muscle or nerve

dysfunction.

5. Soft tissue crepitus (sinus fracture).

6. Abnormal bony mobility.

B. Imaging:

1. Radiographs:

a. Water’s view useful screen in low risk patients.

b. Limited utility for additional films (i.e., facial series).

2. CT imaging:

a. Definitive diagnosis and surgical planning.

IV. MIDFACE FRACTURES

A. Zygomatic arch:

1. General principles:

a. Isolated fractures fairly uncommon.

2. Signs and symptoms:

a. Facial dimpling/depression.

b. Point tenderness.

c. Inability to open mouth (mandibular condyle impingement).

B. Tripod (trimalar) fractures:


a. Fractures occur at articulations with frontal, temporal, and

maxillary bones.

b. Often displaced; if untreated, result in “sunken” facial

asymmetry.


a. Step deformity and point tenderness.

b. Facial flattening.

c. Cheek and/or periorbital edema.

d. Circumorbital ecchymosis.

e. Subconjunctival hemorrhage.

Page 46

Notes


f. Anesthesia of cheek and upper lip (infraorbital nerve), teeth

and gums (dentoalveolar nerves).

g. Enophthalmos/diplopia.

h. Limited mandibular excursion.

i. Overlying subcutaneous emphysema.

j. Intraoral ecchymosis at upper buccal sulcus.

C. Orbit:


a. Blowout fractures secondary to rapid increase in intraorbital

pressure.

b. Classic location is inferomedial orbital border (weakest

point).

c. Orbital soft tissue may be herniated into the maxillary sinus.

i. True entrapment of the inferior rectus is rare.

Ophthalmoplegia commonly resolves when swelling

abates.

ii. Classic radiographic findings include “teardrop sign” and

maxillary sinus air-fluid level.


a. Inferior globe displacement.

b. Vertical diplopia.

c. Infraorbital nerve hypoaesthesia.

d. Globe injury (corneal abrasions, anterior chamber trauma,

scleral rupture).

D. Maxillary:

1. LeFort I = Transverse maxillary fracture:

a. General principles:

i. Fracture lines extend above palate and below zygomatic

process.

ii. Majority are not displaced.

iii. Exceptionally difficult to detect on plain film imaging.

b. Signs and symptoms:

i. Motion of hard palate but not nose.

ii. Dental malocclusion.

iii. Subcutaneous air (sinus fracture).

2. LeFort II = Pyramidal fracture:


i. Bilateral vertical fractures extend through maxillary

sinuses and infra-orbital rims joining across the nasal

bridge.


i. Motion of hard palate and nose but not orbits.

ii. Extensive swelling of the entire midface.

iii. Bilateral subconjunctival hemorrhage.

Page 47

Notes


3. LeFort III = Craniofacial dysjunction:


i. Fractures extend through frontozygomatic sutures, across

the orbits and through the base of the nose and ethmoidal

region.


i. Disjointed lateral orbit rims.

ii. Classic “dishface” deformity.

iii. Motion of entire face relative to skull.

iv. CSF rhinorrhea secondary to sphenoethmoidal

involvement.

Zygomaxillary Complex Fractures with Red Lines Indicating LeFort I, II

and III Patterns

E. Nasal:


a. Most common facial fracture.

b. Most displaced laterally or posteriorly.

c. Clinical diagnosis, radiographs are unnecessary.


a. Nasal bridge deformity.

b. Epistaxis.

c. Hypermobility with crepitus.

d. Periorbital ecchymosis.

3. ED treatment:

a. Control epistaxis.

b. Identify and alleviate septal hematoma:

i. Benzocaine/oxymetazoline or cocaine.

ii. I&D at inferior border.

iii. Pack to prevent reaccumulation.

c. Ice and analgesia.

4. Disposition:

a. Reevaluation in 1 week by PMD or plastic surgeon.

Page 48

Notes


V. MANDIBLE FRACTURES

A. General principles:

1. Commonly two fractures sites (similar to the pelvic ring).

2. Anatomic locations:

a. Condyle: 30%.

b. Angle/Ramus: 30%.

c. Body: 30%.

B. Signs and symptoms:

1. Significant swelling and ecchymosis.

2. Dental malocclusion.

3. Mandible deviation on opening.

4. Trismus.

5. Intraoral laceration (open fracture).

6. Sublingual hematoma.

7. Mental nerve anesthesia.

C. Imaging studies:

1. Radiographs:

a. Panorex: Still the BEST, not readily available.

b. Mandible series: Inadequate, classically miss condylar

fractures.

2. CT mandible: preferred today by many oral surgeons.

D. Specific fractures:

1. Condyle fractures:

a. Jaw deviates toward fracture on maximum opening.

b. Bilateral fractures result in inability to occlude the incisors (+

tongue-blade test).

2. Angle/body fractures:

a. Bilateral angle fractures can result in loss of tongue support

and secondary airway obstruction.

3. Symphysis fractures:

a. Unusual because of overall bone thickness.

b. Evaluate for potential blunt carotid injury.

4. Alveolar fractures:

a. Anterior or incisor areas most common.

b. Focus on maintaining tooth viability.

c. Most require stabilization with wires or arch bars.

Page 49

Notes


E. Treatment:

1. Remove nonviable teeth.

2. Tetanus prophylaxis.

3. Prophylactic antibiotics for open fractures.

4. Reduced by wiring upper and lower teeth in occlusion.

5. Open fixation for edentulous or posterior segments.

VI. AURICULAR INJURIES

A. Auricular hematomas:


a. Blood accumulates between perichondrium (blood supply)

and cartilage (avascular).

b. May occur after blunt or shear force without laceration.

c. Failure to treat results in “cauliflower ear”.

2. Treatment:

a. Aspiration alone often leads to recurrence.

b. Incise along curvature of pinna no greater than 1 cm,

evacuate hematoma, and irrigate cavity.

c. Hold direct pressure for minimum of 5 minutes span.

d. Dress with antibiotic ointment and apply pressure dressing for

48 hour span to prevent reaccumulation.

e. DC with PO antibiotics and recheck in 24 hours.

B. Auricular lacerations:


a. Cartilage involvement is very common.

b. General approach should focus on prevention of skin and

cartilage loss.

c. All cartilage needs to be covered by skin to prevent secondary

chondritis and tissue loss.

2. Treatment:

a. For simple skin lacerations, meticulous closure with 6.0 nylon

is usually sufficient.

b. For large wounds with lacerated cartilage, re-approximate

cartilage with 6.0 nylon and very small knots and then close

the skin as above.

c. Hold direct pressure for minimum of 5 minutes span.

d. Dress with antibiotic ointment and apply pressure dressing for

48 hour span to prevent reaccumulation.

e. DC with PO antibiotics and recheck in 24 hours.

f. Refer patients with significant amount of avulsed skin to

plastic surgeons for a flap closure.

Page 50

Notes


PENETRATING NECK TRAUMA


A. Multiple injuries the norm (several vital tracts in close proximity):

1. Vascular.

2. Respiratory.

3. Neurologic.

4. Aerodigestive (esophagus and oropharynx).

5. Skeletal.

B. External anatomic landmarks:

1. Anterior triangle:

a. Anterior to the SCM and lateral to the midline, extends from

the sternal notch to the base of the skull.

b. Divided into 3 zones based on craniocaudal position.

c. Zone 1:

i. Between sternal notch and cricoid cartilage.

ii. Key structures: subclavian and carotid vessels, trachea,

esophagus.

d. Zone II:

i. Between cricoid cartilage and mandibular angle.

ii. Amenable to readily secure proximal and distal vascular

control.

iii. Key structures: carotid arteries, larynx, esophagus.

e. Zone III:

i. Between mandibular angle and base of the skull.

ii. Key structures: distal carotids, oropharynx.

2. Posterior triangle:

a. Posterior to the SCM and anterior to the lateral border of the

Page 51

Notes


trapezius, extends from the clavicle to the base of the skull.

b. Key structures: vertebral arteries, spinal cord, vertebrae.

C. Fascial planes:

1. Superficial fascia:

a. Overlies the platysma.

b. Minimal clinical significance.

2. Platysma:

a. Thin superficial muscle spanning across SCM muscles.

b. Traumatic violation necessitates aggressive evaluation.

3. Deep cervical fascia:

a. 3 key subdivisions (investing, pretracheal, prevertebral).

b. Limits external bleeding despite significant injury.

c. Hematoma formation may lead to extrinsic compression of

nearby structures.

d. May facilitate the spread of infection into the mediastinum.

II. INITIAL MANAGEMENT

A. Primary survey:

1. Airway: Indications for definitive airway:

a. Acute respiratory distress.

b. Airway compromise from blood or secretions

c. Expanding hematoma.

d. Massive subcutaneous emphysema (can be exacerbated by

continuous BVM).

e. Tracheal deviation.

f. Altered mental status.

2. Breathing:

a. Rule out associated pulmonary trauma (Zone I injuries).

3. Circulation:

a. Hemorrhage can be external, contained, or internal.

b. Control with direct pressure or packing.

c. Avoid disruption of formed clot.

d. Avoid blind clamping (risk for neurological injury).

e. Consider mild Trendelenburg (limit potential for venous air

embolism).

B. Secondary survey:

1. Physical examination:

a. Check for platysma violation.

b. Check for “hard and soft” signs of significant cervical injury.

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Notes


2. Imaging studies:

a. Plain radiographs:

i. Retained foreign body.

ii. Retropharyngeal/subcutaneous air.

iii. Bony/cartilaginous injury.

iv. Intrathoracic injury.

b. CT imaging:

i. Permits the workup of multiple tracts with one study.

ii. Delineates path of bullet/knife and proximity to

underlying structures.

iii. Clinical sensitivity approaching more accepted

modalities.

c. Conventional angiography:

i. Classically the study of choice to rule out arterial injury.

ii. May assist in operative planning.

iii. May be replaced by CT angiography with improving

technology.

3. Endoscopic studies:

a. Esophagoscopy:

i. Combined with contrast esophagram is currently the gold

standard to evaluate for significant esophageal injury.

b. Laryngoscopy:

i. Standard of care for patients with symptoms of LT tract

injury.

ii. Evolving role for CT imaging with improving technology.

Hard and Soft Signs for Operative Intervention

Tract Hard Signs Soft Signs

Vascular Hypotension in ED.

Active arterial

bleeding.

Absent carotid pulse.

Expanding

hematoma.

Carotid thrill or bruit.

Hypotension in field.

History of arterial

bleeding.

Tracheal deviation.

Large hematoma.

Apical capping on CXR.

Laryngotracheal Air/bubbling in

wounds.

Hemoptysis.

Subcutaneous

emphysema.

Stridor.

Dysphonia.

Esophageal None. Hematemesis.

Odynophagia.

Neurologic Lateralizing signs. Vocal cord paralysis.

CN VII palsy.

Unexplained bradycardia

(sympathetic chain).

Page 53

Notes


III. MANDATORY VS. SELECTIVE EXPLORATION OF ZONE II

NECK INJURIES

A. Mandatory exploration:

1. History:

a. Previous to World War II:

i. Expectant management with high mortality (18-35%).

b. World War II onward:

i. Mandatory exploration with decreased mortality (6%).

ii. Increase in negative neck explorations (40-63%).

2. Current indications for emergent operative exploration:

a. Hard signs of vascular injury.

b. Obvious aerodigestive injury.

B. Selective management:

1. Rationale:

a. High rate of negative explorations with mandatory approach.

b. Low energy mechanisms with non-combat civilian wounds.

2. Indications for selective management:

a. Absence of above findings mandating exploration.

b. Stable patient.

3. Pros:

a. Similar overall mortality rates.

b. Fewer negative explorations.

c. Shorter hospital stays.

4. Cons:

a. Potential for undiagnosed injuries vs. mandatory exploration.

b. May delay definitive operation.

c. Requires 24 hour institutional support.

Summary of Work Up by Zone

Zone I Zone II Zone III Posterior

Triangle

Angiogram of

aortic arch and

great vessels.

Esophogram and

esophagoscopy.

Bronchoscopy

with signs and

symptoms of

laryngotracheal

injury.

Angiography of

carotids.

Esophogram and

esophagoscopy.

Bronchoscopy

with signs and

symptoms of

laryngotracheal

injury.

Angiography

of carotids.

Oropharyngeal

exam.

Angiography

of vertebral

arteries.

Page 54

Notes


THORACIC TRAUMA

I. GENERAL PRINICPLES

A. Morbidity/mortality:

1. Second leading cause of traumatic death following traumatic

brain injury.

2. Immediate death on the scene:

a. Cardiac and great vessel rupture.

3. Death within the “Golden Hour” (target of primary survey):

a. Acute airway obstruction.

b. Tension pneumothorax.

c. Massive hemothorax.

d. Open pneumothorax.

e. Flail chest.

f. Pericardial tamponade.

Emergent Life Threats

Diagnosis Key Finding Treatment

Airway Obstruction Can’t talk, can’t breath Endotracheal intubation

Tension PTX Hypotension

JVD

Tracheal deviation

Absent breath sounds

Hyperresonance

Needle thoracostomy

Massive HTX Diminished breath sounds

Dullness to percussion

Chest tube

OR thoracotomy

Open PTX Sucking chest wound Three-sided occlusive

dressing

Chest tube

Flail Chest Paradoxical chest wall

motion

Positive-pressure

ventilation

Cardiac Tamponade Hypotension

JVD

Muffled heart sounds

IV fluid resuscitation

ED pericardiocentesis

OR thoracotomy

B. Initial resuscitation:

1. Airway management:

a. Indications for ETT similar as previously described.

2. Venous access:

a. If central access is necessary above the waist (e.g., pelvic

fracture), then place the line on the side of injury to avoid

trauma to contralateral uninjured lung.

b. With potential injury to the supradiaphragmatic vasculature

(especially the SVC), place IV or central line below the chest

Page 55

Notes


(i.e., femoral line).

II. CHEST WALL INJURIES

A. Rib fractures:


a. Significance of this injury is not fracture itself but associated

injuries (e.g., PTX, HTX):

i. 1st

- 2

nd requires significant force and often associated

with additional injuries.

ii. 4th

– 9th

most commonly involved.

iii. 6th

– 12th

associated with intra-abdominal injury.

b. Typically break at point of trauma or posterior angle (weakest

point structurally).

2. Workup:

a. Upright CXR:

i. Misses fractures in up to 50% of cases.

ii. Useful for evaluating potential intrathoracic injury.

b. Rib film indications:

i. Suspected fracture of 1st-3

rd or 9

th-12

th.

ii. Multiple fractures.

iii. Elderly patient.

iv. Underlying pulmonary disease.

v. Suspected pathologic fracture.

3. Management:

a. Simple fractures:

i. Oral analgesics.

ii. Pulmonary toilet.

iii. Avoid binders/belts or any other restricting agents.

b. Complicated fractures (elderly patients, multiple rib

involvement, underlying cardiopulmonary disease):

i. IV pain control.

ii. Admit for aggressive pulmonary toilet.

B. Sternal fractures:


a. Usually secondary to blunt anterior chest trauma (3-point seat

belt most likely culprit).

b. Most fractures are transverse in orientation.

c. Isolated sternal fractures typically benign (mortality <1%).

d. Concurrent mediastinal hematoma can be life-threatening

(regardless of etiology).

e. Associated complications:

i. Cardiac contusions (1.5 – 6%).

ii. Spinal fractures (< 10%).

iii. Rib fractures (21%).

Page 56

Notes


2. Workup:

a. CXR:

i. Lateral views best for making diagnosis.

b. CT chest:

a. Best for evaluating for suspected secondary mediastinal

injuries.

c. Electrocardiogram:

a. At 0 and 6 hours to evaluate for blunt cardiac injury.

3. Management:

a. Adequate pain control.

b. Pulmonary toilet.

c. Admit complicated cases:

i. Elderly patients.

ii. Underlying cardiopulmonary disease.

iii. Mediastinal hematoma.

iv. Signs of myocardial contusion.

C. Flail chest:


a. Fracture of three or more adjacent ribs at 2 or more sites.

b. Clinically apparent via paradoxical motion of the free chest

wall segment during respiration.

c. Mortality rates of 8-35%.

c. Pre-hospital intubation and positive-pressure ventilation

internally splints the chest wall and masks the diagnosis.

d. Underlying pulmonary contusion is the true problem and the

major source of respiratory compromise.

e. 30% of cases missed within the first 6 hours of evaluation.

2. Workup:

a. CXR:

i. Multiple rib fractures usually identified.

ii. Evaluate for associated PTX/HTX.

b. CT chest:

a. More difficult to appreciate flail segment compared to

CXR.

b. Better delineates presence and severity of underlying

pulmonary contusions.

3. Management:

a. Judicious IV fluid resuscitation.

b. Supplemental 100% O2.

c. Adequate analgesia.

d. Pulmonary toilet.

e. Selective use of endotracheal intubation (increased risk for

secondary pneumonias):

i. Respiratory failure.

ii. Severe shock.

iii. Additional injuries necessitating OR.

Page 57

Notes


III. PULMONARY INJURIES

A. Pulmonary contusion:


a. Found in more than 30-75% of patients with major blunt

thoracic trauma.

b. Most common significant chest injury in children.

c. Pathophysiology is secondary to direct bruising of lung

parenchyma with secondary alveolar edema and hemorrhage.

d. Overzealous fluid resuscitation worsens underlying alveolar

injury with progressive respiratory compromise.

2. Workup:

a. CXR:

i. Areas of patchy consolidation beneath the site of chest

wall injury.

ii. May take several hours of development for accurate

detection.

b. CT imaging:

i. Increased sensitivity to detect early evolving contusions.

c. Arterial blood gasses:

i. Monitor for declining PaO2 or climbing A-a gradient.

ii. May be prognostic and guide decision to intubate.

3. Management:

a. Essentially the same as previously outlined for flail chest.

b. With unilateral lung involvement, consider double lumen

intubation and differential ventilation.

B. Pneumothorax:


a. Most common injury following penetrating chest trauma.

b. Typically accompanied by concurrent hemothorax.

2. Classification:

a. Simple:

i. No persistent communication with the atmosphere.

ii. Hemodynamically stable.

iii. No mediastinal shift.

b. Open pneumothorax:

i. More common with high energy combat wounds.

ii. Persistent communication between the intrathoracic

cavity and the atmosphere.

iii. Chest wall defect greater than 2/3 tracheal diameter

produces “sucking chest wound” and severe respiratory

compromise.

c. Tension pneumothorax:

i. Persistent air leak or chest wall defect with progressive

Page 58

Notes


accumulation of air within the pleural space.

ii. Secondary elevation in intrathoracic pressure leads to

mediastinal shift to the contralateral side, impaired

cardiac preload and outflow, and imminent cardiovascular

collapse.

iii. Clinically evident in patients with severe dyspnea, marked

hypotension, pronounced JVD, and tracheal deviation.

d. Occult pneumothorax:

i. Clinically asymptomatic PTX detected on CT imaging

only.

3. Workup:

a. CXR:

i. Upright full inspiratory film the initial study of choice.

ii. Follow-up expiratory film with high suspicion and

negative initial CXR.

iii. 3 hour repeat CXR in patients with negative initial study

and penetrating trauma.

b. CT imaging:

i. May detect small “occult” PTX missed on initial CXR.

4. Management:

a. Tension pneumothorax:

i. Emergent needle thoracostomy (14G angiocatheter at 2nd

intercostal space, midclavicular line).

ii. Converts tension to open pneumothorax. Follow with

tube thoracostomy.

b. Simple pneumothorax: Indications for chest tube placement:

(*some experts advocate tube thoracostomy for all

pneumothoraces with traumatic etiologies)

i. Moderate-to-large sized pneumothorax.

ii. Respiratory symptoms regardless of the size.

iii. Increasing size on serial imaging.

iv. Patients on ventilator support.

v. Patient requiring general anesthesia.

vi. Associated hemothorax.

vii. Bilateral pneumothorax regardless of size.

c. Occult PTX:

a. Serial observation for development of symptoms.

b. Chest tube placement for patients requiring general

anesthesia.

C. Hemothorax:


a. Accumulation of blood in the pleural space following blunt or

penetrating thoracic trauma.

b. Accompanied by pneumothorax in 25% of cases.

c. Sources of bleeding in order of frequency (highest to lowest)

and clinical severity (lowest to highest):

Page 59

Notes


i. Lung parenchyma.

ii. Intercostal artery.

iii. Great vessel injury.

d. Massive hemothorax is defined as 1500 ml of blood in adult

patients.

2. Workup:

a. CXR:

i. 200 to 300 ml of accumulated blood will result in blunting

of the costophrenic angles on upright CXR.

ii. Supine films may demonstrate only a subtle diffuse hazy

appearance despite up to 1000 ml of fluid.

b. US/FAST:

i. Can detect intrapleural fluid volumes as low as 50 ml.

ii. May also demonstrate subtle findings of PTX (absent lung

sliding/ comet tails).

3. Management:

a. Large bore (36-40F) tube thoracostomy.

b. Strongly consider autotransfusion setup in unstable patients.

c. Indications for OR thoracostomy:

i. Initial thoracostomy tube drainage is > 20 ml/kg of blood

or 1500 ml.

ii. Persistent heavy bleeding at >7mL/kg/hr.

iii. Worsening hemothorax on CXR despite tube

thoracostomy.

iv. Patient remains hypotensive despite adequate blood

product replacement and additional sources of

hemorrhage have been ruled out.

v. Patient decompensates after initial response to

resuscitation.

D. Tracheobronchial injury:


a. Can occur via both blunt and penetrating trauma; MVCs are

the most common etiology.

b. Deceleration injuries with shearing of mobile distal segments

(intrapulmonary) from fixed proximal (trachea) segments vs.

sudden compression of thoracic cage with closed glottis and

secondary blowout.

c. Most (>80%) occur within 2 cm of carina.

d. Symptoms include hemoptysis, dyspnea, subcutaneous

emphysema, and Hamman’s crunch.

e. Up to 10% of cases are asymptomatic; some will present with

an unexplained atelectasis or pneumonia several weeks post-

injury.

2. Workup:

a. CXR:

i. Suspicious findings include large PTX,

Page 60

Notes


pneumomediastinum, deep cervical emphysema, or a

disrupted/obstructed bronchus.

b. Bronchoscopy:

i. Diagnostic procedure of choice.

ii. Perform when injury suspected clinically or

radiographically.

3. Management:

a. Gentle intubation over a bronchoscope (to limit injury

progression).

b. Operative repair.

IV. CARDIOVASCULAR INJURIES

A. Blunt cardiac injury: Spectrum of disease from myocardial

concussion to myocardial contusion to outright ventricular rupture.

B. Myocardial concussion (commotio cordis):

1. Sudden blow to thoracic cage chest during ventricular

repolarization resulting in life-threatening dysrhythmia.

2. Postmortem analysis shows no obvious histopathologic changes.

3. Classic case is young baseball player hit in chest by pitch.

C. Myocardial contusion:


a. Most common and least serious condition.

b. Typical pathophysiology is a direct blow to the anterior chest

or compression between the sternum and vertebrae.

c. Most commonly affects anterior right ventricle, anterior

interventricular septum, and anterior-apical left ventricle.

d. Clinical findings may not be present; suspect in any patient

with moderate to severe upper abdomen or chest trauma.

e. Gold standards for diagnosis, significance, and management

do not exist.

2. Workup:

a. EKG:

i. Tachycardia out of proportion to blood loss.

ii. Dysrhythmias/ectopy (especially PVCs).

iii. Conduction blocks (especially RBBB).

b. Cardiac enzymes:

i. Repeatedly proven to be ineffective and costly.

ii. Utility limited to patients with suspected cardiac ischemia

antecedent to trauma.

c. Echocardiography:

i. Contused myocardium mimics ischemic tissue.

ii. Use in patients with either significant dysrhythmias

and/or cardiac dysfunction.

Page 61

Notes


3. Management:

a. Admit patients with new suspicious EKG abnormalities for

24 hour telemetry monitoring.

b. In unstable patients with echocardiographic evidence of

myocardial contusion, follow standard ACLS protocols minus

the anticoagulation.

Urgent Life Threats: consider during the secondary survey

Dx Key Tx

Rib/sternum fractures CXR

CT for lower ribs

EKG

Respiratory therapy

Pain control

Hospitalize elderly

and sick

PTX Expiratory CXR Chest tube

Observe if occult

Pulmonary contusion CXR findings often

delayed

Careful IVFs

Ventilation

Blunt cardiac injury Mechanism

EKG

Observe

Supportive (ACLS)

Traumatic aortic

injury

Mechanism CTA screen

Angio if equivocal

Diaphragm injury CXR often subtle in

penetrating trauma

DPL

Repair now or have

problems later…

D. Myocardia rupture:

1. Nearly always immediately fatal.

2. Ventricles most commonly involved; concurrent aortic rupture

common.

3. Survivors reach the ED secondary to intact pericardium with

secondary tamponade.

E. Acute pericardial tamponade:


a. Less than 25% of penetrating cardiac injuries survive to reach

the hospital.

b. Most commonly seen with isolated stab wound to the RV

(low pressure leak into the pericardial sac).

c. Requires less than 100 ml of pericardial blood/clot.

d. Exceptionally rare with blunt thoracic trauma.

e. Common clinical findings include hypotension/tachycardia

and JVD.

f. Beck’s triad of hypotension, distended neck veins, and

muffled heart tones is unreliable and typically occurs

immediately before death.

Page 62

Notes


2. Workup:

a. CXR:

i. Cardiomegaly/ “water bottle” silhouette not expected.

ii. Traumatic pneumocardium may suggest external violation

of the pericardial sac.

b. EKG:

i. Sinus tachycardia the most common finding.

ii. Electrical alternans not expected (low volumes required

for acute tamponade).

c. Ultrasound:

i. Subxiphoid view of pericardial sac is standard image for

bedside FAST exam.

ii. Sensitive (>98%) for the detection of pericardial fluid and

tamponade physiology (diastolic collapse of the right

ventricle).

iii. A dilated IVC in a hypotensive patient is a further

suggestive finding.

d. CVP:

i. Levels > 15 cm H2O in the setting of an unstable trauma

patient is the most reliable finding.

3. Management:

a. Aggressive IVF resuscitation to increase filling pressures in

right atrium.

b. Pericardiocentesis (samples as low as 10 ml can be a

temporizing measure for unstable patients when immediate

OR is not an option; high incidence of false positives and

negatives).

c. ED thoracotomy for patients in extremis despite aggressive

IV resuscitation and suspected cardiac injury.

F. Blunt aortic injury (BAI):


a. Majority of patients (80%) will die at the scene.

b. Suspect in patients with sudden deceleration (MVCs, falls) or

high-speed side impact injuries.

c. 90% of injuries occur at the isthmus of the descending aorta

just distal to the takeoff of the left subclavian artery (traction

between the mobile aortic arch and immobile ligamentum

arteriosum).

d. One-third to one-half of patients will have no external signs

of thoracic trauma.

e. Risk increases with age (declining elasticity of vessel wall).

2. Workup:

a. CXR:

i. A widened mediastinum is the most sensitive sign (50-

92%).

ii. Obscured aortic knob.

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Notes


iii. Downwardly displaced left mainstem bronchus.

iv. Displaced nasogastric tube.

v. Widened paratracheal stripe.

vi. Widened right paraspinal interface.

vii. Left pleural apical cap.

b. CT arch angiogram:

i. Screening exam in patients with clinical concern

(mechanism + either abnormal CXR or chest pain).

ii. Modern helical CT ~ 100% sensitive for detecting BAI.

iii. Evaluates for additional thoracic injuries.

c. Transesophageal echocardiography:

i. Alternative to CT in unstable patient.

ii. Can identify intimal flaps and periaortic hematomas.

iii. Can aid in operative planning.

iv. Operator dependent; may not be sensitive enough to rule

out BAI.

d. Aortography:

i. Historically the gold standard; gradually losing favor to

CTA.

ii. Invasive, time consuming, and not readily available at

most institutions.

3. Management:

a. Aggressive BP and HR control (goal systolic 100-120 mmHg,

HR < 60).

b. Expedient operative repair.

V. ESOPHAGEAL INJURIES


1. Lack of a serosal lining grants contents of perforated esophagus

direct access into the mediastinum.

2. High mortality secondary to evolving suppurative mediastinitis

(mortality of 5-25% if repaired within 12 hours; 25-66% if

treatment delayed for more than 24 hours).

3. Most common etiologies:

a. Iatrogenic (rigid endoscope most common offender).

b. Ingested foreign bodies.

c. Caustic ingestions.

d. Blunt (exceptionally rare) or penetrating trauma.

e. Spontaneous/ post-emetic rupture (Boerhaave’s syndrome).

4. Common clinical findings include pleuritic chest pain that is

exacerbated by swallowing and/or neck flexion, odynophagia/

dysphagia, and hematemesis.

5. Hamman’s sign (systolic crunching sound with cardiac

auscultation) can be heard secondary to pneumomediastinum.

Page 64

Notes


B. Workup:

1. CXR:

a. Pneumomediastinum.

b. Subcutaneous emphysema.

c. Left-side pleural effusion.

d. Pneumothorax.

e. Widened mediastinum.

2. Esophagram/esophagoscopy:

a. Combination required to reach 100% sensitivity to rule out

esophageal rupture.

C. Management:

1. NPO.

2. Broad-spectrum antibiotic therapy (targeted at oral flora).

3. Aggressive IV volume replacement.

4. Emergency surgical consultation.

VI. DIAPHRAGMATIC INJURIES


1. More common with penetrating trauma; more obvious with blunt

mechanisms.

2. Right sided and small penetrating injuries can be very difficult to

diagnose.

3. Suspect in any patient with intra-thoracic injury and penetrating

abdominal trauma.

B. Workup:

1. CXR:

a. Initial screening exam.

b. Possible findings:

i. Indistinct left hemidiaphragm.

ii. Focal atelectasis in the left lower lobe.

iii. Hollow viscera/ nasogastric tube located superior to the

diaphragm in the left hemithorax.

2. CT imaging:

a. Inadequate to definitively rule out subtle injuries.

3. DPL:

a. With penetrating thoracoabdominal trauma, RBC counts >

10K/mL necessitate operative evaluation.

Page 65

Notes


C. Management:

1. Operative repair of any detected injuries is the current standard of

care.

2. Delayed clinical presentation (months to years post injury) is

very common:

a. Intrathoracic viscus incarceration.

b. Bowel obstruction.

c. Bowel ischemia.

ABDOMINAL TRAUMA


A. Blunt injuries:

1. High mortality due to difficulty in diagnosis.

2. Direct transmission of energy to abdominal viscera results in

diffuse patterns of injury.

3. Sudden compression injuries (e.g., lap belts) produce rapid

elevations in intraperitoneal pressures and hollow viscus rupture.

a. Direct compression between the forces applied to the anterior

abdominal wall and the posterior thorax/spinal column leads

to contusion and rupture of solid organs (liver, spleen).

4. Sudden deceleration (significant falls) produce both solid and

hollow viscus injuries secondary to traction forces as the more

mobile organs shift relative to their more fixed attachments

(mesentery, vascular pedicles, ligament of Treitze, duodenum and

cecum).

5. Retroperitoneal injury commonly results from falls with vertical

force transmitted up the axial skeleton or from high-speed

horizontal deceleration injury.

B. Penetrating injuries:

1. Gunshot wounds:

a. Direct injuries occur to any structure lying in the actual path

of the missile.

b. Indirect injuries occur from either bone and/or bullet

fragmentation as well as concussive injury along the

secondary blast cavity.

2. Stab wounds:

a. Approximately 70% of anterior abdominal stab wounds

violate the peritoneum; only half of these produce visceral

injury.

b. Injury is confined to path of object; depth and angle often

Page 66

Notes


impossible to predict from history and physical exam.

c. If local wound exploration demonstrates no peritoneal

violation, treat like any similar soft tissue wound.

C. Explosion-related injuries:

1. Both blunt trauma (blast concussion, patient thrown into objects)

and penetrating trauma (shrapnel) patterns are common.

II. INJURY PATTERNS

A. Solid organ injury:

1. Morbidity/mortality secondary to degree of blood loss.

2. The spleen is most commonly involved in blunt trauma, the liver

with penetrating mechanisms.

3. Most common presenting signs are hemodynamic instability and

initial abdominal tenderness progressing to frank rigidity.

4. Kehr’s sign (pain referred to the shoulder due to diaphragmatic

irritation by free intraperitoneal blood) can be a useful early

physical exam finding.

5. Suspect in any patient with injury to the lower ribs, abdomen or

pelvis.

6. Younger patients, pregnant or intoxicated patients, and those with

distracting injury/head trauma may present with minimal initial

symptoms.

B. Hollow viscus injuries:

1. Morbidity/mortality secondary to both blood loss (intraperitoneal

or intraluminal) and septicemia from spilled intestinal contents.

2. Penetrating injury to small bowel most common but may occur

with deceleration injuries.

3. Frequently may have minimal initial symptoms.

4. Peritonitis can take up to 8 hours to develop.

C. Retroperitoneal injury:

1. Duodenal injuries:

a. Hematoma or rupture can occur secondary to crush injuries

(hematoma formation in children is commonly associated

with “handlebar” injuries).

b. Very slow to develop, as hemorrhage or perforation is

initially contained within the retroperitoneum.

c. Symptoms are usually vague and include abdominal pain,

nausea/vomiting, and fever.

d. Complications arise from delayed diagnosis and include

obstruction, septicemia, and hemorrhagic shock.

Page 67

Notes


2. Pancreatic injuries:

a. Classic mechanism is secondary to blunt forces from a

handlebar or steering wheel.

b. Organ disruption causes leakage of proteolytic enzymes

resulting in secondary autodigestion, superinfection, and

abscess formation.

III. WORK UP

A. Laboratory studies:

1. Hemoglobin/hematocrit:

a. Initial hematocrit reflects baseline. Serial determinations

more helpful.

2. Base deficit/lactate:

a. Useful to determine initial degree of hemodynamic insult and

physiologic response to resuscitative efforts.

3. Amylase/lipase:

a. Neither is useful when obtained in a routing fashion.

b. Normal levels do not exclude a major pancreatic injury in

adult patients.

c. Frequently utilized in pediatric patients due to limited

reliability of physical exam and reluctance for CT imaging.

4. Liver function tests:

a. Elevated transaminases can result from hepatic trauma but

degree of elevation cannot estimate severity of liver injury.

b. May have more established role in evaluating pediatric

trauma for similar reasons outlined for pancreatic testing.

B. Radiographs:

1. CXR:

a. Intraperitoneal free air indicates peritoneal violation

(penetrating trauma) or hollow viscus rupture (blunt trauma).

2. AP pelvis:

a. Significant pelvic fractures are frequently associated with

abdominal injury.

3. KUB:

a. Blunt trauma: Routine use not cost-effective.

b. Penetrating trauma: Can help estimate the path of the

projectile via marking the wounds and connecting the dots.

DPL FAST CT

Pros Most sensitive.

Unstable

patients.

Relatively easy

to perform.

Sensitive.

Noninvasive.

Evaluates both chest

and peritoneum.

Rapid.

Sensitive and

SPECIFIC.

Evaluates retro-

peritoneum.

Identifies non-

Page 68

Notes


Repeatable. operative injury.

Cons Too sensitive. Operator and patient

dependent.

Radiation dose.

IV contrast.

Time to perform.

C. CT abdomen/pelvis:

1. Advantages:

a. Readily available.

b. Greater specificity than alternative techniques.

c. Localizes injury/source of hemorrhage.

d. Can help quantify the amount of hemorrhage and determine

the presence of ongoing bleeding.

e. Evaluates retroperitoneum, vertebral column, and lower

thorax.

f. Identifies non-operative injuries.

2. Disadvantages:

a. Decreased sensitivity for certain injuries (diaphragm, small

bowel, mesentery).

b. Exposure to ionizing radiation and IV contrast.

c. Time consuming, requires patient to leave resuscitation arena.

D. DPL:

1. Has been replaced by FAST and CT per ACEP Clinical Policy

noted in references.

2. Advantages:

a. High sensitivity.

b. Relatively fast/technically easy.

c. Low complication rate.

d. No need for patient to leave resuscitation arena.

3. Disadvantages:

a. Lower specificity (negative laparotomy rate approaching

30%).

b. Inability to localize source of hemorrhage.

c. Potential for iatrogenic injury.

d. Examination limited to evaluation of intraperitoneal injury.

e. Inability for serial evaluation.

4. Indications:

a. Blunt trauma indications:

i. Patient too unstable for CT imaging.

ii. Unexplained hypotension with equivocal physical exam.

b. Penetrating trauma indications:

i. Evaluation for peritoneal violation with stab wounds.

ii. Detection of diaphragmatic trauma in patients with

thoracoabdominal trauma.

5. Contraindications:

a. Absolute:

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Notes


i. Criteria necessitating operative laparotomy already met.

b. Relative:

i. Prior abdominal surgeries.

ii. Coagulopathies.

iii. 2nd

/3rd

trimester pregnancies.

iv. Marked obesity.

6. Results:

a. Regardless of etiology, aspiration of 10 ml of gross blood

indicates positive test (should really make you wonder why

you thought you had to tap him anyway).

b. Blunt abdominal trauma and anterior abdominal stab wounds:

i. RBC count > 100K/ml is >90% sensitive for positive

laparotomy.

c. Tangential GSW and penetrating thoracoabdominal trauma:

i. RBC count > 10K/ml indicates need for operative

laparotomy.

d. Less helpful studies include WBC counts, bile and/or Gram

staining, or vegetable matter analysis.

E. FAST exam:

1. Recommended in place of DPL by ACEP Clinical Policy.

2. Accurate bedside screening tool; highly sensitive but poorly

specific.

3. Advantages:

a. Easy, rapid, and repeatable.

b. Non-invasive, free from iatrogenic complications.

c. Does not expose patient to ionizing radiation or IV contrast.

d. Very helpful in patients with relative contraindications to

DPL.

e. Screens for intra-abdominal, pleural and pericardial fluid.

f. Bedside performance allows patient to remain in resuscitation

arena.

4. Disadvantages:

a. Nonspecific study.

b. Inability to localize source of hemorrhage.

c. Operator dependent; difficult in obese patients or those with

extensive bowel gas.

d. No definitive evaluation of retroperitoneum.

e. Inability to detect diaphragmatic injury.

f. Cannot distinguish blood from other sources of

intraperitoneal free fluid (e.g., ascites).

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Notes


NORMAL RUQ VIEW RUQ VIEW WITH FREE FLUID

IN MORRISON’S POUCH

NORMAL SUBXIPHOID SUBXIPHOID VIEW WITH

VIEW FREE FLUID

IV. MANAGEMENT

A. Hemodynamically stable:

1. Absolute indications for operative laparotomy exist.

a. Time permitting, work up additional life-threatening injuries

prior to OR.

2. Absolute indications for operative laparotomy do not exist.

a. Follow workup for potential injury as outlined in figures

below.

b. Address specific injuries as encountered.

c. Observe patient for serial physical exams.

B. Hemodynamically unstable:

1. Aggressive IV resuscitation.

2. Determine source of hemorrhagic shock:

a. Intraperitoneal (+ FAST or DPL).

i. Emergent OR laparotomy.

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Notes


b. Retroperitoneal (+ CT scan).

i. Consider angiogram with embolization based on specific

injury.

3. Antibiotic prophylaxis (GI flora) with hollow viscus perforation.

Work Up by Zones in Penetrating Trauma

Zone Definition Workup

Anterior box

Inferior to sternal

notch and superior

to costal margin.

Medial to bilateral

nipples.

CXR.

Bedside echocardiogram.

Posterior cardiac box

Between medial

border of scapulae.

Superior to costal

margins.

Gunshot wound:

CXR

Arch Angiogram

Esophagus w/up

+/- Bronchoscopy

Stab wound:

CXR

Aortogram*

Esophagus w/up*

* If mediastinum abnormal

on CXR.

Thoracoabdominal

Anterior:

Inferior to

nipples, superior

to costal margins.

Posterior:

Inferior to tips of

scapulae, superior

to costal margins.

CXR

DPL (diaphragm injury)

CT abdomen/pelvis

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Notes


V. PELVIC TRAUMA WORKUP BY MECHANISM

Mechanism Workup

Blunt (significant

fractures)

Retrograde urethrogram (especially with blood at

meatus, scrotal hematoma or high riding

prostate).

Voiding cystogram.

Penetrating Examine the outlet tracts:

GI: Proctoscopy.

GU: Cystogram.

Gyne: Vaginal speculum exam.

Vascular: Consider iliac angiography.

Anterior Abdomen

Inferior to costal

margins, superior to

inguinal ligaments

Anterior to bilateral

midaxillary lines

Gunshot wound:

All GSW that violate

peritoneum go to OR

Stab wounds:

CT abdomen/pelvis

DPL*

* Diminished utility in

most trauma centers

Back and Flank

Inferior to the tips of

the scapulae, superior

to the iliac crests

Posterior to bilateral

midaxillary lines

3° Contrast CT

abdomen/pelvis (PO,

PR, IV)

DPL*

* Diminished utility in

most trauma centers

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Notes


VI. INDICATIONS FOR LAPAROTOMY

Blunt Penetrating

Definitely Anterior abdominal injury

with hypotension.

Abdominal wall disruption.

Frank peritonitis.

Intraperitoneal free air

(CXR).

Diaphragmatic injury (CXR,

DPL).

Significant GI bleeding

(gross blood per NG or

rectal).

CT demonstration of

vascular or viscus injury.

Hemodynamic instability.

Frank peritonitis.

Evisceration.

Retained implement in situ.

Diaphragmatic injury (+DPL).

GI bleeding (gross blood per

NG or rectal).

Intraperitoneal free air (CXR).

Intraperitoneal bullet.

Transperitoneal missile path.

CT demonstration of vascular

or viscus injury.

Maybe Positive DPL or FAST in

stable patient.

Solid organ injury in stable

patient.

Hemoperitoneum without

clear source.

Stab wound with positive

local wound exploration.

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Notes


AIRWAY/MAXILLOFACIAL/PENETRATING NECK/

THORACIC/ABDOMINAL TRAUMA

PEARLS

Airway Management in Trauma

1. Trauma airway management = ACBCs. Always assume cervical

spine injury.

2. Nasal trumpets in awake patients, oral airways only in unconscious

patients with absent gag reflexes.

3. Nasotracheal intubation only if patient is breathing spontaneously

and has no significant midface trauma.

4. 20 mg of etomidate and 100 mg of sux will intubate anyone. But 100

mg of lidocaine, 1 mg of pancuronium, 200 mcg of fentanyl, 200 mg

of thiopental and 100 mg of sux are better in head injury patients.

5. Horizontal surgical cricothyrotomy if you can externally landmark

the cricothyroid membrane. Vertical incision if landmarks are grossly

distorted. Needle cricothyrotomy if patient < 8 years old.

6. Needle cricothyrotomy, LMA, and Combitube do not protect/secure

the airway. These are only temporizing measures until help arrives.

7. Singed face/hair or soot in the airway equals supraglottic injury.

Intubate expediently.

8. Infraglottic burns are typically more subtle but can be just as deadly!

Maxillofacial Trauma

1. Similar to other ring structures (e.g., pelvis), always look for more

than one fracture site when dealing with the mandible.

2. Rule out concurrent globe injury with any orbital fracture.

3. Significant facial fractures (i.e., Lefort II/III) may result in

retropharyngeal hematoma and secondary airway obstruction.

4. Sublingual or buccal ecchymosis is pathognomonic for a mandibular

fracture.

5. Recognize and drain both septal and auricular hematomas on

presentation to avoid significant long-term deformity.

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Notes


Penetrating Neck Trauma

1. Early intubation always leads to easier intubation, especially in cases

of expanding hematomas.

2. Always consider injury to all applicable tracts: airway, vascular,

gastrointestinal and neurologic.

3. Selective management is indicated in stable Zone II injuries when no

hard signs of injury are present and both diagnostic modalities and

surgical expertise are readily available.

4. Both esophagram and esophagoscopy are necessary to reliably

exclude esophageal injury and prevent life-threatening mediastinitis.

Thoracic Trauma

1. Emergent life threats to recognize and treat during the primary

survey include: airway obstruction, tension pneumothorax, massive

hemothrorax, open pneumothorax, flail chest, and cardiac

tamponade.

2. Tension pneumothorax is a clinical diagnosis: JVD, ipsilateral absent

breath sounds and contralateral tracheal deviation.

3. Cardiac tamponade: JVD, diminished heart sounds, and hypotension

(Beck’s triad).

4. Underlying pulmonary contusions are the real problem in patients

with flail chest. Intubate early and avoid overaggressive IV

resuscitation!

5. With any of the following – labored breathing, hemoptysis,

subcutaneous emphysema, tension PTX, and persistent air leak from

chest tube – consider tracheobronchial injury. Confirm with

bronchoscopy.

6. Pneumomediastinum can result from esophageal perforation,

tracheobronchial injury, and interstitial pulmonary emphysema

tracking into the mediastinum.

7. Troponins are typically not helpful in evaluating blunt cardiac injury.

Admit people with abnormal EKGs. Emergent bedside echo in

unstable patients.

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Notes


8. Traumatic aortic injuries surviving to ED presentation are typically

contained by the overlying adventitia but can rupture within 24 hours

if not properly diagnosed. Get the screening CTA and control the BP!

9. Blunt diaphragmatic injury is obvious. Penetrating cases are often

occult. Suspect such injuries in patients who persistently return with

vague upper GI complaints following a thoracoabdominal injury.

10. Rare and generally fatal venous air embolisms occur with combined

pulmonary and vascular injury, especially with concurrent positive

pressure ventilation. Displace air from right ventricle outflow tract

by placing head and left side down (Durant’s maneuver). Use echo

for diagnosis and guidance for removal

Abdominal Trauma

1. Most common solid organ injuries: Blunt trauma – spleen.

Penetrating trauma – bowel and liver.

2. In pediatric patients presenting with handlebar injuries to the

epigastrium, consider pancreatic or duodenal injury.

3. Although less common in clinical practice, be familiar with DPLs:

Absolute contraindications: Need for emergent laparotomy.

Relative contraindications: Prior surgery, pelvic fracture, and

pregnancy.

Criteria for + DPL:

Anterior abdominal SW: > 100,000 RBC/ml

Thoracoabdominal wound: > 10,000 RBC/ml

4. FAST exam gradually replacing DPL. Advantages include

repeatability, non-invasiveness, and quicker time to completion

5. CT imaging: Greater specificity than DPL or FAST. Sensitivity

approaching DPL without high negative lap rate. Evaluates solid

organs, retroperitoneum and pelvis.

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Notes


REFERENCES

1. Tintinalli: Emergency Medicine: A Comprehensive Study Guide, 6th

edition, McGraw, 2004.

2. Marx: Rosen’s Emergency Medicine: Concepts and Clinical

Practice, 6th

edition, Mosby, 2006.

3. ACEP Clinical Policies Committee: Clinical Policies Subcommittee:

Acute Blunt Abdominal Trauma. The Ann Emerg Med 2004: 43(2):

278 – 90. 2006 LLSA REQUIRED READING

08/13

Page 78

Hand and Wrist Injuries

Scott C. Sherman, MD

Assistant Residency Director, Associate Professor of Emergency Medicine, Rush Medical College; Attending Physician, Department of Emergency Medicine, John H.

Stroger Jr. Hospital of Cook County, Chicago

Page 79

Page 80

Notes


HAND AND WRIST INJURIES

I. ANATOMY

A. Surface anatomy: Use the terms volar (palmar), dorsal, radial, and

ulnar. The creases on the volar aspect are named the proximal and

distal palmar crease. The distal palmar crease overlies the mid point

of the proximal finger phalanx.

B. Skin: The skin of the volar hand and fingers is fixed to the

underlying bone by fibrous septa. This helps with grip, limits

movement, and does not allow significant swelling. The dorsal hand

has looser, thinner skin. This allows a fairly extensive space for

swelling from trauma or infection.

C. Nail: The nail complex consists of the eponychium (cuticle),

perionychium (nail edge), hyponychium (under the tip of the nail),

and the nail bed or matrix (under the nail plate).

II. HAND EXAMINATION

A. Neurologic assessment:

1. Digital nerve: Use two-point discrimination with a paper clip.

Normal two-point discrimination is between 2 and 5 mm at the

volar fingertip. Test an uninjured finger to estimate the patient’s

normal ability. Start at 1 cm, and decrease the distance until two

points are no longer felt.

2. Forearm injuries may result in neurologic deficits in the hand. It

is important to document these at the time of the initial exam.

a. Radial nerve: Sensory function is assessed at the dorsal web

space of the thumb and index finger. Motor function is tested

Page 81

Notes


by assessing extension of the wrist or fingers.

b. Ulnar nerve: The sensory function is tested at the volar tip of

the small finger. The ulnar nerve innervates the intrinsic

muscles of the hand. Have the patient spread the digits

against resistance. Another reliable test for the function of

this nerve is to have the patient place the ulnar edge of the

hand on the exam table, and then have them attempt to abduct

the index finger against resistance.

c. Median nerve: Sensory function is assessed at the volar tip

of index finger. Motor strength is best assessed by thumb

abduction (have the patient raise the thumb toward the ceiling

while the dorsal hand is flat on the exam table). This tests the

function of the abductor pollicis, which is reliably innervated

by the motor nerve branch of the median nerve.

B. Tendon assessment:

1. With injuries that lacerate or penetrate, it is important to

document tendon function. Excess flexion occurs with an

extensor tear, while excess extension is seen with flexor tendon

injuries.

2. Each finger should be examined independently for flexion of the

distal phalanx (profundus tendon) and the whole finger

(superficialis tendon). Extension can also be tested. Testing is

performed against resistance. Any weakness or pain might

indicate a partial injury.

3. Open injuries need to be assessed with a bloodless field and

direct inspection of the tendon through a full range of motion.

Flexor digitorum profundus Flexor digitorum superficialis

C. Vascular assessment:

1. Injuries to vascular structures usually do not affect perfusion of

the hand because of extensive anastomoses.

2. If initial inspection reveals a dusky or cool finger or hand, prompt

intervention is needed. Capillary refill and pulse oximetry

waveforms can give some indication of blood flow to injured

digits.

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Notes


D. Anesthesia:

1. Sensory examination must always precede anesthesia.

2. Wrist block includes:

a. Radial nerve: Lateral to radial nerve and skin while on

dorsum of hand.

b. Median nerve: Between the flexor carpi radialis and palmaris

longus tendons at wrist crease.

c. Ulnar nerve: Lateral to the flexor carpi ulnaris tendon.

3. Digit block options include:

a. Half ring block: Each side of the base of the digits.

b. Metacarpal block: Between the metacarpal heads all the way

to the palmar aspect of the hand.

c. Transthecal block: In the center of the proximal digital

crease. Go to bone, pull back slightly, and then inject. Direct

injection into the flexor tendon sheath.

4. Epinephrine injection into the digits has been considered taboo

since the 1950s. A 2005 study of over 3,000 hand surgeries using

the typical concentrations included with local anesthetics

(1:100,000) did NOT find a single case of digital ischemia.

5. An allergy to a local anesthetic is rare and in most cases is due to

preservatives (methylparaben) within the anesthetic. When an

allergy is reported, several options exist:

a. Use an anesthetic from the other class. Amide anesthetics

have two i’s (e.g., lidocaine) in their name. Esters have only

one “i” (e.g., tetracaine).

b. Use Benadryl 0.5%. Mix a 1 mL vial of diphenhydramine 50

mg with 9 mL of saline.

c. Use a 0.1 mL test dose of cardiac lidocaine (100 mg/5 mL),

which does not contain preservatives, and therefore is

unlikely to cause a reaction. If no reaction is noted within 30

minutes, proceed using cardiac lidocaine.

III. WRIST INJURIES

A. All wrist and hand movements depend on the proper alignment and

orientation of the eight carpal bones and their articulations with the

distal forearm and proximal metacarpals. Any disruption of these

structures will disrupt function.

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Notes


B. Scaphoid fracture:

1. Also called the carpal navicular, this is the most commonly

fractured bone of the wrist (60-80%). Usual mechanism is a

fall on an outstretched hand (FOOSH) with the wrist radial

deviated.

2. Pertinent anatomy: Single blood supply, distal end of bone.

Articulates with the lunate, and with the capitate.

3. Exam: Tenderness at anatomic “snuff box” and pain with axial

load to thumb.

4. X-ray: Usually linear waist fracture. Proximal fractures have

greater incidence of non-union with subsequent avascular

necrosis. About 10-20% will have a normal X-ray despite the

presence of a fracture.

5. Treatment: Treat all suspected fractures with thumb spica

immobilization. If no fracture identified, follow-up in 7-10 days

for repeat X-ray. Other modalities include MRI, CT, or bone

scanning.

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Notes


C. Triquetrum fracture:

1. Second most common carpal fracture (5-10%).

2. X-ray: “Dorsal chip” on lateral film. Due to ligamentous

avulsion.

3. Treatment: 4-6 weeks of immobilization.

D. Lunate fracture:

1. Uncommon (1-5%).

2. Pertinent anatomy: 20% have single distal blood supply.

Articulates with scaphoid and capitate.

3. Exam: Tenderness over dorsal radial wrist (lunate fossa). May

have increased pain with axial load on long or index finger.

4. X-ray: Can be occult, as with scaphoid. Usually linear. May

develop Kienböck's disease where the bone undergoes

spontaneous avascular necrosis from repetitive microtrauma.

5. Treatment: Issues are the same as scaphoid fracture. Treat

suspected fractures with immobilization and follow-up.

E. Hamate fracture:

1. Uncommon (2-4%).

2. X-ray: Usually seen as fracture of the hook of the hamate, on the

volar edge of the bone. May need carpal tunnel views.

3. Treatment: Non-union of hook fractures is common. Provide

analgesia and bulky dressing.

F. Distal radius fracture:

1. Colles fracture: Extension fracture of the metaphysis. Common

in children and elderly. 10x more frequent than carpal bone

fractures. Dinner fork deformity. 8% incidence of persistent

neuropathy (median nerve is most common). Goal of closed

reduction includes regaining normal anatomic alignment—volar

tilt (11 degrees), radial tilts (22 degrees), and radial height (11

mm). Sugar-tong splint and referral.

Page 85

Notes


2. Smith fracture: Flexion type or reverse Colles. Less common

than Colles by a factor of 10:1.

3. Hutchinson fracture: Radial styloid fracture. Also known as a

chauffeur’s or backfire fracture. Associated with carpal

ligamentous injury or scaphoid fracture.

4. Barton fracture: Dorsal or volar rim fracture of the radius with

subluxation or dislocation of the carpal bones.

Barton’s Fracture

G. Carpal ligament injury:

1. Scapholunate dissociation: Disruption of the ligaments joining

these bones. Seen as widening of the joint space on X-ray (Terry

Thomas sign). Any space greater than 2 mm is suspicious for

this injury. Left untreated, the patient develops chronic pain in

the wrist. Treatment is surgical.

2. Perilunate dislocation: Dislocation of the joint between the

lunate and the capitate. On the AP view, there is overlap of the

capitate with the lunate. On the lateral view, the lunate remains

articulated with the distal radius, but the capitate is dislocated

Page 86

Notes


dorsally. This dislocation is often seen with associated fractures,

and thus can be missed if not sought carefully. Operative repair is

indicated.

3. Lunate dislocation: This dislocation is similar in presentation to

the perilunate. The AP view reveals that the capitate has rotated,

and assumes a triangular appearance (“piece of pie” sign). On

the lateral view, the lunate is “spilled” from the cup of the distal

radius (“spilled tea-cup” sign). The treatment is open reduction

and fixation.

Piece of pie sign Spilled tea-cup sign

IV. HAND FRACTURES

A. Rotational deformities: It is important to detect and correct any

rotational deformities before healing occurs, as later repair is

difficult.

B. Metacarpals 2 – 5 (index through little finger):

1. Head fractures: Usually due to direct blow, and often

Page 87

Notes


comminuted or crushed. Treatment with hard or bulky splints,

and ortho follow-up.

2. Neck fractures: Classic is “boxer's” fracture. Usually angulated

in volar direction. Treatment varies for index and middle finger

MCs, where anatomic alignment is much more important. Ring

and little finger MCs can tolerate angulation of 30 degrees

without functional impairment.

3. Shaft fractures: Often angulated, sometimes spiral or oblique.

The more proximal the fracture, the more important anatomic

reduction becomes. These should be splinted and referred in a

timely fashion.

4. Base fractures: Uncommon, and often interarticular. Can affect

the carpometacarpal function. The base of the little finger MC

may present with a fracture-dislocation, as the fragment is pulled

by the attachment of the extensor carpi ulnaris. This requires

open fixation.

C. Thumb metacarpal:

1. Base fractures. These are often comminuted and dislocated, as

the abductor pollicis longus tendon pulls the fragments. A single

fracture with this finding is called a Bennett’s fracture; a

comminuted fracture (often “T” or “Y” shaped) is called a

Rolando’s fracture. Treatment is open fixation.

Bennett’s Fracture Rolando’s Fracture

D. Phalanx fractures:

1. Tuft fracture: Crush injuries. Typically torn skin, due to

attachment to bone. Reduction often accomplished by repair of

skin. Nail bed also frequently involved. Repair needed if nail

avulsed and nail bed lacerated. Remember to maintain the

eponychial space to allow continued nail growth. These are open

fractures, if the skin is torn. Antibiotics can be administered,

although infection is uncommon.

Page 88

Notes


2. Shaft fracture: Often spiral or oblique, these will frequently

require fixation. Initial reduction will often not be maintained,

even with splints or buddy taping. Rotation is again important to

detect.

3. Intra-articular fracture: These may need reduction if significant

portions of the joint are involved. “Mallet” finger fracture

occurs with a flexion force applied to the tip of the extending

finger. The force causes an avulsion of the extensor tendon at the

dorsal base of the distal phalanx. The treatment is splinting in

extension for 6 weeks. If greater than 25% of the joint space is

involved, surgical repair may be indicated.

V. FINGER DISLOCATIONS

A. Anatomy:

1. The IP joints of the fingers have both collateral ligaments and the

fibrous volar plate. These structures provide resistance to injury,

but can be subject to large forces when the digit is twisted or

forcibly extended.

2. The MCP joints have unique anatomy that provides strength with

potential range of motion. The transverse metacarpal ligament

provides support by attaching the MCP joints to each other

(except the thumb). There are also collateral ligaments, which are

supported by the lumbrical muscles. The arrangement provides

the ability to abduct when extended, but not when flexed.

B. Interphalangeal joints:

1. The PIP is much more commonly dislocated. These are usually

dorsal. After a digital nerve block, reduction is achieved with

gentle traction. Irreducible dislocations are unusual, but indicate

entrapped soft tissues.

2. These injuries need to be X-rayed, as tiny fragments of avulsed

bone at the joint signify ligament avulsion.

3. The post-reduction exam should also attempt to check for laxity.

4. Splint the joint in 15 – 20 degrees of flexion, for 3-4 weeks.

Some advocate 2 weeks with subsequent buddy taping. Open

Page 89

Notes


injuries need orthopedic consultation for debridement, irrigation,

antibiotics, and close follow-up.

C. Metacarpophalangeal joints:

1. The complex anatomy protects against dislocation, but also leads

to a higher incidence of irreducible dislocations. The most

common dislocations are dorsal, and fall into two broad

categories.

2. “Simple” dislocations have a dramatic appearance clinically,

with marked angulation. These are termed simple because they

are usually easily reduced with closed techniques.

3. “Complex” dislocations appear subtle clinically, but are often

impossible to reduce with closed techniques. This is due to the

interposition of torn ligaments and the arrangement of ligaments

and lumbrical muscles that actually tighten around the head of the

metacarpal as traction is applied, which prevents reduction.

D. Carpometacarpal joints:

1. Similar mechanism to Boxer’s fracture…punching wall.

2. Easy to miss on the PA view…need to look at the lateral

3. Swelling may mask the clinical diagnosis

E. Gamekeeper’s thumb:

1. This injury is a sprain or tear of the ulnar collateral ligament of

the thumb MCP joint from forced radial deviation of the thumb

(e.g., falling with a ski pole in the hand). This results in pain, and

potential laxity with gripping. Recovery is slow and surgery may

be needed. Initial treatment is with a thumb spica splint.

Page 90

Notes


VI. TENDON INJURIES

A. Extensor tendons:

1. More superficial with thinner skin than dorsal tendons. Easily

lacerated. Tendon injury may be “open” or “closed”.

2. Open tendon injuries:

a. Divided into 8 zones. Zone I is over the distal IP joint. Zone

II includes the middle phalanx. The zones of extensor tendon

injury can be more easily remembered by noting that odd-

numbered zones are over joints, while even-numbered zones

are over bones. Zone VII and VIII involve the carpal bones

and distal forearm, respectively.

b. An emergency physician can repair complete tendon injuries

in zones IV, V, and VI. Other complete extensor tendon

ruptures should be referred to a hand surgeon after suturing

the skin and splinting the hand.

c. Partial open tendon ruptures should be referred, but do not

require repair in most instances.

3. Closed extensor tendon injuries:

a. Mallet finger: Tearing of the insertion of the extensor tendon

from the base of the distal phalanx is known as a “mallet

finger,” and is treated with the joint in extension for 6 weeks.

The patient is cautioned not to remove the splint during this

time.

Page 91

Notes


b. Central slip rupture: The central slip of the extensor tendon

is located at the base of the dorsal middle phalanx. At this

location, the tendon splits into three parts, with the central

slip attaching to the bone, and the two lateral parts attaching

to the distal phalanx with the lumbrical muscles. When the

central slip is ruptured secondary to contusion, forced flexion

or dislocation of the PIP joint, the extensor tendon splits and

can slip to either side of the joint. In that position, attempts at

extension actually cause some flexion. The end result is a

“Boutonnière deformity”, where the proximal joint is flexed

while the distal joint is hyperextended.

c. Boxer’s knuckle: Rupture of the extensor hood occurs as a

result of injury to the dorsal aspect of the hand over the MCP

joint. In this scenario, there is disruption of one of the

laterally located sagittal bands that hold the tendon in a

central location. The end result is subluxation of the tendon.

These injuries should be splinted and referred. Splint the hand

in only as much extension as is required to keep the tendon in

its proper position.

B. Flexor tendons:

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Notes


1. There are anatomical “zones” for flexor tendon injuries, with

associated unique problems for healing and repair.

a. Zone 1: From the mid portion of the finger to the insertion of

the profundus tendon. Problems with retraction of the

proximal part and the complex pulley system. The FDP

emerges from the split FDS in this zone.

b. Zone 2: From the distal palmar crease to zone 1, where the

FDS and FDP interweave. This area is known as “no man’s

land” because the complex relationships of multiple tendons,

sheaths, and pulleys make repair difficult. Any scarring leads

to long-term functional deficits. This is the most common

area for injury.

c. Zone 3: Mid palm from level of thenar eminence to proximal

edge of flexor sheath. Easier repair with less pulleys and

better visualization.

d. Zone 4: Carpal tunnel area, multiple tendons usually

involved.

e. Zone 5: Proximal to the carpal tunnel.

2. Flexor tendon injuries require repair by a hand surgeon.

VII. BITE WOUNDS

A. Human bites:

1. Fight bite injuries (i.e., clenched fist injuries) are injuries to

tendons and joints at the MCP sustained following a punch to the

mouth (i.e., tooth).

2. Treatment of fight bite injuries involves surgical debridement,

irrigation, and IV antibiotics. Noninfected bites are managed

with local wound care and oral antibiotics.

3. Amoxicillin clavulanate (Augmentin) remains the drug of choice

for human bites. There are probably over 40 different “bugs” in

the human mouth, but the one to recall is Eikenella corrodens.

B. Dog bites:

1. Potential for significant tissue destruction from large crushing

mechanisms (up to 450 psi). X-ray if any concern of bony injury.

2. Superficial wounds may do well with local care, but deeper

wounds need debridement and antibiotics.

3. Pasteurella multocida is the bacteria to remember. Antibiotic

choices are the same as for human bites.

C. Cat bites:

1. Deeper penetration than dog bites with the inability to cleanse or

irrigate the depth of the wound. The end result is a higher rate of

infection.

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2. Pasteurella multocida. Liberal use of antibiotics.

3. The antibiotic choices are the same as for human bites.

VIII. AMPUTATION

A. Digit amputation:

1. Care of the amputated part involves gentle cleansing if heavily

contaminated, wrapping in moist gauze, with storage in a sealed

plastic bag. The bag is then placed into ice water. Properly

maintained digits have about 12 hours of viability.

2. Classical indications for digit replantation include: between PIP

and DIP, thumb, multiple digits, child, or midpalmar amputation.

However, any amputated part should be considered for

replantation and a hand surgeon should be consulted.

3. It should always be emphasized the re-implanted digit will never

function normally, and will likely have some sensory problems,

as well as chronic stiffness and weakness.

B. Fingertip amputation:

1. Treatment depends on whether bone is exposed.

a. No bone exposed (Zone 1 injuries): heal by secondary

intention after wound care.

Bone exposed (Zone II and III injuries): Rongeur to trim back

the bone, suture soft tissue together, and allow healing by

secondary intention.

IX. INFECTIONS

A. Paronychia:

1. This is an infection of the base of the nail, and can involve the

eponychium and perionychium. Infection may also spread under

the nail in advanced cases. Use a #11 scalpel to lift (incise) the

eponychium until pus is expressed. If there is no abscess,

dicloxacillin and soaks may be sufficient.

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B. Felon:

1. This is an infection of the finger pad due to minor penetrating

trauma. Because the skin is adherent to the bone (fibrous septa),

there is little room for swelling in this area. This leads to a great

deal of pain.

2. A felon is drained with an incision over the most prominent

portion of the abscess. The two recommended incisions are the

volar longitudinal or the high lateral. The “high” lateral is

made just inferior to the nail plate (to avoid the digital nerve) and

on the non-oppositional side of the finger (to avoid a scar that

would come into contact with the thumb). One should avoid

deep, lengthy incisions, which can cause the fingertip to become

unstable because they cut the fibrous septa.

3. Packing is placed and close follow-up is indicated. Antibiotics

are usually prescribed.

C. Flexor tenosynovitis:

1. A serious infection that can follow minor finger injuries in which

the tendon sheath is penetrated.

2. The tendon sheaths allow spread of the infection, and, in the case

of the thumb and little finger, communicate at the level of the

wrist in 50% of the population.

3. The classic presentation are “Kanavel’s signs”:

a. Tenderness along the tendon sheath.

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b. Digit held in slight flexion.

c. Pain with forced extension.

d. Diffuse “sausage like” swelling of the digit.

4. Initial treatment includes splinting, IV antibiotics, and prompt

surgical referral.

D. Deep space infections:

1. Represent 5-15% of hand infections.

2. Five types:

a. Web space: Significant swelling and pain in the web space

and distal palmar regions. Drainage via a longitudinal

incision in the web space.

b. Midpalmar space: Maximal tenderness in the mid palm

with loss of the normal concavity of the palm. Drainage in the

OR.

c. Dorsal subaponeurotic space: Dorsal hand swelling that is

tender to palpation. Requires hand consultation for drainage.

d. Thenar space: Tenderness and swelling within the thenar

space. Thumb is held in abduction. Requires hand

consultation for drainage.

e. Hypothenar space: Rare infection with swelling and

tenderness in the hypothenar area. Requires hand consultation

for drainage.

Deep space hand infections

X. OTHER CONDITIONS

A. De Quervain’s tenosynovitis:

1. Inflammatory condition of the first dorsal wrist compartment

containing the abductor pollicis longus and extensor pollicis

brevis.

2. The patient experiences pain over the radial portion of the wrist.

There is a marked increase in pain with the thumb folded into the

palm and the wrist ulnar deviated (Finkelstein test).

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3. Treatment is NSAIDs and immobilization with a thumb splint.

Injection with local anesthetic and steroid has a success rate of up

to 90%.

B. High pressure injection injuries:

1. Secondary to paint guns, grease guns, or diesel injectors. High

pressures deposit material deep into the finger, and possibly into

the tendon sheath.

2. Usually due to attempts to clear the “blocked” tool with the non-

dominant hand.

3. The initial injury often looks benign, so delayed presentations are

most common. Within hours, the finger starts to become painful,

and vasoconstriction may occur due to the inflammatory response

from the substance.

4. Treatment includes prophylactic antibiotics, tetanus, and incision

and drainage in the operating room for all significant injections.

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HAND AND WRIST INJURIES

PEARLS

1. Two-point discrimination to 4-5 mm implies normal digital nerve

sensory function. Digital nerve is superficial to the digital artery; hence,

an arterial injury would almost necessitate a nerve injury.

2. Radial nerve innervates extensor muscles. Median nerve is responsible

for thumb abduction and flexion of the wrist and IP joint of the thumb.

Ulnar nerve provides grip strength via innervation to the intrinsic hand

muscles.

3. Amides have two "i's" in the generic name: lidocaine, bupivacaine,

mepivacaine, and prilocaine. The esters have only one “i”: cocaine,

procaine, tetracaine, and benzocaine.

4. Allergies to local anesthetics are rare and usually due to preservatives.

If a patient reports an allergy to an amide, consider using an ester,

Benadryl, or a test dose of cardiac lidocaine (no preservative).

5. The scaphoid accounts for 60-80% of carpal bone fractures. It is occult

in 10-20% of initial radiographs, necessitating immobilization when

snuffbox tenderness is present. Avascular necrosis is a common

complication.

6. Triquetrum fracture is the second most common carpal bone fracture

and is best seen on the lateral radiograph.

7. Kienböck’s disease is avascular necrosis of the lunate.

8. Colles fracture is associated with median neuropathy.

9. Scapholunate dissociation is seen on the PA wrist film by noting the

Terry Thomas sign (>3 mm between scaphoid and lunate). Perilunate

dislocation maintains the normal lunate-radius association. Lunate

dislocation (“spilled teacup”) does not.

10. Rotational deformities following fractures to the phalanges or

metacarpals may result in significant hand disability.

11. Complications of partial tendon injuries include delayed rupture,

painful tenosynovitis, triggering, and contraction scarring.

12. Gamekeeper's thumb is an injury to the first MCP ulnar collateral

ligament due to hyperabduction.

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13. Consider a central slip rupture in any patient presenting with an injury

to the PIP joint. Missing this injury may result in a Boutonnière

deformity.

14. Felon is a deep space infection of the fingertip requiring surgical

decompression and antibiotics.

15. Kanavel's four cardinal signs of flexor tendon sheath infection are

finger flexion, diffuse finger swelling, tenderness localized to the flexor

tendon sheath, and pain on passive extension.

16. With human bites, cover for staph, strep, anaerobes AND Eikenella

corrodens.

17. With animal (dog/cat) bites, consider Pasteurella multocida in addition

to the usual oral flora.

18. Digit replantation is favored when the site of injury is between the PIP

and DIP, when the thumb is involved, when multiple digits are

involved, or in a child.

19. De Quervain's syndrome is a tenosynovitis of the first dorsal

compartment. Finkelstein test is nearly diagnostic.

20. High-pressure injection injuries are usually benign appearing, but

frequently harbor significant injury beneath the surface that requires

surgical debridement in many cases.

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Notes


REFERENCES

1. Simon RR, Sherman SC. Emergency Orthopedics. 6th Edition.

McGraw-Hill. New York. 2011.

08/13

Page 100

Upper and Lower Extremity Trauma

Wesley Eilbert, MD, FACEP

Clinical Associate Professor, Department of Emergency Medicine, University of Illinois at Chicago; Attending

Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago

Page 101

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Notes

Upper Extremity Trauma

UPPER EXTREMITY TRAUMA

I. EMERGENT COMPLICATIONS OF FRACTURES AND

DISLOCATIONS

A. Hemorrhage:

1. Primarily a concern with displaced pelvic fractures.

2. Also significant with femoral shaft fractures.

B. Open fractures/dislocations:

1. Open fractures are classified based on the size of the overlying

laceration, the amount of soft tissue damage, and the extent of

contamination.

2. Most will require debridement and irrigation in the OR. Some

small, open fractures (i.e., the phalanges) may be treated in the

ED.

3. Wound cultures are not necessary before antibiotics.

4. An IV first generation cephalosporin (cefazolin), with the

addition of an aminoglycoside for more severe/contaminated

cases is recommended.

5. Open dislocations also require irrigation (usually in the OR) and

IV antibiotics.

C. Neurovascular deficits:

1. The longer a deficit goes untreated, the longer it is likely to

persist and the greater the possibility that it will be irreversible.

Emergent reduction of the offending fracture or dislocation is

indicated.

D. Irreducible dislocations:

1. The longer a joint is dislocated, the more difficult it usually is to

reduce and the more likely it is to be unstable after reduction.

2. With hip dislocations, the risk of avascular necrosis of the

femoral head increases with the length of time of the dislocation.

E. Fat Embolism Syndrome

1. Caused by the presence of fat globules in the peripheral

circulation after long bone fractures - usually of the lower

extremity.

2. Respiratory distress and hypoxemia are the most common

manifestations, usually appearing 1-2 days after the injury.

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3. ARDS, mental status changes, thrombocytopenia and a petechial

rash may occur.

4. Diagnosis is clinical. 50% will have fat globules in the urine.

5. Treatment is supportive, with no specific therapy of proven

benefit.

F. Fracture blisters:

1. Occurs as a result of high energy injuries in areas of little skin

coverage over a fracture. The ankle, elbow, foot and knee are the

most common sites.

2. Are believed to be due to increased underlying tissue pressure,

and may be a marker of compartment syndrome.

3. Treat the same as thermal burn blisters.

G. Compartment syndromes:

1. Occur when tissue pressures is a fascia-enclosed compartment

rise to the point of compromising perfusion. Nerves and muscles

are most susceptible to the resultant ischemia.

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2. The clinical features of compartment syndromes can be

remembered as the six Ps:

a. Pain out of proportion to the injury is the earliest and most

significant finding.

b. Pain with passive stretch of the involved muscle group.

c. Paresis (or weakness) of the involved muscle group.

d. Paresthesias in the distribution of the nerve in the involved

compartment.

e. Pulses intact, unlike arterial injuries where pulses are absent.

f. Pressure (increased) in the involved compartment.

3. Diagnosis is made by measuring the compartment pressure.

Several commercial devices are available for this purpose.

a. Normal compartmental pressure is 0.

b. Compartmental pressures <15 mmHg are generally safe.

Pressures of 20-30 mmHg may cause damage if they persist

for several hours. Pressures of 30-40 mmHg are considered

grounds for fasciotomy.

c. Treatment is emergent fasciotomy of the involved muscle

group.

d. Complications include rhabdomyolysis and hyperkalemia

(especially with large muscle groups). If improperly treated,

loss of nerve and muscle function resulting in ischemic

contracture can occur.

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II. FRACTURE IMMOBILIZATION

A. Basic principles:

1. For injured joints, provide ample length above and below the

joint to immobilize it.

2. For midshaft fractures, immobilize the joint above and the joint

below the fracture.

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III. COMPLICATIONS OF FRACTURE IMMOBILIZATION

A. Casts:

1. Tight cast:

a. Pain is the first and most reliable symptom.

b. Bivalve the cast and the cast padding. The bivalved cast can

be replaced and held in place with an elastic bandage.

c. A new cast should then be placed in 1 to 3 days.

2. Cast sores:

a. Caused by indentation in the cast or a lack of padding.

b. Treat with cast removal and replacement with adequate

padding.

3. Cast cuts:

a. Occur at the cast ends.

b. Treat with bending the cast ends away from the skin with

pliers.

4. Itching under the cast:

a. Treat with oral antipruritic agents or blowing hot air under the

cast with a blow dryer.

b. DO NOT try to scratch under the cast (e.g., with a coat

hanger).

B. External fixation:

1. Pin site infections:

a. Release the skin around the pin with a scalpel, obtain

cultures, clean and irrigate and begin antibiotics (i.e., a first

generation cephalosporin).

2. Pin loosening in the bone frequently occurs and warrants

orthopedic consultation.

C. Internal fixation:

1. Infection is always a potential early complication, and more

common after treatment of an open fracture. Treatment involves

antibiotics and possible removal of the hardware.

IV. SEPTIC ARTHRITIS

A. More common in children under 3 years, the elderly, patients with

HIV and chronic debilitating illnesses and those taking

immunosuppressive medications, IV drug abusers and patients with

prosthetic joints, and after arthrocentesis.

B. Bacterial pathogens reach joint spaces by hematogenous spread

(most common), direct inoculation, and by direct spread from bony

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Notes


or soft tissue infection.

C. Staph aureus is the most common pathogen across all age groups.

D. Neisseria gonorrhea is a common cause in young adults, and usually

causes a polyarthritis.

E. Diagnosis:

1. Patients usually complain of a painful joint, made acutely worse

with movement. The joint is typically swollen and hot.

2. Fever, usually low grade, is present in the majority of cases.

3. Approximately 50% of patients have a serum WBC over 15,000.

An elevated ESR, while nonspecific, is present 90% of the time,

with mean values ranging from 68 to 82 mm/h.

4. Definite diagnosis is by arthrocentesis:

a. WBC is usually elevated - over 50,000 /mm3 in 50%-70% of

patients. The percentage of PMNs is usually higher than

85%.

b. Gram stain will show bacteria 50%-70% of the time.

c. Synovial fluid glucose is typical less than 50.

d. Synovial fluid culture will grow the responsible pathogen

approximately two-thirds of the time. Blood cultures are

positive in less than half of all cases.

F. Treatment:

1. Hospitalization for arthrotomy and irrigation of the joint and IV

antibiotics.

2. Empiric antibiotics:

a. Under 3 months: Nafcillin or oxacillin plus a 3rd

generation Cephalosporin.

b. 3 months to 14 years: Vancomycin plus a 3rd

generation

Cephalosporin.

c. 15 years to 39 years: Ceftriaxone plus Vancomycin.

d. Over 40 years: Nafcillin or Vancomycin.

3. Delay in diagnosis and treatment results in destruction of the

articular cartilage.

V. COMPLEX REGIONAL PAIN SYNDROMES

A. Type I (Reflex Sympathetic Dystrophy):

1. Occurs after prolonged immobilization or disuse (e.g., stroke).

B. Type II (Causalgia):

1. Occurs after peripheral nerve injury – frequently related to a

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Notes


fracture or gunshot wound.

C. Both types present with allodynia (pain from non noxious stimuli)

and a persistent burning or shooting pain.

D. Early signs include edema, warmth, and abnormal localized

sweating.

E. Later signs include periods of edema and warmth alternating with

cold, pale cyanotic skin.

F. Atrophy eventually occurs.

G. Treatment is highly controversial and may include regional

sympathetic blockade.

VI. DISLOCATIONS

A. Sternoclavicular:

1. Relatively rare.

2. Anterior dislocation is more common than posterior.

3. Posterior dislocations can be associated with life threatening

injuries in the mediastinum.

4. Pain with movement of the arm or lateral compression of the

shoulders.

5. Plain X-rays may be difficult to interpret; CT is the study of

choice.

6. Treat with closed reduction:

a. Posterior dislocations should ideally be reduced in the OR.

B. Acromioclavicular:

1. Most occur in young males.

2. Usually caused by a direct blow to the point of the shoulder while

the arm is adducted.

3. Non-displaced sprains and those with minimal displacement

(<5mm) can be treated with a sling.

4. Displaced injuries may require surgical repair, often for cosmetic

reasons.

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C. Shoulder (the most commonly dislocated major joint):

1. Anterior dislocations (95% of all shoulder locations):

a. The most common mechanism is a posterior-to-anterior force

applied to an abducted, extended arm.

b. Axillary nerve injury may occur (5-54%) with resultant

anesthesia over the lateral aspect of the shoulder and deltoid

weakness. Rotator cuff tears occur in 10-15%.

c. 11-50% will have a Hill-Sachs deformity of the humeral

head, 5% have a fracture of the anterior glenoid rim, and 10-

15% have an avulsion fracture of the greater tuberosity.

d. After reduction, immobilize with a sling and swathe.

e. Recurrence is very common (79-100%).

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2. Posterior dislocations (2% of all shoulder dislocations):

a. Classically caused by seizures or electrocution. Also, a fall on

an outstretched, adducted arm.

b. 50% are missed on initial evaluation.

c. Arm is held adducted and internally rotated.

d. Findings on AP X-rays can be subtle. Transscapular (“Y

view”) and axillary views confirm the diagnosis.

e. Fractures of the glenoid rim, greater and lesser tuberosity and

humeral may occur. Neurovascular injury is rare.

3. Luxatio erecta (rare):

a. Arm is locked over head.

b. Almost always associated with tears of the rotator cuff.

c. Injury to the axillary artery and brachial plexus may occur.

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Notes


D. Elbow:

1. Posterior dislocations (most common).

2. Cause by a fall on an outstretched hand.

3. Injuries of the brachial artery occur in up to 8% of cases.

4. Median nerve injury may also occur.

5. Most can be reduced in the ED, then discharged with a posterior

splint and sling.

6. Medial and lateral dislocations occur by the same mechanism as

posterior dislocations and have similar complications and

treatment.

7. Anterior dislocations (rare):

a. Frequently open.

b. Have a high incidence of vascular injury.

VII. FRACTURES

A. Clavicle:

1. The most commonly fractured bone during childhood.

2. 80% occur in the middle 1/3 of the bone.

3. Caused by a direct force applied to the lateral aspect of the

shoulder.

4. Most can be treated with a sling.

a. Associated neurovascular injury is rare.

b. Fractures of the distal clavicle with displacement may require

operative intervention

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Notes


B. Scapula:

1. Relatively rare.

2. Usually due to MVCs or falls.

3. 80% have associated injury to the lung, chest wall or shoulder

girdle.

4. Most are treated with a sling.

5. Surgical intervention may be necessary with displaced fractures

of the glenoid, acromion or coracoid.

C. Humerus:

1. Proximal humerus:

a. Typically occur in elderly, osteoporotic women.

b. Often due to a fall on an outstretched arm and hand.

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Notes


c. Most (85%) are minimally displaced.

d. Fracture lines tend to occur across old epiphyseal lines (i.e.,

the anatomic neck, the greater and lesser tuberosities and the

surgical neck).

e. Injury to the brachial plexus (most commonly the axillary

nerve) and axillary artery can occur, especially with displaced

fractures of the surgical neck.

f. Minimally displaced fractures (85%) can be treated with sling

and swathe.

g. Significantly displaced (>1cm) or angulated (>45º) fractures,

as well as fractures involving multiple parts of the proximal

humerus may require surgical repair.

h. Adhesive capsulitis (“frozen shoulder”) is the most common

complication. Avascular necrosis of the humeral head may

occur with displaced fractures of the anatomic neck.

2. Humeral shaft:

a. Typical occur in young, active men and elderly, osteoporotic

women.

b. Often due to a direct blow or a fall on an outstretched hand

with a torsional force.

c. The most common site of fracture is the middle third.

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Notes


d. Concomitant injury to the axillary artery or vein, or the radial,

ulnar or median nerves (most often the radial nerve) may

occur.

e. The vast majority are treated nonoperatively.

f. Most can be treated in the ED with a sling and swathe. Other

options include a “sugar-tong” splint or a hanging cast for

grossly displaced fractures.

D. Elbow:

1. Since many elbow fractures may be subtle, close inspection of

the lateral elbow film for abnormal fat pads (signifying

intraarticular hemorrhage) is very important. The presence of

any posterior fat pad or an abnormally large anterior fat pad (i.e.,

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Notes


the “sail sign”) usually indicates the presence of intraarticular

skeletal injury.

2. Several important neurovascular structures lie in close proximity

to the elbow joint (i.e., the brachial artery and the median, radial

and ulnar nerves). Evaluation of their function is important after

any elbow injury.

3. Intercondylar T or Y fractures (see picture below):

a. Caused by direct trauma to the elbow that drives the

olecranon against the humeral articular surface, splitting the

distal end.

b. Usually associated with severe soft tissue injury, and

notoriously difficult to treat.

c. Most require ORIF to reestablish articular surface congruity.

d. Patients with severe edema or displaced fractures should be

admitted.

4. Epicondyle fractures:

a. Lateral epicondyle fractures are extremely rare.

b. Medial epicondyle fractures in adults are usually caused by a

direct blow.

c. Use of forearm flexors causes pain.

d. Concomitant ulnar nerve injury can occur.

e. Minimally displaced fractures can be treated with a posterior

mold; displaced fractures may require operative repair;

intraarticular fragments are an indication for surgery.

5. Trochlea fractures usually occur in the setting of posterior elbow

dislocations. Displaced fractures should be treated with internal

fixation.

6. Capitellum fractures also occur primarily with posterior elbow

dislocations and frequently are associated with a radial head

fracture. As with the trochlea, displaced fractures should be

treated with internal fixation.

7. Radial head fractures are the most common fracture of the elbow.

a. Usually from a fall on an outstretched hand.

b. Often associated with other elbow injuries, like capitellum

fractures and elbow dislocations.

c. May be difficult to see on standard X-rays. May only be seen

as an abnormal radiocapitellar line or an abnormal fat pad.

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8. Olecranon fractures are most commonly the result of a direct

blow. They can also occur by a fall on an outstretched hand with

the elbow in flexion and the triceps contracting.

a. A significant percentage of these are open fractures.

b. Triceps function, as tested by elbow extension, is usually

impaired.

c. Associated ulnar nerve injury is common.

d. Best seen on lateral view elbow X-rays.

e. ED management involves immobilization with the elbow in

flexion.

f. Displaced fractures usually require ORIF.

E. Forearm:

1. The radius and ulna are joined together along their entire length

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Notes


by a tough interosseus membrane. Because of this close

relationship, injury to one bone usually has a direct effect on the

other (i.e., a displaced or angulated fracture of one bone causes a

dislocation at the proximal or distal radioulnar joint).

a. Nerve injuries are uncommon with most closed fractures.

b. Due to collateral circulation, vascular compromise is unlikely

if either the ulnar or radial artery remains intact.

c. Forearm fractures are at relatively high risk for compartment

syndrome.

d. Most displaced forearm fractures will require operative

reduction and internal or external fixation.

2. Ulnar shaft fractures (“nightstick fractures”):

a. Due to a direct blow.

b. Non displaced fractures can be treated with a long arm

posterior splint. Displaced fractures require ORIF.

i. X-rays of displaced fractures should be scrutinized for

any evidence of fracture or dislocation of the radius.

3. Monteggia fracture – dislocation:

a. Fracture of the ulnar shaft with a radial head dislocation. The

majority of the time, it’s a fracture of the proximal third of

the ulna with an anterior dislocation of the radial head.

b. Typically due to a forced pronation of the forearm during a

fall on an outstretched hand.

c. The radial head dislocation may be subtle and noted only as a

disruption of the radiocapitellar line.

d. Treatment is with ORIF.

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4. Galeazzi fracture:

a. Fracture of the distal third of the radial shaft with a

dislocation of the distal radioulnar joint.

b. Usually due to a fall on an outstretched hand with the forearm

pronated.

c. The ulna is displaced dorsally on the lateral view X-ray. The

majority will also have an ulnar styloid fracture.

i. Treatment is with ORIF.

VIII. SOFT TISSUE INJURIES

A. Tendonitis:

1. An overuse injury typically due to repetitive movements of the

involved tendon.

2. Occurs most commonly in the hand (flexor and extensor

tendons), the knee (patellar tendonitis), and the foot (flexor

hallucis longus, posterior tibialis and Achilles).

3. There is pain with active or passive movement of the tendon, and

pain with palpation of the tendon.

4. Treatment includes rest (including possible splinting), NSAIDs

and heat.

B. Calcific tendonitis:

1. A self limiting disorder characterized by calcium crystal

deposition within the tendons of the rotator cuff. Most common

in middle age.

2. Presents with pain or a “catching” sensation with shoulder

abduction. Symptoms typically last for 1-2 weeks.

3. Treatment includes NSAIDs, brief sling immobilization and

gentle range-of-motion activities to avoid adhesive capsulitis.

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C. Impingement Syndrome (includes subacromial bursitis, rotator cuff

tendonitis, supraspinatous tendonitis and painful arc syndrome):

1. Caused by repetitive overhead use of the arm resulting in

encroachment of the subacromial space by the humeral head.

2. Causes a dull pain over the anterolateral acromion that is

aggravated with overhead arm use.

3. Initial treatment includes avoidance of aggravating activities (i.e.,

overhead arm use), NSAIDs and gentle range-of-motion activities

to avoid adhesive capsulitis.

D. Rotator cuff tears:

1. May be acute (10%) or chronic (90%).

2. Acute tears are typically traumatic, usually due to forced

abduction with significant resistance (i.e., catching a falling

heavy object) or an anterior shoulder dislocation.

3. Chronic tears are almost always due to repeated compression of

the rotator cuff in the subacromial space caused by repetitive

overhead use of the arm.

4. Physical exam is the key to diagnosis.

5. Disuse atrophy may be present with chronic tears.

6. Weakness and pain are present with active abduction and external

rotation of the upper arm.

7. The drop arm test is positive if the patient is unable to hold or

lower a fully extended arm at 90 degrees shoulder abduction

without dropping it.

8. Treatment in the ED includes support with a sling, ice and

NSAIDs.

9. Complete tears (usually a MRI diagnosis) typically require

surgical repair.

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Notes


E. Bicep tendon rupture:

1. The vast majority occur in the proximal portion of the long head.

2. Typically occurs in middle-aged patients with a history of

chronic bicipital tenosynovitis.

3. Usually described as a pop or snap during contraction against

resistance.

4. Presents with pain over the anterior shoulder and a “Popeye”

appearance of the arm due to distal retraction of the muscle.

Active flexion is still possible due to the coracobrachialis and the

short head.

5. Treat with ice, sling and analgesics.

6. Surgical repair is usually indicated for young active patients.

F. Tennis elbow (epicondylitis):

1. Most involve the lateral epicondyle, though involvement of the

medial epicondyle can occur.

2. Seen in patients whose occupations require repetitive rotary

motion at the elbow, such as pipe fitters and carpenters.

3. Caused by tears in the aponeurosis of the involved tendons or

microavulsion fractures of the epicondyle.

4. The main symptom is a dull ache of the involved epicondyle,

aggravated by grasping or twisting motions.

5. Treat by splinting with the elbow flexed, heat and NSAIDs.

G. Olecranon bursitis:

1. Most commonly caused by repetitive minor trauma. May also be

due to gout or infection (i.e., septic bursitis).

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Notes


2. Presents with pain, tenderness and swelling over the olecranon.

3. Aspiration is diagnostic and therapeutic.

4. Management:

a. Septic bursitis:

i. Bursal aspirate WBC count usually > 10,000.

ii. Treat with antibiotic coverage for skin flora and MRSA.

b. Non infectious bursitis:

i. Bursal aspirate WBC count usually < 1,000.

ii. Treat with a compressive dressing, ice, NSAIDs and

avoidance of the inciting activity.

Page 122

Notes


UPPER EXTREMITY TRAUMA

PEARLS

1. Most open fractures require debridement and irrigation in the O.R.

2. The longer a joint remains dislocated, the more difficult it will be to

reduce and the more likely it is to be unstable after reduction.

3. Pain out of proportion to the injury is the earliest and most significant

finding with compartment syndromes.

4. Midshaft fractures of a bone should have the joint above and the joint

below the fracture included in the immobilization.

5. Staph aureus is the most common pathogen in septic arthritis across all

age groups. N. gonorrhea is a common cause in young adults.

6. Axillary nerve injury and rotator cuff tears may occur with anterior

shoulder dislocations.

7. Transscapular (“Y view”) and axillary views of the shoulder are

necessary to confirm the diagnosis of posterior shoulder dislocation.

8. Posterior dislocations of the elbow are the most common type, and may

have an associated brachial artery or median nerve injury.

9. Clavicle fractures, the most common fracture of childhood, can usually

be treated with a sling alone.

10. A high percentage (80%) of scapular fractures have an associated injury

to the lung, chest wall or shoulder girdle.

11. Proximal humerus fractures typically occur in elderly women and can

usually be treated with a sling and a swathe.

12. The radial nerve is the one most commonly injured with humeral shaft

fractures.

13. The presence of any posterior fat pad or an abnormally large anterior fat

pad on a lateral elbow X-ray indicates the presence of a fracture (radial

head fracture in adult, supracondylar fracture in children).

14. Radial head fractures, while the most common fracture of the elbow,

may be very difficult to detect on standard X-rays. Look for posterior

fat pad or anterior fat pad “sail sign".

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Notes


15. Olecranon fractures usually present with impairment of triceps function

and are frequently complicated by ulnar nerve injury.

16. Due to the interosseus membrane, a fracture of one of the paired

forearm bones usually results in dislocation of a common joint. These

fracture-dislocations are unstable and require ORIF.

17. The majority of rotator cuff tears are chronic and typically present with

weakness and pain on active abduction.

18. Bicep tendon ruptures usually occur during contraction against

resistance and present with a “Popeye” appearance (due to distal

retraction of the muscle) of the upper arm.

19. Tennis elbow (epicondylitis) occurs in patients whose occupations

require repetitive rotary motions of the elbow, and present with pain and

tenderness of the involved epicondyle.

Page 124

Notes


REFERENCES

1. Emergency Orthopedics The Extremities 5th

ed. Simon RR,

Sherman SC, Koenigsknecht SJ McGraw-Hill, 2007.

2. Handbook of Orthopedic Emergencies. Hart RG, Rittenberry TJ,

Uehara DT eds. Lippincott Raven Publishers, 1999.

3. Rosen’s Emergency Medicine. Concepts in Clinical Practice, 7th

Edition

2010, Mosby Elsevier.

4. The Sanford Guide to Antimicrobial Therapy 2011.

5. Tintinalli’s Emergency Medicine. A Comprehensive Study Guide. 7th

Edition.2011, McGraw Hill.

08/13

Page 125

Page 126

Notes

Lower Extremity Trauma

LOWER EXTREMITY TRAUMA

I. HIP & LOWER EXTREMITY

A. Avascular necrosis of the femoral head:

1. Ischemic bone death of the femoral head due to a compromise of

its blood supply.

2. Trauma is the #1 cause – usually after a femoral neck fracture or

hip dislocation. Other causes include: chronic corticosteroid

therapy, sickle cell disease, alcohol abuse, gout and lupus.

Twenty percent of cases are idiopathic.

3. Most common in relatively young males (30-50 years of age is

the peak incidence) and bilateral approximately 50% of the time.

4. Presents with increasing hip, thigh or knee pain with no recent

history of trauma. Decreased range of motion is noted on

physical exam.

5. X-ray shows decreased bone density of the femoral head initially,

followed by bone collapse and loss of head sphericity in the later

stages.

6. Treatment involves surgical removal of part of the core of the

femoral head, or total hip arthroplasty in more advanced cases.

B. Soft tissue injuries of the hip and thigh:

1. Bursitis:

a. Several bursae surround the hip and may become inflamed

due to overuse or excessive pressure. Treatment is with rest,

heat and NSAIDs.

b. Ischiogluteal bursitis often occurs in individuals who sit for

prolonged periods of time on hard surfaces. Tenderness is

present over the ischial tuberosity. In addition to the usual

conservative therapy, these patients should be advised to use

cushioned seating in the future.

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Notes


2. Muscle injuries:

a. Are more common in athletes, poorly conditioned people

engaging in strenuous exercise, and in cold weather.

b. Partial tears present with swelling, ecchymosis, tenderness

and a mild loss of strength.

c. Specific muscle groups:

i. Hamstring injuries are typically due to rapid acceleration

while running and present with sudden, intense pain in the

posterior thigh.

ii. Quadriceps injuries occur when the muscles contract

against the body’s weight (e.g., stumbling to avoid a fall)

and present with pain or an inability to extend the knee.

iii. Iliopsoas strain results from sudden hip flexion against

resistance, and often presents with intraabdominal (lower

quadrant) pain.

d. Partial tears usually respond to conservative therapy (i.e.,

NSAIDs and rest). Complete tears may require surgical

repair.

3. Tendon injuries of the hip (“groin pull”) result from a force to

abduct the hip during contraction of the adducting muscles.

a. Pain and tenderness is noted at the inferior pubic ramus and

ischial tuberosity.

b. Partial tears can be managed conservatively; complete tears

often require surgery.

C. Hip dislocations:

1. The most common cause is motor vehicle accident.

2. Approximately 50% are associated with fractures of the

acetabulum or the femoral head.

3. Need to reduce as soon as possible to decrease complications

(avascular necrosis of the femoral head).

4. Anterior dislocations (10% of all hip dislocations):

a. Patients present with hip flexed, abducted and externally

rotated.

b. May be anterosuperior (pubic) or anteroinferior (obturator).

c. Damage to the femoral artery, vein or nerve may occur, but is

unusual.

d. Treat with closed reduction, usually under general anesthesia.

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Notes


5. Central dislocations (relatively rare):

a. Femoral head is dislocated medially, with a badly fractured

acetabulum.

b. Surgical repair is required (not surprisingly).

6. Posterior dislocations (80-90% of hip dislocations):

a. The classic “dashboard injury”.

b. Presents with hip flexed, adducted and internally rotated.

c. Sciatic nerve injury occurs in approximately 10% of cases.

d. Treatment is with closed reduction, preferably under general

anesthesia.

7. Dislocation of hip prosthesis:

a. Most occur in the first 3 months postoperatively.

b. Reduction may cause damage to the prothesis and should be

attempted only after orthopedic consultation.

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Notes


D. Fractures of the femur:

1. Femoral head fractures:

a. Usually occur with hip dislocation (10-16% of posterior hip

dislocations will have a femoral head fracture).

b. Post-traumatic arthritis and aseptic necrosis of the femoral

head are potential complications.

2. Femoral neck fracture:

a. Most common in elderly women, usually with relatively

minor trauma.

b. Some nondisplaced fractures may be subtle and require MRI

or bone scan for diagnosis.

c. Avascular necrosis of the femoral head in 15% of

nondisplaced fractures and 90% of completely displaced

fractures.

d. All displaced fractures will require surgery.

3. Intertochanteric fracture:

a. Fracture line is between the greater and lesser trochanter.

b. Avascular necrosis is rare.

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Notes


c. The vast majority will require some form of internal fixation.

4. Trochanteric fractures:

a. Greater trochanter:

i. In the young, this is usually secondary to forceful

contraction of the gluteus medius with epiphyseal

separation.

ii. In adults, this usually results from direct trauma to the

area.

iii. Usually treated conservatively with limited weight

bearing.

iv. Surgical fixation is indicated if displaced more than 1 cm.

b. Lesser trochanter:

i. Usually occurs in young athletes.

ii. Caused by powerful contraction of the iliopsoas.

iii. Presents with pain and tenderness in the femoral triangle.

iv. Most can be treated conservatively with gradual weight

bearing.

v. Surgical fixation is indicated if displaced > 2 cm.

c. Subtrochanteric and femoral shaft fractures:

i. These may cause significant blood loss with hematoma

formation.

ii. Shaft fractures are primarily in young patients who have

sustained high energy trauma and have a high incidence

of concomitant injuries.

iii. Fat emboli syndrome is a concern with shaft fractures.

iv. Treat initially with a traction splint and, ultimately, ORIF.

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Notes


E. Knee injuries:

1. Dislocations:

a. The knee joint:

i. A true orthopedic emergency.

ii. The majority are anterior or posterior. Can also be lateral,

medial or rotary.

iii. 30–40% have popliteal artery injury. While there is no

consensus as to the diagnostic approach to detect popliteal

artery injury, some type of vascular assessment must be

done (i.e., arteriography, ultrasound, arterial-brachial

indicis, etc.).

iv. 35% have peroneal nerve injury.

v. Some dislocations will reduce spontaneously prior to

presentation. Stress radiographs or arthrograms may aid in

the diagnosis.

vi. Immediate reduction is indicated.

b. The patella:

i. The vast majority are lateral.

ii. Risk factors include a high riding patella (patella alta) and

excessive genu valgum (“knock knees”).

iii. The typical patient is an obese female who experiences a

sudden twisting on an extended or slightly flexed knee.

iv. Reduce with knee extended and hip flexed, and then

immobilize the knee in full extension.

v. Superior or intra-articular dislocations warrant orthopedic

consultation.

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Notes


2. Fractures:

a. The Ottawa Knee Rules: X-rays are necessary if one of the

five conditions are present:

i. Age older than 55 years.

ii. Inability to transfer weight from one foot to the next, four

times at the time of injury and in the emergency

department.

iii. Inability to flex the knee to 90 degrees.

iv. Patellar tenderness with no other bony tenderness.

v. Tenderness of the fibular head.

b. Femoral condyle (supracondylar, intercondylar, unicondylar):

i. Usually secondary to direct trauma.

ii. Associated neurovascular injury is relatively uncommon.

c. Tibial spine:

i. Usually present with associated damage to the cruciate

ligaments.

ii. Incomplete or nondisplaced fractures should be

immobilized in extension. Completely displaced fractures

require open reduction.

d. Tibial tuberosity:

i. The insertion site for the quadriceps.

ii. Caused by a sudden force to flex the knee while

quadriceps is contracted.

iii. If tubercle is incompletely avulsed, can immobilize

extension. Complete avulsions require operative repair.

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Notes


e. Tibial plateaus:

i. Caused by direct force (most commonly to the lateral

knee that compresses the femoral condyle into the

articulating surface of the tibia).

ii. More common in the elderly.

iii. 7–15% will have associated ligamentous injury.

iv. Can be difficult to detect. Oblique views may be helpful.

Sometimes only a fat-fluid level is present on X-ray.

v. If fracture fragment is depressed 5 mm or more, surgery is

indicated.

f. Patellar fractures:

i. Can be caused by direct trauma or contraction of the

quadriceps during violent flexion of the knee.

ii. X-ray findings can be confused with a secondary patellar

ossification site (usually in the superolateral aspect).

These anomalies are usually present bilaterally.

iii. Other than small avulsion fractures of the rim, these are

considered intra-articular fractures.

iv. If overlying skin is open, these require debridement and

irrigation in the OR.

v. Non-displaced transverse fractures can be treated

conservatively with immobilization in extension.

vi. Displaced fractures require open reduction and internal

fixation. Severely comminuted fracture may warrant total

patellectomy.

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Notes


3. Ligamentous injuries:

a. Most present with hemarthroses.

b. 1st degree sprain: no instability but pain with stress testing.

c. 2nd

degree sprain: pain and mild instability.

d. 3rd

degree sprain: marked instability (complete ligament

disruption).

e. Medial collateral ligament (MCL):

i. Caused by a valgus force to knee.

ii. If laxity is felt with valgus stress with knee in 30 degree

flexion, check for laxity while in full extension. If this is

present, damage to other structures (i.e., cruciate

ligaments) is present.

iii. The “terrible triad”: rupture of ACL and MCL with tear of

the medial meniscus.

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Notes


f. Lateral collateral ligament (LCL):

i. Isolated injuries to this are uncommon.

ii. Caused by a varus stress.

iii. May have associated common peroneal nerve injury.

g. Anterior cruciate ligament (ACL):

i. Usually a non-contact injury. Often caused by stopping

abruptly or making a sharp turn while running.

ii. Patients frequently hear a “pop,” then knee gives out.

iii. Diagnosed by a positive anterior drawer (not very

sensitive) or Lachman (more sensitive).

h. Posterior cruciate ligament (PCL):

i. Not a commonly torn ligament.

ii. Usually caused by pretibial trauma to the hyperflexed

knee (as in the “dashboard injury”).

iii. Diagnosed by a positive posterior drawer sign.

i. Isolated ligament injuries can be treated as follows:

i. First degree: ice, compressive wrap, non weight bearing.

ii. Second degree: ice, immobilization, non weight bearing.

iii. Third degree: orthopedic consultation, some may not

require immediate intervention.

4. Meniscal injuries:

a. Can occur primarily or with associated ligamentous injuries.

b. May present with locking of the joint during flexion or

extension, clicking or popping during activity or effusion

after activity.

c. A positive McMurray or Apley test may be present.

d. Arthroscopy or MRI is used for definitive diagnosis.

5. Quadriceps/patellar tendon rupture:

a. Caused by forceful contraction of quadriceps or falling on a

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Notes


flexed knee.

b. Risk factors include chronic steroid use, hyperparathyroidism,

and long-term dialysis.

c. Complete ruptures require surgical repair.

F. Distal leg:

1. Fractures of the tibial shaft:

a. Have a high rate of open fractures and healing complications.

b. All displaced fractures require hospitalization for circulatory

observation due to high incidence of compartment

syndromes.

c. Closed fractures with minimal or no displacement (e.g., a

spiral fracture secondary to excessive rotation while skiing)

can initially be managed with a long leg splint with 10 to 20

degrees of knee flexion.

2. Fractures of the fibular shaft:

a. Isolated fractures of the fibular shaft are uncommon.

b. Usual mechanism is a direct blow.

c. Fracture of head or neck may injure common peroneal nerve.

d. Treatment is symptomatic. A short leg walking cast may be

used for comfort.

e. Maisonneuve fracture:

i. Rupture of deltoid ligaments of the ankle or distal tibial

fracture with a proximal fibular fracture.

ii. Caused by forceful external rotation of the foot.

iii. Most can be treated with cast immobilization. Any ankle

instability warrants operative repair.

3. Shin splints:

a. Exercise-induced pain over the medial aspect of the tibia.

b. Often occurs in runners, military recruits, and those with flat

feet.

c. May be a repetitive trauma induced periostitis of the tibia.

d. Diagnosis is made clinically.

e. A bone scan may be performed to rule out stress fracture.

f. Treatment is avoidance of the repetitive trauma.

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Notes


G. The ankle:

1. Inversion injuries typically cause sprains, while eversion injuries

characteristically cause fractures.

a. 75% of all ankle injuries are sprains and 90% of these involve

the lateral ligaments. The anterior talofibular ligament is the

most commonly injured lateral ligament.

b. Standard X-ray views include AP, lateral and mortise (15

degree of internal rotation) views.

c. The ankle can be thought of as a ring consisting of the tibia,

fibula and talus bound together by medial (deltoid) ligaments,

lateral ligaments and tibiofibular ligaments. Any two breaks

in the ring (e.g., a fracture of both malleoli, a malleolus and a

ligament, or two ligaments) leaves the joint unstable.

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Notes


2. Ligamentous injuries:

a. Lateral collateral ligaments:

i. Usually injured by internal torsion.

ii. Laxity on anterior drawer testing of the ankle indicates

tear of the anterior talofibular ligament.

iii. Laxity noted with inversion testing indicates a tear of the

anterior talofibular and caneofibular

ligaments.

b. Medial collateral ligaments:

i. Usually injured by eversion stress.

ii. Almost always associated with fracture of the fibula

(Maisonneuve) or separation of the tibiofibular

syndesmosis.

c. Treatment:

i. 1st degree sprains can be treated with rest, ice,

compression dressing and elevation.

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Notes


ii. 2nd

degree sprains require immobilization and non weight

bearing.

iii. 3rd

degree sprains warrant immobilization and orthopedic

consultation.

3. Fractures:

a. The Ottawa Ankle Rules: X-rays are necessary if there is pain

in the malleolar region and any of the following findings:

i. Bone tenderness at the posterior edge of the distal 6 cm or

the tip of the lateral malleolus.

ii. Bone tenderness at the posterior edge of the distal 6 cm or

the tip of the medial malleolus.

iii. The patient is unable to bear weight for at least four steps

both immediately after the injury and in the emergency

department.

b. Often occur with associated ligamentous injury.

c. Definitive treatment (open versus closed) is variable with the

primary goal being stability of the talus within the joint.

4. Dislocations (not a common injury):

a. May be posterior (most common), anterior, lateral or

superior.

b. Most are associated with malleolar fractures and almost half

are open dislocations.

c. Emergent reduction is indicated.

d. There is a relatively high incidence of vascular injury and

avascular necrosis of the talus.

5. Achilles tendon rupture:

a. Most commonly in middle-aged men engaging in athletics.

b. May be due to forceful dorsiflexion of the ankle or direct

blows to a taut tendon.

c. Often described as being “kicked in the back of the leg”.

d. Even with complete rupture, some active plantar flexion may

be present.

e. A Thompson’s test (calf squeeze) aids in the diagnosis.

f. Complete ruptures should be repaired surgically.

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Notes


H. The foot:

1. The forefoot: phalanges and metatarsals.

2. The midfoot: the cuneiforms, cuboid and navicula.

3. The hindfoot: calcaneus and talus.

4. Calcaneal fractures:

a. Usually secondary to a fall from a height.

b. Bilateral 10 – 20% of the time. Associated lumbar spine

injuries 10% of the time and other injuries to the involved

extremity 26% of the time.

c. Most fractures are through the body.

d. May see a decrease in Bohler’s angle on lateral film, and

special calcaneal views may aid in the diagnosis.

e. Notoriously difficult to treat, often with long term morbidity.

5. Talus fractures:

a. Often secondary to hyperdorsiflexion of the foot.

b. The lateral view of the foot is most helpful.

c. At risk for avascular necrosis, especially if fracture through

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Notes


neck with dislocation of the body.

d. Usually require early reduction if any displacement is present.

6. Midfoot fracture:

a. A rare occurrence. Usually involve the navicula.

b. Usually due to direct trauma (crush injuries).

c. Non displaced fractures can be treated with a walking cast;

displaced fractures require orthopedic consultation.

7. Tarsometatarsal (Lisfranc) fracture/dislocations:

a. Can be caused by direct (car running over foot) or indirect

(excessive axial load onto plantar flexed foot) trauma.

b. Very often associated with fracture of the base of the second

metatarsal (this is where forefoot “locks into” the mid foot).

c. Most reliable radiographic finding is separation of the first

and second metatarsals.

d. Notoriously difficult to reduce.

e. Admission for observation for circulatory compromise of the

foot (a major complication) is indicated.

8. Metatarsal fractures:

a. Stress fractures of the 2nd

and 3rd

metatarsals occur with

frequent “pushing off” (i.e., “the march fracture”) since they

are subjected to the greatest stress during this activity.

b. Other fractures are secondary to direct blows or twisting type

injuries.

c. Can usually be treated conservatively with a short leg splint

and non weight bearing.

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Notes


9. Fractures of the base of the 5th

metatarsal: the most common type

of metatarsal fracture.

a. Tuberosity fracture:

i. Secondary to inversion, with avulsion of the peroneus

brevis insertion.

ii. Can be treated conservatively with immobilization and

non weight bearing.

b. Jones fracture:

i. Now thought not to be an avulsion fracture.

ii. Fracture line is distal to the insertion of the peroneus

brevis.

iii. Usually treated with screw fixation.

10. Phalangeal fractures:

a. Usually secondary to direct (crushing) trauma.

b. If displaced, can usually be reduced after digital anesthesia.

c. Fractures of the big toe may require more immobilization

(i.e., walking boot cast) given its increased role in weight

bearing.

11. Soft tissue injuries:

a. Plantar fasciitis is an overuse syndrome caused by repetitive

stretching of the plantar fascia, commonly occurring in

runners.

i. Presents with pain in arch or heel worsened by stair

climbing and tenderness along medial edge of fascia.

ii. Usually responds to rest, NSAIDs and possibly padded

heel cups.

b. Turf toe is a sprain or tear of the first MTP joint capsule

caused by repetitive pushing off from a hard surface (i.e.,

repeated hyperextension of the great toe).

i. Initial treatment is conservative and the use of a

supportive shoe to lessen the hyperextension.

12. Calcaneal spurs:

a. Occur on the plantar aspect of the calcaneus at the attachment

of the plantar aponeurosis.

b. Presents as heel pain with walking or standing and local

tenderness to palpation.

c. Treated with rest, NSAIDs and padded heel cups.

13. Puncture wounds:

a. 8-15% progress to cellulitis or localized abscess.

b. Associated osteomyelitis is due to pseudomonas aeruginosa

Page 143

Notes


93% of the time.

c. Surgical debridement and parenteral antipseudomonal

antibiotics are indicated if osteomyelitis is present.

Page 144

Notes


LOWER EXTREMITY TRAUMA

PEARLS

1. 80-90% of hip dislocations are posterior and often secondary to motor

vehicle accidents. A significant percentage (10%) of these will have

associated sciatic nerve injury.

2. Femoral head fractures commonly occur with hip dislocations.

3. Trauma (usually femoral neck fracture or hip dislocations) is the #1

cause of avascular necrosis of the femoral head.

4. Femoral shaft fractures can cause a large amount of blood loss and

hematoma formation.

5. A high percentage of knee dislocations have an associated popliteal

artery injury. Arteriography after knee dislocation is generally warranted.

6. Most patellar dislocations can be reduced with the knee extended and hip

flexed.

7. Tibial plateau fractures depressed 5 mm or more require surgical repair.

8. Tears of medial collateral ligament are frequently associated with

concomitant injury to the anterior cruciate ligament and the medial

meniscus.

9. Isolated injuries to the anterior cruciate ligament are often non-contact

injuries.

10. Any patient unable to actively extend his/her knee after falling on it

while flexed should be evaluated for possible quadriceps/patellar tendon

rupture.

11. Fractures of the tibial shaft have a high incidence of compartment

syndromes and healing complications.

12. A Maisonneuve fracture is a rupture of the deltoid ligaments of the ankle

or a fracture of the distal tibia with a proximal fibular fracture.

13. Inversion ankle injuries typically cause ligament sprains, while eversion

injuries characteristically cause fractures.

14. The majority of ankle injuries are ligament sprains, and the vast majority

of these involve the lateral ligaments.

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Notes


15. Ankle dislocations have a relative high incidence of vascular injury and

avascular necrosis of the talus.

16. Even with complete Achilles tendon rupture, the patient may have some

active plantar flexion.

17. Calcaneal fractures are often bilateral (10 – 20%), associated with

lumbar spine injuries (10%) and other injuries to the involved extremity

(26%).

18. Tarsometatarsal (Listranc) fracture/dislocations are very often associated

with a fracture of the base of the second metatarsal. Frequently, a

separation of the first and second metatarsals is seen on X-ray.

19. A tuberosity fracture of the base of the fifth metatarsal is due to avulsion

of the peroneus brevis insertion.

20. A Jones fracture of the fifth metatarsal is distal to the peroneus brevis

insertion and is not thought to be an avulsion fracture.

21. Metatarsal stress fracture (i.e., “March fractures”) usually involves the

second or third metatarsals.

22. Osteomyelitis in the foot secondary to puncture wounds is caused by

Pseudonomas aeruginosa the majority of the time.

Page 146

Notes


REFERENCES

1. Clinical Procedures in Emergency Medicine. 5th Edition. 2010,

Saunders Elsevier.

2. Emergency Medicine. The Core Curriculum. 1998, Lippincott-Raven

Publishers

3. Emergency Orthopedics. The Extremities. 5th Edition. 2007, McGraw-

Hill

4. Rosen’s Emergency Medicine. Concepts in Clinical Practice, 7th

Edition

2010, Mosby Elsevier.

5. Textbook of Pediatric Emergency Medicine. 6th Edition. 2010,

Lippincott, Williams, and Wilkins

6. Tintinalli’s Emergency Medicine. A Comprehensive Study Guide. 7th

Edition.2011, McGraw Hill.

08/13

Page 147

Page 148

Urology/GU Trauma

Wesley Eilbert, MD, FACEP

Clinical Associate Professor, Department of Emergency Medicine, University of Illinois at Chicago; Attending

Physician, Department of Emergency Medicine, University of Illinois Hospital and Health Sciences System, Chicago

Page 149

Page 150

Notes

Urology/GU Trauma

UROLOGY/GU TRAUMA

I. NON-TRAUMATIC PROBLEMS

A. Paraphimosis:

1. The inability to reduce the proximal foreskin over the glans,

resulting in distal venous congestion. This can progress to

arterial compromise, gangrene, and amputation from the foreskin

acting as a tourniquet around the glans.

2. Most common cause is a circular scar in the prepuce from

preexisting phimosis which is then retracted behind the glans

cutting off blood supply.

3. This is a true urologic emergency.

4. May be iatrogenic (i.e., foreskin not reduced after placement of a

urinary catheter).

5. Attempt to reduce the foreskin often requires penile nerve block

with 1% lidocaine (without epinephrine) to be successful.

6. Techniques to reduce edema of the glans:

a. Place glans in rubber glove filled with ice water.

b. Manual compression of the glans.

c. Several punctures of the glans with a small needle to drain

edema fluid.

7. If all else fails, the constricting band may be released by cutting a

small dorsal slit or ultimately by circumcision.

B. Phimosis:

1. A constriction of the foreskin, with the inability to retract it over

the glans.

2. Usually not a true urologic emergency.

3. Often confused with:

a. Balanitis.

b. Balanoposthitis.

c. Paraphimosis.

4. Physiologic phimosis occurs in 96% of uncircumcised newborns,

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and resolves itself by the age of 3.

5. Caused by infection, poor hygiene or trauma that results in

scarring.

6. If causing urinary outlet obstruction, you can dilate the meatus

with forceps.

7. Topical steroids have been proven beneficial.

8. Definitive treatment is circumcision.

C. Priapism:

1. A prolonged, often painful erection occurring without sexual

stimulation.

2. CBC and coagulation studied are indicated.

3. Immediate IV fluids and analgesia are given.

4. High flow priapism (less common) is caused by increased

arterial blood flow due to an arterial-cavernosal shunt usually

formed as a result of a groin or straddle injury.

a. This type does not cause ischemia; is usually painless and is

at low risk for permanent complications.

b. Can usually be treated with arterial embolization.

5. Low flow priapism is due to a decreased penile venous outflow.

a. Causes include sickle cell disease (the most common cause in

children), leukemic infiltration, spinal trauma, medications

(usually phenothiazine, SSRI or antihypertensives) and illicit

drugs (cocaine and marijuana). In adults, usually it is

idiopathic.

b. Corpus cavernosum is hard but the glans and corpus

spongiosum is soft. (Pathophysiology usually involves

sludging of RBCs in the corpus cavernosum.)

c. Treatment in sickle cell patients includes oxygen,

alkalinization, hydration, pain control and, ultimately,

exchange transfusion.

d. Other treatment options include local anesthesia through a

dorsal penile nerve block, parenterally administered

vasodilators such as terbutaline or hydralazine, and

cavernosal aspiration and irrigation – often with

phenylephrine or epinephrine added to the irrigation solution.

e. If priapism recurs after aspiration of blood, surgical shunting

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is needed.

f. If left untreated, corporal fibrosis and erectile dysfunction

may result.

g. Treatment within 4-6 hours = low morbidity.

h. Treatment after 24 hours = high morbidity.

D. Hydrocele:

1. A collection of fluid in the tunica vaginalis.

2. May be communicating – open to the peritoneal cavity, or

noncommunicating.

3. Many are present at birth and may worsen with crying.

Congenital hydroceles often resolve spontaneously by age 18

months.

4. Reactive hydroceles may be caused by testicular tumors, torsion

or epididymitis/orchitis.

E. Varicocele:

1. Due to abnormal dilatation of the spermatic cord veins.

2. Often described as a “bag of worms” palpable superior and

posterior to the testicle, and more pronounced in the upright

position.

3. 85% - 95% are left-sided.

4. Intraabdominal pathology causing compression of the inferior

vena cava should be suspected with right-sided varicoceles.

5. Surgical resection may be performed for symptomatic relief.

F. Testicular torsion:

1. Peak incidence at 13 years; however, there is a bimodal age

distribution between the teens and the first year of life. Torsion

can occur at any age.

2. At-risk testes align in a horizontal rather than a vertical axis (i.e.,

the “bell-clapper deformity”— see Figure 3). This is caused by

malformed tunica vaginalis in infants and incomplete attachment

of the gubernaculum in adults. Both of these malformations leave

the testicles free to rotate.

3. Classically a sudden onset of lower abdominal or testicular pain.

4. Involved testicle is firm, tender, swollen and higher in the

scrotum than the other testicle.

5. Cremasteric reflex is typically absent, which is highly sensitive

for testicular torsion. SURGICAL EXPLORATION SHOULD

NOT BE DELAYED FOR DIAGNOSTIC STUDIES,

especially if symptoms are <12 hours old.

6. Newer color Doppler ultrasound has sensitivities of 90%-100%

and specificity of 100%; helpful in indeterminate cases.

7. Manual detorsion may be attempted by “dialing out” or “opening

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a book” (i.e., medial to lateral direction). This is done for acute

pain relief and some return of blood flow; it is not a definitive

treatment and surgery is still indicated even if successful.

8. Testicular salvage rate of >90% if de-torsed within 4 hours, 20%

within 12 hours, and almost 0% if de-torsed after 24 hours.

Figure 3: “Bell-clapper” deformity

G. Torsion of the testicular appendage:

1. Torsion of the appendix testis, a remnant of the Müllerian duct.

2. Average age is 10 years.

3. Sudden onset of testicular pain, but usually more gradual than

testicular torsion. A tender nodule may be palpated.

4. The blue dot sign may be seen on cranial portion of testes or

epididymis.

5. Cremasteric reflex normally present, helps to differentiate

from testicular torsion.

6. Doppler ultrasound, or alternatively, nuclear scintigraphy can be

used to confirm the diagnosis.

7. Treatment is conservative. The appendages will autoamputate

within a week.

H. Epididymitis (Inclusion for its similarity in presentation to torsion):

1. Rarely occurs before puberty. Caused by retrograde spread of

urethral and bladder pathogens.

2. Under age 35, chlamydia and gonorrhea are the main

pathogens. Over age 35, it’s E. coli.

3. Presents with lower abdominal and testicular pain, usually with a

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low grade fever. Pain may be relieved with scrotal elevation

(Prehn’s sign).

a. Can be difficult to distinguish from torsion. Negative Prehn’s

sign can help to distinguish from epidydimitis but is

insensitive. (see Figure 4)

b. Erythema and edema of the hemiscrotum may be noted. The

epididymis is usually swollen and tender. A reactive

hydrocele may be present.

4. UA, urine culture, and urethral STD cultures should be sent.

5. UA may not show evidence of infection.

6. Empiric treatment:

a. If presumed sexually acquired: single dose ceftriaxone plus

doxycycline for 10 days.

b. If presumed not sexually acquired: Cipro/levofloxacin for 10

days OR ofloxacin for 10 days.

c. Also: bed rest, scrotal elevation (athletic supporter), ice

packs, NSAIDs, urologic follow-up.

7. Complications: orchitis, abscess formation and infertility.

Figure 4: Torsion

versus epidydmitis

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I. Acute urinary retention:

1. Most common cause is prostatic hypertrophy. Other causes

include: multiple sclerosis, diabetes, urethral stricture, spinal cord

compression and drugs (antihistamines, anticholinergics, TCAs

and sympathomimetics).

2. “An intact sensory exam, anal sphincter, and bulbocavernosus

reflex differentiates chronic outlet obstruction from the sensory

or motor neurogenic bladder” (Tintinalli, 2004).

3. A normal-sized prostate on physical exam does not eliminate it as

a cause of obstruction.

4. To decompress the bladder, start with a 16Fr or 18Fr catheter.

If the obstruction is at the level of the prostate, a 16Fr Coude-

catheter can be tried. Ultimately, a suprapubic cystostomy may

be needed.

5. BUN/Cr and UA should be sent to check renal function and for

infection respectively.

6. “Spontaneous, complete drainage of a distended bladder can be

accomplished rapidly without the need for repeated clamping of

the catheter” (Tintinalli, 2004). Rapid decompression may cause

transient gross hematuria or hypotension, but this is usually

insignificant.

7. Postobstructive diuresis may occur. For this reason, patients

should have urinary output measured for 4-6 hours after

catheterization. Postobstructive diuresis warrants admission for

IVF and monitoring of electrolytes.

J. Fournier’s gangrene:

1. A necrotizing fasciitis of the perineum, usually involving the

penis and scrotum, but can also affect women.

2. Main risk factor is immunosuppression, especially diabetes.

3. Often proceeded by perineal trauma (i.e., scratches, burns, anal

intercourse).

4. Perineal and genital pain and itching is followed by fever, toxic

appearance and perineal swelling. Subcutaneous crepitance is

often present. CT may show edema and gas in scrotal skin.

5. A polymicrobial infection, usually aerobic and anaerobic, with

bacteria from the distal colon.

6. Treat with aggressive fluid resuscitation, appropriate antibiotics

(ticarcillin/clavulanate or ampicillin/sulbactam or piperacillin

plus gentamicin plus metronidazole), and, most importantly,

immediate urologic consultation and surgical debridement.

7. Elasticity of genital skin allows for surgical closure even if 60%

of skin is lost; more than 60% loss with require grafts.

8. Mortality rate of 13-22%.

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K. Renal calculi (kidney stones):

1. Incidence may be as high as 10% -12%. Three times more

common in males.

2. Usually occur in between the ages of 20 and 50 years.

3. Risk factors include: arid climates, family history, sedentary

lifestyle, a history of hyperparathyroidism, milk-alkali syndrome,

sarcoidosis, history of recurrent UTIs, and HIV medications

(protease inhibitors).

a. Types of stones:

i. Calcium. Calcium oxalate or calcium phosphate stones

comprise 75% of all kidney stones.

ii. Struvite (magnesium-ammonium-phosphate) stones

account for 15% of stones. These occur exclusively in

patients with UTIs caused by urea-splitting organisms.

iii. Uric acid stones make up 10% of renal calculi. These are

radiolucent.

iv. Cystine stones are rare and due to inborn errors in

metabolism.

b. Clinical features:

i. Classically, a sudden onset of a colicky pain in the flank,

radiating laterally around the abdomen and into the groin.

Pain may radiate to the testicle. Nausea and vomiting are

common.

c. Patient unable to find a position of comfort - writhing in bed.

d. Abdomen is minimally tender, if at all.

4. Diagnostic studies:

a. Hematuria, gross or microscopic is present in 85% of cases.

b. Urinary pH >7.6 many indicate the presence of urea-splitting

organisms (struvite stones).

c. “Unenhanced helical CT is best radiographical test for

diagnosing urolithiasis in patients with acute flank pain”

(Miller, 2007). Sensitivity and specificity >94%.

d. Intravenous pyelogram (IVP) is not as sensitive as CT, but

has the advantage of evaluating kidney function.

i. The most reliable and earliest indicator of a calculus is a

delay in the appearance of the contrast on the affected

side.

ii. Other signs of a calculus: visualization of the entire ureter

(columnization), dilatation of the collecting system,

extravasation of the contrast out of the collecting system.

e. Ultrasound causes no radiation exposure, making it the study

of choice in pregnant patients. It is only modestly sensitive

and specific for kidney stones, though 98% sensitive for

detecting hydronephrosis.

f. Abdominal plain films can determine whether stones are

radio-opaque and can be used to monitor disease activity.

5. Treatment should be with NSAIDs (which also help decrease

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ureteral spasm) and narcotics.

a. Indications for admission include: obstruction with infection,

uncontrolled pain, persistent vomiting, urinary extravasation

out of the collecting system, and a solitary or transplanted

kidney.

b. Outpatient treatment includes increased fluid intake and

straining of urine. If the stone is obtained, it should be taken

to the urologist for analysis.

c. The most important predictor of stone passage is its size.

90% of stones <4 mm pass spontaneously, while only 10% of

those >6 mm do. Stones in the distal ureter have a greater

likelihood of passage than those more proximal.

d. Shock wave lithotripsy can be used to fragment stones <2 cm

but is contraindicated for staghorn calculi.

e. Ureteroscopy with instruments for fragmentation or removal

can be used where lithotripsy fails.

f. Percutaneous nephrolithotomy can be used to create an access

tract into the collecting system but is invasive and used only

as a last resort.

g. Alpha blockers with corticosteroids have been investigated

as agents to aid expulsion of stones based on the idea that

they inhibit basal ureteral tone and decrease peristaltic

frequency.

h. Irreversible renal damage begins to occur if obstruction

persists beyond two weeks.

L. Urinary tract infections (UTIs):

1. Uncomplicated UTIs occur in otherwise healthy, reproductive –

aged women who are not pregnant. E. coli is the pathogen in

>80% of cases.

2. Complicated UTIs occur in males, and females with risk factors

for complicated infections (i.e., premenarchal, post menopausal,

pregnant, diabetic or with structural abnormalities) These patients

are frequently infected with more resistant organisms.

3. The diagnostic standard is 105 CFUs/ml on culture.

4. On urinalysis, the presence of > 5 WBCs/hpf on a centrifuged

specimen is abnormal.

5. Antimicrobial agents should be chosen according to local

resistance patterns. In general, nitrofurantoin, quinolones and 3rd

generation cephalosporins have the lowest resistance rates.

6. Uncomplicated cystitis can be treated with 3 day antibiotic

therapy. A urine culture does not need to be sent.

7. Complicated cystitis and all pyelonephritis should be treated with

10- 14 days of antibiotics, and a urine culture should be sent.

8. Indications for inpatient treatment of pyelonephritis include:

pregnancy, excessive vomiting, immunocompromise and

obstruction (e.g., kidney stone)

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II. GU TRAUMA

A. Penile injuries:

1. Penile amputation should be treated with reimplantation if the

distal penis is in satisfactory condition and the ischemia time is

<12-24 hours. Chances or reimplantation can be increased by

proper handling of amputated portion:

a. Penis wrapped in saline soaked gauze and put in sterile bag.

b. Immerse bag in ice slush until surgery can be performed.

2. Penile “fracture” or traumatic rupture of the tunica albuginea

and underlying corpus cavernosum occurs when an erect penis

impacts forcibly on a hard surface such as the pubic bone (often

during vigorous intercourse).

a. Often a snapping sound is heard, with localized pain,

detumescence and a progressive penile hematoma.

b. Most require surgical repair of the torn tunica albuginea.

“Egglant deformity” (see Figure 5) on physical exam with

swollen ecchymotic penis.

c. About 1/3 of penis fractures also involve an underlying

urethral injury so a retrograde urethrogram should be

performed.

d. Treatment: surgical exploration.

3. Superficial penile and scrotal lacerations may be closed with 4-0

absorbable sutures.

4. Penile skin trapped in a zipper can be treated with lidocaine

infiltration followed by mineral oil application to help free the

skin. Otherwise, wire cutting pliers can be used to divide the

median bar of the zipper, causing it to fall apart.

Figure 5: Eggplant deformity

B. Scrotal injuries:

1. The mobility of the testes combined with their tough, fibrous

capsule make their rate of injury low.

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Urology/GU Trauma

a. Penetrating injuries to the scrotum should be operatively

explored.

b. All blunt testicular injuries should undergo color Doppler

ultrasound examination to evaluate the integrity of the testes.

2. “Testicular fracture” or rupture:

a. Caused by a deforming force rupturing the tunica albuginea,

which functions to protect the seminiferous tubules.

b. Difficult to distinguish from a scrotal contusion or

hematoma. c. Usually follows assault or sports injury.

d. Risk can be as high as 50% following major blunt trauma to

testicles.

e. Ultrasonography aids in diagnosis, but definitive diagnosis is

made surgically.

f. Treatment is early surgical correction and medically managed

cases result in atrophy, necrosis, and infection.

C. Urethral trauma:

1. Urethral trauma is suggested by the presence of a pelvic fracture,

blood at the urethral meatus, a high-riding or absent prostate

on rectal exam, or a perineal, scrotal or penile hematoma. Also,

these patients have acute urinary retention with a palpable

bladder.

a. A Foley catheter should never be placed if urethral trauma is

suspected without first performing a retrograde urethrogram.

b. A retrograde urethrogram (see Figure 6) is performed by

placing the end of a Toomey syringe into the urethral meatus

for a snug fit and then injecting 60 mL of contrast into the

urethra over 30-60 seconds. A radiograph of the length of the

urethra is taken during the injection of the last 10 mL of

contrast. Extravasation of contrast outside of the urethra with

concomitant bladder filling distinguishes a partial urethral

laceration from a complete disruption (where no contrast

reaches the bladder).

Figure 6:

Retrograde

urethrogram

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Urology/GU Trauma

2. Anterior (10%) urethral injuries (those below the urogenital

diaphragm) are usually secondary to direct trauma (e.g., kicks

and straddle injuries).

3. Posterior (90%) urethral injuries (those above the UG

diaphragm) are typically associated with pelvic fractures, which

often cause prostatomembranous urethral disruption (sign: high-

riding or absent prostate on DRE). Quick diagnosis and treatment

of these injuries significantly lowers chances of incontinence and

erectile dysfunction.

4. Partial urethral lacerations are usually managed with an

indwelling urethral catheter. Attempted placement of this

catheter in the ED is controversial.

5. Complete urethral disruption requires placement of a suprapubic

catheter for bladder drainage pending definite surgical repair.

6. Urethral strictures, erectile dysfunction, and incontinence are the

main long-term complications.

D. Bladder injuries:

1. Usually associated with blunt trauma, pelvic fractures, and

deceleration with compression of the bladder (as in MVCs).

There is a high incidence of associated life-threatening non-

urologic injuries.

2. Evaluation of potential bladder injury should take place only after

potential urethral injuries have been ruled out (i.e., do the

urethrogram before the cystogram).

3. Suspicion of bladder injury should arise with the presence of

gross hematuria, especially in the setting of a pelvic fracture.

98% of patients with bladder rupture have gross hematuria.

4. Symptoms are non-specific and include suprapubic pain and

inability to void.

5. Retrograde cystogram or retrograde CT cystography are the

diagnostic procedures of choice for suspected bladder injury.

a. Retrograde cystogram is performed by allowing 300-400 mL

of contrast to flow by gravity from a Toomey syringe through

a Foley catheter into the bladder. If the bladder contracts

before the instillation of 300 mL, 50 mL more of the contrast

should be inserted with hand pressure. The Foley catheter is

then clamped, and AP and lateral radiographs of the bladder

taken. The Foley is then unclamped, the bladder drained, and

a postevacuation film taken.

b. Retrograde CT cystography is performed in the same fashion

but using CT for imaging.

c. With extraperitoneal bladder perforations, the extravasated

dye is seen in the area of the pelvic outlet (see Figure 7) but

does not enter the peritoneal cavity.

d. With intraperitoneal perforations, the contrast enters the

peritoneal space and outlines the intraperitoneal structures.

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Urology/GU Trauma

e. Extraperitoneal bladder ruptures will usually heal

spontaneously in 14 days with Foley catheter drainage.

f. Intraperitoneal bladder ruptures require surgical repair.

Figure 7: Cystograms in bladder rupture

E. Ureteral injuries:

1. Rare and usually occur secondary to penetrating trauma. Often,

several non-urologic injuries are also present.

2. Much more likely to be iatrogenic from gynecological, vascular,

or complex urological procedures.

3. Hematuria, flank pain and a palpable mass in the lower

abdomen are the classic features. Often there is a delay in

making this diagnosis and hematuria is not sensitive for ureteral

injury.

4. These are usually diagnosed by CT with contrast or retrograde

pyelogram. IVP may be used though is less sensitive.

5. If the cause is penetrating trauma, a ureterocuteneous fistula may

form.

6. Most are treated surgically.

F. Renal injuries:

1. The most common of all urologic injuries; usually due to blunt

trauma. History is important to distinguish blunt from penetrating

traumas.

2. More than 80% of those patients with kidney injuries have other

concurrent injuries, often life-threatening.

3. Contusions account for over 90% of renal injuries. Kidney

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Urology/GU Trauma

lacerations and pedicle injuries each make up <5% of all renal

injuries.

4. The main indications for imaging the kidneys after blunt trauma

are:

a. Gross hematuria.

b. Microscopic hematuria with multiple injuries or

hemodynamic instability (shock).

c. A mechanism that includes rapid deceleration.

5. Any penetrating trauma with the potential for renal injury

warrants an imaging study, even in the absence of hematuria.

Hematuria, often present, does not correlate with severity of

injury.

6. CT with IV contrast is the imaging procedure of choice for

potential renal injuries. IVP may be used if CT is not available or

if the patient’s instability does not allow time for CT (i.e., a “one

shot” IVP in the ED or OR).

7. Renal contusions are managed non-operatively.

8. Renal injuries are graded from I-V (see Figure 8). Higher grade

injuries are more likely to require surgical repair.

9. Indications for operative intervention for renal injuries

include:

a. Uncontrolled renal hemorrhage.

b. Penetrating injuries.

c. An avulsed major renal vessel.

d. Extensive urine extravasation.

e. Shattered kidney or lacerations extending through to the

collecting system.

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Urology/GU Trauma

Figure 8: Grades of Renal Trauma

Page 164

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Urology/GU Trauma

UROLOGY/GU TRAUMA

PEARLS

Urology

1. Definitive treatment of phimosis is circumcision.

2. Sickle cell anemia is the most common cause of priapism in children.

3. Color flow Doppler ultrasound of the scrotum is as accurate as

radionuclide scanning and much faster to rule out torsion.

4. Don’t delay surgical exploration of a potential testicular torsion for

diagnostic studies, since the salvage rate markedly decreases after 4

hours of ischemia.

5. Manual detorsion may be attempted, medial to lateral.

6. Epididymitis under age 35 is usually caused by gonorrhea or chlamydia.

Over 35, E. coli is the main pathogen.

7. BPH is the #1 cause of acute urinary retention in men.

8. Patients catheterized for acute urinary retention should be observed for

4-6 hours for postobstructive diuresis.

9. Treatment of Fournier’s gangrene involves aggressive fluid resuscitation,

antibiotics, and, most importantly, surgical debridement.

10. The majority of kidney stones contain calcium.

11. Struvite stones (staghorn calculi) are infection stones associated with a

high urinary pH.

12. Stones caused by indinavir are radiolucent.

13. The most common site of ureteral stone impaction is the ureterovesical

junction.

14. Helical CT is the preferred imaging study for kidney stones.

15. Ultrasound is good to diagnose ureteral hydronephrosis and obstruction.

It is poor for imaging the stone itself.

16. 90% of kidney stones <4 mm in size will pass spontaneously, while only

10% of those >6 mm will.

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Urology/GU Trauma

GU Trauma

1. A retrograde urethrogram should be performed before inserting a Foley

catheter if urethral injury is suspected.

2. 95% of patients with bladder rupture will have gross hematuria.

3. Retrograde cystogram or retrograde CT cystography are the diagnostic

procedures of choice for suspected bladder injury.

4. Extraperitoneal bladder ruptures usually heal spontaneously (with Foley

catheter drainage), while intraperitoneal ruptures require operative

repair.

5. Indications for imaging the kidneys after blunt trauma are: gross

hematuria, microscopic hematuria in the presence of multiple injuries or

hemodynamic instability, and a mechanism that includes rapid

deceleration.

6. CT with IV contrast is the imaging procedure of choice for potential

renal injuries.

7. The majority of renal injuries occur in the presence of other, usually

life-threatening injuries.

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REFERENCES

1. Benway, Brian. "Bacterial Prostatitis". Urologic Clinics of North

America 2008: 23-32.

2. Coley, Brian. "The Acute Pediatric Scrotum". Ultrasound Clinics

2006: 485-496.

3. Engineer R, Peacock WF: Urologic Stone Disease, in Tintinalli JE,

Kelen GD, Stapczynski JS (eds): Emergency Medicine: A

Comprehensive Study Guide 6th

ed., McGraw-Hill Inc., 2004, 620-

625.

4. Escobar JI, Eastman ER, Harwood-Nuss AL: Selected Urologic

Problems, in Marx JA, et al (eds): Rosen’s Emergency Medicine:

Concepts and Clinical Practice 5th

ed., Mosby Inc., 2002, 1400 –

1433.

5. Frenkl, Tara Lee. "Sexually Transmitted Infections". Urologic

Clinics of North America 2008: 33-46.

6. Galejs, Laris. "Diagnosis and Treatment of the Acute Scrotum".

American Family Physician Februrary 15, 1999: 817-824.

7. Hartke, David. "Anomalies of the Penis". Journal of Men's Health

and Gender September 2006: 244-249.

8. Howes DS, Bogner MP: Urinary Tract Infections and Hematuria, In

Tintinalli JE (Ed. In Chief): Emergency Medicine: a Comprehensive

Study Guide 7th

ed., McGraw-Hill Inc., 2011, 630-640.

9. Levy F, Kelen GD: Genitourinary Trauma, in Tintinalli JE, Kelen

GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive

Study Guide 6th

ed., McGraw-Hill Inc., 2004, 1622-1629.

10. McCollough M, Sharieff G: Genitourinary and Renal Tract

Disorders, in Marx JA, et al (eds): Rosen’s Emergency Medicine:

Concepts and Clinical Practice 7th

ed., Mosby Elsevier, 2010, 2200-

2217.

11. Miller, Nicole. "Management of Kidney Stones". British Medical

Journal March 3, 2007: 468-472.

12. Nicolle, Lindsay. "Uncomplicated Urinary Tract Infections in Adults

Including Uncomplicated Pyelonephritis". Urologic Clinics of North

America 2008: 1-12.

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13. Norris, Donald. "Urinary Tract Infections: Diagnosis and

Management in the Emergency Department". Emergency Medicine


14. Rosenstein, Daniel. "Urologic Emergencies". Emergency Medicine


15. Samm, Bill. "Urologic Emergencies". Postgraduate Medicine

October 1996: 187-200.

16. Schneider RE: Genitourinary Procedures, in Roberts JR, Hedges JR

(eds): Clinical Procedures in Emergency Medicine 3rd

ed., W.B.

Saunders Company, 1998, 947 – 987.

17. Selius, Brian. "Urinary Retention in Adult: Diagnosis and Initial

Management". American Family Physician March 1, 2008: 643-650.

18. Tracy, Chad. "Diagnosis and Management of Epidydimitis".

Urologic Clinics of North America 2008: 101-108.

19. Turgut, Ahmet. "Acute Painful Scrotum". Ultrasound Clinics January

2008: 93-107.

08/13

Page 168

Stroke and Seizures

E. Bradshaw Bunney, MD, FACEP

Associate Professor and Residency Director, Department of Emergency Medicine, University of Illinois at Chicago

Page 169

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Notes

Stroke and Seizures

STROKE AND SEIZURES

Stroke Epidemiology, Diagnosis and Management

I. INTRODUCTION

A. Objectives:

1. Describe the epidemiology and pathophysiology of acute stroke.

2. Describe the clinical presentation of the various stroke

syndromes.

3. Delineate the current management of acute hemorrhagic strokes.

4. Delineate the current management of acute ischemic strokes.

B. Epidemiology of stroke:

1. Third leading cause of death in the U.S.

2. 550,000 new strokes per year.

3. 150,000 deaths per year.

C. Types of stroke:

1. 85% of strokes are ischemic:

a. 2/3 thrombotic.

b. 1/3 embolic.

2. 15% are hemorrhagic:

a. 2/3 intracerebral.

b. 1/3 subarachnoid.

D. Mortality rates:

1. For all strokes, 25% of patients over 70 years will die within 30

days.

2. African Americans have 2x the incidence and mortality vs. other

groups.

II. PATHOPHYSIOLOGY

A. Circulation:

1. Normal blood flow is 40-60cc/100g brain/min.

2. At < 20cc/100g/min neurons stop firing; membrane integrity is

maintained.

3. At < 10cc/100g/min membrane failure occurs.

4. Collateral circulation leaves a large area with 10-20cc/100g/min.

The area perfused between 10-20cc/100g/min is called the

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Stroke and Seizures

penumbra.

5. It is the preservation of the neurons in the penumbra that is the

goal of therapies such as thrombolytics and neuroprotective

agents.

B. Glucose:

1. Within 5 min, ATP is depleted and lactate production increases

leading to acidosis.

2. If more glucose is given, there is an increase in lactate through

anaerobic metabolism.

3. Thus it is important to have strict glucose control and avoid using

D50W.

C. Pre-hospital issues in the treatment of stroke:

1. Public education is a priority.

a. Average arrival time after the onset of symptoms is 12-24

hours.

b. Barsan et al found that arrival times after the onset of

symptoms were different based on who the patient called first

(911 vs. hospital vs. private physician).

c. Kothari et al found that using 911, race (white) and living

with someone were independently associated with arrival

within 3 hours of the onset of symptoms.

2. EMS response and assessment:

a. Porteous et al found that dispatchers classified calls in which

“stroke” was used by the caller as “CVA” only 48% of the

time. In 61 patients with documented stroke, the EMS calls

were retrospectively reviewed and the dispatch code of

“CVA” was used in only 31% and ambulances were

dispatched at “low priority” in 59%.

b. Kothari et al have validated their Prehospital Stroke Scale

which uses 3 items from the NIH Stroke Scale (facial palsy,

best motor arm, and best language).

c. Kidwell et al have also developed a prehospital stroke screen.

III. STROKE SYNDROMES

A. Anterior cerebral artery:

1. Paralysis of the opposite leg, worse than the arm paralysis.

2. Sensory deficit paralleling paralysis.

3. Altered mental status; confusion.

4. Bowel or bladder incontinence.

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B. Middle cerebral artery (most common):

1. Paralysis opposite body, arm, face, worse than legs.

2. Sensory deficit paralleling paralysis.

3. Blindness in lateral half of visual field (hemianopsia).

4. Dysphasia.

5. Agnosia (inability to recognize objects).

C. Posterior cerebral artery:

1. Hemianopsias.

2. 3rd nerve paralysis.

3. Cortical blindness.

4. Altered mental status.

D. Vertebrobasilar artery:

1. Vertigo, nystagmus.

2. Facial numbness/paresthesias.

3. Contralateral loss of pain and temperature.

4. Bilateral spasticity.

5. Syncope, drop attacks.

E. Cerebellar infarction:

1. Nausea and vomiting.

2. Headache.

3. Nuchial rigidity.

4. Central vertigo.

5. Drop attacks.

6. 1/3 of ischemic infarcts develop cerebellar edema.

7. Hemorrhagic cerebellar infarcts are a surgical emergency.

8. Brainstem impingement leads to altered consciousness.

9. Pathologic respiratory pattern.

10. Stable period of 6 - 12 hours.

F. Lacunar infarction:

1. 20% of all infarctions.

2. Risk factors are those with small vessel disease (i.e. diabetes,

hypertension).

3. Areas most highly affected include:

a. Basal ganglia.

b. Pons.

c. Thalamus.

4. These infarcts are subcortical, so rarely have cognitive deficits.

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G. Transient ischemic attack (TIA):

1. Focal symptoms: usually weakness or numbness.

2. Usually not: dizziness, syncope or altered mental status.

3. Lasting < 24 hours.

4. Majority last 10 - 15 minutes.

5. 20% have a stroke within one month.

6. 50% have a stroke within five years.

H. Risk factors for stroke:

1. Same as atherosclerotic vascular disease:

a. Hypertension.

b. Heart disease.

c. Elevated cholesterol.

d. Diabetes.

e. Cigarette smoking.

I. Clinical assessment:

1. ABCs.

2. Altered mental status protocol.

3. Glucose check, not D50W.

4. Level of consciousness.

5. AVPU.

6. Glasgow coma scale.

J. While assessing the patient, keep in mind:

1. 10-20% of strokes has brain stem compression.

2. 5% of strokes have an acute seizure.

K. Ancillary tests:

1. CBC.

2. Chemistry.

3. PT/PTT.

4. EKG.

5. CT scan.

IV. HEMORRHAGIC STROKES

A. Epidemiology:

1. 15% of all strokes.

2. 2/3 intracerebral.

3. 1/3 subarachnoid.

4. 30 day mortality rate is 50%.

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5. Usually occur during working hours.

6. Headache is a symptom in only 50% of patients.

7. 85% of SAH patients have headache.

B. Pathophysiology of cerebral hemorrhage:

1. Strong correlation with hypertension.

2. Usually in the middle cerebral artery distribution.

3. 2/3 is in the basal ganglia.

4. Microaneurysm which is susceptible to changes in blood pressure

(cocaine).

C. Pathophysiology of subarachnoid hemorrhage (SAH):

1. 3/4 occur in the Circle of Willis-Berry Aneurysm.

2. Most occur before age 50.

3. Aneurysm, AVM.

D. Clinical assessment:

1. ABCs.

2. Altered mental status: unconsciousness.

3. Respiratory pattern:

a. Cheyne-Stokes respirations may indicate a large ICH.

b. Deep irregular respirations may indicate a putamen

hemorrhage.

c. Normal respirations may be seen in a cerebellar hemorrhage.

4. Pupils:

a. Pinpoint pupils may indicate a pontine hemorrhage.

b. Dilated pupils may indicate a putamen hemorrhage.

c. Gaze preference to the side of the lesion.

E. Ancillary tests:

1. Same as ischemic strokes.

2. EKG: increased sympathetic outflow causes increased

dysrhythmias.

3. PT/PTT for coagulopathy.

F. CT scan:

1. 95% of ICH can be seen on CT.

2. Will miss the very small and those in the 5-9 day window.

3. 90% of SAH can be seen on CT.

4. LP on all negative CT scans for SAH.

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G. SAH CT scan findings:

1. High density hemorrhage injury.

2. Interhemispheric fissure.

3. Third ventricle.

4. Ambient cistern.

5. Sylvian fissure.

V. TREATMENT OF HEMORRHAGIC STROKE

A. Introduction:

1. If intubation is necessary, remember ICP. Pre-treat with

lidocaine.

2. Lower hypertensive blood pressure to a diastolic of 100-110.

3. Nitroprusside, labetalol, esmolol and nicardapine.

4. Head of the bed to 45 degrees. FASTEST TO DECREASE

ICP. 5. Hyperventilation should only be used if a neurosurgeon is going

to perform a definitive procedure within hours of the initiation.

Hyperventilate to a CO2 of 25-30 mmHg.

6. Diuretic: mannitol 20% solution 0.25g-1.0g per kg.

7. Steroids generally not used in hemorrhagic stroke.

8. Phenytoin at the discretion of the neurosurgeon.

9. Nimodipine useful in SAH.

B. Nimodipine:

1. Ca channel blocker.

2. Greater effect on cerebral arteries: lipophilic.

3. Decreases neurological deficits in SAH.

4. Used in SAH Hunt and Hess Grades I-III.

5. Most common adverse reaction is decreased BP.

6. 60 mg PO every 4 hours.

C. Treatment: Surgery:

1. Usually not helpful in ICH.

2. Used in large ICH to prevent herniation or hydrocephalus.

3. Recommended in SAH: timing is controversial.

4. Recommended in cerebellar hemorrhage.

VI. TREATMENT OF ISCHEMIC STROKE

A. Treatment: Hypertension:

1. Because of impaired cerebral autoregulation, treatment of

hypertension is controversial.

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2. Treatment should be begun if the patient is a candidate for

thrombolytic therapy or shows signs of:

a. Hypertensive encephalopathy.

b. Aortic dissection.

c. Severe hypertension.

d. Myocardial infarction.

B. Treatment: Anti-coagulation:

1. Prevent thrombus propagation and further embolization.

2. Proven in cardiac arrhythmia.

3. Useful in TIA to decrease the number of recurrent ischemic

events.

4. Unfractionated heparin:

a. International Stroke Trial: 2 doses (5,000 and 12,500 IU SQ

BID), 19,435 subjects, no improvement in outcome at 6

months, significantly more intracerebral bleeds (especially

the 12,500 IU group).

b. Risk of bleed in large stroke reported as high as 14%.

5. Low-molecular weight heparin:

a. Kay et al (using Nadroparin) found in 306 subjects that both

4100 IU SQ daily and 4100 IU SQ BID, given within 48

hours of the onset of symptoms, were effective in improving

outcomes at 6 months compared to placebo. There was no

difference among the three groups in regards to death or

bleeding related complications.

b. TOAST trial found in 1281 subjects, that Org 10172 given

within 24 hours of the onset of symptoms, lead to improved

outcomes at 7 days but similar outcomes at 3 months when

compared to placebo.

C. Treatment: Anti-platelet agents:

1. Cyclooxygenase: thromboxaneA2; platelet aggregation.

2. Aspirin inhibits Cyclooxygenase for the life of the cell.

3. Aspirin decreases the stroke risk by 20% when taken prior to

symptom onset.

4. International Stroke Trial when combined with the Chinese Acute

Stroke Trial shows a decrease in 10 deaths or recurrent strokes

per 1000 at 2-3 weeks when aspirin (300 mg) was given within

48 hours.

D. Thrombolytic agents for stroke:

1. TPA clinical trials:

a. NINDS:

i. 3 hour window for enrollment, many within 90 minutes.

ii. TPA dose was 0.9 mg/kg.

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iii. 624 patients enrolled.

iv. Part 1: No significant improvement in 24 hours though

secondary analysis showed a significant improvement in

the median NIHSS (42 point scale of specific neurological

deficits) at 24 hours.

v. Part 2: Significant improvement in outcome at 3 months

overall and in each of the four components; NIHSS,

Barthel Index (activities of daily living), Modified Rankin

Scale (comparison to pre stroke function) and Glasgow

Outcome Scale (level of independent living).

vi. Increased bleeding was found in the TPA group, but 3

month mortality was no different.

vii. The overall conclusion was those treated with TPA were

30% more likely to have little or no disability at 3 months.

Follow up has shown this to continue to 6 months and 1

year. Ischemic stroke lesion size, as measured on CT,

was reduced in the TPA treated group.

b. ECASS III:

i. Prospective, randomized, placebo controlled study.

ii. Is tPA efficacious in the treatment of ischemic stroke in

the 3 – 4.5 hour window?

iii. Primary outcome = mRS 0 - 1 at 90 days.

iv. Study mandated by the European Medicines Agency

(EMEA), pharmaceutical approval agency.

v. Inclusion:

18 – 80 years old.

Symptoms > 30 min.

vi. Exclusion:

NIHSS > 25.

Prior stroke and diabetes.

Oral anticoagulation use.

Seizure at onset of symptoms.

BP > 185/110 not easily controlled, no IV drips.

vii. N = 821

viii. Median time to treat = 3:59.

ix. Differences between tPA and placebo groups:

NIHSS 10.7 v. 11.6 p=0.003.

History of stroke 7.7 v. 14.1 p=0.03.

x. Primary outcome mRS 0-1

tPA 219/418 (52.4%).

Placebo 182/403 (45.2%).

P = 0.04.

OR 1.34 (CI 1.02 – 1.76).

Absolute improvement 7.2%.

xi. Criticisms:

Fewer diabetics compared to NINDS.

tPA 14.8% v. 22%, placebo 16.6% v. 20%.

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Much lower mean NIHSS.

tPA 10.7 v. 14, placebo 11.6 v. 14.

No history of prior stroke and diabetes allowed.

E. TPA eligibility:

1. Age 18 or older.

2. Diagnosis of ischemic stroke with measurable neurological

deficits.

3. Time of symptom onset to drug administration less than 3 hours.

4. Need a separate protocol if going to treat in the 3-4.5 hour

window.

F. TPA exclusion criteria:

1. Similar to cardiac TPA:

a. Head injury within 3 months.

b. Surgery within 2 weeks.

c. GI or GU bleeding within 3 weeks.

2. Currently on anti-coagulants.

3. Platelet count <100,000.

4. Improving symptoms.

5. Post treatment blood pressure >185/110.

6. Isolated or mild neurological deficits.

7. Blood glucose <50 or >400 mg/dl.

8. Recent myocardial infarction.

9. Seizure related to the stroke no longer an exclusion.

10. Clinical presentation suggestive of subarachnoid hemorrhage.

G. TPA protocols:

1. Administered within 3 hours from the onset of symptoms, not

arrival in ED.

2. Head CT.

3. 0.9 mg/Kg to a maximum of 90 mg.

4. 10% bolus over 1-2 min.

5. 90% infusion over 1 hour.

6. Facilities to handle bleeding complications.

7. Patients who receive TPA should not receive anti-platelet or anti-

coagulant therapy for 24 hours.

H. Time goals:

1. Door to emergency physician - 10 minutes.

2. Door to CT- 25 minutes.

3. Door to CT reading - 45 minutes.

4. Door to TPA - 60 minutes.

5. Door to ICU bed - 2 to 3 hours.

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Seizures

I. EDUCATIONAL OBJECTIVES

A. Describe the epidemiology of acute seizures.

B. Define the principles of diagnosis and management of acute seizures

in the emergency department (ED).

C. Determine the utility of new acute seizure therapies in improving

patient outcomes.

D. Discuss current guidelines, issues, and unanswered clinical questions.

II. EPIDEMIOLOGY

A. Seizure disorders:

1. 6/1000 prevalence; 2.5 million in U.S.

2. 147,000 newly diagnosed seizure patients/year.

3. 28% of patients with epilepsy visit an ED annually.

4. 82,000 hospitalizations/year.

B. Acute symptomatic seizures:

1. CVD, trauma, infection, AED withdrawal account for 60% of

cases.

2. Toxic, metabolic: 15% of cases.

C. Status epilepticus (SE):

1. 50,000 -150,000 cases annually.

2. 50 cases per 100,000 population.

3. Infants and elderly: greatest risk.

4. 20% of patients with epilepsy will have SE by age 5.

5. Etiology: 1/3 acute insult; 1/3 chronic epilepsy; 1/3 new onset.

III. OUTCOMES

A. Seizures:

1. Injury/death: 15%.

2. Head contusions/lacerations common.

3. Mortality:

a. 1.2% of all seizures.

b. 3% to 26% in SE.

c. 10 times higher in adults (vs children).

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d. Highest with hypoxic or ischemic insult.

B. SE:

1. Duration > 60 min: 10-fold greater 30-day mortality (32% vs

2.7%).

2. Worse outcome associated with longer duration, refractory to 1st

drug.

IV. SEIZURE CLASSIFICATION

A. Status epilepticus: definition:

1. Needed for epidemiologic and clinical trials.

2. Historical definitions:

a. Two seizures within 30 min without a lucid interval.

b. One seizure >30 min duration.

3. More recent definitions more aggressive:

a. Two seizures over any interval without a lucid interval.

b. One seizure of >10 min duration.

B. Status epilepticus: classification:

1. Generalized convulsive SE:

a. Primarily and secondarily generalized.

b. Overt: GTC (Generalized Tonic Clonic) or major motor SE

subtle: myoclonic SE, "electrical" SE.

2. Nonconvulsive SE: epileptic twilight state.

a. Complex partial SE.

b. Absence SE: spike-wave stupor.

3. Simple partial SE:

a. No impairment of consciousness.

C. Refractory status epilepticus:

1. Lack of response to first-line drugs: benzos, phenytoin,

phenobarbital.

2. 2000 - 6000 cases yearly in U.S.

3. 6% - 9% of all SE cases, suggests progressive CNS disorder.

4. 20-30% mortality.

V. CEREBRAL CHANGES IN SE

A. CNS injury independent of systemic effects.

B. Neuronal injury due to repetitive firing and excessive metabolic

needs.

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C. CNS injury will occur even if systemic disturbances are treated

(fever, hypertension, motor activity).

D. Early in SE, BP and CBF (cerebral blood flow) are increased.

E. Late in SE, BP and CBF are decreased.

VI. SYSTEMIC CHANGES IN SE

A. BP: early hypertension, followed by hypotension.

B. Fever: 49% have temperature >100.5 Fo.

C. Lactic acidosis: 30% will reach blood pH <7.00.

D. Hypercarbia: 84% will have increased pCO2.

E. Catechols: levels within 30 min.

F. Leukocytosis without bands.

G. CSF pleocytosis: 2%-18% have >5 PMNs.

VII. POST-ICTAL PHYSICAL FINDINGS

A. Focal findings:

1. Anisocoria, Todd's paralysis.

2. Plantar response, hyperreflexia.

3. Evidence of trauma (e.g., tongue lacerations).

B. Altered mental status should improve within 20-30 min.

VIII. LABORATORY TESTING

A. Basic metabolic tests:

1. 2.4% of seizures due to chemistry derangements.

2. Full workup with comorbidity, age extremes.

B. AED (Anti Epileptic Drug) levels.

C. Toxicologic and ETOH screens (when indicated).

D. Accu-Chek, pulse oximetry, rhythm strip, pregnancy test.

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IX. COMPUTED TOMOGRAPHY (CT)

A. Abnormal CT most likely:

1. Abnormal neurologic exam after recovery.

2. Malignancy history.

B. Abnormal CT less likely:

1. Alcohol-related seizure.

C. Focal seizure alone does not increase likelihood of positive CT.

D. Initial CT should be non-contrast.

X. MAGNETIC RESONANCE IMAGING (MRI)

A. Intractable epilepsy: 25% positive CT, 50% positive MRI.

B. May not be appropriate in ED due to off-site location.

C. After a negative non-contrast CT in the ED.

XI. EMERGENT ELECTROENCEPHALOGRAM (EEG)

A. ACEP Clinical Policy: Acute Seizures (Non-SE)

1. Detailed evaluation for prolonged AMS.

2. Directed workup for uncomplicated, self-limited seizures.

3. Follow-up care with primary care MD.

4. Review driving precautions.

XII. PHARMACOTHERAPY OF ACUTE SEIZURES

A. Benzodiazepines:

1. GABA inhibition of repetitive neuronal firing.

2. 79% control of SE in 47 studies.

3. Lorazepam vs diazepam:

a. Adult SE.

i. Comparable efficacy in seizure termination.

b. Pediatric seizures.

4. Lorazepam may be more effective:

a. Intubation more common with diazepam in SE (73% vs

27%).

5. Emulsified diazepam (Diastat).

6. Diazepam emulsified injection:

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a. Less local irritation than diazepam.

b. Seizure termination in 5 to 7 min.

c. No significant respiratory depression.

d. PR dose: 0.25 to 0.5 mg/kg.

B. Phenytoin:

1. Overview:

a. Stabilizes membrane Na+ channels.

b. Regulates Ca++ channels.

c. Effective in generalized seizures and SE.

d. Seizure termination in 40% to 80% of patients.

e. 18 mg/kg loading dose results in therapeutic (10 /mL) levels

up to 24 h.

f. Constant infusion preferred over slow IVP use.

2. Oral phenytoin loading regimens:

a. 18 mg/kg oral load:

i. 64% achieve level of 10 mg/mL by 8 h

ii. Mean phenytoin level does not exceed 10 mg/mL until

after 4 h

b. Delayed absorption may relate to large loading dose or

phenytoin preparation.

c. Delay in achieving therapeutic level did not result in seizure

recurrence in 8 h.

3. High-dose phenytoin therapy:

a. Initial Rx for GCSE:

i. Maximal benzodiazepine dose.

ii. 20 mg/kg phenytoin load.

b. Additional half load of phenytoin:

i. Give 10 mg/kg for a total 30 mg/kg dose.

c. Phenytoin level may exceed 10 to 20 mg/kg.

d. Higher therapeutic levels may be required in refractory SE.

C. Fosphenytoin (Cerebyx): Phosphate-ester prodrug:

1. Water soluble prodrug.

2. Complete conversion in vivo to phenytoin:

a. Therapeutic free phenytoin levels within 2.7 minutes (IV).

3. Conversion comparable in all demographic groups and all disease

states.

4. Available for rapid IV infusion (up to 150 mg PE/min in SE).

5. Available for IM use.

6. Dosing is equivalent to phenytoin dosing.

7. Limited need for monitoring.

8. Drug level testing: 2h after IV, 4h after IM.

9. Perioral and perineal paresthesias and pruritus, not an allergic

reaction.

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D. Barbiturates:

1. Phenobarbital:

a. Barbiturate crosses blood-brain barrier slowly.

b. Long half life (21-42 h).

c. Enhances GABA inhibition.

d. Infuse at 100 mg/min up to 10 mg/kg.

e. Monitor for:

i. Respiratory depression.

ii. Hypotension.

f. Good drug for SE treatment.

g. Third-line therapy for refractory GCSE.

h. Stops seizure motor activity and suppresses EEG burst

patterns.

i. Loading dose: 5 mg/kg infused at 25 mg/min.

j. Maintenance infusion: 2.5 mg/kg/h .

k. Intubation, ventilatory support, hemodynamic and EEG

monitoring required.

E. Other agents:

1. Lidocaine:

a. Membrane stabilizing effect at Na+/K+ pump.

b. Reduces neuronal excitability.

c. Possible role in refractory GCSE.

d. Use only as third-line agent.

e. Load at 1.5 mg to 3 mg/kg.

2. Propofol:

a. Third-line agent, after benzodiazepines, phenytoin,

phenobarbital.

b. Anesthetic agent; GABA mechanism.

c. Provides burst suppression.

d. Loading dose: 2 mg/kg.

e. Requires continuous infusion.

f. EEG monitoring required.

g. Hypotension, respiratory depression, acidosis.

3. IV valproic acid (Depacon):

a. IV valproate now available.

b. Restores valproate level quickly.

c. French study tested IV valproate in SE:

i. GCSE and partial SE.

ii. 19/23 patients (83%) controlled in 20 minutes.

iii. EEG control achieved.

4. Not indicated for SE in U.S,

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XIII. PRIMARY CAUSES OF DRUG-INDUCED SEIZURES

A. Cocaine:

1. Consider multiple etiologies (inhalation, body stuffing).

2. Indirect CNS causes: ischemia, hemorrhage, vasculitis.

3. Diagnostic work-up low yield with brief seizures, rapid return to

normal CNS status.

4. Treatment: benzodiazepines.

5. Avoid beta blockers.

B. Isoniazid (INH):

1. Inhibits pyridoxine kinase:

a. Enzyme that forms pyridoxal phosphate.

b. Cofactor in GABA formation.

2. Administer pyridoxine on gram for gram basis:

a. Unknown overdoses, give 5 g IVP, repeat q 5 h X 6.

b. Acidosis and refractory seizures improved with pyridoxine.

3. Rx: GABA agonists (benzodiazepines, barbiturates).

C. Theophylline:

1. Seizures common in chronic ingestions.

2. Treat with benzodiazepines, barbiturates.

3. Phenytoin probably not effective.

4. Enhance elimination:

a. Multiple doses of activated charcoal.

b. Hemodialysis or hemoperfusion.

D. Cyclic antidepressants:

1. Seizure (39%) and coma (61%) common in TCA deaths.

2. Seizures more likely when QRS > 100 msec.

3. Rx: benzodiazepines:

a. Consider pentobarbital or propofol in refractory SE.

b. Phenytoin, physostigmine, NaHCO3 of limited value.

E. Alcohol withdrawal seizures:

1. Epidemiology:

a. 61% occur within 24 hours of last drink.

b. Peak incidence by 12 hours of last drink.

c. Generalized seizures common, 60% recur.

d. 44% Of GCSE cases due to alcohol.

e. Prolonged post-ictal state, but good outcome in

alcohol-withdrawal SE.

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2. Diagnosis and treatment:

a. Baseline chemistries to evaluate specific etiologies.

b. CT for head trauma, deteriorating mental status, or focal

neurologic finding.

c. EEG required excluding idiopathic seizures (if not performed

previously).

d. IV D5NS, thiamine, K, Mg, lorazepam.

e. Avoid progression of disease to DTs.

3. Phenytoin use:

a. Phenytoin not effective in preventing seizure recurrence

within 6 hours.

b. Decision to load with phenytoin multifactorial:

i. Not preferred for simple, uncomplicated seizures.

ii. Must be considered in seizures refractory to optimal

benzodiazepine therapy.

iii. May be advisable without knowledge of patient's medical

and seizure history.

XIV. EPIDEMIOLOGY OF POST-TRAUMATIC SEIZURES

A. Adult high-risk criteria: 20% incidence:

1. Glasgow Coma Scale < 10.

2. Intracranial hemorrhage.

3. Penetrating injury or depressed skull fracture.

B. Pediatric high-risk criteria: 39% incidence:

1. Loss of consciousness.

2. Glasgow Coma score 3 to 8.

3. Abnormal CT scan.

C. Phenytoin in post-traumatic seizures:

1. One-year, placebo controlled trial in severe TBI:

a. Phenytoin associated with fewer seizures within 7 d vs

placebo (3.6% vs 14.2%).

b. Late-onset seizure rate similar in both groups (28% and 21%)

at 1 and 2 .

2. Mortality rates similar (24% and 21%) by 2nd year.

3. Absence of late effect not due to mortality, low phenytoin levels,

or treatment crossover.

XV. REFRACTORY SE MANAGEMENT

A. Goal of treatment: achieve an EEG with burst-suppression pattern.

B. Pentobarbital: 5 mg/kg, load at 25 mg/min.

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C. Propofol: 2 mg/kg load, 7 to 10 mg/kg/h maintenance.

D. Lorazepam and midazolam IV.

E. Chloral hydrate, lidocaine, valproate.

F. Inhalation anesthetics less useful.

G. Neuromuscular blockade not an anticonvulsant.

XVI. EPILEPSY FOUNDATION OF AMERICA SE TREATMENT

PROTOCOL

A. EFA: Drug Recommendations:

1. Adequate dosing of each drug.

2. Benzodiazepines, phenytoin, phenobarbital.

3. Benzodiazepine for active seizures (>50% will respond).

4. High-dose phenytoin (up to 30 mg/kg).

5. Blinded, placebo-controlled, comparative trial.

XVII. VETERANS ADMINISTRATION (VA) TRIAL OF SE

A. 5-year double-blind study in 16 VA and 4 university hospitals.

B. N = 581 patients in GCSE or subtle SE randomized to:

1. Phenytoin, 18 mg/kg.

2. Diazepam, 0.15 mg/kg, then phenytoin, 18 mg/kg.

3. Phenobarbital, 15 mg/kg.

4. Lorazepam, 0.1 mg/kg.

C. Outcome: no clinical and electrical seizures 20 to 60 min after onset

of infusion.

D. Lorazepam superior to phenytoin alone, all others equal in SE.

E. All equally poor in refractory SE.

XVIII. CONCLUSIONS: EMERGENCY MANAGEMENT OF

SEIZURES

A. Seizures and SE are medical emergencies.

B. Optimal outcome depends on early interventions.

C. Appropriate drugs.

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D. Dosing based on mg/kg requirements.

E. Knowledge of new drugs and protocols will allow for advances in

seizure care and patient outcomes.

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STROKE AND SEIZURES

PEARLS

Stroke

1. 50% of TIAs go on to CVAs in five years.

2. Gaze is TOWARD the affected side in intracerebral lesions and AWAY

from the affected side in brain stem abnormalities.

3. Cerebellar hematomas require immediate neurosurgical evaluation.

4. Pontine hemorrhages result in pinpoint pupils.

5. Anterior cerebral artery infarct produces weakness in the contralateral

leg more than arms and face.

6. Middle cerebral artery infarct (the most common infarct) produces

weakness in the contralateral arm and face more than the leg.

7. TIAs last less than 24 hours.

8. The easiest way to lower the intracranial pressure is to put the head on

the bed at 45 degrees.

9. TPA must be administered within 3 hours of the ONSET of symptoms

when treating an ischemic stroke.

10. The dose for TPA for ischemic stroke (0.9 mg/kg, max 90 mg) is

different from that used to treat a myocardial infarction.

Seizures

1. SE mortality exceeds 30% when seizures occur for longer than 60

minutes.

2. SE occurs when there is a seizure of greater than 10 minutes duration or

two seizures without a lucid interval.

3. CNS neuron injury can occur even if the systemic effects of seizures

(fever, motor activity, hypertension) are controlled.

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Stroke and Seizures

4. Mental status changes should begin to resolve within 20-30 minutes of a

seizure. Failure of the mental status changes to begin to resolve within

this time period suggests subtle SE.

5. Subtle SE is electrical SE without the associated motor activity. It is a

late manifestation of prolonged SE and is associated with a high

mortality.

6. Subtle SE can only be diagnosed by EEG monitoring. EEG monitoring

should be considered with prolonged altered mental status, after

neuromuscular paralysis, and with pentobarbital coma or general

anesthesia.

7. All first-line therapies for seizures are about 80% effective when used

quickly in appropriate doses (based on mg/kg dosing).

8. Seizures caused by INH overdoses must be treated with pyridoxine

in order for control to be achieved by standard seizure therapies.

9. Alcohol withdrawal seizures are best controlled and prevented with

lorazepam.

10. Seizures associated with eclampsia are best treated and prevented with

magnesium sulfate.

11. Greater than 50% of psychogenic seizure patients will have at least

one neurogenic seizure, such that therapy should only be withheld if the

diagnosis of psychogenic seizures is confirmed clinically.

12. When IV access is not available, rectal diazepam, IM midazolam and

IM fosphenytoin all can be used to control seizures.

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Stroke and Seizures

SUGGESTED READINGS

1. Kasner SE, Grotta JC: Emergency identification and treatment of acute

ischemic stroke. Ann Emerg Med 1997; 30:5: 642-653.

2. Marler JR, Winters Jones P, Emr M Eds: Proceedings of a national

symposium on rapid identification and treatment of acute stroke. The

National Institute of Neurological Disorders and Stroke, NIH, Bethesda,

Maryland, August 1997.

OTHER REFERENCES

3. Andersen M, Meden P, et al: Effects of Citicoline combined with

thrombolytic therapy in a rat embolic stroke model. 23rd International

Joint Conference on Stroke and Cerebral Circulation. Stroke 1998;

29:1:279.

4. Broderick JP: Guidelines for medical care and treatment of blood

pressure in patients with acute stroke. Proceedings of a national

symposium on rapid identification and treatment of acute stroke. The

National Institute of Neurological Disorders and Stroke, NIH, Bethesda,

Maryland, August 1997.

5. Chiu D, Krieger D, et al.: Intravenous tissue plasminogen activator for

acute ischemic stroke. Stroke 1998; 29:1:18-22.

6. Clark WM, Williams BJ, et al.: Randomized efficacy trial of Citicoline

in acute ischemic stroke. 23rd International Joint Conference on Stroke

and Cerebral Circulation. Stroke 1998; 29:1:287.

7. del Zoppo GJ, Higashida RT, et al.: PROACT: A phase II randomized

trial of recombinant pro-urokinase by direct arterial delivery in acute

middle cerebral artery stroke. Stroke 1998; 29:1: 4-11.

8. Diener HC: The failure of NMDA antagonists. Acute stroke current

approaches to management 1997; 5: 12-14.

9. Dumo P, Fagan SC, et al.: Thrombolysis in acute ischemic stroke. Am J

Health Syst Pharm 1997; 54:19: 2213-2217.

10. Hacke, W., Kaste, M, et al., Thrombolysis with Alteplase 3 to 4.5 Hours

after Acute Ischemic Stroke, M.D, NEJM 2008;359:1317-29

11. Hanston L, Wessel T: Therapeutic benefit of Lubeluzole in ischemic

stroke. 23rd International Joint Conference on Stroke and Cerebral

Circulation. Stroke 1998; 29:1:287.

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Notes

Stroke and Seizures

12. Kaste J, Mau J, et al.: Risk/benefit assessment for mortality and handicap

in 615 ECASS randomized and treated patients. A post-hoc analysis.

23rd International Joint Conference on Stroke and Cerebral Circulation.

Stroke 1998; 29:1:288.

13. Kay R, Wong KS, et al.: Low-molecular-weight heparin for the

treatment of acute ischemic stroke. NEJM 1995; 333:24: 1588-1593.

14. Kidwell CS, Saver JL, et al.: High accuracy of emergency medical

technician identification of stroke using the Los Angeles prehospital

stroke screen (LAPSS). 23rd International Joint Conference on Stroke


15. Kothari R, Brott T, et al.: Accuracy in the diagnosis of stroke. Stroke

1995;26: 12: 2238-2241.

16. Kothari RU, Pancioli A, et al.: Cincinnati prehospital stroke scale:

validity and reproducibility. 23rd International Joint Conference on

Stroke and Cerebral Circulation. Stroke 1998; 29:1:313.

17. Kothari RU, Sauerbeck L, et al.: Acute stroke: delays to presentation and

the patients perceptions. 23rd International Joint Conference on Stroke


18. Kwiatkowski TG, Libman R, et al.: The NINDS rt-PA stroke study:

sustained benefit at one year. 23rd International Joint Conference on

Stroke and Cerebral Circulation. Stroke 1998; 29:1:288.

19. Lyden, P, Thrombolytic therapy for acute stroke – not a moment to lose.

NEJM 2008; 395:13:1393

20. Multicenter Acute Stroke Trial-Italy (MAST-I) Group: Randomized

controlled trial of streptokinase, aspirin, and combination of both in

treatment of acute ischemic stroke. Lancet 1995; 346: 1509-1515.

21. Multicenter Acute Stroke Trial-Europe study group: Thrombolytic

therapy with streptokinase in acute ischemic stroke. NEJM 1996; 335:3:

145-150.

22. Nassissi D: Acute stroke. Emergency management and future

interventions. Mt Sinai J Med 1997; 64:4-5: 241-248.

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Stroke and Seizures

23. Porteous GH, Corry M, et al.: Emergency medical dispatcher

identification of stroke and TIA victims. 23rd International Joint

Conference on Stroke and Cerebral Circulation. Stroke 1998; 29:1:314.

24. Quality standards subcommittee of the American Academy of

Neurology: Practice Advisory: Thrombolytic therapy for acute ischemic

stroke- summary statement. Neurology 1996; 47: 835-839.

25. TenBroeke M, Vincent A, et al.: Lubeluzole: Molecular reversal of

Nitric Oxide induced programed cell death. 23rd International Joint


26. The European Cooperative Acute Stroke Study (ECASS): Intravenous

thrombolysis with recombinant tissue plasminogen activator for acute

hemispheric stroke. JAMA 1995; 274: 1017-1025.

27. The International Stroke Trial (IST): a randomized trial of aspirin,

subcutaneous heparin, both or neither among 19435 patients with acute

stroke. Lancet 1997; 349: 9065: 1569-1581

28. The NINDS rt-PA Stroke Study Group: Tissue plasminogen activator for

acute ischemic stroke. NEJM 1995; 333:24: 1581-1587.

29. The NINDS rt-PA Stroke Study Group: Effect of rt-PA on ischemic

stroke lesion size by computed tomography: preliminary results from the

NINDS rt-PA stroke trial. 23rd International Joint Conference on Stroke


30. TOAST investigators: Usefulness of a low molecular weight heparinoid

in improving outcomes at 7 days and 3 months after stroke. 23rd

International Joint Conference on Stroke and Cerebral Circulation.

Stroke 1998; 29:1:286.

31. von Kummer R, Meier D, et al.: Extent of ischemic lesion and

hemorrhage in ECASS II. 23rd International Joint Conference on Stroke


32. Zhang R, Chopp M: Administration of anti-CD18 antibody extends the

therapeutic window for thrombolysis in rats. 23rd International Joint


08/13

Page 194

Psychiatric Emergencies

E. Bradshaw Bunney, MD, FACEP

Associate Professor and Residency Director, Department of Emergency Medicine, University of Illinois at Chicago

Page 195

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Notes


PSYCHIATRIC EMERGENCIES

I. INTRODUCTION

A. 10-15% of patients seen in the ED have psychiatric problems.

B. 50% of patients seen in the ED between midnight and 8 A.M. have a

current or past psychiatric history.

C. 50% of psychiatric patients have a substance abuse problem.

II. OUTLINE OF PRESENTATION

A. Psychiatric evaluation in the ED, including mental status

examination.

B. Discussion of approach to violent patient.

C. Discussion of approach to suicidal patient.

D. Review of specific psychiatric conditions: organic v. functional (now

termed mental disorders due to general medical condition and mental

disorders with no medical etiology); delirium; dementia;

schizophrenia; depression; mania; anxiety disorders.

E. Psychiatric medications used in the ED.

III. PSYCH EVALUATION IN EMERGENCY DEPARTMENT

A. As with any patient, the first priority is to diagnose and treat any life

threatening medical problems that may be causing the patient’s

behavioral disorder (i.e., hypoglycemia, shock, drug or alcohol

overdose or withdrawal, CVA, hypoxemia, etc.). The ED physician

must first rule out organic cause of patient’s symptoms. If the ED

physician does not, then the psychiatrist most likely will not. Only

15% of new patients at an inpatient psychiatric facility receive a

physical exam.

B. General: Make patient feel comfortable. Developing a rapport with

the patient is the best way of avoiding problems later, such as the

need for restraints.

1. Have patient remain dressed (comfortable), at least initially.

2. Have patient sit in chair rather than on cart.

3. ED physician should sit in a chair next to patient and not stand

above the patient.

4. ED physician should introduce him/herself and ask open-ended

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question such as: What can you tell me about what is going on?

5. Allow patient time to reply!

C. History:

1. Past medical, psych and surgical history, with any recent

problems, i.e., recent infections, trauma, stresses.

2. Medication history, both prescribed and OTC. Always ask about

compliance.

3. Living situations, i.e., married, divorced, separated, widowed.

Home situation: Lives alone? With family? On street? Any

change in family dynamics, i.e., recent separation or death in

family?

4. Employment situation: Is patient employed? What does he do?

Any exposure at work to chemicals? Any recent change in work

situation, i.e., fired, recent lay-off, demotion?

5. Review any past psych history, hospitalizations, suicide attempts,

violence, imprisonment, alcohol or other drug abuse, detox

history. A past psych history is important as it weighs against an

organic cause and toward recurrence of functional disorder.

6. Review of symptoms, with eye toward recent changes, i.e.,

change in weight, sleep pattern, eating habits, mood, headaches,

confusion, speech difficulty, loss of consciousness.

7. One of the most important bits of historical information is why is

the patient coming in now? What has changed to prompt

admission to the ED at this time?

8. Validate history, when possible, with patient’s family or friends.

9. Pay attention to your emotional responses to patient, i.e., counter

transference. What is your gut reaction to patient?

D. Physical examination:

1. Age of patient: most functional psychosis, like schizophrenia,

begins early in life, whereas those patients who present with first

behavioral problem in their late 40s and beyond generally have

an organic problem.

2. Vital signs: any deviation from normal vital signs suggests an

organic cause until proven otherwise.

3. Other physical findings that suggest an organic cause:

diaphoresis, ataxia, nystagmus.

IV. MENTAL STATUS EXAMINATION (MSE)

A. General: MSE should be part of assessment of every psych patient.

Serves as baseline, but primarily used to differentiate organic from

functional illness and helps to establish specific psych diagnosis.

Historically, ED physicians do not perform MSE as frequently as

they should and do not pick up cognitive impairment well when it is

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present. The MSE is THE test to diagnose changes in cognitive

function. An abnormal MSE suggests an organic etiology and thus a

potentially treatable and reversible condition.

B. The MSE is composed of the following parts: general observations,

affect, attention, language and speech, orientation, memory,

visual/spatial and conceptualization.

1. Observation: Is the patient clean, unkempt, disheveled, or

inappropriately dressed for the season? Unkempt and disheveled

patients may be seen with dementia, delirium, schizophrenia or

severe depression.

2. Affect: This is the examiner’s impression of the patient’s

emotions. Is the patient emotionally labile? Are the emotions

blunted? Chronically depressed or schizophrenic patients may

have blunted or flat affect, and manic patients often have labile

affect.

3. Attention: Perform serial 7’s, which is a test of attention and not

intellectual function. Also test attention by having patient

identify a specific letter when the examiner recites random

letters. Patients with dementia, delirium, depression and mania

all have altered attention span.

4. Language and speech: Any form of aphasia suggests an organic

cause. Tests of language include asking patient to name two

common objects like watch or pencil or to repeat a simple phrase

such as “I would like to go home.” Also can test language and

speech by having patient read a simple command and then obey

it, such as having examiner write out “close your eyes” and

instructing the patient to do this. Disorders of language are part

of dementia and organic diseases. Manic patients have loud, fast

and pressurized speech while depressive patients may have slow,

soft and flat speech patterns.

5. Orientation: This is the area most often examined in the ED.

Disorientation is found with dementia and other organic diseases.

Most patients with schizophrenia and other functional behavioral

disorders are well oriented.

6. Memory: Impairment of memory is often seen with dementia and

depression, but with depression the patient can recall if he or she

is given time. Dementia affects deeper storage areas the least, so

that patients with dementia can recall long ago events better than

recent events. Test short-term or recent memory by having

patient repeat three words and then repeat them again after five

minutes. Test remote or long-term memory with questions

concerning birth dates, addresses, and confirmable life events like

birth dates of children or anniversaries. Dementia patients have

defects primarily in short-term memory. Long-term memory

defects suggest other organic etiology.

7. Visual-spatial: Have patient draw a clock with time set at ten

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after eleven. Patients with organic non-dominant hemispheric

lesion often cannot perform this test well. MOST ACCURATE

ONE. 8. Conceptualization: This is proverb interpretation, reasoning and

abstraction. Ask patient to interpret proverb like “grass is always

greener on other side of fence.” Can test reasoning and

abstraction by questions about similarities: “How are arm and

leg alike?” Can also test by asking about similarities between

pairs - apple/grape or refrigerator/stove. Delirium and dementia

are accompanied by decreased level of cortical function.

Depressed patients have diminished ability to perform

abstraction. Proverbs are one area of cognitive function where

chronic schizophrenics do not do well.

9. To summarize, the MSE is used to differentiate organic from

functional illness. Most organic diseases have an abnormal MSE,

while most functional problems have a relatively normal MSE.

In one study, non-psychiatrists missed over half of patients with

cognitive impairment.

V. VIOLENCE IN THE EMERGENCY DEPARTMENT

A. Signs and symptoms of potential violence: Any patient can become

violent, but patients with organic disorders such as dementia,

delirium, and chemical intoxication have high incidence of violence,

as do functional disorders such as mania and schizophrenia. The

following is a list of “early warning signs” of violence:

1. Patient exhibits or threatens violence.

2. Patient makes ED staff anxious or fearful.

3. Behavior alternates between shouting and dozing and between

cooperation and belligerence.

4. Patient expresses fear of losing control.

5. Patient is uncooperative, hostile, agitated and unable to sit still.

Pacing and muttering.

6. Intoxicated with alcohol or other chemicals or withdrawing.

7. Past history of violence. “Frequent flyer” known to police or ED

staff for violence or impulsive behavior.

8. Patient has tense, rigid posture, is easily startled and suspicious.

9. Tattoos that suggest relationship to violent organization or gang.

B. How to avoid precipitating violence:

1. Avoid eye contact with patient.

2. Do not block exits and leave the door to the room open.

3. Maintain a safe distance from potentially violent patient; do not

invade patient’s “space.”

4. Adopt passive, non-confrontational posture and attitude, and

allow patient to ventilate his feelings. Develop a therapeutic

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alliance with the patient.

5. Treat the patient as you expect him to behave.

6. Offer food or drink.

7. Do not make challenging, provocative, or belligerent remarks.

8. If a patient acts out, tell patient directly that “your behavior is

frightening others and we cannot allow such behavior.”

9. Do not turn your back on a potentially violent patient. Never

underestimate the potential for violence.

C. ACEP has summarized the hospital responsibilities to ensure safety

and security for patients and staff in the ED:

1. Provide adequate security personnel, physical barriers,

surveillance equipment, and other security systems.

2. Coordinate these security systems with local law enforcement.

3. Have written protocols in the ED for dealing with violence.

4. Educate staff on preventing, recognizing and dealing with

potentially violent situations.

D. Initial management of the uncooperative, violent patient: If, in spite

of reasonable measures by ED staff, the patient’s conduct continues

to escalate, the ED physician should try to enlist the help and

influence of the patient’s family or friends. If this does not work, a

show of force should be used. This includes:

1. Placing 4-5 security officers in clear view of the patient.

2. The ED physician should then notify the patient in a firm but

non-threatening voice that the continuation of the patient’s

uncontrolled and disruptive behavior will not be allowed, and that

the patient will be restrained by “the team” unless he lies down

now on the ED cart and cooperates with the medical staff.

3. When the decision is made to restrain a patient, the restraints

used should be the least restrictive necessary.

E. Seclusion: The placing of a patient alone in a locked room from

which he/she cannot leave is seclusion.

1. It is considered a form of restraint and therefore needs to be

monitored, usually by video surveillance, and the reason for

seclusion documented in the same way as other restraints. This is

often considered the least restrictive form of restraint but many

emergency departments do not have the necessary room to allow

for seclusion.

2. The specific room in which a patient is secluded must be

observable, devoid of any potentially harmful objects and meet

the local health code for such rooms.

3. If the patient does not respond to seclusion, then physical

restraints may be necessary.

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F. Physical restraints: Physical restraints should be used if, in the ED

physician’s medical opinion, the patient is a danger to himself, other

patients or the staff.

1. Also can use “good faith” restraints to allow evaluation and

treatment of an uncooperative incompetent patient. More suits

are brought for failure to restrain than are brought for improper

detention and restraint. If restraints are to be used, they should be

used properly and restraints must be adequate.

2. Use of physical restraints:

a. Team approach, ideally with six members, one for each

preassigned extremity, one for head, and one to apply

restraints. The team members should remove all objects from

themselves which could be used as weapons by the violent

patient, i.e., ID pins, reflex hammers, pagers, stethoscopes

around neck of staff, etc. Team should advance as a unit

from all directions, restraining their pre-assigned extremity.

Team members should wear protective gear, at least gloves,

to minimize possible exposure.

b. Generally, all violent patients need four limb restraints.

c. Explain to the patient that the restraints are being applied for

his protection and the protection of others, as he cannot seem

to control his behavior. Do not negotiate. Emphasize the

therapeutic reasons for the restraints, not the punitive.

d. The patient should be restrained on his side or prone to avoid

aspiration, and to minimize likelihood of patient’s biting or

spitting.

e. Can apply soft cervical collar that may also restrict patient’s

range of motion and minimize head banging and biting.

f. Patient should be kept in open area where he can be observed

and monitored. Change position of restrained extremities

often and check for neurovascular function.

g. Undress patient and search for concealed weapons or

chemicals.

h. The ED physician must document fully the reasons the

restraints were necessary.

i. Make the entire restraint procedure a team effort, like a

cardiac code, with pre-assigned functions. Should have

rehearsals for the restraint team.

G. Chemical restraints:

1. If the patient is willing to take medication prior to the use of

physical restraints, then give them. Often patients just want to get

back on their medications in order to feel better (stop the voices)

and so will take medication with better cooperation than physical

restraints.

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2. Chemical restraints can also be used after physical restraints if

the patient continues to struggle against the restraints and shows

persistence of uncontrolled behavior. Gather as much history,

physical exam, and laboratory information as possible after

physical restraints and before chemical restraints, as medications

may alter the patient’s behavior, rendering diagnosis difficult.

3. Consider contacting the psych consult before chemically

restraining the patient, as consult may wish to see and examine

the patient before drugs are used.

4. Medications to consider for chemical restraint: (more information

on psych medications at end of outline)

a. Neuroleptics such as Haldol (Haloperidol). Dosage is 2.5-10

mg IM or IV every 30-60 minutes to effect.

b. Atypical antipsychotics such as Risperdal (risperidone) oral

liquid or dissolving tablet 2-4 mg, and Geodon (ziprasidone)

IM 10-20 mg. Onset of action 30-40 minutes.

c. Benzodiazepines such as Ativan (Lorazepam). Dosage is 1-2

mg IV or IM every 30 minutes to effect.

d. The combination of neuroleptics and benzodiazepines has a

synergistic effect and are often used together.

H. Legality of restraints:

1. “Restraints are justified to protect others or self in the judgment

of the health professional,” Supreme Court decision, 1982,

Youngberg v. Romero.

2. The ED physician must ensure that restraints are not negligently

performed. There have been several cases of inpatient

death/suicide while patients were in restraints and unsupervised.

3. In general, there have been many more malpractice suits lost by

ED physicians for having NOT detained a patient who then went

on to commit suicide than there have been suits for unlawful

imprisonment. Documentation of the reason for restraints is

mandatory.

VI. SUICIDE

A. Frequency: Eighth leading cause of death in U.S. Third leading

cause of death in adolescents. Second leading cause of death for

college students. Leading cause of death in young African American

women. Over 30,000 deaths per year are directly attributable to

suicide. Suicide rate highest in older population, but increasing

fastest in the 15-24 age group. Women attempt suicide three times

more often than men, but men complete suicide three times more

frequently than women. Two-thirds of men who commit suicide use

firearms; firearms have overtaken drug overdose as leading method

of completed suicide in women.

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B. Risk factors for suicide. In addition to sex and age, the following are

considered risk factors for suicide:

1. Depression. Patients with clinical depression have a lifetime

probability of suicide of 25-30% and have a suicide rate thirty

times that of general population.

2. Previous attempt. 50% of patients who commit suicide have

previously attempted to do so.

3. Ethanol abuse. Alcoholics, with poor judgment and impulse

control, have a 15-20% lifetime risk of suicide. Twenty percent

of all suicides have a history of alcoholism.

4. Rational thinking loss. Over 90% of patients who commit

suicide have had some type of psychiatric disorder.

Schizophrenics, acting on their delusions or hallucinations, have

a 10-20% lifetime risk of suicide.

5. Separated, widowed, or divorced. Loss, especially recent, of

significant other, with subsequent social isolation, is risk factor

for suicide. Married, with children, have lowest suicide rate,

followed by those never married, then divorced and widowed.

Young widowed men have greatest risk.

6. Organized plan. Patients with well-delineated specific plan at

greater risk than those with only vague thoughts of suicide.

Consider risk/rescue ratio. If risk of death is high and likelihood

of rescue low, then there is a high risk/rescue ratio, which

suggests extreme risk for repeat attempt, i.e., patient who shoots

himself while alone in a motel room has high risk of death and

low rescue likelihood. So a high risk/rescue ratio suggests a

repeat attempt is probable. Low risk and high likelihood of

rescue, as with patient who takes 4 OTC antihistamines and then

calls their parents, has low risk of death and high likelihood of

rescue, so low risk/rescue ratio and decrease risk of repeat suicide

attempt.

7. No social supports. Lack of close family or friends or other

social support such as ethnic, or religious affiliations or

employment-friendships increase suicide risk.

8. Sickness. Chronic, debilitating and painful illnesses increase

suicide risk.

9. Mnemonic of SAD PERSONS for increased suicide risk:

S = sex (male)

A = age (older)

D = depression

P = previous attempt

E = ethanol abuse

R = rational thinking loss

S = separated, widowed, or divorced

O = organized plan

N = no social supports

S = sickness

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One point for each factor; over three is high risk for suicide.

10. No Harm Contracts: These are written or verbal agreements

between the patient and the health professional. They state that

the patient will not cause harm to himself or others, and if he

feels he will not be able to fulfill the contract (i.e., he is going to

hurt himself), he will come in to the ED first. These can be very

dangerous. They may give the physician a false sense of

reassurance about the patient’s suicide risk. They are NOT

legally binding. They afford little or no protection in suicide

malpractice suits.

VII. ORGANIC VS. FUNCTIONAL

A. DSM IV - Diagnostic and Statistical Manual of Mental Disorders.

This is a book of official diagnostic nomenclature and criteria for

mental diseases published by the American Psychiatric Association.

The last edition, the DSM IV, was published in 1994. The Study

Guide to the DSM IV by Dr. Fauman is an excellent addition with

clinical vignettes to illustrate most conditions.

B. Differentiating organic vs. functional psychiatric illness. In general,

ED physicians do a poor job of ruling out organic illness. Over 30%

of patients sent to psych units after being medically cleared are later

found to have organic basis for their behavioral disorder. It is very

important to rule out organic pathology as these illnesses are

potentially reversible. Organic disease is suggested by following

historical findings:

1. Psychosis appearing for the first time in patients over 45 or under

12. Most functional illnesses start in late teens to early 40s; a

younger or older patient with new onset of aberrant behavior is

suggestive of organic pathology.

2. Acute onset. Sudden change in patient’s behavior, without

history of prior psychiatric illness, suggests organic pathology.

3. History of medical disease. Diabetes, hypertension, organic heart

disease, pulmonary, thyroid, or hepatic pathology suggests

organic basis.

4. History of recent trauma. Must rule out intracranial pathology,

pulmonary emboli, or other sequelae of recent trauma as etiology

of patient’s psychiatric illness.

5. Recent hospitalization and/or surgery. Suggests possibility of

complications arising from the medical condition.

6. Medications. Recent changes in medications or possible side

effects of medications suggestive of organic basis. Inquire about

OTC medication use.

7. Visual hallucinations. Organic illness producing psychiatric

symptoms generally produces visual hallucinations, if

hallucinations are present at all. Functional illness tends to

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produce auditory hallucinations, which can be bizarre or well

organized.

8. Drug and alcohol abuse. History of chemical abuse is more often

found with organic illness.

9. History of urinary or fecal incontinence, ataxia, headache, speech

pathology, seizures or diaphoresis suggests an organic cause.

C. Following physical findings suggestive of organic basis:

1. Vital signs. Abnormal vital signs should always suggest organic

basis.

2. Eye and EOM pathology. Nystagmus, pupillary abnormalities

and scleral icterus suggest an organic cause.

3. Neurologic and musculoskeletal disturbances. Ataxia, tremors,

cranial or peripheral nerve deficits suggest organic basis.

4. Endocrine disease. Evidence of goiter, carpopedal spasm,

diaphoresis, and skin pigmentation suggest organic illness.

5. MSE - Abnormalities in the MSE suggests organic involvement.

VIII. DELIRIUM

A. General: This is an organic illness, the essential feature of which is

disturbance of consciousness - defined as reduced clarity of

awareness of environment, disorientation, decreased alertness, and

impaired cognitive function. Acute onset. All symptoms are variable

and may change over hours.

B. Characteristic findings of delirium:

1. Reduced ability to maintain attention to external stimuli;

manifested by examiners having to repeat questions, because of

poor attention span of patient. Also by patient responding with

same answer to all questions, called perseveration.

2. Disorganized thinking, manifested by rambling, irrelevant or

incoherent speech.

3. Reduced level of consciousness. Difficulty keeping awake

during exam or decreased awareness of self and environment.

DIFFERENT FROM DEMENTIA. 4. Perceptual disturbances in form of delusions or hallucinations.

Hallucinations generally visual and ill-defined, non-complex,

such as colors or black spots.

5. Disturbances of sleep-wake cycle with insomnia or daytime

sleepiness.

6. Increased or decreased psychomotor activity. Patient either

pacing or lying dormant.

7. Disorientation. In MSE, the patient is poorly oriented.

8. Memory impairment. In MSE, the patient cannot recall three

objects after five minutes or inability to recall anniversary or

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children’s ages.

9. Clinical features develop acutely over hours or days and

symptoms fluctuate within the day. This fluctuation is one of the

hallmarks of delirium.

10. Should be evidence of general medical condition or substance

intoxication or withdrawal.

11. Causes of delirium:

a. Chemicals: substances most frequently producing delirium:

anticholinergics, clonidine, lidocaine, caffeine, Antabuse,

amphetamines, cocaine, and alcohol use and withdrawal.

b. CNS: SAH, tumors, subdurals, CVA.

c. Infections: meningitis, encephalitis, TB, sepsis.

d. Endocrine: hyperthyroidism.

e. Metabolic: hypoglycemia, electrolyte imbalance, hypoxemia,

hyperthermia, and acid/base disturbance.

12. Treatment of dementia: focused on diagnosing and treating

underlying organic abnormality.

IX. DEMENTIA

A. General: An organic disorder with multiple etiologies. The essential

feature is impairment in short-term and long-term memories,

personality, judgment or language sufficient to interfere with

occupation or social functioning. Insidious onset.

B. Other findings with dementia:

1. Apraxia. Impaired ability to execute motor activities despite

intact motor abilities, i.e., can’t wave good-bye.

2. Aphasia. Difficulty producing names of objects or individuals.

Patient refers to objects as “things” or “it”.

3. Agnosia. Failure to recognize objects. Can’t recognize chairs or

pencils.

4. Abstract thinking impaired. In MSE, the patient is unable to find

similarities and differences between word pairs such as arm/leg

or car/bus.

5. Impaired judgment. Patient unable to organize or plan.

6. Personality changes.

7. No clouding of consciousness as with delirium and onset is

gradual with dementia.

C. Specific organic etiology such as:

1. Substance-inducing dementia due to sedatives, steroids,

anticholinergics, digitalis, oral hypoglycemics, diuretics,

cimetidine, beta blockers, chronic alcohol abuse.

2. Alzheimer’s disease.

3. Vascular dementia, formerly called multi-infarct dementia.

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Notes


4. Dementia due to AIDS.

5. Dementia due to head trauma.

6. Parkinson’s disease, Pick’s disease, Creutzfeldt-Jacob disease.

7. General medical conditions: CNS tumors, subdurals,

neurosyphilis, CNS abscess, hypercalcemia, B1 and B12

deficiency, thyroid disease, and hypoglycemia.

8. Depression: In addition to above organic causes of dementia, can

get dementia from depression. This must be considered in every

case, as this is one of the most treatable causes of dementia.

9. In elderly patient with no prior psychiatric history who presents

with cognitive disturbance, think of dementia and then look for

organic cause.

X. SCHIZOPHRENIA

A. General: Functional illness, which generally starts gradually in

adolescence or early adulthood, rarely after 40. Symptoms have to

have been present for at least six months, with signs of delusions,

hallucinations or disorganization persisting for one month.

B. Characteristic features:

1. Delusions. Erroneous beliefs, with themes of persecution, or

religious or grandiose overtones. Persecutory delusions are most

common with patients believing that they are being followed,

tricked, spied upon, controlled by devices, etc. May be bizarre,

i.e., stranger has removed patient’s internal organs and replaced

them with his own. But some delusions can be well organized

and plausible, i.e., delusion that IRS is after them.

2. Hallucinations. May occur in any sensory modality, but usually

auditory, and generally well organized, i.e., patient hears voices

conversing in pejorative manner about the patient.

3. Disorganized thinking also called loosening of associations.

Suggested by speech patterns with derailment, or slipping from

one topic to another, or completely disorganized so that speech is

not comprehensible, called “word salad.”

4. Disorganized behavior. Disheveled appearance, unusual or

inappropriate dress, and inappropriate sexual behavior such as

public masturbation.

5. Flattening of affect and speech.

6. For a significant portion of the time since the onset of the

disturbance, one or more major areas of functioning such as

work, interpersonal relations, or self-care are markedly below the

level prior to onset of disease.

7. Disturbance not due to substance-effect or general medical

condition.

8. Generally, the cognitive function is intact, so most of mental

status exam is normal.

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Notes


a. Duration of symptoms longer than 6 months.

b. Schizophreniform are the same symptoms but lasting fewer

than 6 months.

c. Brief reactive psychosis is an acute break after an emotional

or traumatic event, usually lasting less than 2 weeks.

C. Management: If agitated, suicidal, homicidal or violent, may need

physical and then chemical restraints with admission.

XI. DEPRESSION

A. General: This is affective, functional disorder, characterized by

disturbance of mood, which is not due to physical condition. This is

most common of all psychiatric disorders with estimates that 15% of

all adults suffer serious depressive symptoms in a given year and 15-

20% of Americans suffer a major depression during their lifetime.

Occurs twice as commonly in women. Suicide rates are high in this

disorder. Can see frank psychosis with depression.

B. Clinical findings (should have five or more present for at least two-

week period):

1. Depressed mood most of day, every day.

2. Markedly diminished interest in hobbies, sports or

activities/endeavors that previously gave pleasure to patient.

3. Significant weight gain or loss of more than 5% of body weight

in one-month period, generally associated with vague somatic

complaints, such as headache, back pain, etc.

4. Insomnia or hypersomnia nearly every night.

5. Psychomotor agitation or retardation. Patient either can’t sit still

or has slow thinking, body movement, and speech pattern.

6. Fatigue or loss of energy.

7. Feeling of worthlessness or excessive/inappropriate guilt.

8. Diminished ability to think or concentrate associated with

indecisiveness. Lack of attention may lead to poor memory

testing in mental status examination, and may be confused with

dementia.

9. Preoccupation with thought of death and suicidal ideation.

Depression is one of major risk factors in SAD PERSONS

mnemonic for suicide.

10. Must be more than mild unhappiness. These symptoms must

cause clinically significant distress or impairment in social or

occupational areas of life.

11. Not due to physiologic effects of substance or general medical

condition.

C. Management: Must rule out organic causes and evaluate patient’s

suicide risk. Admit if any question of suicidal ideation.

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Notes


D. IN SAD CAGES - mnemonic for common features of depression:

IN = interest decreases in everything

S = sleep disorder

A = appetite alteration

D = dysphoric mood

C = concentration decreases

A = affect blunted

G = guilt

E = energy diminishes

S = suicide risk

XII. MANIA

A. General: Affective, functional mood disorder. Mean age at onset is

early 20s. Usually begins suddenly with rapid escalation of

symptoms over a few days. Must be managed carefully by ED staff

as they usually appear very pleasant and likable, but may turn violent

suddenly when demands are thwarted. Mania, like the other affective

disorder, depression, can present with frank psychosis.

B. Characteristic findings in manic patients:

1. Abnormal and persistently elevated, expansive, or irritable mood

lasting at least one week.

2. During this period of mood disturbance, three or more of the

following symptoms are present:

a. Inflated self-esteem or grandiosity that may reach delusional

proportions.

b. Decreased need for sleep.

c. Extremely talkative, with loud, pressured, rapid speech

patterns.

d. Flight of ideas. Abrupt changes in topics with no connections

between them.

e. Distractibility. Patient easily distracted by surrounding

objects, people and even the environment.

f. Increased activity or psychomotor agitation. Excessive

participation in multiple activities such as multiple new

business ventures, new political goals, etc.

g. Excessive involvement in pleasurable activities that have a

high potential for painful consequences. Reckless driving,

spending sprees, sexual indiscretions.

h. Symptoms sufficiently severe so as to cause marked

impairment in occupation or social activities.

i. Not result of general medical condition or chemicals.

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Notes


C. Management of mania: These patients must be viewed as risk for

violent behavior in spite of their likeable and ingratiating

personalities, as they have extreme emotional lability. Thus most of

these patients should be admitted to prevent harm to themselves or

others. They may need physical or chemical restraints. Lithium is

generally the accepted treatment for mania, but this takes days to

work and is rarely used in the ED.

XIII. BIPOLAR DISORDER

A. General: Patient has cycles of both mania and depressive episodes.

Formerly called manic-depressive.

XIV. ANXIETY DISORDERS

A. General: Prototype is panic attack. Anxiety disorders are increasing

in frequency and now approach depression as the leading mental

health problem in the country.

B. Characteristic features of panic attack:

1. Essential feature is discrete period of intense fear or discomfort.

These attacks start very suddenly and build to a peak rapidly in

10 minutes or less. Often accompanied by a sense of imminent

danger or doom, and an urge to escape. Not due to chemical or

general medical condition.

2. Should be associated with at least four of the following 13

somatic or cognitive symptoms:

a. Palpitations or rapid heart rate.

b. Sweating.

c. Trembling or shaking.

d. Shortness of breath or sense of smothering.

e. Feeling of choking.

f. Chest pain or pressure.

g. Nausea or abdominal pain.

h. Dizziness or lightheadedness.

i. Fear of losing control.

j. Fear of dying.

k. Paresthesias.

l. Chills or hot flashes.

C. Panic Disorders: If a patient has recurrent panic attacks followed by

at least one month of persistent fear of another panic attack, this is

panic disorder. Panic disorders classified as with or without

agoraphobia, which is anxiety about being in places or situations in

which panic attacks might occur and from which escape is difficult

or embarrassing, i.e., being in a crowd or being in line, or in plane,

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Notes


train, etc. Most serious complication of panic disorder is suicide,

which may reach 20% of patients with panic disorders. Of course,

must rule out organic pathology, as many of the above symptoms are

present with organic diseases, i.e., myocardial infarction, pulmonary

emboli, hypoglycemia, etc.

XV. PSYCHIATRIC MEDICATIONS

A. Antipsychotics/neuroleptics:

1. Act on dopamine subtype 2 receptors. The degree to which they

block or antagonize this receptor determines the potency.

a. Low potency: Chlorpromazine (Thorazine) Chlorprothixene

(Taractan), mesoridazine (Serentil), thioridazine (Mellaril).

b. Medium potency: Loxapine (Loxitane), molindone (Moban),

perphenazine (Trilafon).

c. High potency: fluphenazine (Prolixin), haloperidol (Haldol),

pimozide (Orap), trifluoperazine (Stelazine), thiothixene

(Navane).

2. Adverse effects associated with neuroleptic medication.

3. Extrapyramidal symptoms:

a. Dystonia: Brief or sustained abnormal postures that include:

torticollis, oculogyric crisis, laryngeal spasm, facial

grimacing, opisthotonos, accompanied by panic or anxiety.

Treated with diphenhydramine (Benadryl) 25 – 50 mg

PO/IM/IV or benztropine (Cogentin) 1 - 2 mg PO/IV.

b. Parkinsonism: Shuffling gait, bradykinesia, mask-like facies,

resting tremor, rigidity.

c. Akathisia: Motor restlessness which includes pacing, rocking,

shifting from one foot to another.

4. Other adverse effects:

a. Tardive dyskinesia: Involuntary buccolinguomasticatory

movements including lip smacking, tongue protrusion,

grimacing and chewing. Occurs after chronic use of

neuroleptics.

b. Neuroleptic malignant syndrome: Hyperthermia, rigidity,

altered mental status, autonomic instability. Treated with

supportive care, antipyretics, fluids and consider Dantrolene.

B. Atypical antipsychotic are combined dopamine and serotonin

antagonists. Generally have significantly less extrapyramidal side

effects. Also have a decreased incidence of prolonged QT syndrome

though this is not universal.

1. Clozapine (Clozaril) blocks serotonin (5-HT2A) receptors as well

as D2 receptors.

a. Works well on those resistant to neuroleptics or those prone

to the extrapyramidal side effects of neuroleptics.

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Notes


b. Adverse effects: Agranulocytosis (1-2%), seizures (1-6%),

hypersalivation.

2. Risperidone (Risperdal):

a. Considered first line in some patients.

b. Adverse effects: orthostatic hypotension, it has some alpha

adrenergic blockade.

3. Ziprasidone (Geodon):

a. Currently the only IM atypical antipsychotic on the market.

b. QT prolongation similar to the classic neuroleptics.

4. Olanzapine (Zyprexa):

a. Adverse effects: sedation and anticholinergic effects.

5. Quetiapine (Seroquel):

a. Not used in the ED because it carries a recommendation of

slow titration and so cannot be used at the doses needed to

change behavior abruptly.

C. Antidepressants:

1. MAOIs: phenelzine (Nardil), tranylcypromine (Parnate); block

the metabolism of norepinephrine, serotonin and dopamine

throughout the CNS.

a. Adverse effects: food (those that contain Tyramine) and drug

interactions exaggerate peripheral sympathetic responses,

hypertension, tachycardia, diaphoresis, and headache.

Exaggerate central serotonin response.

b. Serotonin syndrome- hyperpyrexia, CNS depression,

hypertonicity. Treated with supportive care, fluids, consider

Cyproheptadine.

2. TCAs block many different receptors.

a. Adverse effects: block sodium channels leading to QRS

widening, arrhythmias, and seizures, block muscarinic

receptors leading to anticholinergic toxidromes and seizures,

adrenergic antagonism leading to hypotension.

3. Selective Serotonin Reuptake Inhibitors (SSRIs): fluoxetine

(Prozac), fluvoxamine (Luvox), paroxetine (Paxil), sertraline

(Zoloft) act by inhibiting serotonin reuptake. The order of

potency is paroxetine > sertaline > fluvoxamine > fluoxetine.

a. Adverse effects: fewest adverse effects of all antidepressants.

GI distress, sexual dysfunction, hyponatremia (SIADH).

4. Venlafaxine (Effexor) similar mechanism to TCAs but has much

more serotonin effect than norepinephrine and little effect on α

adrenergic and Muscarinic receptors.

a. Adverse effects: well tolerated, tremor and hypertension at

higher doses.

5. Bupropion (Wellbutrin) inhibits the uptake of Dopamine and to a

smaller extent norepinephrine.

a. Adverse effects: sexual dysfunction and seizures.

6. Nefazodone (Serzone): serotonin 2 receptor antagonist and

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Notes


reuptake inhibitor.

a. Adverse effects: sedation, dry mouth, constipation, and

lightheadedness.

7. Mirtazapine (Remeron) acts on autoreceptors to increase

norepinephrine and serotonin release.

a. Adverse effect: sedation, dry mouth, weight gain.

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Notes


PSYCHIATRIC EMERGENCIES

PEARLS

1. The first and most important part of assessing patients for psychiatric

illness is to rule out a medical emergency, e.g., hypoglycemic, post-ictal

state, drug-induced state, etc.

2. Assume organic illness until proven otherwise, as they are potentially

reversible.

3. Visual and tactile hallucinations which wax and wane suggest organic

illness, such as delirium tremors.

4. Auditory hallucinations which are stable and fixed suggest functional

disease, such as schizophrenia.

5. Look for evidence of a potentially violent patient: past history of

violence, agitated state, verbal threats, pressured speech, and lability.

6. In dealing with a potentially violent patient, avoid confrontation, offer

food or drink, and make a show of force which clearly overpowers and

outnumbers the patient when applying restraints.

7. Depression is the most common psychiatric disorder.

8. Women attempt suicide more often than men; men complete suicide

more often than women.

9. Those at greater risk for suicide include those who live alone with little

social support. Widowed men are at greatest risk.

10. Depression, schizophrenia and alcoholism are major risk factors for

suicide.

11. Patients with mania are potentially violent and frequently have wild

mood swings.

12. Historical findings significant for an organic rather than primary

psychiatric basis: onset after age 40, headache, recent trauma,

incontinence, systemic illness, recent hospitalization, recent medication

change, hallucinations that are visual or tactile rather than auditory,

known alcohol or drug abuse.

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Notes


13. Abnormal vital signs, neuro deficits, signs of autonomic excess, and

delirium suggest organicity.

14. Neuroleptics side effects include: autonomic anticholinergic properties,

extrapyramidal side effects, dystonic reactions, tardive dyskinesia,

neuroleptic malignant syndrome.

15. Document the reasons for restraining the patient.

16. Night shifts have the highest incidence of patients with psychiatric

illness.

17. Disorientation is more commonly found with organic illnesses, such as

delirium; whereas functional psychiatric patients, such as

schizophrenics, generally retain orientation.

18. Mnemonic for potentially suicidal patients: “SAD PERSONS.”

19. Delirium has a rapid onset with fluctuating symptoms during the day.

20. Dementia generally has a gradual onset.

21. Mnemonic for depression: “IN SAD CAGES.”

22. Anxiety disorders, such as panic attacks, are increasing in frequency and

can be associated with suicide.

23. MSE is for differentiating between organic and functional illnesses.

24. Restraints should always be the least restrictive possible that protects

the patient and staff but also gives the patient as much autonomy as

possible.

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Notes


REFERENCES

1. Violence Prevention in Emergency Medicine, Foresight, Issue 47,

Winter 1997, ACEP.

2. DSM-IV. Diagnostic and Statistical Manual of Mental Disorders,

American Psychiatric Association, 1994.

3. Olshaker JS, Browne B, et al. Medical Clearance and Screening of

Psychiatric Patients in the Emergency Department. Academic

Emergency Medicine, 1997;4:124-128.

4. Armitage DT, Townsend GM. Emergency Medicine, Psychiatry, and

the Law. Emergency Medicine Clinics of North America.

1993;11:869-887.

5. Hill HF III. Use of Restraints. In: Emergency Medicine Risk

Management. A Comprehensive Review, 1991:381-385.

6. Tueth, MJ. Predicting Suicide in the Emergency Department.

American Journal of Emergency Medicine. 1996;14:434.

7. Kane JM. Schizophrenia. New England Journal of Medicine.

1996;334:34-41.

8. Hutzler JC, Rund DA. Behavioral Disorders: Emergency Assessment

and Stabilization. In: Emergency Medicine-A Comprehensive Study

Guide. Tintinalli JE, Ruiz E, et al. 4th ed. 1996:1334-1340.

9. Kim SW. Panic Disorder: In: Emergency Medicine-A Comprehensive

Study Guide. Tintinalli JE, Ruiz E, et al 4th ed. 1996:1348-1350.

10. Henneman, PL, et al. Prospective Evaluation of Emergency Department

Medical Clearance. Annals of Emergency Medicine. 1994;24:672.

11. Hoffman DP, Dubovsky SL. Depression and Suicide Assessment.

Emergency Med. Clinics of North America. 1991;9:107-121.

12. Weissman MM, et al. Suicidal Ideation and Suicide Attempts in Panic

Disorder. New England J of Medicine. 1989;321:1209.

13. Patterson WM, Dohn Hospital, et al. Evaluation of Suicidal Patients:

The SAD PERSON Scale. Psychosomatics. 1983;24:343-349.

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Notes


14. Schmidt T. Suicide. In: Rosen P, Barkin R, et al. Emergency

Medicine-Concepts and Clinical Practice. 3rd ed. 1992:2066-2072.

15. Geldmacher DS, Whitehouse PJ. Evaluation of Dementia. New England

Journal of Medicine. 1996;335:330-336.

16. Hall RC, Gardner ER, et al. Physical Illness Manifesting as Psychiatric

Disease. Archives of General Psychiatry. 1980;37:989-995.

17. Centers for Disease Control. Suicide Among Older Persons. JAMA.

1996;275:509.

18. Lessmeier TJ, et al. Unrecognized Paroxysmal Supraventricular

Tachycardia: Potential for Misdiagnosis as Panic Disorder. Archives

Internal Medicine. 1997;157-537.

19. Alexopoulos, G.S. Treatment of Agitation in Older Persons with

Dementia. Postgraduate Medicine, April 1998.

08/13

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Intensive



MiscellaneousTopics

Page 219

Page 220

Pulmonary Emergencies

Matthew Jordan, MD, FACEP

Clinical Assistant Professor, University of Illinois College of Medicine; Department of Emergency Medicine, Presence Resurrection Medical Center

Page 221

Page 222

Notes


PULMONARY EMERGENCIES

I. ASTHMA

A. Definition:

1. A chronic inflammatory disorder characterized by reversible

airway obstruction and/or increased airway broncho-constrictive

response to multiple stimuli.

2. Reversible airway obstruction secondary to an inflammatory

response.

B. Epidemiology:

1. 15 million in U.S. (5% of population).

2. 1.5 million ED visits.

3. 500,000 hospitalizations.

4. 5,500 deaths.

5. D/I costs totaled 11.3 billion.

6. Prevalence:

a. Children > adults.

b. Females > males.

c. African-Americans > Caucasians.

C. Disturbing trend:

1. Incidence and prevalence of asthma are increasing across all

races, gender, and age strata.

2. Mortality increased in U.S. in 1980s to early ’90s.

3. Most substantial increase was among children.

4. Mortality rates in African-Americans are consistently higher.

5. Factors contributing to these trends include poor initial

assessment; use of OTC medications which delays treatment; and

consistent under-use of corticosteroids.

D. Pathophysiology:

1. Was historically felt to be a combination of IgE mediated and

cholinergic effects.

2. Focus now is upon inflammatory response, both immediate and

delayed.

3. Usually begins with some type of “trigger”:

a. Allergens.

b. Environmental antigens.

c. Exercise.

d. Menstruation.

e. Medications (aspirin).

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Notes


f. Gastroesophageal reflux.

E. Pathology:

1. Events above lead to:

a. Recurrent bronchoconstriction.

b. Congestion.

c. Edema.

d. Mucous production.

2. Chronic disease ultimately leads to cell damage and irreversible

airway damage.

F. Risk factors for death from asthma:

1. History of severe/sudden attacks.

2. Prior intubation.

3. Prior ICU admission.

4. Two or more admissions in previous year.

5. Three or more ED visits in previous year.

6. Use of >2 MDI short acting B2 agonist per month.

7. Illicit drug use.

8. Recent withdrawal from systemic corticosteroids.

9. Serious psychiatric or psychosocial problems.

G. Presentation:

1. Clinical triad of wheezing, dyspnea, and cough.

2. Ominous signs:

a. “Silent” chest.

b. Agitation/lethargy.

c. Paradoxical respirations.

d. Cyanosis (very late finding due to left shift of oxyhemoglobin

dissociation curve in respiratory alkalosis).

e. Diaphoresis.

3. Possible signs of severe attack:

a. Tachypnea.

b. Tachycardia.

c. Pulsus paradoxus >10.

d. Accessory muscle use.

e. Inability to speak >3-4 word sentences.

f. PEFR <50% of P/SFB.

g. ALL OF THE ABOVE MAY BE ABSENT EVEN IN A

SEVERE ATTACK.

4. Poor initial predictors of severity:

a. Patient’s perception of attack.

b. Intensity of wheezing.

c. Pulse ox.

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Notes


H. Diagnostic evaluation:

1. Spirometry:

a. Forced expiratory volume in 1 second (FEV1).

b. Peak expiratory flow rate (PEFR) (L/s):

i. Easy to perform at bedside/home.

ii. Initial reading can predict disposition with >85%

sensitivity/specificity.

iii. Absolute number not useful; need to calculate percent of

predicted (P) (based on height/weight) or percent of

symptom free best (SFB).

iv. Severity assessment can be made based on initial PEFR:

Mild = >80% P/SFB.

Moderate = 50 – 80% P/SFB.

Severe = <50% P/SFB.

2. Arterial blood gas:

a. Measures gas exchange, not pulmonary function; has not

demonstrated usefulness in clinical decision making.

b. Demonstrates ventilatory failure.

3. Chest radiography:

a. Will be abnormal in 1/3 of all patients.

b. Usually show concomitant disease (pneumonia,

pneumothorax, etc.).

4. CBC, ESR, ECG, etc., rarely useful in acute exacerbations of

patients with known disease.

I. Differential diagnosis:

1. “All that wheezes is not asthma”:

a. CHF.

b. COPD.

c. Pneumonia.

d. Foreign body.

e. Tumor.

f. Croup.

g. Aspiration.

h. Pulmonary embolism.

2. Be especially cautious in the elderly patient with no previous

history of asthma/COPD/smoking:

a. “Cardiac asthma”- in acute pulmonary edema, fluid in alveoli

increases wall tension with collapse during inspiration/

exhalation which causes wheezing.

b. Incidence greater than “new asthma” in patients >60 years.

c. B-agonist induced tachycardia may increase myocardial

oxygen demand and worsen ischemia.

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Notes


J. Treatment:

1. Goals are to ensure oxygenation, reverse obstruction, relieve

inflammation, reduce relapse, and treat concomitant disease.

2. Oxygen - always good/never bad - should be placed on patients at

presentation.

3. β-agonist:

a. Increase cyclic-AMP- causes bronchodilatation and increases

mucociliary clearance.

b. Can be β-selective or non-selective, injected or inhaled,

nebulized or MDI, standard or long acting.

c. Selective: Albuterol sulfate, Metaproterenol, Pirbuterol,

Terbutaline.

d. Non-selective: Epinephrine.

e. Long acting: Salmeterol (Serevent), Formoterol - no role in

acute treatment at this time.

f. Many studies demonstrate similar efficacy of using nebulized

agent vs. MDI in acute exacerbation; however, MDIs require

patient compliance/proper use.

g. Standard dose of Albuterol (adult) is 2.5mg per nebulized

treatment.

h. Albuterol has R and S isomer:

i. S isomer has no bronchodilatory activity and may induce

bronchial hyper-reactivity.

ii. Levalbuterol (Xopenex)- R isomer only now available but

no strong evidence of superior clinical efficacy yet.

iii. IV Albuterol not used in U.S.; used extensively

elsewhere. Efficacy is controversial. SQ Epinephrine is

less efficacious than nebulized Albuterol. Epinephrine

(SQ) should be used only in patients with inadequate

ventilation for nebulizer therapy. Caution advised in

patients with heart disease.

4. Corticosteroids:

a. Inhibit recruitment of inflammatory cells and release of

proinflammatory mediators.

b. May restore β-2 responsiveness (controversial).

c. Standard of care in moderate to severe attack.

d. Has been shown to significantly reduce relapse.

e. Onset of action around 6 hours.

f. No benefit to IV vs. oral.

g. No benefit to “high dose” (>2mg/kg prednisone).

h. Standard dose (adult):

i. Prednisone (40-60 mg).

ii. Methylprednisolone (60-125 mg).

5. Anticholinergic agents:

a. Reverse large airway bronchoconstriction and may have

additive effect on β-2 response.

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Notes


b. Nebulized ipratropium bromide (Atrovent) is most studied

drug and only approved in U.S.

c. Standard dose (adult) is 0.5 mg per nebulized treatment.

d. Studies show that these agents are probably most efficacious

in moderate to severe exacerbations.

6. Magnesium sulfate:

a. Relaxes bronchial smooth muscle.

b. Majority of studies show benefit of use in severe attacks.

c. Dose: 1-3 gm slow IV infusion or push.

7. Heliox:

a. Mixture of helium (60-80%) with oxygen (20-40%).

b. Reduces gas density, airway resistance, and non-laminar

flow.

c. Reduces work of breathing.

d. Studies on outcome data vary - consider in severe attack.

8. Leukotriene modifiers:

a. Diminish bronchoconstriction.

b. Zafirlukast (Accolate) and montelukast (Singulair) currently

recommended for maintenance treatment.

c. Use in acute exacerbations is evolving (not currently

recommended for ED use), but multiple ongoing and

completed trials show improved PFTs and decrease relapse

with use.

9. Ketamine:

a. Causes bronchodilation, so good choice as induction agent for

intubation.

10. Methylxanthines:

a. Mechanism of action is unclear.

b. Have a very narrow therapeutic window.

c. Not recommended for use in acute exacerbations at this

time.

K. Ventilatory support:

1. Noninvasive (CPAP, BiPAP):

a. Some data show benefit to use but no large randomized

controlled studies have shown reduced intubation, relapse,

etc.

b. Currently not recommended as standard of care.

2. Intubation:

a. <1% of asthmatics will require.

b. Indications:

i. Absolute - apnea, coma.

ii. Relative - hypercarbia, depressed level of consciousness,

exhaustion.

c. Rapid sequence orotracheal intubation has lowest

complication rate and highest success rate.

i. Lidocaine (1.5 mg/kg) given 3 minutes prior to

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Notes


neuromuscular blocking agent may reduce bronchospasm.

ii. Ketamine is preferred induction agent.

d. Mechanical ventilation:

i. Need to reduce/eliminate auto-PEEP.

Inhaled volume exceeds exhaled volume.

Leads to air-trapping, pneumothorax, and decreased

right heart filling.

ii. Permissive hypercapnia (hypoventilation):

Goal is to oxygenate and reduce airway pressure while

tolerating increased pCO2.

Low tidal volumes (5-7 cc/kg).

Short inspiration/long expiration.

Paralyze patient to rest muscles and reduce vent

cycling.

Allow elevated pCO2 to 60-80, pH to 7.1.

L. Disposition:

1. Multifactorial based on patient's response to therapy.

2. Socioeconomic status, expectation of compliance, etc.

3. 10-20% of all patients will relapse to ED within two weeks.

4. Response to treatment using PEFR % is best clinical tool.

a. Patients >70% P/SFB without persistent symptoms and with

access to medication and follow-up care can be safely

discharged home.

b. Patients <50% P/SFB should be admitted regardless of

symptoms.

c. Patients with persistent symptoms and/or P/SFB between 50-

70% are in the gray zone - consider admission, close medical

follow-up, or observation unit if available. Err on the side of

admission.

M. Pregnancy and asthma:

1. Asthma complicates 4% of all pregnancies.

2. 35-45% of these women required hospitalization in one study.

3. Treatment generally does not change; β-agonist and

corticosteroids are considered safe.

4. Hyperventilation of pregnancy:

a. Leads to an expected elevation of pO2 and decrease of pCO2.

b. This means that a pO2 <70 mmHg or pCO2 >35 mmHg is

significant and may represent hypoxemia and/or respiratory

failure in the pregnant patient.

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Notes


II. CHRONIC OBSTRUCTIVE PULMONARY DISEASE

A. Definition:

1. Best described as a spectrum of three diseases alone and in

combination and their resultant pathologic condition:

a. Chronic asthma (airway reaction).

b. Chronic bronchitis (airway inflammation).

c. Emphysema (airway collapse).

2. The combination of these entities ultimately leads to airway

destruction.

B. Epidemiology:

1. In U.S., approximately 10% of those over 55 y.o. are affected.

2. 4th

leading cause of death.

3. ONLY one of the top five causes of death that is increasing in

prevalence.

4. Mortality rate for women is increasing.

C. Predisposing factors:

1. Cigarette smoking accounts for 80-90% of all cases.

a. Age of starting and total pack-years is predicative of

mortality.

b. Only 15% of all smokers develop clinically significant

COPD.

2. Environmental and occupational causes are probably significantly

under-recognized and under-reported.

3. Alpha1-antitrypsin deficiency is only proven genetic risk factor.

D. Pathophysiology:

1. Very complex and progressive mechanism but generally a cycle

of recurrent bronchoconstriction and mucous plugging leading to

airway obstruction, impaired elastance and destruction.

E. Presentation:

1. Asthma - see above.

2. Emphysema - pink puffer:

a. Abnormal permanent enlargement of the airspaces distal to

the terminal bronchioles.

b. Very thin, secondary to chronic tachypnea.

c. Alert, anxious.

d. Pursed lips on expiration increases intraluminal bronchial

pressure (auto-PEEP).

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Notes


e. Hunched forward which increases accessory muscle

efficiency.

f. Hyperresonant lungs and diminished breath sounds.

3. Chronic bronchitis - blue bloater:

a. Productive cough on most days for three months over two

years where other causes have been eliminated.

b. Heavyset, no tissue wasting.

c. Plethora and cyanosis secondary to polycythemia and

hypoxemia.

d. JVD and anasarca often present secondary to corpulmonale.

e. Cough, purulent sputum, rhonchi.


1. Clinical observation directs most treatment.

2. FEV1 is superior to PEFR in predicting outcome - multiple

guidelines established in the pulmonary literature - usefulness in

ED questioned.

3. ABG allows monitoring of hypercarbia, especially if patient is

aware of baseline levels.

4. Pulse oximetry allows constant monitoring of oxygenation;

however, most COPD patients expected to be below 95%.

Comparison to patient’s baseline is most useful (with O2 on if

that is normal for patient).

5. Chest radiography - will demonstrate some abnormality in most

cases (hyper-inflated lung fields, decreased vascular markings) -

most useful for diagnosing coexisting pathology.

6. ECG - used to diagnose concomitant cardiac disease - continuous

cardiac monitoring probably more important.

G. Treatment:

1. Goals of treatment:

a. Ensure tissue oxygenation.

b. Assist gas exchange.

c. Reverse bronchospasm.

d. Treat concomitant disease.

2. Oxygen induced hypercapnia is very controversial (both its

mechanism and its effect, deleterious or not, on treatment). pCO2

does rise in oxygen administration, but minute ventilation

changes very little. All sources, however, suggest limiting O2 as

tolerated with a goal of 60 mmHg pO2, or 90% oxygen

saturation. Nasal canula or Venturi masking at a fixed FiO2 is

recommended.

3. Pharmacotherapy is similar to that of acute asthma (see above).

a. Increased efficacy of anticholinergics has been shown.

b. Methylxanthines probably have expanded role here in acute

exacerbations:

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Notes


i. Increases diaphragm strength.

ii. Improves spirometry.

iii. However, data doesn’t demonstrate clinical efficacy.

iv. Aminophylline - load 5mg/kg over 10-15 minutes in

acutely ill patients not previously taking (Rosen).

4. Empiric antibiotics:

a. Controversial topic in acute bronchitis but most studies

support their use in COPD (some texts suggest treatment in

every exacerbation even in the absence of pneumonia

symptoms).

b. Those with signs/symptoms of CAP should be treated per

protocols (see below).

H. Ventilatory support:

1. Noninvasive assisted ventilation:

a. CPAP, BiPAP, IPAP recruit alveoli, reduce dead space - all

have been shown to be efficacious.

b. Little difference in efficacy of above in multiple studies.

c. Patient must be cooperative, not vomiting, protecting airway.

2. Intubation:

a. Indications are similar to asthma.

b. Pressure support method has been used extensively and is

described as being most comfortable for the patient and may

accelerate weaning.

c. Permissive hypercapnia has shown to cause the least amount

of ventilator complications.

d. Neither of the above has shown to improve outcome as

compared with volume-cycled modes.

I. Disposition:

1. There is limited role for discharge of patients with acute

exacerbation of COPD secondary to:

a. Limited pulmonary reserve.

b. High likelihood of comorbid disease.

c. High incidence of relapse.

2. Patients considered for discharge home should have:

a. Home O2 as needed.

i. Adequate bronchodilator treatment with appropriate

knowledge and use of device.

b. Corticosteroid dosing.

c. Close follow-up and/or home care.

d. If available, and FEV1 of >50% predicted.

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Notes


III. PNEUMONIA

A. Epidemiology:

1. 6th

leading cause of death in U.S.

2. 1 million hospitalizations annually.

3. D/I cost of $23 billion per year.

4. Frequency of atypical, resistant, and opportunistic infections is

increasing secondary to:

a. Immune compromised and immunosuppressive states.

b. Improper antibiotic use.

c. Increase in foreign travel.

5. Good news is that morbidity and mortality can be drastically

reduced by prompt diagnosis and initiation of appropriate therapy

in the ED.

B. Pathophysiology:

1. Organisms inhaled or aspirated.

2. Hemategenous seeding also possible but less common.

3. Inflammatory response in alveoli:

a. Air space fills with WBC, bacteria, and exudate.

C. Clinical features (atypical agents follow this pattern less frequently

and general have vague symptoms):

1. Cough (80-90%).

2. Fatigue (90%).

3. Fever (75%).

4. Sputum production (60%).

5. Pleuritic chest pain (40%).

D. Predisposing factors:

1. Nursing home, chronic care residences.

2. Chronic lung disease - COPD, CHF, cancer.

3. Systemic disease - diabetes, valvular heart disease.

4. Immune compromised states - HIV, SS, leukemia, chemotherapy.

5. Chest wall disorders - trauma, post-op pain, neuropathies.

6. Aspiration risks - intoxication, seizure, syncope, sedatives,

debilitated.

7. Impaired mucociliary clearance - smoking, age.

8. Iatrogenic - indwelling catheters, bronchoscopy, intubation.

E. Patient history:

1. Very important to obtain a thorough history.

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Notes


2. May give clues to etiologic agents which vary depending on

patient’s:

a. Age.

b. Comorbid disease.

c. Travel.

d. Season of illness.

e. Symptoms.


1. WBC count:

a. Usually not predicative of outcome or disposition.

b. >15,000 increases the probability that the patient has a

pyogenic bacterial etiology.

c. Less useful at extremes of age - look for a left shift in the

absence of elevation, especially in the elderly.

d. May be most useful to look for immune compromised state-

absolute neutropenia necessitates IV therapy.

2. Sputum cultures:

a. Theoretically, should be the most useful information;

however, therapy must begin prior to results.

b. Gram staining can be done, but correlation to ultimate culture

results is poor (<40%).

3. Blood cultures:

a. Again, most useful before antibiotics.

b. Considered a Quality Indicator; however, few are positive

and results rarely change the antibiotic chosen.

4. Chest radiography:

a. Most useful diagnostic tool.

b. May give important clues to causative agent while ruling

in/out other pathology.

i. Must be used along with clinical picture, and should never

rule out diagnosis of pneumonia as symptoms usually

precede radiographic findings.

ii. Dehydration, leukopenia, immune compromised states,

and elderly status all delay appearance of infiltrate.

5. ABG/pulse oximetry:

a. Used to determine oxygenation and ventilation status.

b. Respiratory failure more common at extremes of age.

6. Tests specific for agent may be needed:

a. Legionella DFA, urinary antigen testing.

b. Mycoplasma ELISA testing.

c. Pneumoniae IFA.

G. Specific etiologic agents:

1. Streptococcus pneumoniae:

a. Gram+, lancet shaped, encapsulated.

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Notes


b. Most common cause of CAP.

c. Winter and early spring.

d. Splenectomized/immune-compromised patients prone to

severe, rapidly progressive illness.

e. Drug resistant Strep is becoming much more common (15-

20% in Chicago area) (see below).

f. Classic picture:

i. Single shaking rigor.

ii. Pleuritic chest pain.

iii. Rust colored sputum.

iv. Single lobar infiltrate - usually in the lower lobes or right

middle lobe (effusions present in 10-25%).

2. Haemophilus influenzae:

a. Gram-, pleomorphic rods, +/- encapsulated.

b. Winter and early spring.

c. Becoming most common in elderly and debilitated.

d. Classic picture:

i. Elderly or debilitated patient, possibly from nursing

home.

ii. Cough and severe SOB, green sputum.

iii. Diffuse rales without consolidation.

iv. Patchy, multilobar infiltrate.

3. Klebsiella pneumoniae:

a. Gram-, encapsulated rods.

b. Common in alcoholics, diabetics, COPD.

c. Fall and winter.

d. Upper lobe infiltrates.

e. Classic picture:

i. Alcoholic/non-domiciled.

ii. Sudden cough with multiple shaking chills.

iii. Severe SOB with cyanosis.

iv. Sputum thick, progressing to currant jelly-like (thick,

dark, caused by necrotizing nature of illness).

v. Elevated WBC count.

vi. RUL infiltrate +/- empyema.

4. Staphylococcal pneumoniae:

a. Gram+, in clumps.

b. Less common but can be very severe in nature.

c. Classic picture:

i. Debilitated patient with antecedent mild URI.

ii. Purulent sputum.

iii. Hemoptysis.

iv. Empyema, abscess formation.

5. Mycoplasma pneumoniae:

a. Gram-, but don’t stain well (smallest free living organism).

b. Seen often in older children and young adults.

c. Classic picture:

i. Adolescent.

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Notes


ii. Prolonged constitutional symptoms: Arthralgias,

cephalgias, ear ache, URI, bullous myringitis.

iii. Diffuse rhonchi, possibly wheezing.

iv. Diffuse interstitial infiltrate, sometimes with bilateral

lower lobe small consolidations or effusions.

6. Legionella pneumophila:

a. Summer/fall.

b. Smokers, diabetics, COPD, immune compromised, those who

sleep or work near incubation sites such as cooling towers,

compressors.

c. Probably underdiagnosed and more common cause of CAP

than expected.

d. Male > females.

e. Gastrointestinal symptoms very common.

f. Classic picture:

i. Middle aged male, smoker.

ii. Multiple constitutional symptoms - fever, cough,

cephalgia, diaphoresis, arthralgias.

iii. Severe nausea and watery diarrhea.

iv. Progresses to confusion/mental status change.

v. High fever with relative bradycardia.

vi. Lower lobe patchy infiltrate - 30% may have effusions.

7. Chlamydia pneumoniae:

a. Now called Chlamydophile pneumoniae.

b. Obligate intracellular parasite - resembles gram but usually

not well seen in gram stain.

c. Probably accounts for 8-10% of all CAP but underdiagnosed

due to difficulty in isolating.

d. Classic picture:

i. Similar to Mycoplasma - multiple constitutional

symptoms.

ii. Mucoid green sputum.

iii. Focal infiltrate.

8. Viral pneumonias:

a. Influenza A and B.

b. Often responsible for outbreaks (esp. nursing homes).

c. Usually self limiting, but may cause secondary bacterial

pneumonia.

d. Classic picture:

i. Fever, myalgias, coryza, non-productive cough.

ii. Diffuse patchy infiltrates.

iii. Treatment with antiviral medications is usually only

indicated in patients with severe underlying illness,

immune compromised states, or with evidence of severe

disease (hypoxia). Must be initiated in first days of

illness to be effective.

9. Animal exposure and pneumonia:

a. Bat caves = Histoplasma capsulatum.

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Notes


b. Turkeys, ducks, chickens = Chlamydia psittaci.

c. Rabbits = Francisella tularensis.

d. Cattle, sheep, goats = Coxiella burnetti.

e. Rodent feces = hantavirus.

10. Aspiration pneumonia:

a. Is separate and secondary entity of ‘aspiration’ which is the

inhalation of ingested material and/or gastric contents causing

a local inflammatory response.

b. Classic picture:

i. Debilitated patient with impaired glottic reflex or

receiving tube feedings.

ii. Choking or spasmodic cough productive of very foul

smelling sputum.

iii. RLL infiltrate is most common if patient was upright

when he/she aspirated.

iv. Anaerobic coverage needed (ESFQ, clindamycin,

ticarcillin, piperacillin).

c. Prevention is key:

i. Debilitated patients should be placed upright.

ii. Prokinetic agents and antacid should be used.

iii. If observed, immediate bronchoscopy to remove large

material.

d. Antibiotic treatment prior to symptoms is controversial.

e. Steroids are not indicated and have shown to be of no benefit.

11. Nursing home acquired:

a. Higher incidence of Chlamydia pneumoniae.

b. Influenza outbreaks leading to S. aureus, Klebsiella.

12. Nosocomial acquired:

a. Higher incidence of Klebsiella and Pseudomonas species.

H. Disposition criteria:

1. Multiple guidelines have been developed to predict severity

(Pneumonia Severity Index, CURB 65) but these should not

supersede clinical judgment.

2. Absolute indications for admission are:

a. Severe hypoxia.

b. Immune compromised state.

c. Failed appropriate outpatient treatment.

d. Unable to tolerate p.o. antibiotics.

3. Relative criteria for admission are:

a. Comorbid disease.

b. Limited supportive care.

c. Elderly.

I. Treatment:

1. Empiric treatment recommendations have been set forth by

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Notes


numerous organizations including:

a. American Thoracic Society.

b. Centers for Disease Control and Prevention.

c. Infectious Disease Society of America.

d. Antibiotic Selection for CAP 2010 Consensus Report.

2. There is general but not absolute consensus in these reports.

3. Recommendations all generally accept the following:

a. Atypical organisms are increasing.

b. Drug resistant S. pneumo considered.

c. Early administration is key to reduce morbidity and mortality.

d. Based on age, comorbid factors, etc.

e. Now divided into 2 broad classes.

f. Community Acquired (CAP).

g. Health Care Associated (HCAP).

4. CAP vs. HCAP:

a. Acute care hospital > 1 days in last 90 days.

b. Nursing home residence in last 90 days.

c. Output chemo or abx in last 30 days.

d. Home wound care in last 30 days.

e. Dialysis center in last 30 days.

f. Known close contact with MRD organism.

CAP Treatment Recommendations

First Alternative

Outpatient

Healthy,<60 y.o Azithromycin Clarithromycin

ESFQ, Doxycycline

Erythromycin

>60 y.o. Pcn + β-lactam inhib ESFQ

Comorbid disease Plus a macrolide

Inpatient Non-ICU 3

rd Gen Ceph ESFQ

Plus a macrolide

HCAP Treatment Recommendations

4th

Gen Ceph or Pip/Tazo + Vancomycin + Cipro or Aminoglycoside

J. Drug resistance:

1. Emergence of drug resistant S. pneumoniae (DRSP) prompted

recommendation of ESFQ as second line agent in order to reduce

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Notes


likelihood of FQ resistant species.

2. Unfortunately, fluoroquinolone resistant species now emerging.

3. Resistant pseudomonas also emerging.

4. Recommendation guidelines likely to change again in near future.

IV. TUBERCULOSIS

A. Epidemiology:

1. 6 percent of deaths worldwide.

2. Leading infectious cause of death above age 5.

3. Increase in U.S. from 1984-1992:

a. HIV predominant.

b. Homeless, drug abuse, immigration.

c. Multi-drug resistance.

d. Receiving immunosuppressive therapy (TNF inhibitors).

4. Control programs improved in 1992.

5. Yr 2000 = 16,377 cases.

B. Pathophysiology:

1. Mycobacterium tuberculosis:

a. Slow-growing aerobic rod.

b. Acid-fast property.

c. Transmission through inhalation of droplet nuclei.

2. Host defense:

a. Immune-competent:

i. Rare - all organisms killed in lung.

ii. Usual - transport to regional lymph nodes:

Tubercles (granulomas) formed by Macrophages.

Tubercles are evidence of primary infection.

May necrose and calcify = Ghon complex.

b. Some organisms spread through body:

i. Remain dormant in low oxygen areas.

ii. Latent infection.

iii. + Tuberculin test.

3. Immune-compromised:

a. Latent infection may reactivate when host’s immune system

can no longer contain foci of spread:

i. 5% within 2 yrs of primary infection.

ii. 5% over lifetime.

iii. 7-10% in HIV +.

b. At risk groups:

i. Extremes of age.

ii. Immune compromised disease states.

iii. Cancer of solid organs.

iv. Leukemia.

v. Transplant patients.

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Notes


vi. DM.

vii. Renal failure.

4. Clinical features:

a. Primary infection:

i. Usually asymptomatic and identified by PPD.

ii. Can be a pneumonitis.

iii. In immune-compromised, may be rapidly progressive and

fatal.

b. Reactivation:

i. Systemic:

Fever.

Night sweats.

Malaise, fatigue.

Weight loss.

ii. Pulmonary:

Hemoptysis.

Cough.

Pleurisy.

Dyspnea.

c. Miliary TB - results from initial wide hematogenous spread

during primary infection with seeding of multiple organs:

i. Hepato - and splenomegaly.

ii. Diffuse lymphadenopathy.

iii. Pancytopenia.

iv. Hyponatremia.

v. CXR shows numerous small nodules.

d. CNS - tubercles can form in meninges during primary

infection – Rich Foci:

i. Rupture of Rich Foci- tuberculous meningitis.

ii. CSF may show low glucose and mononuclear cells.

5. Diagnosis:

a. Tuberculin skin test (Mantoux) - subcutaneous injection of

0.1 ml of purified protein derivative (PPD):

i. Delayed-type hypersensitivity reaction.

ii. Read at 48-72 hours - positive if:

>5 mm in immune-compromised host, suspicious

CXR, or individual in close contact with TB patient.

>10 mm in IV drug user, high prevalence groups,

chronic lung disease, children< 4 year old.

> 15 mm in general healthy population.

b. Chest radiograph - use as screening tool after positive PPD or

patient with signs/symptoms of disease.

c. Primary infection - parenchymal infiltrates, isolated hilar or

mediastinal adenopathy.

d. Reactivation - cavitary and non-cavitary lesions of the

upper lobe of the lung.

e. Microbiology:

i. Gold standard - blood or sputum for culture.

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Notes


ii. Acid-fastness may provide presumptive diagnosis but

40% of culture + are AF neg.

6. Treatment:

a. 2011 CDC recommendations:

i. Four regimens are recommended:

Minimum of four drug therapy for 8 weeks (INH,

EMB, PZA, RIF).

Continued 2 drug therapy for minimum of 18

weeks.

All regimens maintain INH (Isoniazid) and

Rifampin or Rifapentine throughout treatment.

ii. Choice of regimens based on patient compliance, local

practices.

iii. All therapy is prolonged in immune-compromised

patients.

iv. Hepatitis is the most common side effect (INH, RIF,

PZA).

b. Multi-drug resistance:

i. Peaked during TB resurgence and most cases were co-

infected with HIV.

ii. Incidence now decreasing with improved surveillance.

iii. Foreign born persons currently account for >70% of new

cases.

iv. Most treatment regimens involve 4-6 drugs for 18-24

months.

V. HEMOPTYSIS

A. Expectoration of blood from the respiratory tract below the level of

the larynx:

1. Most cases are not life threatening, but frightening to patients.

2. Cause is not identified in up to 25% of patients. Mild = < 20ml in

24 hours; moderate = 20-600ml; severe = > 600ml.

B. Epidemiology:

1. 25% rule:

a. In industrialized countries:

i. 25% = infectious (non-tubercular).

ii. 25% = neoplasm.

iii. 25% = miscellaneous (identified cause, not a or b).

iv. 25% = idiopathic (no identified cause, sometimes referred

to as cryptogenic hemoptysis).

2. These percentages vary by patient demographic.

a. Risk factors for neoplasm:

i. Male (60/40).

ii. Smoking.

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Notes


iii. Age >40.

b. Rare in children:

i. Cystic fibrosis.

ii. Congenital heart disease.

iii. Infection.

C. Common causes of hemoptysis:

1. Infectious - bronchitis, pneumonia, lung abscess, tuberculosis.

2. Neoplastic - lung cancer, bronchial adenoma.

3. Cardiovascular - pulmonary embolism, mitral stenosis,

congestive heart failure, pulmonary hypertension.

4. Alveolar hemorrhage syndromes - Bechet syndrome,

Goodpasture syndrome, Wegener granulomatosis.

5. Hematologic - uremia, platelet dysfunction, anticoagulant

therapy.

6. Traumatic - foreign body aspiration, ruptured bronchus.

7. Iatrogenic - bronchoscopy, lung biopsy.

8. Inflammatory - cystic fibrosis, bronchiectasis.

D. Diagnosis:

1. Chest radiograph:

a. 70% will be abnormal in all cases.

b. 80-90% abnormal in patients with neoplasm.

2. CT - limited data suggest CT is more efficient than bronchoscopy

at identifying cause and has significantly lower complications.

3. Bronchoscopy - allows for biopsy, and better identifies luminal

tumors.

E. Treatment:

1. Immediate airway stabilization as needed:

a. 8.0 ETT or larger to allow bronchoscopy.

b. If bleeding is massive, advancement of ETT into mainstem

bronchus of non-bleeding lung.

2. Position patient with bleeding lung down to minimize soiling of

normal lung.

3. Bronchoscopy as needed.

4. Antibiotic/antiviral/antitubercular treatment as needed.

5. FFP or platelet concentrates to correct any identified

coagulopathies.

6. Cough suppression with codeine or opioids.

7. Emergency consultation w pulmonologist and/or thoracic

surgeon.

8. Bronchial artery embolization.

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Notes


PULMONARY EMERGENCIES

PEARLS

Asthma

1. Defined as reversible airway obstruction secondary to an inflammatory

response.

2. Incidence is increasing across all strata, highest among children.

Mortality rates higher in African-Americans.

3. Usually begins with some type of trigger.

4. Patient’s perception of exacerbation, intensity of wheezing, and pulse

oximetry are poor predictors of severity.

5. Bedside spirometry at presentation can predict response/disposition with

>85% sensitivity and specificity. Chest radiography usually shows

concomitant disease.

6. ABG is usually not useful in clinical decision-making.

7. Nebulized Beta specific agonist much more efficacious than Beta non-

specific given SQ.

8. R isomer of Albuterol available, but no strong evidence of clinical

superiority.

9. Corticosteroids and anticholinergics should always be used in moderate

to severe exacerbations. Steroids should be started early secondary to

lag in response time.

10. Leukotriene modifiers may develop role in acute exacerbations.

11. Magnesium and Heliox should be considered in severe exacerbations.

12. Mechanical ventilation by permissive hypercapnia should be used; goal

is to reduce auto-PEEP.

13. Disposition should be based on response to therapy by spirometry

measurement and compared to predicted or symptom free best.

14. Treatment does not change in the pregnant patient.

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Notes


COPD

1. Is a spectrum of diseases including chronic asthma, chronic bronchitis,

and emphysema.

2. Is the only one of the top five cause of death increasing in prevalence.

3. Cigarette smoking accounts for 80-90% of cases but only 15% of all

smokers develop clinically significant disease.

4. The emphysema patient (pink puffer) develops increasing lung

destruction, expanding chest cavity, weight loss, and sits hunched

forward with pursed lips.

5. The chronic bronchitis patient (blue bloater) develops polycythemia,

plethora and cyanosis, hypertension, and cor pulmonale.

6. FEV1 is best tool to predict outcome.

7. Chest radiography will be abnormal in most cases.

8. Oxygen administration should be limited to keep patient’s pO2 greater

than 60 mmHg.

9. Pharmacotherapy similar to asthma.

10. Methylxanthines probably efficacious in these patients.

11. Liberal use of empiric antibiotics probably warranted.

12. Non-invasive assisted ventilation very useful to recruit alveoli and

reduce dead space.

13. Limited role for discharge of patients in acute exacerbation.

Pneumonia

1. Frequency of atypical, resistant, and opportunistic infections is

increasing.

2. Morbidity and mortality can be drastically reduced by early recognition

and intervention.

3. History can give important clues to etiologic agent involve.

4. Sputum cultures always recommended but EP must begin empiric

therapy prior to results.

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Notes


5. Chest radiography may give important clues to etiology.

6. Streptococcus - single shaking rigor, rust colored sputum, pleuritic chest

pain.

7. Haemophilus -debilitated, green sputum, diffuse rales.

8. Klebsiella - alcoholic, multiple chills, cyanosis, high WBC count,

currant jelly sputum.

9. Staphylococcus - debilitated patient after mild URI, purulent sputum,

empyema.

10. Mycoplasma - young adult, constitutional symptoms, bullous

myringitis.

11. Legionella - gastrointestinal symptoms, mental status change, relative

bradycardia.

12. Chlamydia- constitutional symptoms, mucoid green sputum.

13. Nosocomial and nursing home patients have higher incidence of

Klebsiella, Pseudomonas, Chlamydia, and Influenza outbreaks.

14. Empiric treatment early is key; must include atypical coverage.

15. Drug resistant Strep species are increasing. Empiric recommendations

will probably change as result.

Tuberculosis

1. Increase in cases in 1980s due to HIV epidemic.

2. Host defense leads to formation of tubercles and dormant organism in

low oxygen areas.

3. Latent infection reactivates in immune-compromised states.

4. Primary infection is usually asymptomatic and identified by PPD.

5. TB skin test is read differently for different at-risk groups. The greater

the risk of disease, the smaller the induration needs to be for positive.

6. CDC suggests multiple regimens based on patient compliance; all utilize

3-4 drugs initially and INH and Rifampin/Rifapentine throughout

therapy.

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Notes


7. Hepatitis is the most common side effect of therapy.

8. Immune-compromised patients and those with muti-drug resistant

strains require prolonged therapy.

Hemoptysis

1. Most cases are not life threatening.

2. 25% of cases are neoplasm.

3. Chest radiograph will be abnormal in ¾ of patients.

4. Immediate airway stabilization is most important treatment in life-

threatening cases.

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Notes


REFERENCES

1. Marx JA, Hockberger RS, Walls RM, et al. Rosen’s Emergency

Medicine: Concepts and Clinical Practice, 7th

edition.

2. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A

Comprehensive Study Guide, 7th edition.

3. Harwood-Nuss A, Wolfson AB, et al. The Clinical Practice of

Emergency Medicine, 5th edition.

4. Emergency Medicine. The Core Curriculum. 2008.

5. Rivers CS, et al. Preparing for the Written Board Exam, 5th

Edition.

08/13

Page 246

Environmental Emergencies

Jay Sharp, MD, FACEP

Emergency Medicine Board Review Intensive Course Committee; Core Faculty, Emergency Medicine

Residency, Presence Resurrection Medical Center; Attending Physician, Presence Resurrection Medical Center

Page 247

Page 248

Notes


ENVIRONMENTAL EMERGENCIES

I. HIGH-ALTITUDE ILLNESS

A. General characteristics:

1. The environment at altitude:

a. Decreased barometric pressure.

b. Decreased partial pressure of O2.

c. Hypobaric hypoxia.

d. Physiologic responses: Increased ventilation, RBC

production, BP/HR/CO.

2. Incidence of altitude illness is dependent on:

a. Rate of ascent.

b. Final altitude.

c. Sleeping altitude.

d. Duration at altitude.

e. Individual susceptibility.

3. AMS incidence:

a. Up to 67% incidence with rapid ascent (1-2 days) >14,000 ft.

b. 0% incidence for skiers visiting resorts and sleeping < 9000

ft.

c. 15-20% of people that ascend to 8500-9000 feet from sea

level in one day.

4. HAPE (High Altitude Pulmonary Edema) incidence:

a. <1-2%.

b. Affects 0.01% skiers in Colorado (8-12,000 ft) each year.

c. 1 in 50 climbers of Mt. McKinley (20,000 ft).

d. Varies with rate of ascent.

5. HACE (High Altitude Cerebral Edema) incidence <1%.

B. Clinical manifestations:

1. Acute mountain sickness (AMS):

a. Signs and symptoms:

i. Generally benign and self-limited.

ii. Symptoms may become debilitating.

iii. Onset 4-12 hours after ascent.

iv. Headache.

v. Anorexia/nausea/vomiting.

vi. Fatigue.

vii. Weakness. viii. Dizziness.

ix. Lightheadedness.

x. Difficulty sleeping due to periodic breathing.

xi. Presence of ataxia a useful sign of progression of AMS to

HACE.

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Notes


b. Differential diagnosis:

i. Viral syndrome.

ii. Exhaustion.

iii. Alcohol hangover.

iv. Carbon monoxide poisoning.

c. Treatment:

i. Mild cases usually self-limited.

ii. Symptomatic treatment.

iii. Halt ascent until symptoms resolve.

iv. Oxygen – in severe cases; 2L/min by mask/NC especially

at night.

v. Simulated descent with Gamow Medical Tent.

vi. Acetazolamide:

Drug of choice for prevention and treatment.

Mechanism:

•• At higher elevations, arterial oxygenation

decreases, resulting in hyperventilation and a

pronounced respiratory alkalosis that limits the

medullary respiratory center’s response to fully

compensate for hypoxemia.

•• Causes renal excretion of bicarbonate.

•• Improves ventilatory response to the high altitude

and thus arterial oxygenation.

•• Combats fluid retention.

75% effective in preventing AMS at 14,000 feet.

Dose - 250 mg BID starting 24 hrs prior to ascent.

Aspirin or acetaminophen for headache.

Prochlorperazine for nausea.

vii. Dexamethasone:

Effective in prevention/treatment.

Used only for treatment due to possibilities of side

effects.

Dose 4-8 mg QID.

d. Prevention:

i. Graded ascent – climb high, sleep low.

ii. Avoid increase in sleeping altitude greater than 2,000 feet

when over 8,000 feet.

iii. Acetazolamide for prevention.

iv. Avoid alcohol and sleeping pills.

2. High-altitude cerebral edema (HACE):

a. Signs and symptoms:

i. Life-threatening.

ii. Occurs in presence of AMS or HAPE:

Seen rarely as an isolated entity.

iii. Onset:

May occur 12 hours after the onset of AMS.

Usually requires 1-4 days for development.

iv. Ataxia.

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Notes


v. Severe headache.

vi. Altered mental status (confusion/drowsiness/stupor/

coma).

vii. Nausea/vomiting. viii. Seizure.

ix. Focal neurologic deficit.

b. Differential diagnosis:

i. Cerebrovascular accidents/transient ischemic attacks.

ii. Focal neurologic signs suggest a vascular lesion.

c. Treatment:

i. ABCs.

ii. Immediate evacuation to lower altitude.

iii. Oxygen - 2-4 L/min.

iv. Dexamethasone - 4-8mg IV/IM/PO.

v. Bed rest with elevation of head at 30 degrees and in

severe cases, aggressive management of elevated

intracranial pressure.

3. High-altitude pulmonary edema (HAPE):

a. Pathophysiology:

i. Noncardiogenic pulmonary edema.

ii. Precise pathophysiology unknown; combination of

alveolar leakage with overperfusion; impaired endothelial/epithelial barrier; intense pulmonary artery

vasoconstriction causing pulmonary hypertension.


i. Fatigue.

ii. Weakness (occurs 2-4 days after ascent).

iii. Dyspnea at rest (early).

iv. Cough (dry at first, then productive).

v. Tachypnea.

vi. Rales – first heard in right axilla.

vii. Cyanosis. viii. Severe respiratory distress and death may occur.

c. Radiographs:

i. CXR in HAPE:

Reveal fluffy (alveolar) infiltrates which are patchy in

distribution, with areas of clearing between the

patches; peripheral location rather than central.

Unilateral or bilateral infiltrates (right midlung field

being most common).

X-ray findings generally correlate with severity of

disease and degree of hypoxemia.

Cardiomegaly, bat-wing distribution of infiltrates, and

Kerley B lines (typical of cardiogenic pulmonary

edema) are absent in HAPE.

d. Differential diagnosis:

i. Pneumonia.

ii. High-altitude bronchitis and pharyngitis.

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Notes


iii. Pulmonary embolism:

More rapid onset.

Pleuritic chest pain.

e. Treatment:

i. ABCs:

Endotracheal intubation for impending respiratory

failure, hyperventilation or airway protection.

Continuous positive airway pressure (CPAP).

ii. Supplemental oxygen:

Lowers pulmonary artery pressure and respiratory

rate.

Raises oxygen saturation.

iii. Descent:

Immediate descent for moderate/severe symptoms.

iv. Mild cases may be managed without descent if:

Lowers pulmonary artery pressure.

Adequate oxygen supplies available.

Serial medical examinations possible.

Immediate descent for any deterioration in clinical

status.

v. Bed rest (to avoid exercise induced pulmonary

hypertension).

vi. Medications:

Sildenafil (Viagra®):

•• Selective phosphodiesterase-5 inhibitor.

•• Reduces pulmonary hypertension at rest and

during exercise while maintaining gas exchange

and systemic blood pressure.

Nifedipine:

•• For prevention and treatment.

•• Lowers hypoxic pulmonary hypertension by

reducing pulmonary vascular resistance.

•• Does not quickly improve oxygenation.

Lasix, morphine, acetazolamide used with varying

success.

II. DECOMPRESSION SICKNESS


1. Gas laws:

a. Henry’s law:

i. Amount of gas that will dissolve in a solution is directly

proportional to the partial pressure of that gas.

ii. Increases in partial pressure result in larger amount of gas

dissolved in tissue.

iii. Decreases in partial pressure result in gas coming out of

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Notes


solution.

b. Dalton’s law:

i. Total pressure exerted by a mixture of gases is equal to

the sum of the partial pressure of each of the component

gases.

c. Sequence:

i. Increases in ambient pressure cause an increase in

partial pressure of nitrogen inspired.

ii. Nitrogen accumulates in the tissues in higher and

higher concentrations the longer pressures remain

elevated.

iii. Decompression sickness (DCS) results when ambient

pressure keeping nitrogen in solution decreases too

rapidly on ascent, preventing gradual removal of the

excess body burden of nitrogen.

iv. As the nitrogen removal gradient is overwhelmed,

tissues become supersaturated, and bubble formation

occurs.

2. Etiology:

a. Bubble location determines clinical effects:

i. Blood flow obstruction and tissue ischemia from

intravascular bubbles.

ii. Tissue distention and compression from interstitial

bubbles.

iii. Compression of arterioles, nerves, and lymphatics.

iv. Endothelial damage leading to stimulation of coagulation

and clotting cascades.

v. Bubbles sensed as foreign by host defenses lead to the

release of chemotactic and other factors.

b. Risk factors for DCS:

i. Greater depth, longer bottom time, and quicker rate

of ascent.

ii. Use of dive tables/computers do NOT eliminate DCS.

iii. Increased incidence with age and weight (body fat),

hypothermia, dehydration, exercise, multiple dives in a

day.

c. Airplane flight can precipitate DCS due to lower cabin

pressure.



a. Cutaneous:

i. Scarlatiniform, erysipeloid or mottled rash.

ii. Peau d’orange appearance due to lymphatic obstruction.

b. Musculoskeletal:

i. Pain:

Classic bends.

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Notes


Dull deep aching.

Often in a joint (elbow and shoulder most

common).

Not exacerbated by movement or reproduced with

palpation.

No external physical signs.

c. GI:

i. Nausea/vomiting.

ii. Abdominal pain.

d. Pulmonary:

i. Dyspnea.

ii. Chokes (triad of substernal pressure, cough, dyspnea):

Due to large bubbles in the pulmonary tree.

e. CNS:

i. Weakness/fatigue.

ii. Numbness/paresthesia.

iii. Agitation.

iv. Headache.

v. Dizzy.

vi. Vertigo.

vii. Convulsion.

viii. Bowel/bladder incontinence.

ix. Lethargy.

x. Visual disturbance.

xi. Staggers:

Vestibular system and the posterior column

involvement.

f. Time after surfacing to presentation of DCS:

i. 50% - symptoms within 1 hour.

ii. 95% - symptoms within 12 hours.

iii. 60% of neurologic DCS within 10 minutes.

2. Treatment:

a. ABCs.

b. Provide normobaric (100%) oxygen via mask or ETT:

i. Increase inert gas (nitrogen) elimination from the tissues

reducing gas bubble size.

ii. Increase oxygen delivery to the injured tissue.

c. Early recompression in hyperbaric chamber:

i. For all DCS except for cutaneous.

ii. Arrange transportation to nearest hyperbaric facility.

iii. Aircraft capable of full pressurization of flight below

1,000 feet are best suited for transfers.

iv. Prophylactic chest tube for simple pneumothorax to

prevent conversion to tension pneumothorax.

v. Fill endotracheal and foley catheter balloons with water or

saline to avoid shrinkage/damage during recompression.

d. IV rehydration with 0.9% NS:

i. Diver usually dehydrated due to diuretic effect of

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Notes


pressure, exercise, breathing dry compressed air.

ii. Increased fluid assists with off-gassing and dissolution of

nitrogen.

e. Water recompression:

i. Returning injured diver/patient to a depth where

symptoms are ameliorated.

ii. Extremely difficult.

iii. Need large amount of surface support.

iv. Controversial.

v. Use as a last resort only.

f. Divers Alert Network (DAN):

i. Based at Duke University Medical Center.

ii. Provides a 24 hour emergency hotline for medical

consultation on the treatment of dive related injuries and

for referrals to hyperbaric chambers.

www.diversalertnetwork.org

800-446-2671.

919-684-4DAN (4326).

III. BAROTRAUMA


1. Injury to the body as a result of the expansion and contraction of

gas in an enclosed space.

2. Boyle’s law states that at a constant temperature, pressure (P)

is inversely related to volume (V):

a. PV=K (constant) or P1V1=P2V2.

b. Increase of pressure mandates a reduction of volume by same

factor.

3. Gas filled cavities in the body subject to expansion/

contraction:

a. Lung.

b. Middle ear.

c. Sinus.

4. Solid and liquid filled spaces distribute the pressure equally.

5. Volume changes experienced during ascent are greatest in the

few feet nearest the surface.

6. Key points:

a. For barotrauma of descent, unless an air filled cavity has

ruptured, no progression of the disease expected upon return

to normal atmospheric pressure.

b. If patient transport requires air evacuation, maintain air cabin

pressure at one atmosphere or fly below 1,000 feet to avoid

aggravating barotrauma.

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Notes



1. Middle ear (barotitis media):

a. General:

i. Barotrauma of descent.

ii. Most common type of barotrauma.

iii. Seen in 30% of inexperienced divers and 10% of

experienced divers.

iv. Results from inadequate equalization of pressure between

the middle ear and the external ear canal.

v. Eustachian tube provides the sole route of pressure

equalization for the middle ear.


i. Begins as a clogged sensation.

ii. Increasingly painful as the pressure differential across the

tympanic membrane (TM) increases.

iii. Progresses to rupture of the TM.

iv. Tympanic membrane appearance: Teed Grading System:

0 – Symptoms without otologic findings.

1 – Erythema and mild retraction of the TM.

2 – Erythema of the TM with mild hemorrhage within

the TM.

3 – Gross hemorrhage throughout the TM.

4 – Grade 3 changes plus gross hemorrhage within the

middle ear (hemotympanum).

5 – Free blood in middle ear plus TM performation.

c. Treatment:

i. Decongestants.

ii. Antihistamines for allergic component.

iii. Antibiotics for TM rupture.

iv. Prevent with decongestants prior to dive.

2. Inner ear/ Labyrinthine window rupture:

a. General:


ii. Results from forceful attempts at equalizing middle ear

pressure.

iii. Increased middle ear pressure can raise intracranial

pressure and cause rupture of the round or labyrinth

windows allowing perilymph to enter the middle ear.


i. Sudden, severe vertigo, disorientation during dive.

ii. Tinnitus.

iii. Sensorineural hearing loss in the affected ear.

iv. Nystagmus.

c. Treatment:

i. Bed rest.

ii. Avoidance of straining.

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Notes


iii. Prompt surgical repair advocated by some.

3. Mask squeeze:

a. General:


ii. Air volume in mask decreases with increasing ambient

pressures, resulting in rupture of capillaries.

iii. Easily prevented by exhaling through nose into mask to

equalize pressures.


i. Skin ecchymosis.

ii. Subconjunctival hemorrhage.

iii. Lid edema.

iv. Hyphema – rarely.

c. Treatment:

i. Most cases are asymptomatic.

ii. Resolves spontaneously after days to weeks.

iii. Cold compresses and analgesics if needed.

4. Paranasal sinuses:

a. General:


ii. Nasal ostia act as a valve to regulate sinus pressure.

iii. If the ostia fail to allow pressure equalization, congestion,

edema, and hemorrhage can occur.


i. Sinus congestion.

ii. Pain.

iii. Epistaxis.

c. Treatment:

i. Decongestants.

ii. Antibiotics for severe cases.

5. External objects:

a. General:

i. Air pockets in dive suit/mask expand/contract.


i. Tight fitting dive suit – edema and erythema of the skin.

c. Treatment – none; resolves with time.

6. Teeth (barodontalgia):

a. General:

i. Air trapped inside a filling.

ii. Can occur with ascent or descent.


i. Severe tooth pain.

7. Gastrointestinal (aerogastralgia):

a. General:

i. Barotrauma of ascent.

ii. Swallowed air in the GI tract expands as external pressure

decreases.


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Notes


i. Excessive belching.

ii. Flatulence.

iii. Abdominal distention.

8. Pulmonary (Pulmonary Overpressurization Syndrome):

a. General:

i. Occurs with ascent.

ii. Lungs expand against a closed glottis.

iii. Cause for arterial gas embolism [see below].

iv. Divers with decreased lung compliance/increase lung

volumes at increased risk (COPD, asthma).


i. Dyspnea.

ii. Cough with frothy red sputum; subcutaneous emphysema.

iii. Delayed symptoms including a bull neck appearance,

dysphagia, and changes in voice character.

iv. Specific clinical manifestations depend on the location

and amount of air that accumulates:

Pneumomediastinum.

Pneumothorax.

Tension pneumothorax.

c. Treatment:

i. Treatment varies based on clinical findings and severity

of injury.

ii. 100% oxygen for ill appearing patients.

iii. Intubation for patients with massive subcutaneous

emphysema of the neck.

iv. Immediate needle thoracostomy for evidence of tension

pneumothorax.

IV. ARTERIAL GAS EMBOLISM


1. Extreme manifestation of pulmonary barotraumas.

2. Overpressurization of lung tissue causes pleural tear with air

entering the vascular circulation:

a. Air bubbles tend to rise and enter the cerebral vessels where

they can occlude vascular flow.

b. Boyle’s law: pressure x volume=constant.

c. Trapped air (in lungs with closed glottis) expands on ascent.

3. Arterial embolism can also occur via pulmonary AV shunts, or as

paradoxical embolism via a patent foramen ovale (up to 18% of

the adult population).

4. Etiology:

a. Breath holding during ascent:

i. Symptoms attributable to a shower of bubbles and

multiple blood vessel involvement.

b. Iatrogenically during placement of CVP lines, cardiothoracic

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Notes


surgery, or hemodialysis.

c. Penetrating wounds to heart with emergent repair of cardiac

wound.



a. Cerebral:

i. Dive related stroke.

ii. Second leading cause of dive related death (after

drowning).

iii. Two main presentations:

Apnea and full cardiopulmonary arrest.

Any combination of neurologic deficits.

iv. Presentation depends on the arterial distribution of the gas

embolism.

v. Change in level of consciousness/loss of consciousness

(40%).

vi. Sensory loss (20%).

vii. Motor deficit (20%).

viii. Paraplegia (10%).

ix. Seizure (4%).

x. Visual changes.

xi. Aphasia.

xii. Paresthesias.

xiii. Timing of presentation.

10% during the ascent.

80%<5 min. after surfacing; must occur within 10

min. of ascent.

10% 5-10 min. after surfacing.

xiv. Spontaneous improvement minutes after the initial

deficits may occur:

High incidence of relapse.

Improvement may be transiently related to postural

changes that affect the distribution of the bubbles

flowing to the brain.

b. Pulmonary:

i. Shortness of breath.

ii. Bloody, frothy sputum.

iii. Subcutaneous air.

c. Cardiac:

i. Myocardial infarction due to air in the coronary vessels.

ii. Reduced cardiac output due to air trapped in ventricle.

iii. Hamman’s sign: crepitus on auscultation of the heart.

d. Renal:

i. Renal infarction due to air embolism.

2. Treatment:

a. Initial stabilization:

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Notes


i. ABCs.

ii. 100% oxygen by tight fitting mask.

iii. Intubation for ventilation/protection of airway required.

iv. IV access with volume augmentation.

b. Recompression treatment:

i. All cases of AGE must be referred for recompression

treatment (hyperbaric oxygen therapy).

Rapidly increasing ambient pressure to reduce

intravascular bubble volume and to restore tissue

perfusion.

Slow decompression to avoid the reformation of

bubbles.

ii. Rapid transport:

Arrange transportation to nearest hyperbaric facility.

Aircraft capable of full pressurization or flight below

1,000 feet are best suited for transfers.

iii. Prophylactic chest tube for simple pneumothorax to

prevent conversion to tension pneumothorax during

recompression.

iv. Over 50% of victims of AGE have complete functional

recovery.

c. Controversies:

i. Trendelenburg positioning patients with cerebral AGE is

not effective.

ii. Hypothesized that elevation of the legs could cause the air

bubble to migrate away from the cerebral circulation and

that increased hydrostatic pressure in brain will shrink

bubbles.

iii. Trendelenburg positioning may increase injury by

increasing the intracerebral pressure and worsen cerebral

edema.

d. Cautions:

i. Patients who experience sudden neurologic recovery can

relapse quickly as bubble positions change.

V. ELECTRICAL INJURY


1. Amperage (electron flow):

a. Most directly related to injury.

b. Varies directly with voltage and indirectly with resistance:

Ohm’s Law I=V/R. (I=current in amp; V=voltage in volts;

R=resistance in ohms).

i. Decrease in resistance (with moisture) results in worse

injury.

Increase in voltage leads to worse injury.

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Notes


c. Narrow margin of safety:

Milliamperes at 60 Hz

Effect

0.2-2

tingling sensation

1-4

pain

6-22

inability to let go/tetanic contractions

30-50

diaphragm/intercostal tetany

100

VFib

1000

ventricular standstill

2. Voltage:

a. Unit of electromotive force or electric pressure that causes

current to flow.

b. Force or push of electrons.

c. Often only parameter known in electrical injury.

3. Resistance:

a. Varies depending on skin properties.

b. Varies according to diagram.

c. High voltage will cause resistant tissues (fat, tendons, bone)

to heat up and coagulate.

Source

Voltage

Automobile

12V

Telephone line

65V

Home

110V or 220V

Residential/industrial area lines

7620V

Cross country power lines

>110,000V

Skin Type

Resistance in Ohms

Heavily calloused

1,000,000

Average

5,000-30,000

Moist

1-2,000

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Notes


Tissue of least resistance

Nerve

Blood

Muscle

Skin

Fat

Bone

Tissue of most resistance

4. Watt:

a. Unit of electrical power delivered to tissue when one ampere

flows through one ohm for one second.

b. Energy defined in watt-second.

c. One joule=one watt-second.

5. Type of current:

a. Alternating current 3x more dangerous than direct

current.

b. Alternating current at 60 cycles/second causes muscle tetany

and grasping of source since flexors stronger than extensors

and may cause respiratory muscle tetany.

c. Direct current causes muscle contraction which pushes victim

away from the source.

6. Duration:

a. Longer duration – worse injury.

b. Skin resistance falls with continued contact with source.

c. Resistance does not return to previous high level immediately

after withdrawn from source.

7. Current pathway determines damage:

a. Current through thorax - heart damage.

b. Current through head - brain injury.

c. Degree of cross section diameter inversely proportional to

injury.

B. Clinical presentation:


a. General:

i. Crush-type trauma involving deep tissues which may be

extensive relative to small skin burns.

b. Cardiac:

i. Dysrhythmias:

PVC.

Sinus tachycardia.

Atrial fibrillation.

Ventricular fibrillation:

•• Most common cause of death.

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Notes


•• Induced by alternating current at levels of 50 to

60 Hz (household current).

Asystole results from direct current.

Myocardial damage.

Occurs rarely.

Generally epicardial, not transmural.

Patch-like damage does not follow distribution of

coronary arteries.

ECG will not show standard injury patterns.

c. Respiratory:

i. Respiratory arrest may occur from:

Electrical brain injury causing respiratory center

inhibition.

Tetanic contraction of chest wall muscles and/or

diaphragm.

Prolonged paralysis of respiratory muscles.

Post-cardiac arrest respiratory arrest.

d. Neurologic:

i. Acute:

Respiratory arrest, amnesia, altered mental status,

seizures, coma, quadriplegia, localized paresis.

ii. Delayed:

Ascending paralysis, transverse myelitis, amyotrophic

lateral sclerosis.

e. Vascular:

i. Venous thrombosis.

ii. Compartment syndrome secondary to edema.

f. Renal:

i. Renal failure secondary to myoglobinuria.

g. Musculoskeletal (forceful muscle contraction from electro-

stimulation cause):

i. Vertebral column fracture.

ii. Posterior shoulder dislocation.

iii. Fractures or dislocations secondary to falls.

iv. Compartment syndrome.

h. Ophthalmologic:

i. Cataracts (onset 4-6 months post injury).

ii. Corneal burns, intraocular hemorrhage, uveitis, retinal

injuries and optic nerve atrophy.

i. Dermatologic.

i. Thermal burns from current arcing or clothes burning.

ii. Kissing burns from flexor surface arcing as current exits

and reenters the skin.

iii. Entry/exit wounds.

j. Pediatric considerations:

i. Fetus much less resistant to electrical shock than mother.

ii. All pregnant patients must undergo a period of fetal

monitoring.

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Notes


iii. Oral commissure burn:

Results from child biting an electrical cord.

Associated with bleeding from the labial artery 7-

10 days post injury.

May heal with significant contractures.

C. Diagnosis:

1. Essential work-up:

a. ECG - indications:

i. High voltage electrical injury.

ii. Presence of risk factors: decreased skin resistance, tetany,

current path across heart.

iii. Large body surface burns.

iv. LOC/AMS.

v. Findings often non-diagnostic since injury pattern patchy

rather than following coronary vessels.

vi. Normal ECG associated with absence of late arrhythmias.

b. Urinalysis for myoglobin.

c. Cardiac monitor:

i. Controversy abounds on the subject of the need for 24

hour monitoring.

ii. Prolonged monitoring is not necessary in asymptomatic

patients with a normal ECG with no arrhythmias, and an

exposure to <240 volts.

iii. Indications:

Abnormal ECG.

LOC.

Dysrhythmia.

Significant burn size.

2. Laboratory:

a. Determined by the nature of the injury.

b. For most exposures to household current, no testing indicated.

c. Creatinine kinase (CK) indications:

i. Positive urine myoglobin.

ii. High voltage exposures.

d. Troponin and CK MB indications:

i. Abnormal ECG.

ii. Dysrhythmia.

e. Electrolytes, BUN, Cr:

i. For high voltage exposures.

ii. Provides baseline renal function.

iii. Hyperkalemia occurs due to cell death.

iv. Metabolic acidosis with significant injury.

3. Differential diagnosis:

a. Thermal burns from electrical arcing flash injuries.

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Notes


D. Treatment:

1. Pre-hospital:

a. Caution:

i. Care must be exercised in removing patients to ensure

that rescuers do not contact live electrical sources.

ii. Spinal precautions for transport.

iii. Standard BLS/ACLS care.

iv. Remove smoldering clothes.

b. Initial stabilization:

i. ABCs.

ii. Standard ACLS measures for arrhythmias.

iii. Spine immobilization when indicated.

2. ED treatment:

a. IV fluid resuscitation:

i. Larger fluid volumes required due to extensive third

spacing in injured muscle.

ii. As much as 7ml/kg/% body burn.

iii. Rapid administration to reach urine output of 1ml/kg/hr.

iv. Titrate to urine output and CVP measurement.

b. Foley catheter.

c. Prevent renal failure from myoglobulinuria:

i. Maintain good urine output.

ii. IV bicarbonate increases solubility of myoglobin in urine.

iii. Furosemide/mannitol.

iv. Monitor renal function.

d. Immobilize/reduce fractures and dislocations.

e. Local wound care for thermal burns.

f. Tetanus prophylaxis.

3. Admissions criteria:

a. Documented LOC.

b. Dysrhythmias observed on monitor.

c. Abnormal ECG.

d. Suspicion of deep tissue burns.

e. Myoglobinuria.

f. Acidosis.

g. Significant skin burns/associated injury.

VI. LIGHTNING INJURIES


1. Voltage – several million to 2 billion.

2. Acts as direct current which causes asystole and respiratory

arrest.

3. Due to the brief duration (1-100 milliseconds) of lightning:

a. Current passes over the skin rather than through the body

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Notes


(flashover).

b. Deep tissue injuries are rare.

c. Some experimental evidence that the current may enter the

cranial orifices- eyes, ears, nose, mouth.

i. May explain myriad of eye and ear symptoms.

4. Mechanisms of injury:

a. Direct strike - strikes victim directly.

b. Splash injury - moves from one object to victim of lesser

resistance to current flow.

c. Contact injury - holding object that is hit or splashed by

lightning.

d. Ground strike - current moves through ground and may injure

multiple victims.

e. Blunt injury due to direct explosive effect.

f. Thermal burning - objects worn by victim heat up or clothes

catch on fire.



a. Cardio-respiratory.

b. Cardiac asystole:

i. Due to direct current injury.

ii. May resolve spontaneously as the heart’s intrinsic

automaticity resumes.

c. Respiratory arrest:

i. Due to paralysis of medullary respiratory center.

ii. May persist longer than cardiac asystole and lead to

hypoxia induced Vfib.

d. Acute myocardial infarction rare.

e. Shock.

f. Neurogenic (spinal injury).

g. Hypovolemic (trauma).

h. Mottled or cold extremities:

i. Due to autonomic vasomotor instability.

ii. Usually resolves spontaneously in a few hours.

i. Neurological injuries:

i. Confusion.

ii. Memory defects.

iii. Alteration of level of consciousness (>70% of cases).

iv. Flaccid motor paralysis.

v. Seizures.

vi. Fixed dilated pupils due either to serious head injury or

autonomic dysfunction.

j. Traumatic injuries:

i. Head or spine.

ii. Fractures, dislocations, muscle tears and compartment

syndromes.

Page 266

Notes


iii. Ruptured tympanic membrane with ossicular

disruption (up to 50%).

iv. Burns:

Discrete entrance and exit wounds uncommon.

Thermal burns due to evaporation of water on skin,

ignited clothing, heated metal objects (buckles or

jewelry).

Feathering (fern-like) burns:

•• Cutaneous imprints from electron showers that

track over skin.

•• Pathognomonic of lightning injury.

•• Resolve within 24 hours.

k. Ophthalmologic injuries:

i. Cataracts occur days to years post injuries.

ii. Corneal lesions.

iii. Intraocular hemorrhages.

iv. Retinal detachment.

C. Diagnosis:

1. Confirmatory history from bystanders or rescuers of the

circumstances of the injury:

a. Consider lightning strike in unwitnessed falls, cardiac arrests

or unexplained coma in an outdoor setting when a

thunderstorm was present.

2. Laboratory:

a. CBC for baseline Hct.

b. Urinalysis for myoglobin.

c. Electrolytes for acidosis.

d. BUN, Cr for baseline renal function.

e. CK and CKMb and Troponin fraction for muscle/cardiac

damage.

3. Imaging/special tests:

a. CXR.

b. C-spine radiograph.

c. CT head for altered mental status or significant head trauma.

d. ECG should be performed in all cases:

i. Non-specific ST changes common.

ii. QT prolongation.

iii. Acute myocardial infarction rare.


a. Other causes of coma, cardiac dysrhythmia, or trauma:

i. Hypoglycemia.

ii. Intoxication.

iii. Drug overdose.

iv. Cardiovascular disease.

v. CVA.

Page 267

Notes


D. Treatment:

1. Pre-hospital:

a. Controversies:

i. Field triage should rapidly focus on providing ventilatory

support to unconscious victim(s) or those in cardio-

pulmonary arrest.

ii. Prevents reversible asystolic cardiac arrest from

degenerating into hypoxia induced Vfib.

iii. Conscious victims are at lower risk of imminent demise.

b. Cautions:

i. Spine immobilization for:

Cardiopulmonary arrest (suspected trauma).

Significant mechanical trauma.

Suspected loss of consciousness at any time.

ii. Cover superficial burns with sterile saline dressings.

iii. Immobilize injured extremities.

iv. Rapid extrication prevents exposure to repeat lightning

strike.

c. Initial stabilization:

i. ABCs.

ii. Standard ACLS measures for cardiac arrest.

iii. Diligent primary and secondary survey for traumatic

injuries:

Maintain cervical spine precautions until cleared.

Treat altered mental status with glucose, naloxone,

and thiamine as indicated.

Hypotension requires volume expansion and pressor

agent.

2. ED treatment:

a. IV access for medication administration.

b. Volume expansion:

i. Do not follow burn treatment formulas as flashover

burns are rarely the cause of fluid loss.

ii. Occult deep burn injury is rare when compared to other

types of electrical current injury.

iii. Titrate volume administration to urine output; fluid

loading may be dangerous with head injuries.

c. Clean and dress burns.

d. Tetanus prophylaxis.

e. Treat myoglobinuria with:

i. Diuretics, such as furosemide or mannitol.

ii. Alkalinization of urine to a pH of greater or equal to 7.45.

iii. Maintain urine output with IV fluid administration.

f. Compartment syndrome:

i. Must be distinguished from vasospasm, autonomic

dysfunction, and paralysis which are usually self-limited

phenomena.

Page 268

Notes


ii. Delay fasciotomy if possible since it will rarely be

necessary.

3. Admission criteria:

a. Seriously injured and post-cardiac arrest victims.

b. History of change in mental status/altered level of

consciousness.

c. Myoglobinuria.

d. Acidosis.

e. History of dysrhythmias or ECG changes:

i. May not resolve spontaneously.

ii. 24-48 hour observation period discriminates potentially

unstable cases.

VII. NEAR DROWNING


1. Definitions:

a. Drowning:

i. Death by suffocation after submersion in a liquid.

ii. Death within 24 hours of the accident.

b. Near drowning:

i. Survival, or at least temporary survival, following a

submersion accident.

ii. Survival beyond 24 hours.

2. Stages of drowning:

a. Stage I:

i. Unexpected submersion with struggle.

ii. Aspiration of small amount of water.

iii. Laryngospasm.

b. Stage II:

i. Increased hypoxia and panic.

ii. Large volume of water swallowed.

c. Stage III:

i. Wet drowning: (85-90% of cases).

ii. Laryngospasm relaxes due to persistent hypoxia.

iii. Aspiration of large volumes of water or gastric contents if

victim vomits.

iv. Dry drowning: (10-15% of cases):

Aspiration of small amount of water.

Further laryngospasm.

Severe hypoxia leading to seizure or death.

3. Physiologic responses:

a. Saltwater drowning:

i. Protein-rich fluid pulled into the alveoli causing

pulmonary edema and hypoxia.

ii. Reduced circulating blood volume with elevated

hemoglobin and sodium.

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Notes


b. Freshwater drowning:

i. Affects surface-tension properties of surfactant making

the alveoli unstable.

ii. Collapse or atelectasis of alveoli.

iii. Intrapulmonary shunting of alveoli.

iv. Hypotonic fluid absorbed quickly into the circulation and

redistribution into the body.

v. Hemodilution and fluid overload.

vi. Reduced hemoglobin and serum electrolytes.

vii. Lysis of red cells leads to hyperkalemia.

4. Pathophysiology:

a. Aspiration:

i. Small volume of water usually aspirated.

ii. Significant electrolyte changes uncommon.

iii. Grossly contaminated water may further increase

pulmonary injury/infection.

b. Hypoxemia:

i. Metabolic lactic acidosis.

ii. Multisystem organ dysfunction.

iii. Myocardial dysfunction.

iv. Coagulation abnormalities (DIC).

v. Renal failure.

vi. CNS dysfunction.



a. Cardiovascular:

i. Cardiopulmonary arrest – apneic and pulseless.

ii. Cyanosis.

b. Pulmonary:

i. Dyspnea.

ii. Cough.

iii. Copious pulmonary secretions.

c. CNS:

i. Loss of consciousness.

ii. Hypoxic induced cerebral injury or cerebral edema.

d. Other:

i. Evidence of trauma.

ii. Cervical spine injury.

e. Hypothermia:

i. More common in young children due to larger body

surface to mass ratio and less subcutaneous fat.

ii. Decreases the metabolic rate.

iii. Survival and full recovery possible after prolonged

submersion in cold water (66 minutes-record).

iv. Diving reflex:

Young children may be more susceptible.

Page 270

Notes


Potentiated by fear.

Triggered by submersion of face in cold water.

Bradycardia ensues with redistribution of blood flow

to the heart and brain.

C. Treatment:

1. Prehospital:

a. Cautions:

i. Avoid further aspiration.

ii. Apply cricoid pressure during bag-to-mask ventilation

until airway is secured by intubation.

iii. Strict C-spine precautions.

b. Controversies:

i. Abdominal thrusts to remove water:

Not appropriate to remove water from the lungs.

Increased risk of aspiration.

Only useful if foreign body is lodged in airway.

2. Initial stabilization:

a. ABCs.

b. Remove wet clothing.

c. Obtain accurate core temperature:

i. Initiate rewarming (see Hypothermia section).

3. ED treatment:

a. Correct hypoxemia:

i. Titrate to oxygen saturation.

ii. Intubate and provide mechanical ventilation with positive

end-expiratory pressure to maintain oxygenation.

b. Evaluate and treat traumatic injuries.

c. Correct acidosis:

i. Administer sodium bicarbonate if pH<7.1.

d. Cardiopulmonary arrest:

i. Initiate ACLS measures and continue resuscitation until

core temperature > 32oC, or until spontaneous pulse and

respirations return.

e. Importance of admission:

i. Pulmonary edema may develop as long as 12 hours later.

ii. Delayed neurologic abnormalities.


a. ICU:

i. Patients who required CPR or artificial ventilation.

ii. Abnormal chest radiograph.

iii. ABG abnormalities.

b. Admit observation status:

i. Submersion for >1 minute.

ii. History of cyanosis or apnea.

iii. Patients who required brief assisted ventilation.

Page 271

Notes


5. Discharge criteria:

a. Questionable history of submersion:

i. Observe in ED for 6-8 hours.

ii. No signs or symptoms of respiratory distress or change in

neurologic status.

VIII. HYPOTHERMIA


1. Description:

a. Definition - body temperature <35°C.

2. Etiology:

a. Decreased heat production:

i. At age extremes.

ii. With endocrine failure and malnutrition.

b. Impaired thermoregulation:

i. Central CNS conditions affecting the hypothalamus.

ii. Spinal cord transection.

c. Increased heat loss:

i. Immersion in cold water and wet clothes.

ii. Burns.

iii. Alcohol – increased vasodilation/altered behavior.

d. Medications/toxins decrease the body’s ability to respond to

cold stress.

B. Clinical presentations:


Temp C Signs/Symptoms

35 (95°F)

maximum shivering

34

amnesia/dysarthria

33

ataxia/apathy

32

stuporous

31 (88°F)

shivering ceases

30

Afib

28 (82°F)

Vfib

27

reflexes/voluntary motion cease

24

significant hypotension

Page 272

Notes


19 EEG flat

18 (64°F) asystole

15.2

lowest accidental hypothermia survival

a. Cardiovascular.

i. Early tachycardia followed by bradycardia:

Caused by decreased spontaneous depolarization of

pacemaker cells.

Refractory to atropine.

ii. Cardiac cycle lengthens resulting in increased intervals.

iii. Osborn J Wave= Hypothermic Hump:

Repolarization abnormality seen at the junction of the

QRS and ST segments at temperatures less than 32 C.

iv. Dysrhythmia:

All atrial/ventricular dysrhythmia encountered below

32 C.

v. Core temperature after drop:

Decline in a temperature after removal from the cold.

Most common during active external rewarming

where peripheral vasoconstriction and A-V shunting

are reversed.

b. CNS system:

i. Linear decrease in cerebral metabolism of 6-7% per

degree C from 35-25 C.

c. Respiratory system:

i. Progressive respiratory depression with CO2 retention.

d. Renal system:

i. Paradoxical large initial diuresis due to:

Relative central hypovolemia.

Cold induced defects in distal tubular reabsorption of

sodium and water.

ii. Renal blood flow depressed 50% at 27-30 C.

e. Pediatric considerations:

i. Infants have a large body surface to mass ratio and are at

greater risk for hypothermia.

C. Responses to hypothermia:

1. 32.2-35°C:

a. Thermogenesis preserved via shivering/endocrine

mechanisms.

2. 24-32.2°C:

a. Vasoconstriction preserved.

b. Shivering/endocrine mechanisms fail.

3. <24°C:

a. All heat conservations mechanisms fail.

Page 273

Notes


D. Diagnosis:


a. Accurate core temperature confirms diagnosis.

2. Laboratory:

a. ABG:

i. Temperature correction not needed.

b. CBC:

i. Hematocrit rises due to decreased plasma volume.

ii. Leukopenia does not imply absence of infection.

c. Electrolytes, BUN/Cr:

i. Vary during rewarming – recheck frequently.

d. PT, PTT, and platelets:

i. Prolonged clotting times with thrombocytopenia common.

e. Toxicology screen:

i. Alcohol/drug ingestions – common risk factors.


a. CXR – pneumonia common complication.

E. Treatment:

1. “No one is dead until warm and dead”:

a. Near normal recovery of Norwegian hypothermic man who

was successfully resuscitated using warmed IV fluids and

heated peritoneal lavage after 6 hours of CPR.

2. Prehospital:

a. Cautions:

i. Prolonged palpation/auscultation for cardiac activity.

ii. Apparent cardiovascular collapse may be depressed

cardiac output often sufficient to meet metabolic

demands.

iii. Do not want to induce Vfib with unwarranted chest

compressions.

b. Controversies:

i. CPR not recommended if:

Electrical rhythm present without palpable pulse

or blood pressure with short transport time.


a. ABCs:

i. Supplemental oxygen.

ii. Oral and naso-tracheal intubation are safe.

iii. Cardiac monitor.

iv. Warmed D5.9NS preferred over lactated ringers.

b. Remove wet clothing and begin passive external rewarming.

c. Administer Narcan, D50W (or Accu-Cheks), and thiamine

with an altered mental status.

d. Obtain accurate core temperatures using rectal temperature.

Page 274

Notes


4. ED treatment:

a. Cardiac arrest resuscitation:

i. Vfib induction occurs with rough handling, chest

compressions, hypoxia, and acid/base changes.

ii. CPR is less effective due to decreased chest wall

elasticity.

b. Defibrillation:

i. Defibrillation is rarely successful at temperatures <30°C.

ii. Defibrillate 1 to 3 times and then again post

rewarming.

iii. Direct current results in myocardial damage.

c. Arrhythmia management:

i. Atrial fibrillation:

Common below 32°C.

Usually converts spontaneously with rewarming.

ii. Malignant ventricular arrhythmias:

Bretylium drug of choice if available.

Medication most effective > 30 C.

Avoid lidocaine and procainamide B (may incr. Vfib).

4. Rewarming techniques:

a. Faster rewarming rates (1-2 C/hr) generally have better

prognosis than slower rewarming rates (<0.5 C/hr).

b. Active rewarming is necessary at core temperatures below

32 C:

i. Internal thermogenesis (shivering extinguished)

insufficient to increase the body temperature.

c. Passive external rewarming:

i. Ideal technique for the majority of healthy patients with

mild hypothermia.

ii. Cover the patient with dry insulating material.

iii. Endogenous thermogenesis must generate an acceptable

rate of rewarming.

d. Active external rewarming:

i. Delivers heat directly to the skin.

ii. Associated with core temperature afterdrop.

iii. Safe in previously health young acutely hypothermic

victims.

e. Active core rewarming techniques:

i. Airway rewarming (complete humidification at 40-

45 C):

Administer to all patients.

ii. Heated IVF (40-42 C):

High flow rates to deliver warmed fluid.

Heat one liter of crystalloid in a microwave set at high

for two minutes.

iii. Heated gastric irrigation via NG or OG tubes:

Not recommended.

Page 275

Notes


Low amount of surface area.

Aspiration risk if the airway has not been secured.

iv. Pleural irrigation (0.9% NS at 40-42 C):

Use in severe hypothermia without cardiac activity.

One or two chest tubes.

Contraindicated in patients with a cardiac rhythm

since the chest tube may induce Vfib.

v. Heated peritoneal lavage (0.9% NS at 40-45 C):

Use in unstable hypothermic patients or stable patients

with severe hypothermia whose rewarming rates are

<1 C/hr.

One or two catheters.

Advantageous in patients with an overdose or

rhabdomyolysis.

vi. Hemodialysis:

Initiate for patients with drug overdoses or severe

electrolyte disturbances.

vii. Cardiopulmonary bypass:

Treatment of choice in severe hypothermia especially

for those patients in cardiac arrest.

Complications include:

•• Hemolysis.

•• Vascular injury.

•• Air embolism.

•• Coagulopathies.


a. Moderate to severe hypothermia (<32 C).

b. Young healthy patients with no co-morbid illness who have

mild accidental hypothermia (32-35 C) that responds well to

warming:

i. Admit to an observation area.

ii. Discharge if asymptomatic after 8-12 hours.


a. Young healthy patients with no co-morbid illness.

b. Very mild accidental hypothermia (>35 C) that responds well

to warming.

c. Safe, warm environment to go to after discharge.

IX. FROSTBITE


1. Definitions:

a. Frostnip:

i. Mildest form of cold injury.

ii. Transient numbness and paresthesias resolve after

rewarming.

Page 276

Notes


iii. Due to superficial and reversible ice crystal formation

with intense vasoconstriction without tissue destruction.

iv. Warming results in freedom from epidermal/dermal

damage.

b. Chilblain:

i. Usually located on face, anterior tibia, dorsum of

hands/feet.

ii. Chronic vasculitis of dermis provoked by repeated

exposures to cold temperature above freezing.

iii. Secondary to sympathetic instability and vascular

hypersensitivity to cold with microvascular

stasis/thrombosis.

iv. Localized erythema, cyanosis, plaques and vesicles.

c. Trenchfoot:

i. Feet exposed to wet conditions and temperatures between

0-20°C.

ii. Neurovascular damage occurs without ice crystal

formation.

iii. Hyperemia may be present for up to 6 weeks.

iv. Pallor, mottling, paresthesias, pulselessness, paralysis,

numbness and cramps.

d. Frostbite:

i. Freezing of skin/subcutaneous tissues.

2. Frostbite injury:

a. Inability to physiologically compensate for cold that produces

injury.

b. Factors include:

i. Duration of contact, humidity, wind, altitude, clothing,

medical conditions, behavior, and individual variability.

c. Prefreeze state:

i. Tissue cooling, increased viscosity, capillary constriction-

dilation cycle.

d. Frozen state:

i. Extracellular ice crystal formation, intracellular

dehydration and hyperosmolarity, fluid crossing cell

membrane.

e. Ischemic and vascular complications:

i. Reperfusion injury, leaky endothelium, coagulation from

stasis, leakage of prostaglandins and free radicals,

vasoconstricting and AV shunting, necrosis/gangrene.

f. Three zones of injury:

i. Zone of coagulation:

Most severe, distal region of damage; irreversible.

ii. Zone of hyperemia:

More superficial, proximal region; least cellular

damage; recovers in < 10 days.

iii. Zone of stasis:

Middle ground; severe, possibly reversible cell

Page 277

Notes


damage.



a. Penis, fingers, toes, ears and nose most commonly affected.

b. Initial appearance of an injury often fails to predict

eventual depth or outcome.

i. Devitalized tissue demarcates as the injury evolves over

weeks to months.

2. 1st degree frostbite:

a. Partial skin freezing.

b. Erythema, edema, hyperemia.

c. Lack of blisters or necrosis.

d. Stinging/burning/throbbing.

e. Prognosis – excellent.

3. 2nd

degree frostbite:

a. Full thickness skin freezing.

b. Substantial edema over 3-4 hrs.

c. Erythema.

d. Formation of clear blisters (6-24hrs) that desquamate and

form eschar.

e. Numbness/aching/throbbing.

f. Prognosis – good.

4. 3rd

degree frostbite:

a. Damage extends into subdermal plexus.

b. Hemorrhagic blisters form.

c. Skin necrosis, blue-gray discoloration.

d. “Block of wood”.

e. Burning/throbbing/shooting pains.

f. Prognosis – poor.

5. 4th

degree frostbite:

a. Extension into subQ, muscle, bone, and tendon.

b. Little edema.

c. Mottled, nonblanching cyanosis.

d. Forms deep, dry, black eschar.

e. Deep aching joint pain.

f. Prognosis – extremely poor.

6. Post-rewarming appearance:

a. Post-rewarming edema begins within 3 hours lasting 5 days.

b. Large, clear blebs form within 6-24 hours.

c. Small, hemorrhagic blebs form after 24 hours:

i. Associated with deeper injury.

d. Eschar forms in 9-15 days.

e. Mummification in 3-6 weeks.

f. Persistent mottling and anesthesia despite edema after

rewarming are unfavorable prognostic indicators.

Page 278

Notes


C. Treatment:

1. Pre-hospital:

a. Protect and immobilize frostbitten area during transport.

b. Remove restrictive or wet garments.

c. Avoid dry rewarming of the frostbitten limb if there is a

likelihood of refreezing of the injury:

i. If the evacuation will be delayed, and suitable facilities

are available, field rewarming in warm (40-42°C) water

can be attempted.

d. Rubbing, manipulating the limb or applying snow while it is

still frozen is contraindicated.

e. Hypothermia:

i. Common in frostbite victims.

ii. Avoid rough handling to minimize possibility of cardiac

dysrhythmias in the seriously hypothermic patient.

f. Look for evidence of intoxication, head injury, trauma,

hypoglycemia, cardiac, or neurologic problems as underlying

etiologies and treat them appropriately.


a. ABCs.

b. Identify and correct hypothermia.

c. IV fluid volume expansion with 0.9% NS for severe frostbite.

d. Protect frostbitten areas from excessive handling or dry

warming during resuscitation.

3. ED treatment:

a. If the injury is less than 24 hours old and has not yet been

rewarmed:

i. Initiate rapid thawing of the injured extremity for 10-

30 minutes in 40-42°C water.

ii. Stop treatment when the limb is warm, red, and pliable.

iii. Monitor water temperature closely to prevent thermal

injury.

b. Analgesia.

c. NSAID (ibuprofen):

i. Combat the effects of prostaglandins on skin necrosis.

d. Aloe vera topical cream:

i. Combats the arachidonic cascade.

ii. Recommended for all intact blisters.

e. Blister debridement or aspiration:

i. Indicated for clear blebs (removes thromboxane and

prostaglandins).

ii. Contraindicated for hemorrhagic blebs (exposes

deeper structures to dehydration and infection).

f. Tetanus prophylaxis.

g. Antibacterial prophylaxis:

i. Consider during the hyperemic recovery phase (at least 2-

3 days) in severely frostbitten areas.

Page 279

Notes


ii. Against streptococci, staphylococci and Pseudomonas

species (cephalosporin, penicillinase-resistant penicillin,

quinolone).

iii. Topical antibacterial agents interfere with the use of aloe

vera cream and should be considered a second line

approach.

h. Elevation and splinting of frostbitten area.

i. Two to four times daily dressing change.

j. Avoid vasoconstrictive agents (including tobacco).

k. Amputation after 3-4 weeks.

l. Admit all but the most isolated and superficial cases.

m. Investigational treatments:

i. Dextran, heparin, calcium channel blockers, hyperbaric

oxygen therapy not effective consistently.

ii. Alpha blockers such as phenoxybenzamine – under study.

iii. Medical or surgical sympathectomy –beyond the scope of

the emergency department.

iv. Topical methylprednisolone 1% cream – not as effective

as aloe vera.

X. HEAT-RELATED ILLNESS


1. Mechanism:

a. Continuum of increasingly severe illnesses secondary to

overwhelming heat stress.

b. Begins with dehydration and electrolyte abnormalities and

progresses to thermoregulatory dysfunction and multi-system

organ failure.

c. Heat dissipation:

i. Body temp: heat production vs. heat loss (or gain).

ii. Conduction: heat exchange b/t two surfaces in contact.

iii. Convection: heat exchange b/t a surface and a gas or

liquid.

iv. Radiation: transfer of heat b/t body and environment

through electromagnetic waves.

v. Evaporation: one-way heat flow from body to

environment.

d. Heat regulation:

i. 3 distinct systems of control:

Thermosensors: temperature sensitive structures found

in skin, spinal cord, limb muscles, and preoptic area of

anterior hypothalamus.

Central integrative area: interprets data from

thermosensors; probably located in hypothalamus or

spinal cord.

Thermoregulatory effectors: structures that respond to

Page 280

Notes


physiologic changes to decrease temperature

(peripheral vasodilatation and sweating - most

important).

2. Heat stroke:

a. Loss of thermoregulatory function, severe CNS dysfunction,

and multi-system organ failure.

b. Classic heat stroke:

i. Occurs in those with compromised homeostatic

mechanisms (elderly, debilitated).

ii. Develops over days to weeks.

iii. Severe dehydration.

c. Exertional heat stroke:

i. Occurs in younger, athletic individuals with a

combined environmental and exertional heat stress.

ii. Develops over hours.

iii. Internal heat production overwhelms dissipating

mechanisms.

iv. May be sweating.

3. Heat exhaustion:

a. Fluid and electrolyte depletion.

b. Thermoregulatory function is maintained.

4. Heat cramps:

a. Secondary to excessive sweating and sodium loss.

B. Etiology:

1. Circulatory insufficiency:

a. Age extremes.

b. Dehydration.

c. CHF.

d. Obesity.

e. Diuretics.

f. Laxatives.

2. Pharmacologic causes:

a. Sympathomimetics.

b. LSD.

c. MAO inhibitors.

d. PCP.

e. Anticholinergics.

f. Antihistamines.

g. Drug or alcohol withdrawal.

3. Excessive head load:

a. Environmental.

b. Fever.

c. Exertional.

d. Lack of acclimatization.

4. Decreased cardiovascular function:

a. Beta-blockers.

Page 281

Notes


b. Sympatholytics.

5. Pediatric:

a. Children are at increased risk of heat illness due to increased

body surface area to mass ratio.

C. Clinical presentation:


a. Heat edema:

i. Swelling of dependent areas of body.

ii. Resolves after acclimatization.

b. Heat syncope:

i. Consequence of a reduced “effective” blood volume.

ii. Brief and responds to horizontal positioning and

improved venous return.

c. Heat cramps:

i. Cramps in heavily exercised muscles.

ii. During or after exercise.

iii. Primarily in lower extremities.

d. Heat tetany:

i. Carpal-pedal spasm (secondary to hyperventilation).

e. Heat exhaustion:

i. Core temp: <104°F.

ii. CNS: headache, fatigue, malaise, agitation.

iii. CV: mild tachycardia, dehydration.

iv. Pulmonary: tachypnea.

v. Renal: elevated BUN/Cr due to dehydration.

vi. GI: nausea, vomiting.

f. Heat stroke:

i. Core temp: >105°F.

ii. CNS: severe confusion/lethargy, coma, seizure, ataxia

or focal deficits.

iii. CV: tachycardia, hypotension.

iv. Pulmonary: tachypnea.

v. GI: nausea, vomiting, diarrhea.

vi. Skin: dry and hot in classic heat stroke; moist/sweating

with exertion/ heat stroke.

vii. Renal: acute oliguric renal failure due to rhabdomyolysis/

dehydration. viii. Liver: hepatic failure.

D. Diagnosis:


a. Accurate core temperature.

b. Obtain history of heat exposure.

c. Heat exhaustion – diagnosis by exclusion of other causes.

2. Laboratory (for heat stroke and heat exhaustion):

Page 282

Notes


a. CBC:

i. Leukocytosis might point toward infection.

b. BMP:

i. Hypernatremia with severe dehydration.

ii. Acute renal failure.

iii. Hyperkalemia with severe heat stroke.

c. UA:

i. Myoglobin present in rhabdomyolysis.

ii. Bacteria/WBC.

d. LFTs:

i. Hepatic necrosis.

e. PT/PTT/DIC panel:

i. Clotting abnormalities.


a. ECG indicated in elderly or those at cardiac risk.

b. CT head for altered mental status.

c. CXR for ARDS, aspiration pneumonia.


a. Febrile illness/sepsis.

b. Thyroid storm.

c. Pheochromocytoma.

d. Malignant hyperthermia.

e. Cocaine.

f. PCP.

g. Anticholinergics.

h. MAO inhibitors.

i. Meningitis.

j. Encephalitis.

k. Cerebral falciparum malaria.

l. Delirium tremens.

E. Treatment:

1. Pre-hospital:

a. Institute cooling measures for severe heat illness:

i. Remove from heat stress.

ii. Disrobe patient.

iii. Ice packs to axilla, groin, and neck.

iv. Cover body with wet sheet.

b. IV 0.9% NS at TKO - 500 cc fluid bolus if hypotensive.

c. If altered mental status – glucose (or accucheck), thiamine,

naloxone.


a. ABCs.

b. Immediate/rapid cooling if temperature >40 C.

3. ED management:

a. Cooling measures: initiate for body temperature >40 C.

i. Evaporative:

Page 283

Notes


Extremely effective (0.05-0.3 C/min).

Spray disrobed patient with fine mist of warm

water (prevents shivering).

Airflow with fans blow over patient.

ii. Conductive:

Ice packs to groin/axilla combine with evaporative

adjunctive treatment above.

Iced or cold water immersion very effective

(0.13 C/min) but impractical.

Iced peritoneal lavage and cardiopulmonary bypass

for refractory cases.

iii. To avoid hypothermia, stop cooling therapy at 39 C.

b. Supportive measures:

i. Rehydration for heat stroke:

Initial rehydration with 0.5-1.0 L 0.9% NS.

Avoid overhydration may contribute to development

of ARDS.

Peds: 20 cc/kg bolus.

ii. Glucose/naloxone/thiamine for altered mental status.

iii. Chlorpromazine to stop shivering.

iv. Benzodiazepine for seizure.

v. Analgesics and oral or IV hydration with electrolyte

containing fluid for heat cramps.

vi. Reassurance/calming measures/rebreathing in closed

system (bag or non-rebreather without oxygen) for

hyperventilation heat tetany.

vii. Lower extremity elevation/removal from heat stress for

heat edema.


a. Heat stroke to the ICU.

b. Heat exhaustion:

i. Severe electrolyte abnormalities.

ii. Renal failure/evidence of rhabdomyolysis.

iii. Elderly.

XI. RADIATION INJURY


1. Description:

a. Acute Radiation Syndrome results after a major portion of the

body is irradiated by deeply penetrating radiation with a dose

usually >1 Gy.

b. Measuring radiation:

i. Rad (radiation absorbed dose) is a measure of energy

imparted to matter.

2. 1 rad=100ergs/g.

a. 1 Gray (Gy), the SI (International System of Units) Measure=

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Notes


100 rad.

3. Types of exposure:

a. External contamination:

i. Follows irradiation from an external source (e.g.,

radiation therapy).

ii. Radioactive material in contact with a patient’s clothing

or skin.

iii. Must remove radioactive material.

iv. Contain radioactive material to prevent further

contamination.

v. No contamination hazard.

b. Internal contamination:

i. Inhalation or ingestion of radioactive material.

ii. Treat as heavy metal ingestion.

4. Etiology:

a. Alpha, beta, X- and gamma rays emitted during the decay of

unstable isotopes:

i. Responsible for acute radiation syndrome.

b. Alpha particles:

i. Equivalent to a helium nucleus and derived from the

decay of certain nuclides of heavy elements.

ii. Penetration limited to the epidermis.

iii. Contamination treated by skin cleaning.

c. Beta particles:

i. Electrons or positrons ejected at high velocity from a

nucleus undergoing beta decay.

ii. Skin penetration of 8 mm causes thermal-like burns.

iii. Clothing blocks penetration.

iv. Measured by radiation meters.

v. Removed by skin cleaning.

d. Gamma rays:

i. Primary cause of radiation injury.

ii. Deeply penetrating high energy wave similar to X-rays.



a. Tissues with greater rates of cellular division more

radiosensitive.

b. GI and heme systems most vulnerable.

2. Skin:

a. With increasing radiation exposure develop:

i. Epilation.

ii. Erythema.

iii. Dry desquamation.

iv. Wet desquamation.

b. Erythema that develops within 48 hours usually progresses to

ulceration or chronic radiodermatitis.

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Notes


c. Treat as thermal burn.

3. Gastrointestinal:

a. Anorexia/nausea/vomiting/diarrhea.

b. Dehydration due to transudation of plasma into the GI tract.

c. Major source of septicemia when combined with bone

marrow suppression.

d. Higher doses result in an earlier onset and more protracted

course:

i. <0.5 Gy - onset >6 hrs.

ii. <2 Gy - onset 2-6 hrs.

iii. >4 Gy - onset <2 hrs.

iv. >10 Gy - onset <30 min.

4. Hematopoetic:

a. Pancytopenia due to bone marrow suppression:

i. Anemia.

ii. Thrombocytopenia with doses exceeding 2-4 Gy after

about 4 weeks.

iii. Lymphopenia/neutropenia causing fever and increased

risk of infection.

b. Bone marrow depression develops after a latent phase.

5. Central nervous system:

a. Headache.

b. Altered mental status.

c. Vertigo.

d. Occurs after massive exposure – associated with near 100%

mortality within 48 hours; survivable if exposure is limited to

the head.

C. Diagnosis:


a. Radiation monitoring to insure decontamination.

2. Laboratory:

a. CBC/platelet count:

i. Baseline important.

ii. Absolute lymphocyte count (ALC) at 48 hours

correlates with prognosis:

>1200/mm3 -good prognosis.

300-1200/mm3 -fair prognosis.

<300 mm3 -poor/critical prognosis.

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Notes


3. Illness categorization:

D. Treatment:

1. Pre-hospital:

a. Activate plan when predefined criteria met.

b. Early notification of type of incident to receiving hospital.

c. Transport after decontamination if medically stable.

d. Site decontamination.

2. Remove/bag clothing and leave at scene for disposal.

3. Clean with soap and water:

a. Protective clothing includes respirators, rubber gloves and

shoe covers for rescue personnel.


a. Field decontamination except for patients in extremis.

b. ABCs:

i. 0.9% NS IV fluid bolus for extensive thermal

burns/hypotension.

c. General principles:

i. Irradiated, non-contaminated victim is not radioactive and

poses no risk to health care workers.

ii. Contaminated victims are unlikely to represent a

significant risk of radiation exposure to health care

workers and the treatment of serious medical problems

take priority over radiation concerns.

Degree

Gy

Clinical Scenario

Treatment/

Disposition mild

<2

mild GI for 24 hours

ALC(48h)2,000

discharge if

asymptomatic; follow

daily CBC and platelets moderate

2-4

moderate GI for 4 days

ALC(48h)1,200

admit for supportive care

and observation severe

4-10

severe GI for 7 days

ALC(48h)<1,200

symptomic anemia

infections common

admit for reverse

isolation, antibiotics,

transfusions, consider

bone marrow transplant

about 50% mortality fatal

>10

GI and CNS within

30 mins

ALC(48h)<300

admit for palliative

measures; death expected

within 1 week

Page 287

Notes


5. ED management:

a. Protect all hospital personnel:

i. Cover skin with gown.

ii. Use radiation survey monitors to prevent contamination.

iii. Set up containment and decontamination areas with

running water and drainage.

b. Irrigate open wounds with saline followed by 3% hydrogen

peroxide if contamination persists.

c. Irrigate contaminated eyes and ears.

d. Gently scrub skin with soap and water 3 minutes (do not

abrade).

e. GI decontamination for ingestions:

i. Whole-bowel irrigation and activated charcoal within 2

hours of exposure.

f. Pulmonary decontamination:

i. Consider bronchoalveolar lavage.

g. Supportive treatment:

i. IV fluids to replace GI losses.

ii. Antiemetics and analgesics.

iii. Monitor for need of reverse isolation.

iv. Cover severe burns with sterile dressing.

v. Early and broad spectrum antibiotics for fevers or other

signs of infection.

vi. Early surgery for associated trauma to reduce risk of

infection and bleeding.

h. Potassium iodine to prevent thyroid uptake of radioactive

iodine-131 ingestion:

i. Indications: >100 rad for adult/ >50 rad for child.

ii. Blocks 90% I-131 if given within 1 hr; 50% if given

within 5 hr.

i. Chelating agents for radioactive heavy metals:

i. Aluminum reduces absorption of strontium.

ii. Barium reduces and precipitates radium.

iii. EDTA precipitates lead.

iv. Penicillamine for lead, copper, cobalt.

v. Prussian blue for thalium, cesium, rubidium.

vi. DTPA for transuranics, heavy metals.

vii. Deferoxamine for plutonium, iron. viii. Water diuresis for tritium, Na+ ,K+.

ix. Dimercaprol for mercury, arsenic, bismuth, chromium,

nickel, lead.

j. For expert assistance contact Radiation Emergency

Assistance Center in Tennessee: (615) 481-1000 (24 hr/day).


a. Exposure to a dose of radiation >1Gy.


a. Asymptomatic patients with dose of radiation less than 1 Gy

with close laboratory follow-up.

Page 288

Notes


XII. BURNS

A. Degree of injury:

1. 1st degree:

a. Red skin, no blisters, painful.

b. Heal over several days with no scarring.

2. 2nd

degree:

a. Superficial partial thickness:

i. Epidermis and superficial dermis.

ii. Pink, moist, tender, thin blisters, heal in 2 weeks.

iii. Very painful to the touch.

iv. Scarring is minimal and usually full return of function.

b. Deep partial thickness.

c. Extends into dermis (damage to hair follicles and sweat and

sebaceous glands).

d. Red, blanched white, decreased 2pt discrimination.

e. Thick walled blisters, usually ruptured, heal in 4 weeks.

f. Scarring is common; surgical debridement and skin grafting

may be necessary.

3. 3rd

degree:

a. Full thickness, destroyed epidermis/dermis.

b. White leathery appearance, clotted vessels, numb.

c. < 1cm heal by contraction.

d. Skin grafting for larger lesions.

4. 4th

degree:

a. Full thickness with destruction of all deep structures.

b. Extensive debridement and reconstructive surgery.

B. Burn size - % body surface area:

1. The Rule of Nines:

a. Front and back of torso – 18% BSA each.

b. Each leg – 18% BSA each.

c. Each arm – 9% BSA each.

d. Head – 9% BSA.

e. Perineum – 1% BSA.

2. Back of patient’s hand is ~1% BSA.

C. Burn categories:

1. Major:

a. Full thickness: >10% TBSA.

b. Partial thickness: >25% TBSA adults; >20% TBSA >50 yr or

<10 yr.

c. Miscellaneous: face, hands, feet, perineum, chemicals,

electrical, complicated by inhalational injury, increased co-

Page 289

Notes


morbidities.

d. Disposition:

i. Transfer to a burn unit.

2. Moderate:

a. Full thickness: 2-10% TBSA.

b. Partial thickness: 15-25% TBSA adults; 10-20% TBSA >50

yr or <10 yr.

c. Disposition:

i. Admit to the hospital.

ii. Burn unit unnecessary.

3. Minor:

a. Full thickness: <2% TBSA.

b. Partial thickness: 15% TBSA adults; <10% TBSA >50 yr or

<10 yr.

c. Disposition:

i. Outpatient management.

D. Treatment:

1. Keep burns clean.

2. Wash/dress area with cool water:

a. No ice.

3. Pain meds:

a. Morphine.

4. IV fluids if >20% TBSA 2nd or 3rd degree burns:

a. IV through unburned skin.

b. Parkland formula:

i. LR @ 4 cc/kg / %TBSA burn IV 1st 24 hrs.

ii. ½ in first 8 hrs.

iii. ½ in next 16 hrs.

iv. Maintain UO @ 0.5 – 1.0 cc/kg/hr.

5. Special situations:

a. If suspect inhalational injury:

i. Check CN level.

ii. Check COHb level.

Half-life of carbon monoxide is:

•• 4-5 hours at room air.

•• 80-90 minutes with 100% oxygen

supplementation.

•• 20-30 minutes with hyperbaric oxygen treatment.

Indications for hyperbaric oxygen treatment include:

•• Persistent symptoms after 4 hours of oxygen

treatment.

•• CO level greater than 15-40.

•• Any history of syncope.

•• Any neurovascular or cardiovascular impairment.

•• Pregnant women who are symptomatic or with a

level exceeding 15.

Page 290

Notes


b. Pediatric “Parkland formula”:

i. Galveston formula.

ii. D5/LR 5000cc / m2 TBSA burned + 2000 cc / m2 IV in

24 hrs.

iii. ½ in first 8 hrs.

iv. ½ over next 16 hrs.

c. FT circumferential burns:

i. Perform escharotomy.

6. Wound care:

a. Shur-Clens or sterile saline for cleaning.

b. Debride blisters: not on palms or soles.

c. Apply Silver sulfadiazine: not on face.

d. dPT > 10y and < 64y.o., Td.

e. Cover with sterile gauze or specialized burn dressings.

Page 291

Notes


ENVIRONMENTAL EMERGENCIES

PEARLS

1. The range of illness due to high altitude includes acute mountain

sickness, pulmonary edema, cerebral edema, and retinal hemorrhage.

The most serious of these is high altitude cerebral edema.

2. Acute mountain sickness is manifested by headache, nausea, vomiting,

exertional dyspnea, and difficulty sleeping. It lacks specific physical

findings. It can be avoided by gradual ascent, and is usually self-

limited. Acetazolamide and dexamethasone are useful for prevention

and treatment.

3. High altitude pulmonary edema is a noncardiogenic permeability edema

that may be life-threatening. In contrast to acute mountain sickness,

victims have physical signs and symptoms of pulmonary edema.

Immediate descent is important.

4. High altitude cerebral edema is the least common but most serious form

of altitude illness, manifested by ataxia and mental status changes and

sometimes focal deficits. Immediate descent is mandatory. Steroids,

oxygen, and elevation of head may be beneficial.

5. Three gas laws should be understood to explain the pathophysiology of

dysbarism:

Dalton’s Law: The total pressure of a mixture of gases is equal

to the sum of the partial pressures of each gas.

Henry’s Law: The amount of gas which is dissolved in any

solution is proportional to the pressure of the gas with which it is

in equilibrium (i.e., in descent, with an increase in pressure, a

greater amount of gas dissolves in solution. In ascent, with a

decrease in pressure, gas dissipates from the solution.)

Boyle’s Law: At constant temperature, the volume of a gas

varies inversely with pressure. (PV=nRT).

6. Barotrauma which occurs in descent is frequently the result of a

pressure imbalance of a gas contained in a closed space, such as sinuses

or ear. The result may be ear squeeze with rupture of the TM, round or

oval window, or hemorrhage into a closed space such as the sinuses.

7. Barotrauma from ascent is the most serious dysbaric illness. It results

from gas coming out of solution as the pressure decreases (“the bends”)

or air emboli. Decompression sickness occurs when ascent is too rapid

Page 292

Notes


and gas bubbles form. It is a multisystem disorder which may include

skin rashes, edema, periarticular joint pain, spinal cord ischemia,

pulmonary venous embolism, cerebral embolism (as discussed above.)

Treatment requires immediate 100% oxygen and recompression in a

hyperbaric chamber.

The onset of decompression illness may be delayed for up to 12-24

hours after surfacing.

8. Risk factors for decompression illness include too rapid ascent, obesity,

fatigue, alcohol use, dehydration, heavy exertion, and respiratory tract

infections.

9. Skin is a good resistor of electrical flow, although moisture decreases its

resistance. Nerve and blood tissue are least resistant to electrical flow.

Bone is most resistant.

10. Alternating current is more dangerous than direct current, causing

tetany, sometimes preventing the patient from letting go of the electrical

source.

11. The amount of tissue injury sustained from an electrical injury is usually

much greater than would be expected from any visible burn. Muscle

necrosis, hyperkalemia, hyperphosphatemia, metabolic acidosis, and

renal failure should be anticipated. Treatment involves volume loading

to achieve a urine output of 1 cc/kg/hr, urinary alkalinization to

facilitate excretion of myoglobin.

Cardiac arrhythmias, fractured bones, neurological complications

should be searched for and anticipated.

12. Electrical cord bite injuries may be complicated by late bleeding from

the labial artery when the eschar separates 7-10 days post injury.

13. In contrast to electrical injury, lightning injuries are usually flash-over

with superficial skin burns. Many injuries may be mild; however, a

massive countershock can cause cardiac asystole, and paralysis of the

medullary respiratory center can cause apnea. If the victim is thrown

from the force of the shock, multiple blunt trauma may result in any

number of injuries. Other common injuries include cataract formation

and TM rupture.

14. 10-20% of drowning deaths are “dry drownings” which occur from

laryngospasm without aspiration of fluid.

15. Fresh water aspiration may differ from salt water drowning but usually

only when more than 22 cc/kg of water are aspirated. Fresh water

Page 293

Notes


drownings with significant aspiration may be complicated by surfactant

washout with atelectasis, an increase in total plasma volume with a

decrease in serum lytes, hemolysis with hyperkalemia. Salt water

drowning with significant aspiration will cause a decrease in plasma

volume and an increase in serum lyte concentrations.

16. Postimmersion syndrome or secondary drowning refers to the

development of ARDS preceded by a relatively asymptomatic period of

hours to days. It usually occurs in significant drowning events with

transient hypoxia or aspiration that are effectively resuscitated. All

patients should have ABGs and CXRs done to determine anyone at risk.

17. Hypothermia may be due to decreased heat production (hypothyroidism,

adrenal insufficiency), increased heat loss (burns, ETOH), or impaired

thermoregulation (CVA, drug overdoses.)

18. Osborn J waves are one sign of hypothermia, occurring at temperatures

less than 32oC.

19. Mild hypothermia can be managed by passive external rewarming

techniques (remove wet clothes, apply warm covers.)

20. Active core rewarming techniques should be employed for temperature

less than 32oC including warmed humidified oxygen, heated IVFs (40-

42oC), and possibly heated peritoneal dialysis and cardiopulmonary

bypass.

21. Rapid rewarming in a water bath at 40-42oC is the treatment of

choice for frostbite.

22. Early debridement is contraindicated in frostbite.

23. Heat exhaustion is a clinical syndrome of headache, nausea, malaise,

tachycardia, orthostasis, and muscle cramps but normal mental status.

Treatment is rest in a cool environment with rehydration.

24. Heat stroke is characterized by altered mental status, confusion, possibly

progressing to seizures and coma. Classical “dry” heat stroke occurs in

the elderly or very young; exertional “wet” heat stroke occurs in the

young, fit individuals, usually overzealous athletes.

25. Treatment of heat stroke is supportive with rapid cooling best

accomplished by spraying the body with a fine mist and placing near

fans to increase evaporative loss.

Page 294

Notes


26. Ionizing radiation includes:

Alpha particles: penetrate only the epidermis.

Beta particles: penetrate skin to about 8 mm.

May decay to more dangerous gamma rays.

Gamma rays: deep penetration with deep tissue injury.

27. Tissues which are most radiosensitive are those with the fastest rate of

cellular division, especially G1 and hematopoietic cells.

28. The mean lethal dose of acute radiation exposure is 350 rads.

29. A 48 hour lymphocyte count is prognostic in acute radiation illness: a

value less than 300 is critical with predictable bone marrow failure.

30. The half-life of carbon monoxide is:

4-5 hours at room air.

80-90 minutes with 100% oxygen supplementation.

20-30 minutes with hyperbaric oxygen treatment.

31. Indications for hyperbaric oxygen treatment include:

Persistent symptoms after 4 hours of oxygen treatment.

CO level greater than 15-40.

Any history of syncope.

Any neurovascular or cardiovascular impairment.

Pregnant women who are symptomatic or with a level

exceeding 15.

Page 295

Notes


REFERENCES

1. Auerbach, PJ. Wilderness Medicine 5th

Ed. Philadelphia. Mosby

Elsevier 2007.

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of Children with Household Electrical Injuries. Ann Emerg Med

1995;25:5:612-617.

3. Bartlett RB. Diving Emergencies in Critical Decisions in Emergency

Medicine. Vol 10. Num 10. Lesson 20. Published by ACEP.

4. Bortsch P, Maggiorini M, Ritter M, Noti C, Vock P, Oelz O.

Prevention of high-altitude pulmonary edema by nifedipine. N Engl J

Med. 1991:325:1284-1289.

5. Bradley ME. Pulmonary Barotrauma. In Bove AA, Davis JC. Diving

Medicine. 2nd

Ed. Philadelphia. WB Saunders. 1990; 188-91.

6. Britt LD, Dascombe WH, Rodriguez A: New horizons in management

of hypothermia and frostbit injury. Surg Clinics of NA. 1991; 71(2)

345-70.

7. Browne, B.J.and Gaasch, W.R., Emergency Medicine Clinics of North

America, 10:2:211-30, 1992.

8. Cooper MA, Andrew CJ, Holle RL: Lightening Injuries, Auerbach PS

(ed): Wilderness Medicine 5th

Ed., Mosby Elsevier, 2007, pp.67-108.

9. Danzl DF et al: Accidental hypothermia. NEJM. 1994;331(26), 1756-

60.

10. DeNicola LK, Falk JL, Swanson ME, Gayle MO, Kissoon N:

Submersion injuries in children and adults. Crit Care Clinics.

1997;13:477-502.

11. Edmonds C, Lowry C, Pennefather J. Diving and Subaquatic Medicine.

Butterworth-Heinemann. Oxford 1992.

12. Fields AI: Near-drowning in the Pediatric Population. Crit Care Clinics

1992;8:113-129.

13. Fish, R., Electric Shock, Part II: Nature and Mechanisms of Injury,

Journal of Emergency Medicine, Vol. 11, pp.457-462, 1993.

14. Fontanarosa, P., Electrical Shock and Lightning Strike, Annals of

Emergency Medicine, 22:2 Part 2 February 1993, pp 378-386.

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15. Garcia, C. Smith, G., Cohen, D., Fernandez, K., Electrical Injuries in a

Pediatric Emergency Department, Annals of Emergency Medicine,

26:5, November 1995, pp.604-608.

16. Ghofrani HA, et al: Sildenafil Increased Exercise Capacity during

Hypoxia and Low Altitudes and at Mount Everest Base Camp. Annals

of Internal Medicine 141:3; Aug, 2004, pp169-177.

17. Grissom CK, Roach RC, Sarnquist FH, Hackett PH. Acetazolamide in

the treatment of acute mountain sickness: Clinical efficiacy and effect

on gas exchange. Ann Int Med. 1992: 116:6:461-465.

18. Heifetz In. Radiation Accidents. In Harwood-Nuss, A et al: The

Clinical Practice of Emergency Medicine, Philadelphia, 1996, J.B.

Lippincott Company.

19. Honigman B, Theis MK, McLain J, Roach RC, Yip R, Houston C et al.

Acute mountain sickness in a general tourist population at moderate

altitudes. Ann Int Med. 1993: 118:8:587-592.

20. Jerrard DA. Diving Medicine. In Emergency Medicine Clinics of North

America. Vol 10. Num 10 May 1992.

21. Jerrard DA. Diving Medicine. In Emergency Medicine Clinics of North

America. Vol 10. Num 2 May 1992.

22. Jolly BT, Ghezzi KT: Accidental hypothermia. Emerg Med Clinics NA.

1994; 10, (2); 311-327.

23. Kizer KW, Van Hoesen KB. Diving Medicine. Auerbach PA (ed.)

Wilderness Medicine. 5th

Ed. Philadelphia. Mosby Elsevier; 2007.

1599-1638.

24. Lavelle JM, Shaw KN, Seidl T, Ludwig S: Ten-year Review of

Pediatric Bathtub Near-drownings: Evaluation for Child Abuse and

Neglect. Annal Emerg Med, 1995;25:344-348.

25. Lee-Chiong TL, Stitt JT: Heat Stroke and Other Heat-Related Illnesses.

Postgraduate Medicine 1995 Jul;26-36.

26. Lichtenberg R, et al, Cardiovascular Effects of Lightning Strikes,

Journal of the American College of Cardiology, 21:2:531-6, 1993.

27. Madsen J, Hink J, Hyldegaard O. Diving Physiology and

Pathophysiology. Clinical Physiology (1994) 14, 597-626.

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28. Markovchick, V, Radiation Injuries. Marx JA, Hockenberger RS, Walls

RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical

Practice, 6th

ed, Philadelphia, Mosby Elsevier, 2006. pp. 2316-2325.

29. Moon RE, Vann RD, Bennett PB. The Physiology of Decompression

Illness. Scientific American. August 1995.

30. Olshaker JS: Near Drowning. Emrg Med Clin NA, 1992; 10:339-349.

31. Price TG, Cooper MA: Electrical and Lightning Injuries, Marx JA,

Hockenberger RS, Walls RM, et al (eds): Rosen’s Emergency


ed, Philadelphia, Mosby

Elsevier, 2006, pp. 2267-2278.

32. Primavesi, R. Electrical Injuries: Current Issues, Canadian Journal of

CME June 1996, pp. 85-96.

33. Quan L, Wentz KR, Gore EJ, Copass MK: Outcome and Predictors of

Outcome in Pediatric Submersion Victims Receiving Prehospital Care

in King County Washington. Peds, 1990;86:586-593.

34. Raymond LW. Pulmonary Barotrauma and Related Events in Divers.

Chest. 1995; 107;1648-52.

35. Simon HB: Hyperthermia. New England Journal of Medicine . 1993

Aug 12;329 (7) 483-7.

36. Smith RM, Neuman TS. Elevation of Serum Creatine Kinase in Divers

with Arterial Gas Embolism. NEJM. 1994;330:19-24.

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08/13

Page 298

Gynecological and Obstetrical Emergencies

Collette Wyte, MD, FACEP

Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Oakland University, William Beaumont School of Medicine, Royal Oak, Michigan

Page 299

Page 300

Notes

Gynecological Emergencies

GYNECOLOGICAL EMERGENCIES

Vaginitis

I. TRICHOMONIASIS

A. Epidemiology:

1. Trichomonas vaginalis is an anaerobic flagellate protozoan.

2. Does NOT normally inhabit the GU tract.

3. It is transmitted sexually.

a. Incidence increases with number of sexual partners.

b. Men are usually asymptomatic.

B. Pathophysiology:

1. Infection may cause vaginitis, urethritis, cervicitis and cystitis.

a. Vaginitis is the primary infection in women.

b. Cervicitis:

i. Occurs in 13%.

ii. Associated with "strawberry cervix".

c. Urethra infected in up to 90%.

2. Coexisting infections:

a. Gonorrhea in up to 50%.

b. Bacterial vaginosis.

3. Complications:

a. Polymicrobial PID.

b. During pregnancy:

i. Premature rupture of membranes.

ii. Preterm labor.

iii. Post-partum endometritis.

C. Presentation:

1. Profuse vaginal discharge, pruritus and irritation.

2. May complain of dysuria and dyspareunia.

D. Diagnosis:

1. Speculum exam reveals vaginal discharge:

a. Often not the classic green frothy discharge.

b. Usually discharge is grey in color and profuse.

c. Frothy discharge only present in 10%.

2. Strawberry cervix:

a. "Flea-bitten" appearance due to punctate submucosal

hemorrhage.

b. Only present in 2%, but denotes cervicitis.

3. Definitive diagnosis:

Page 301

Notes


a. Culture - prolonged incubation time, so not used much.

b. Wet-mount slide:

i. Rapid and practical.

ii. Positive for trichomonads in 60-80%.

iii. See motile trichomonads microscopically.

iv. Trichomonads are about the same size as leukocytes,

which are usually also present.

c. KOH prep - will emit a fishy odor if trichomonads are

present.

d. Gonorrhea and Chlamydia cultures should also be sent.

4. Bimanual examination will reveal no cervical motion

tenderness or adnexal or uterine tenderness in a patient with

isolated vaginitis.

E. Treatment:

1. Metronidazole:

a. Anti-protozoan drug.

b. Dosage:

i. 2 grams orally as a single dose.

ii. 500 mg twice a day for 7 days.

iii. Single dose therapy usually initial course of choice.

c. Produces a disulfiram-type reaction if taken with

alcohol.

d. Patients should refrain from drinking alcohol for at least

24 hours after taking Metronidazole.

e. Reoccurrence rates are low.

f. Class B in pregnancy.

2. Tinidazole:

a. 2 gm orally as a single dose.

b. Class C in pregnancy.

c. Avoid alcohol for 72 hours.

3. All sexual partners need to be seen and treated prior to

further sexual activity as the organism is found in 70% of

partners of an infected patient.

4. During pregnancy:

a. Treat symptomatic women only.

b. Metronidazole 2 g PO x 1.

c. Data does not indicate that treating asymptomatic pregnant

women lessens the risk of complications.

II. BACTERIAL VAGINOSIS

A. Epidemiology:

1. Previously referred to as nonspecific vaginitis, Haemophilus

vaginalis, Gardnerella vaginalis or corynebacterium vaginale.

2. Preferred term now is bacterial vaginosis.

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Notes


3. Microbial etiology is controversial:

a. Polymicrobial.

b. Overgrowth of normal flora.

4. Not inherently transmitted sexually.

B. Complications:

1. Polymicrobial PID.

2. During pregnancy:

a. PROM.

b. Preterm labor.

c. Postpartum endometritis.

C. Presentation:

1. Patient will complain of a profuse watery and odiferous vaginal

discharge.

2. Usually not a purulent discharge (unlike Trichomonosis).

3. Dysuria, dyspareunia and abdominal pain are rare.

D. Diagnosis:

1. Speculum exam often reveals profuse, watery, grayish

malodorous vaginal discharge.

2. There is usually little or no inflammation (unlike Trichomonas

or Candida).

3. Gonorrhea and Chlamydia cultures should also be sent.

4. Wet prep will reveal many small bacteria with absence of white

blood cells (unlike Trichomonas).

5. May see "clue cells" - epithelial cells studded with these tiny

bacteria.

6. Gram stain may reveal gram negative coccobacilli instead of

normal Lactobacillus which are gram positive.

7. Amine (fishy) odor released when vaginal discharge is mixed

with KOH.

8. pH of vaginal fluid greater than 4.5.

E. Treatment:

1. Antibiotics effective against anaerobic bacteria.

a. Metronidazole:

i. 500 mg two times per day for 7 days.

ii. Metronidazole gel 0.75% (5g) intravaginally daily for

5 days.

b. Clindamycin:

i. 2% vaginal cream 5 g intravaginally qHS for 7 days.

ii. 300 mg po bid for 7 days.

iii. 100g ovules intravaginally qHS x 3 days.

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Notes


2. In pregnancy:

a. Metronidazole 250 mg po tid for 7 days.

b. Metronidazole 500 mg po bid for 7 days.

c. Clindamycin 300 mg po bid for 7 days.

d. Do not use topical agents during pregnancy.

e. It has been shown that treatment during pregnancy lowers

the complication rate for BV in symptomatic women and

in asymptomatic women at high risk for preterm labor.

3. Reoccurrence rates are high no matter which therapy chosen.

4. Treatment of sexual partners is currently not indicated.

III. VULVOVAGINAL CANDIDIASIS

A. Epidemiology:

1. Candida albicans is a fungal infection.

2. Although Candida species normally inhabits the

gastrointestinal tract, it is usually NOT found in the vulva or

vagina.

3. Under certain conditions, Candida may proliferate and invade

the epithelium of the vagina or vulva.

4. Predisposing conditions to Candida vulvovaginitis include:

a. Pregnancy.

b. Immunosuppression.

c. Medication:

i. Oral contraceptives.

ii. Antibiotics.

iii. Corticosteroids.

d. Diabetes mellitus.

e. Hormonal - luteal phase of menstrual cycle.

5. Isolated Candida infection is not usually sexually transmitted.

B. Presentation:

1. Whitish vaginal discharge with pruritus and tissue irritation.

2. Not odoriferous (unlike bacterial vaginosis or Trichomonas).

3. Patient may complain of dysuria and vulvovaginal burning.

C. Diagnosis:

1. Speculum examination reveals a white curdy discharge.

2. Vulvar erythema is the most common sign.

3. Abdominal and bimanual examination should be unremarkable.

4. Cultures - impractical because of time constraints.

5. Wet mount reveals white blood cells without clue cells.

6. KOH prep:

a. Of the discharge or scrapings of the border of the vulvar

irritation.

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b. Classically demonstrates pseudohyphae or branching

dendritic chains.

D. Treatment:

1. Clotrimazole:

a. 100 mg vaginal tablet x 7 days.

b. Two 100 mg vaginal tablets x 3 days.

c. 1% cream - 5g intravaginally x 7 - 14 days.

d. Cream applied locally to the vulva may lessen symptoms.

2. Miconazole nitrate:

a. 200 mg suppository intravaginally q HS x 3.

b. 100 mg vaginal suppository x 7 days.

c. 2% cream - 5g intravaginally x 7 days.

d. 1,200 mg vaginal suppository x 1 dose.

3. Butoconazole intravaginal agent:

a. 2% cream – 5 g intravaginally x 3 days.

b. 2% cream sustained release – 5 g intravaginally x 1 dose.

4. Nystatin intravaginal agent 100,000 unit vaginal tablet daily x

14 days.

5. Tioconazole intravaginal agent – 6.5% ointment 5 g

intravaginally x 1 dose.

6. Terconazole intravaginal agent:

a. 0.4% cream 5 g intravaginally x 7 days.

b. 0.8% cream 5 g intravaginally x 3 days.

c. 80 mg vaginal suppositories – 1 daily x 3 days.

7. Fluconazole (Diflucan) - 150 mg PO x 1 dose.

8. Partners should be referred for diagnosis and treatment only if

symptomatic.

9. Pregnancy:

a. Incidence increases 10-20 times in the pregnant patient.

b. Treat with topical azoles for seven days.

Genital Ulcers

I. HERPES SIMPLEX TYPE 2

A. Epidemiology:

1. The prevalence of HSV-2 in the U.S. remains very high.

2. Overall, 16.2% of Americans between the ages of 14 and 49

(or 1 in 6) are infected with HSV-2, while black women have a

prevalence rate of 48% (CDC, 2010).

3. Spread primarily through sexual contact.

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Notes


B. Pathophysiology:

1. Following the initial attack, the virus harbors in dorsal nerve

root ganglia of the affected site.

2. The viral disease is then reactivated in up to 50% of cases by

emotional or physical stress.

C. Presentation:

1. Primary herpetic infection:

a. Begins 3-7 days after contact with the virus.

b. Vulvovaginal pain, fever, malaise and myalgias.

c. Tender nonfluctuant, bilateral inguinal

lymphadenopathy. d. 2-4 mm clear fluid vesicles with erythematous bases.

e. These vesicles then rupture and form small ulceration.

f. Usually lasts from 2-6 weeks.

2. Reoccurrence:

a. Occur in up to 50% of cases.

b. Heralded by a tingling sensation in the genitals.

c. Usually less painful and there is no systemic illness or

tender lymphadenopathy after the primary infection.

d. Duration is much shorter than with the primary

infection.

D. Diagnosis:

1. Classic lesions.

2. Tzanck smear:

a. Multinucleated giant cells with intranuclear inclusion

bodies.

b. Only 40-50% as sensitive as viral cultures.

3. Viral cultures specific for Herpes Simplex Type 2.

4. PCR assay for HSV DNA is the most sensitive method.

E. Treatment:

1. Symptomatic treatment:

a. Burrow's solution.

b. Sitz baths.

c. Bed rest.

d. Analgesics.

2. Specific treatment:

a. Primary Herpes Simplex:

i. Acyclovir (Zovirax):

200 mg po 5 times daily or 400 mg tid for 7-10

days.

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Notes


Shortens the duration of pain.

Decreases the viral shedding.

Shortens the systemic symptoms.

ii. Famciclovir:

250 mg po tid for 7-10 days.

iii. Valacyclovir:

1 g po bid for 7-10 day. .

b. Recurrent Herpes Simplex - episodic therapy:

i. Acyclovir:

400 mg po tid for 5 days.

800 mg po bid for 5 days.

800 mg po tid for 2 days.

ii. Famciclovir:


500 mg po x 1, then 250 mg bid for 2 days.

1000 mg orally twice daily for 1 day.

iii. Valacyclovir:


1 g po once daily for 5 days.

c. Topical acyclovir - not therapeutic.

d. Severe disease – acyclovir 5-10 mg/kg IV tid until clinical

resolution.

II. CHANCRE

A. Smooth, painless ulcer.

B. Forms at the site of initial inoculation in primary syphilis.

C. Syphilis review:

1. Primary syphilis:

a. Three week incubation period.

b. Chancre forms at the site of initial inoculation.

c. Smooth, painless ulcer.

2. Secondary syphilis:

a. 4-10 weeks after the primary chancre.

b. Macular pink rash on trunk, extremities including palms

and soles, sparing the face.

c. Condyloma lata on moist intertriginous areas.

d. Fever, malaise generalized lymphadenopathy, mucous

patches.

3. Latent syphilis:

a. Tests are positive, but patient is asymptomatic.

4. Tertiary syphilis:

a. 10 years after initial chancre.

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Notes


b. Neurosyphilis, cardiovascular, auditory, ophthalmologic or

gummatous syphilis.

D. Diagnosis:

1. Wear gloves, as all primary and secondary syphilitic lesions are

highly infectious.

2. Dark-field examination for spirochetes from material aspirated

from chancres, condyloma lata or mucous patches.

3. Nontreponemal (NT) serologic tests:

a. VDRL, RPR, ARF.

b. Good screening tool.

c. Many false positives.

d. Useful in following treatment as test reverts back to

negative when syphilis infection is eradicated.

4. Treponemal serologic tests:

a. FTA-ABS, MHA-TPH, HATTS.

b. Very specific - useful to confirm the diagnosis if NT test

+.

c. Once the test has turned positive, remains positive for life.

d. Therefore not useful in following management.

E. Treatment:

1. Primary, secondary and latent (less than 1 year) syphilis:

a. Benzathine Pen G 2.4 million U I.M. for one dose therapy.

b. Penicillin allergic:

i. Tetracycline 500 mg orally QID x 14 days.

ii. or Doxycycline 100 mg orally BID x 14 days.

2. Tertiary or latent (greater than 1 year) syphilis:

a. Benzathine Pen G 2.4 million U IM per week x 3 weeks.

b. Penicillin allergic: Tetracycline or Doxycycline for 28

days if latent, Infectious Disease consult if tertiary.

3. Pregnancy - Penicillin (desensitize if allergic).

4. Neurosyphilis – Penicillin G 3-4 million units IV every 4 hours

for 10-14 days.

5. Children:

a. Benzathine pen G 50,000 units/kg IM, up to the adult dose

of 2.4 million units in a single dose for primary, secondary

and early latent syphilis.

b. Benzathine pen G 50,000 units/kg IM per week x 3 weeks,

up to the adult dose of 7.2 million units for late latent and

tertiary syphilis.

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Notes


III. CHANCROID

A. Painful genital ulcers.

B. Hemophilus ducreyi.

C. Inguinal lymphadenopathy.

D. Rule out Herpes Simplex and Syphilis.

E. Treatment:

1. Azithromycin 1 gram PO x 1.

2. Ceftriaxone 250 mg IM.

3. Erythromycin base 500 mg tid x 7 days.

4. Ciprofloxacin 500 mg bid x 3 days.

Genital Warts

I. CONDYLOMA ACUMINATA

A. Caused by the human papillomavirus.

B. Painless, nonpruritic, pedunculated or sessile warts.

C. Sexually transmitted:

1. 25% of sexual partners of the index case will get the lesions.

2. Risk increased even further in immunocompromised patients.

3. 12-34% of patients with genital warts also have gonorrhea,

chlamydia or syphilis infections.

4. Associated with cervical neoplasia.

D. Diagnosis - by site, biopsy all tissue removed.

E. Treatment:

1. Provider - Podophyllin, cryotherapy, laser therapy,

Trichloroacetic acid or Bichloracetic acid 80-90%.

2. Patient - Podofilox 0.5% solution or gel, Imiquimod 5% cream,

Sinecatechins 15% ointment.

II. CONDYLOMA LATA

A. Warty lesions caused by syphilis.

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Notes


B. Wart is smoother and moister than Condyloma acuminatum.

Bartholin Abscess

I. CHARACTERISTICS

A. Very painful.

B. Contains mixed bacterial pathogens from the vagina.

C. Gonorrhea implicated in @ 10% of cases.

II. TREATMENT

A. Incision and drainage of the cyst or abscess in the emergency

department.

B. Placement of a Word catheter after the I & D.

C. A CO2 laser may be used alternatively to recreate a duct orifice.

Cervicitis

I. NEISSERIA GONORRHEA

A. Pathophysiology:

1. Gram negative intracellular diplococci.

2. Causes 5 different patterns of disease in women:

a. Asymptomatic carriers.

b. Cervicitis.

c. Pelvic Inflammatory Disease (PID):

i. Up to 20% of patients with GC develop PID.

ii. 33-80% of patients with PID have GC.

d. Disseminated gonorrhea - hematogenous spread:

i. Migratory septic arthritis.

ii. Arthritis-Dermatitis syndrome:

Fever, chills.

Polyarticular arthritis or arthralgias.

Rash.

Tenosynovitis of extensor tendons of hands,

wrists and ankles.

iii. Meningitis – rare.

iv. Endocarditis – rare.

v. Perihepatitis.

vi. 80% of disseminated GC occurs in women.

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Notes


vii. ≈ 66% develop within the first week following the last

menses.

e. Ophthalmitis.

B. Presentation:

1. Purulent endocervical discharge.

2. Usually symptomatic soon after menses begins.

3. Lower abdominal pain.

C. Diagnosis:

1. Gram negative intracellular diplococci on gram stain:

a. 95% specific.

b. Less than 60% sensitive. So do not rule out GC if gram

stain inconclusive.

2. Culture on Thayer-Martin plate with 3-5% CO2.

3. Finding other pathogens on microscopy also does not rule out

GC:

a. 35% of patients with GC also had Trichomoniasis.

b. 19% of patients with GC also had Candida vaginalis.

4. Nucleic acid amplification and hybridization testing more

sensitive than culture.

D. Treatment:

1. Urethral, cervical, rectal or pharyngeal gonorrhea:

a. Ceftriaxone 250 mg IM - 1 dose.

b. Cefixime 400 mg PO - no longer recommended by CDC.

c. Fluoroquinolone no longer recommended due to high

resistance rates.

2. Ophthalmologic:

a. Ceftriaxone 1 gram IM - 1 dose.

b. Saline irrigation.

3. All patients with GC should be tested for Chlamydia if reliable

for follow up, or treated with doxycycline (100 mg bid for 7

days) or Azithromycin (1 gram orally x 1 dose).

4. Cephalosporin allergy:

a. Azithromycin 2 grams orally as a single dose, but high

level of resistance developing.

b. Fluoroquinolone if antimicrobial susceptibility is

documented by culture.

II. CHLAMYDIA TRACHOMATIS

A. Pathophysiology:

1. Most common of all the STDs.

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Notes


2. Obligate intracellular parasite.

3. Causes 5 patterns of disease in women:

a. Asymptomatic.

b. Acute urethral syndrome - pyuria without bacteria.

c. Cervicitis.

d. PID.

e. Lymphogranuloma venereum:

i. Small painless vesicle which then ulcerates.

ii. Tender, ulcerated inguinal lymphadenopathy.

B. Presentation:

1. Mucopurulent cervical discharge; may be watery and non-

purulent.

2. Cervical erythema.

3. Usually less symptomatic than with Gonorrhea.

C. Diagnosis:

1. Gram stain that shows > 10 PMN leukocytes without bacteria.

2. Direct fluorescent monoclonal antibody test of cervical

exudate.

3. Chlamydia culture.

4. Nucleic acid amplification and hybridization testing more

sensitive than culture.

D. Treatment:

1. Urethritis or cervicitis:

a. Doxycycline 100 mg PO bid for 7 days.

b. OR Azithromycin 1 gram PO - 1 dose.

c. OR Erythromycin 500 mg PO qid for 7 days.

d. OR Ofloxacin 300 mg PO bid for 7 days.

e. OR Levofloxacin 500 mg daily for 7 days.

f. In pregnancy:

i. Azithromycin 1 gram PO for 1 dose.

ii. OR Amoxicillin 500 mg tid for 7 days.

2. Lymphogranuloma Venereum:

a. Doxycycline 100 mg PO bid for 21 days.

b. OR Erythromycin 500 mg PO qid for 21 days.

Pelvic Inflammatory Disease

I. EPIDEMIOLOGY

A. Most common serious infection in reproductive-aged women in the

U.S.

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Notes


B. 2.5 million patient visits annually for PID.

C. 250,000 hospitalizations annually.

D. 150,000 surgical procedures for complications of PID annually.

E. Estimated annual cost: $3.5 billion/year.

II. PATHOPHYSIOLOGY

A. PID is an acute clinical syndrome attributed to ascent of

microorganisms from the vagina and cervix to the following

structures:

1. Endometrium – endometritis.

2. Fallopian tubes – Salpingitis.

3. Ovaries – Oophoritis.

B. May progress to tuboovarian abscess or pelvic peritonitis.

C. PID usually begins as a cervical infection with Neisseria gonorrhea

and/or Chlamydia trachomatis.

D. The resulting cervicitis alters the vaginal-cervical

microenvironment, leading to overgrowth of endogenous and

anaerobic flora.

E. Thus PID is a polymicrobial disease. Common pathogens are:

1. Neisseria gonorrhea.

2. Chlamydia trachomatis.

3. Anaerobic bacteria:

a. Peptococcus.

b. Peptostreptococcus.

c. Bacteroides.

4. Escherichia coli.

III. PRESENTATION

A. Risk factors:

1. Previous history of PID.

2. Multiple sexual partners.

3. Intrauterine conception device (IUD) usage.

4. Adolescence:

a. Inverse proportion of incidence to age.

b. 75% of cases occur between the ages of 15-25.

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Notes


5. Instrumentation of the uterine cavity:

a. Dilation and curettage.

b. Endometrial biopsy.

c. Hysterosalpingography.

d. Cervix cautery or cryotherapy.

B. Symptoms:

1. Lower abdominal pain - usually bilateral.

2. Purulent vaginal discharge - present in over 50% of patients.

3. Abnormal vaginal bleeding - from endometritis.

4. Fever and general malaise.

5. Nausea and anorexia.

6. Most common symptoms begin shortly after menses- when

there is decreased defense by the cervix to ascending

pathogens.

7. Dysuria without frequency or urgency.

C. Physical findings:

1. Lower abdominal tenderness.

2. Cervical motion tenderness (Chandelier sign).

3. Adnexal tenderness bilaterally.

4. Adnexal mass may be present if patient has a tuboovarian

abscess.

5. Purulent cervical discharge- if absent, this does not preclude

the diagnosis of PID.

6. Fever - but a temperature above 38 degrees (100.4F) is only

present in 1/3 of patients.

IV. DIAGNOSIS

A. Criteria for empiric treatment of PID:

1. CDC minimum criteria:

a. Cervical motion tenderness.

b. OR Adnexal/uterine tenderness.

c. In a patient with lower abdominal or pelvic pain, at risk for

STDs and no other cause for the illness is identified.

2. Other supporting evidence for PID:

a. Abnormal cervical mucopurulent discharge.

b. Leukocytosis in vaginal secretions.

c. Temperature greater than 38.3 degrees C (101 F).

d. White blood cells and bacteria in peritoneum.

e. Laparoscopy.

f. Culdocentesis.

g. Inflammatory mass detected by bimanual examination or

sonography.

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Notes


h. Erythrocyte sedimentation rate over 15 mm/h.

i. Elevated C-reactive protein.

B. Testing for N. gonorrhea or Chlamydia trachomatis:

1. Gram stain of cervical secretions:

a. Gram-negative intracellular diplococci – N. gonorrhea.

b. Vaginal flora.

2. Culture and sensitivity of cervical secretions:

a. Chocolate agar or Thayer Martin plate – N. gonorrhea.

b. Chlamydia trachomatis.

3. Nucleic acid amplification and hybridization testing:

a. More sensitive than culture.

b. Can be run on cervical secretions or urine.

C. HCG determination:

1. To rule out pregnancy.

2. Very unusual (i.e., reportable) to have PID and pregnancy

because after implantation, a mucous plug forms that prevents

spread of infection from the lower to the higher genital tract.

D. Leukocytosis – not always present.

E. Pelvic ultrasound - to rule out tuboovarian abscess or other pelvic

abscess if patient unresponsive to antibiotic therapy after 48-72

hours or if unilateral symptoms in a toxic-appearing patient.

F. Culdocentesis - purulent fluid from the posterior cul-de-sac.

V. COMPLICATIONS OF PID

A. Chronic pelvic pain.

B. Dyspareunia.

C. Infertility.

D. Ectopic pregnancy.

E. Tuboovarian abscess:

1. Walled off abscess originating in the infected fallopian tube,

which may then extend to involve the fimbriae and the ovary as

well.

2. Patients appear septic, have exquisite unilateral adnexal

tenderness and usually have a mass or fullness appreciated on

bimanual examination.

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Notes


3. This is primarily an anaerobic infection and generally needs to

be drained surgically and treated with parenteral antibiotics.

F. Fitz-Hugh-Curtis Syndrome:

1. Perihepatitis secondary to PID.

2. Occurs in 8-10% of patients with PID.

3. It is most commonly associated with Chlamydia trachomatis

(but also associated with N. Gonorrhea).

4. Purulent discharge from the fallopian tube ascends to the tissue

adjacent to the liver, in the right colic gutter.

5. Causes adhesion formation between the liver capsule and the

abdominal wall.

6. Patients usually complain only of sudden, severe, sharp RUQ

pain; this may be pleuritic and may be referred to the right

shoulder.

7. The RUQ pain may be so severe that patients do not complain

of vaginal discharge or bilateral lower pain.

8. Thus the presence of RUQ pain in a woman of childbearing

age mandates a pelvic exam to rule out perihepatitis.

9. Physical exam will reveal vaginal purulent discharge, bilateral

lower quadrant AND right upper quadrant abdominal

tenderness.

10. The patient with Fitz-Hugh-Curtis usually has systemic illness,

including fever, chills, nausea, vomiting and generalized

malaise.

11. Elevated liver enzymes.

VI. TREATMENT

A. 25-50% of patients with culture-proven N. Gonorrhea are co-

infected with Chlamydia, so treat for both.

B. Indication for admission include any of the following criteria:

1. Suspected tuboovarian abscess.

2. Temperature greater than 101 F (38.3 C).

3. Pregnancy.

4. Patient unable to hold down fluids (and thus oral antibiotics).

5. Evidence of Fitz-Hugh-Curtis:

a. RUQ tenderness.

b. Elevated liver function studies.

6. Peritonitis.

7. Patient unreliable for oral antibiotic therapy and follow-up.

8. Patient who fails outpatient management.

9. Uncertain diagnosis and in whom surgical emergencies such as

appendicitis, ovarian torsion, etc., cannot be excluded.

10. Patient who appears septic.

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Notes


11. Prepubertal children (rule out sexual abuse).

12. Patients with IUD in place.

13. Consider admission for the nulliparous patient.

C. In-patient management:

1. Gonorrhea is notoriously Penicillin and Fluoroquinolone

resistant.

2. Chlamydia is rarely resistant to current therapy.

3. Cefoxitin 2 grams IV q 6 hours or Cefotetan 2 grams IV q 12

hours.

4. WITH: Doxycycline 100 mg PO or IV q 12 hours.

5. Treat with IV antibiotics for approximately 24 hours after the

patient improves, then continue oral Doxycycline (100 mg bid)

to complete a 14 day course.

6. Alternatives regimens:

a. Clindamycin 900 mg IV q 8 hours AND Gentamicin 2

mg/kg load followed by 1.5 mg/kg q 8 hours.

b. OR Ampicillin/Sulbactam 3 g IV qid PLUS

Doxycycline 100 mg bid PO/IV for 14 days.

D. Outpatient management:

1. Ceftriaxone 250 mg IM once PLUS Doxycycline 100 mg bid

for 14 days with/without Metronidazole 500 mg PO bid x for

14 days.

2. OR Cefoxitin 2 gm IM with Probenecid 1 gm PO PLUS

Doxycycline 100 mg bid for 14 days with/without

Metronidazole 500 mg bid for 14 days.

3. Discharge instructions to include:

a. No sexual activity (intercourse, oral, etc.) until all sexual

partners have also been seen and treated and the patient

and partners have had a negative culture after antibiotic

therapy is complete.

b. Referral numbers for follow up for both the patient and

their partners with specific instructions that their partners

need to be evaluated also.

c. 72 hour follow up, or sooner if patient develops any signs

or symptoms that would necessitate admission (see 6-B

above).

Pelvic Pain

I. GENERAL

A. Pelvic pain must be differentiated from pain of gastroenteric or

urologic origin.

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Notes


B. Pelvic pain is the second most common gynecologic presenting

complaint (abnormal vaginal bleeding is the first).

C. It is important that a pregnancy test be done on all women of

reproductive age presenting with abdominal pain or abnormal

vaginal bleeding.

D. If the patient is pregnant, ectopic pregnancy must then be ruled out.

E. If the patient is not pregnant, the following differential diagnosis of

pelvic pain should be entertained: PID, ovarian mass complications,

fibroids, mittelschmerz, and endometriosis.

II. PID

A. PID is the most common cause of pelvic pain.

B. See above section on PID.

III. OVARIAN CYST OR MASS

A. Pathophysiology:

1. Types of ovarian masses:

a. Functional cysts - most common:

i. Follicular cysts occur the first two weeks of the

menstrual cycle.

ii. Corpus luteal cysts occur the last two weeks of the

menstrual cycle.

b. Benign and malignant cystic and solid ovarian masses.

2. Ovarian enlargement due to cystic and solid ovarian masses are

usually asymptomatic unless one of five things occur:

a. Cyst rupture.

b. Torsion of the ovary.

c. Intratumor hemorrhage.

d. The mass pushes on contiguous structures.

e. The bulk of the mass is so large that the patient

experiences abdominal pain, ascites and abdominal

enlargement.

B. Ruptured ovarian cyst:

1. Presentation:

a. Patient develops sudden, sharp, severe unilateral pain.

b. Often rupture occurs during intercourse, exercise or an

aggressive pelvic examination.

c. Signs of peritonitis may be evident:

i. Hemorrhagic corpus luteum cyst rupture - will

Page 318

Notes


develop peritonitis from hemoperitoneum.

ii. Ruptured dermoid cyst may produce a chemical

peritonitis - with fever, ileus and distention.

d. Signs and symptoms may quickly abate after rupture of a

simple follicular cyst.

e. Unilateral adnexal tenderness and possible fullness will be

elicited on bimanual pelvic examination.

2. Diagnosis:

a. hCG testing - to rule out ectopic pregnancy rupture.

b. Hg/Hct may be lowered in patients with ruptured

hemorrhagic corpus luteal cyst.

c. Pelvic ultrasound may demonstrate free fluid in the

posterior cul-de-sac. The type of fluid, however, may not

be differentiated by sonographic examination.

d. Culdocentesis may be diagnostic - see Table 1.

e. Laparoscopy may be necessary for diagnosis in a patient

with peritoneal findings.

TABLE 1

Culdocentesis Diagnosis of Pelvic Pathology

3. Treatment:

a. Observation - ruptured follicular cyst.

b. Gynecology consult and possible surgery:

i. Ruptured hemorrhagic corpus luteal cyst.

ii. Ruptured dermoid cyst.

C. Ovarian torsion:

1. Pathophysiology:

a. Occurs if limited enlargement of an ovarian mass occurs.

i. Stretching of the mesovarium from the enlarging

mass, to the point that it effectively acts as a pedicle.

ii. The "pedunculated" mass, then may twist on its

pedicle.

iii. Ovarian blood supply then becomes compromised.

iv. Leading to painful ischemic degeneration of the

ovary.

Pathology Fluid Aspirated

Ectopic pregnancy Nonclotting blood

Ruptured hemorrhagic corpus luteum Nonclotting blood

Leaking corpus luteum cyst Serosanguineous fluid

Acute pelvic inflammatory disease Purulent material

Perforated intestinal viscus Particulate matter

Ruptured ovarian dermoid cyst Lipid-laden fluid

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Notes


v. Eventual gangrenous necrosis of the ovary.

b. Torsion is more likely to occur if there is a solid tumor or a

dense cystic tumor of the ovary.

c. Ovarian torsion can occur at any age.

d. 15% of cases occur in premenarchal girls.

e. Complications:

i. Scarred fallopian tube.

ii. Thrombosis of infundibulopelvic vessels with possible

resultant pulmonary embolization.

iii. Ovarian abscess and/or necrosis.

iv. Peritonitis and shock.

2. Presentation:

a. Torsion may produce intermittent, recurrent attacks of

colicky pain, nausea, vomiting and low grade fever.

b. Or, torsion can present with signs and symptoms of an

acute abdominal process (rebound tenderness with

rigidity, etc.).

c. Pain is often described as sudden, sharp and severe.

d. Unilateral lower quadrant tenderness is most common, but

may progress to diffuse abdominal tenderness.

e. Adnexal fullness and tenderness is usually evident on

pelvic exam.

f. Associated nausea and vomiting are frequently present.

3. Diagnosis:

a. hCG testing - to rule out ectopic pregnancy.

b. Pelvic sonography – color flow Doppler is diagnostic.

c. Laparoscopy - may be necessary since it may be

impossible to differentiate appendicitis, ovarian torsion,

and ovarian cyst rupture or intratumor hemorrhage with

peritonitis pre-operatively.

4. Management:

a. Urgent gynecologic consultation.

b. Laparotomy:

i. Important that the ovarian mass not be de torsed until

clamping of the more proximal vascular pedicle

occurs; to prevent thrombi dislodgement and

pulmonary embolization.

ii. Salvage rate for the torsed ovary is low.

IV. MITTELSCHMERZ

A. Pathophysiology:

1. Unilateral adnexal pain at the time of ovulation.

2. Secondary to rupture of a follicle with ovum extrusion or from

bleeding from the follicle site itself, resulting in a limited

hemoperitoneum and thus local irritation.

3. Occurs in up to 25% of ovulating women.

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4. Less common after the third decade of life.

B. Presentation:

1. Unilateral pain, usually lasting a few hours, but may last for 3

days.

2. Sharp, well localized abdominal tenderness without peritoneal

findings.

3. Withdrawal spotting may be present.

4. Malaise and nausea may be present.

C. Diagnosis:

1. hCG testing.

2. Observation - symptoms should abate.

D. Treatment:

1. Nonsteroidal anti-inflammatory agents.

2. Reassurance.

3. Ovulation suppression therapy if symptoms are severe.

V. UTERINE FIBROIDS

A. Incidence:

1. Most common tumor of the uterus.

2. Occur in ≈ 20% of women over age 35.

3. More common in black women.

4. Tend to occur at an earlier age in black women.

5. New tumors rarely develop after menopause.

6. There may be some regression in size after menopause.

B. Complications:

1. Sarcomatous transformation to cancerous leiomyosarcoma

occurs in less than 1% of patients.

2. Red degeneration or carneous degeneration:

a. Hemorrhagic necrosis of fibroid may occur during

pregnancy because the tumor outgrows its blood supply.

b. May mimic other obstetrical emergencies such as abruptio

placenta.

c. May produce pain, fever, leukocytosis.

d. Treatment is symptomatic: bed rest and analgesics.

C. Presentation:

1. Patients may complain of heaviness or fullness of the abdomen.

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2. Rarely cause pain, unless complication such as torsion,

ischemia, necrosis or hemorrhage occur.

3. May cause pressure effects:

a. Difficulty voiding.

b. Stress urinary incontinence.

c. Urinary retention.

d. Constipation.

e. Neuropathy if impinge on nerve roots.

4. Most common symptom is increasingly heavy and longer

lasting menstrual bleeding.

5. Physical examination may reveal a palpable mass or an

enlarged and irregular uterus.

D. Diagnosis:

1. hCG testing.

2. Pelvic ultrasound will reveal a uterine mass.

3. Hg/Hct - patients with hypermenorrhea secondary to fibroids

will often be anemic.

E. Treatment:

1. Gynecology referral.

2. Possible elective leiomyectomy or hysterectomy.

VI. ENDOMETRIOSIS

A. Epidemiology:

1. Occurs in 8-15% of all menstruating women.

2. 75% of patients are diagnosed between the ages of 25-45.

3. More common among women in whom pregnancy has been

delayed.

4. More common in upper socioeconomic groups.

5. Relatively common cause of pelvic pain and infertility.

B. Pathophysiology:

1. Growth of endometrial tissue in extra-uterine locations -

endometrium normally lines the uterine cavity.

2. Sites of ectopic endometrial tissue:

a. Ovaries = most common.

b. Uterine ligaments, rectovaginal septum, pelvic

peritoneum, umbilicus, laparotomy scars, hernia sacs,

vagina, vulva, cervix, pleura of lung, lymphatics (rare).

3. Advanced disease may involve all peritoneal organs.

4. Tissue responds to hormonal stimulation at the ectopic sites,

just as normal endometrium does.

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a. Why patients classically get symptoms at the time of

menstruation.

b. Useful in therapy.

5. Complications:

a. Distortion of pelvic structures.

b. Adhesion formation.

c. Infertility - from peritubal adhesions.

C. Presentation:

1. Causes secondary dysmenorrhea in older women.

2. Patients present with chronic abdominal pain, dyspareunia,

abnormal vaginal bleeding or infertility.

3. History of repeated attacks.

4. Although there are no absolute classic symptoms,

dysmenorrhea is common.

5. Dyspareunia occurs when there is involvement of the

uterosacral ligaments.

6. Infertility is common, which is unfortunate since one of the

best treatments of endometriosis is pregnancy.

7. Severity of symptoms correlates poorly with extent of

endometriosis.

8. Physical exam findings:

a. No abnormal findings may be present.

b. Fixed retroverted uterus.

c. Ovarian masses (chocolate cysts).

d. Uterosacral nodularity.

e. Recto vaginal nodularity.

D. Diagnosis:

1. Diagnosis can be suspected on the basis of history and

physical.

2. Definitive diagnosis is made by visualization with laparoscopy

or by biopsy.

E. Treatment:

1. Analgesics.

2. Gynecology referral.

3. For patients who want to preserve reproductive function:

a. Danazol (Danocrine):

i. Methyl sterone derivative.

ii. Medically produces a "menopausal" state.

b. High dose estrogen.

c. Progesterone.

d. Combined oral contraceptives:

i. Continuous usage.

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ii. Produces a "pseudopregnancy" state.

e. Pregnancy - will stop the cyclic endometrial changes and

lead to regression of endometriosis.

4. For symptomatic patients whose families are complete:

a. TAH-BSO may be considered.

b. Bilateral oophorectomy will stop the hormonal cycling.

Vaginal Bleeding

I. DEFINITIONS

A. Amenorrhea – Bleeding absent for 6 months or more in a non-

menopausal woman.

B. Dysmenorrhea – Painful menstruation.

C. Dysfunctional uterine bleeding – Ovulatory or anovulatory

bleeding, diagnosed after the exclusion of pregnancy, medications,

iatrogenic causes, genital tract pathology, and systemic disease.

D. Menorrhagia – Bleeding occurring at regular intervals, but with

heavy flow (≥80 ml) or duration (≥7 days).

E. Metrorrhagia – Bleeding among premenopausal women at irregular

intervals.

F. Midcycle spotting – Bleeding absent for 6 months or more in a non-

menopausal woman.

G. Postmenopausal bleeding – Recurrence of bleeding in a menopausal

woman at least 1 year after cessation of cycles.

II. DIFFERENTIAL DIAGNOSIS

A. Newborn:

1. Maternal estrogen withdrawal (lasts 3-4 days).

2. Bleeding disorders.

B. Children:

1. Foreign bodies.

2. Trauma (red flag).

3. Precocious puberty (ovarian, adrenal or CNS tumors).

4. Zebra: sarcoma botryoides.

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C. Menarche:

1. Anovulatory DUB.

2. Blood dyscrasias (ITP).

D. Postmenopausal:

1. Endometrial cancer.

2. Estrogen therapy.

3. Atrophic vaginitis.

4. Anatrophic endometrium.

5. Polyps.

E. Reproductive years:

1. Disturbances of pregnancy.

2. Fibroids (menorrhagia; fullness or pressure but no pain).

3. Cervicitis/PID.

4. IUD/foreign body.

5. Breakthrough bleeding from BCP usage - need reassurance

only.

6. Post-partum hemorrhage (>500 ml):

a. Retained products.

b. Uterine atony.

7. Endometritis (post Ab or perinatal).

8. Trauma.

9. Metabolic:

a. Hyperthyroid.

b. Hypothyroid.

c. Cushing's.

10. Nutritional extremes.

11. Cancer:

a. Endometrial.

b. Cervical.

c. Vaginal.

d. Ovarian.

12. Polyps:

a. Cervical.

b. Endometrial.

13. Blood dyscrasia:

a. Thrombocytopenia.

b. Coumadin prescription.

c. Hypermenorrhea.

d. Polymenorrhea.

14. Endometriosis or adenomyosis (with pain).

15. Psychogenic factors (stress).

16. Dysfunction uterine bleeding - DUB (85% anovulatory).

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III. WORK-UP

A. Laboratories:

1. Hg/Hct.

2. Rh if pregnant.

3. HCG.

4. Quantitative B-HCG for follow up if pregnant.

5. T&C.

6. Consider PT/PTT/platelets.

B. Pelvic ultrasound.

IV. TREATMENT

A. ABCs - unusual to have severe hemorrhage in the non-pregnant

patient, but can occur with:

1. Cervical cancer.

2. Post-operative hemorrhage.

3. Dysfunctional uterine bleeding in adolescents.

B. Gynecology referral or urgent consult if severe bleeding.

C. All patients over the age of 35 with dysfunctional bleeding and all

post-menopausal women with bleeding other than withdrawal

bleeding from estrogen therapy, should have timely gynecologic

follow-up for endometrial sampling (endometrial biopsy or

dilatation and curettage sampling).

V. DISPOSITION - ADMIT

A. Hemodynamic instability.

B. Suspect child abuse.

C. Children needing GA for PE or repair.

D. All significant third trimester bleeds.

E. Cancer work-up in patient likely to be lost to follow-up.

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Sexual Assault by History

I. INTRODUCTION

A. Definition:

1. Varies from state to state.

2. Most statutes define rape as the "carnal knowledge of a female

forcibly and against her will".

3. Evidence must support the allegations that:

a. Force or threat of force was involved.

b. The action was against the will of the accuser.

c. A sexual act (carnal knowledge) actually occurred.

B. Revised laws:

1. Most states have expanded the traditional rape statutes:

a. Marital rape.

b. Date rape.

c. Shield laws - prevent past sexual practices of the victim

from being introduced as evidence.

2. Because of changing law and also inter- and intra-state

variability, it is important for each emergency department to

have access to applicable statutes for their jurisdiction.

C. Violent crime.

D. Legal aspects:

1. Burden of proof is on the accuser.

2. Defendants charged with rape are four times less likely to be

convicted than defendants charged with other crime.

3. Rape is a legal term, not a medical diagnosis.

II. INCIDENCE

A. In the United States, it is estimated that one out of every 6 women

is raped in her lifetime.

B. In the United States, a rape is reported every 2-5 minutes.

C. It is estimated that only one in five rapes of adult women are

actually reported.

D. Sexual assault is the fastest growing violent crime in the United

States.

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E. Over 300,000 women and 92,000 men are raped each year in the

United States; more than 1/3 of all lifetime rapes occur before the

age of 12, while more than half occur before the age 18.

F. 5-6% of sexual assault victims are male.

III. ROLE OF THE EMERGENCY PHYSICIAN

A. Evaluate for any life threatening injury.

B. Assessment and treatment of physical injuries.

C. Prevention of venereal disease and pregnancy.

D. Collection of evidence.

E. Recognition and management of emotional trauma.

IV. HISTORY

A. History of the assault:

1. Should not be exhaustive.

a. Patient may not remember details accurately while she is

so emotionally distraught.

b. May later prove confusing in court.

2. Important information to gather:

a. Date and time of the assault.

b. Areas of the body affected:

i. Physical trauma.

ii. Sexual contact.

c. Location in which the attack occurred.

d. Perpetrator:

i. Known to victim in up to 80% of cases.

ii. Number of assailants.

iii. Description - will be done by police.

e. Threats of violence should be noted.

f. Use of weapons, restraints, foreign bodies, etc. should be

documented.

g. Type of sexual acts:

i. Vaginal, oral or anal penetration or attempt at

penetration.

ii. Did perpetrator wear condom?

iii. Did ejaculation occur?

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Notes


B. Historical data surrounding the incident:

1. Post assault clean-up:

a. Douching.

b. Bathing/showering.

c. Defecation.

d. Urination.

e. Change of clothes.

f. Brush teeth.

2. Pre-assault factors:

a. Gravidity, parity, LMP.

b. Contraceptive usage.

c. Date of last consensual intercourse.

3. Past medical history:

a. Allergies.

b. Medications.

c. Past medical or surgical diseases.

V. PHYSICAL EXAMINATION

A. Clothing should be placed in a paper bag and transferred to the

police as evidence when they arrive.

B. Modesty of the patient should be respected.

C. Skin:

1. Carefully examine for scratches, bruises, teeth marks, rope

marks, burns, etc.

2. Special attention to neck, oral mucosa, face, lips, perineum,

medial thighs, breasts and wrists.

D. Cervical spine tenderness:

1. Strangulation.

2. Battering/falls.

E. Wood's lamp for identification of seminal fluid in areas where

ejaculation may have occurred, but fluorescence is not

pathognomonic of semen (urine and other stains also fluoresce).

F. Photograph physical findings with the patient's permission.

G. Pelvic examination:

1. External genitalia:

a. Trauma.

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Notes


b. Semen?

c. Hymen - intact, absent, traumatized.

2. Speculum exam:

a. Gentle exam using a narrow speculum (when possible)

moistened with warm tap water.

b. No lubricant jelly for speculum exam - interferes with

studies.

c. Search for vaginal or cervical lacerations.

d. Posterior fornix secretions:

i. Aspirate.

e. Place in sterile receptacle.

f. Wet mount of cervix and vagina for sperm and

Trichomonas.

g. GC and chlamydia cultures.

3. Bimanual examination.

H. Rectal examination - as indicated.

I. Penis and testicle examination in male victims.

VI. EVIDENCE COLLECTION

A. Sexual assault kit.

B. Non pelvic collections:

1. May be done by nursing staff.

2. Combings of victim's scalp and pubic hair.

3. Victim's plucked scalp and pubic hair samples.

4. Buccal swabs - saliva sample.

5. Foreign matter:

a. Hair, fibers, soil or vegetation.

b. Found on victim's body or clothing.

6. Fingernail scrapings.

C. Collections to be obtained during pelvic examination:

1. Vagina and cervix secretions:

a. Smears.

b. Swabs.

2. Wet mount of cervix and vagina for sperm:

a. Sperm present.

b. Motile or not.

3. Cervical cultures or FDA-approved nucleic acid amplification

tests for GC and Chlamydia.

4. Smears and swabs of other affected areas:

a. Oropharynx.

b. Anus.

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5. Chain of evidence must be maintained:

a. Proper labeling.

b. Proper documentation.

VII. LABORATORY ANALYSIS IN THE EMERGENCY DEPARTMENT

A. ABO analysis.

B. Syphilis serology.

C. hCG:

1. Unless assault occurred in remote past, +hCG denotes previous

pregnancy prior to the assault.

2. + hCG will alter management.

D. Nucleic acid amplification tests should be sent with results

forwarded to the patient's gynecologist or referral physician.

E. Wet mount:

1. Check for trichomonads, hyphae or clue cells.

2. Check for sperm - note motility on record.

F. HIV testing may be discussed:

1. Referral for testing and reporting of results.

2. If drawn in emergency department, a plan for reporting results

and possible counseling should be determined in consultation

with the patient's private or referral physician.

VIII. TREATMENT

A. Pregnancy prophylaxis:

1. Establish a current negative hCG.

2. Low probability of pregnancy from rape – about 1%.

3. The 1% risk of pregnancy and the available choices of

pregnancy prevention and risks of each should be told to

patient.

4. Victim's options:

a. Do nothing.

b. Therapeutic abortion if hCG negative now, but becomes

positive in 1-2 weeks.

c. Hormonal therapy:

i. Needs to be started within 72 hours of the assault:

Ovral 2 tabs q 12 hours x 2 doses.

Most common ED management.

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Feminization of male fetus - theoretical risk.

ii. Plan B: 0.75 mg q 12 hr x 2 – OTC progesterone only.

iii. Premarin 50 mg IV qd x 2 doses.

d. Reluctance of physician to prescribe above:

i. Gynecology consultation.

B. Sexually transmitted disease prophylaxis:

1. Gonorrhea:

a. 2-13% incidence after sexual assault.

b. Ceftriaxone 250 mg IM x 1 dose (**2010 change).

c. Cefixime 400 mg orally x 1 dose – no longer

recommended.

d. Penicillin allergic: Azithromycin 2 gm orally as a single

dose.

e. Pregnant patient: Ceftriaxone 250 mg IM.

2. Chlamydia:

a. Post rape incidence @ 5-10%

b. Azithromycin 1 gm orally as a single dose.

c. Doxycycline 100 mg bid x 7 days.

d. Pregnant patient:

i. Azithromycin 1 gram orally as a single dose.

ii. Amoxicillin 500 mg tid for 7 days.

iii. Erythromycin base 500 mg qid for 7 days.

3. Trichomonas:

a. Metronidazole 2 grams orally x 1 dose.

b. No treatment in asymptomatic first trimester pregnant

patient but ensure timely follow-up.

4. Syphilis:

a. 0.1% incidence after sexual assault.

b. Draw baseline VDRL, with referral for repeat testing at 6,

12 and 24 weeks.

c. Prophylaxis probably not routinely indicated.

5. HIV.

6. Hepatitis B:

a. Hepatitis B vaccine if unvaccinated.

b. Repeat doses at 1-2 and 4-6 months.

c. Hepatitis B immunoglobulin not necessary for prophylaxis

unless offender is known to have acute Hepatitis B and

victim is not vaccinated.

IX. EMOTIONAL SUPPORT

A. Important to treat the patient with respect and provide a safe and

calming environment.

B. Expedite care when possible, and allow the victim to have support

persons present at her request.

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C. Rape crisis counselors are very helpful.

D. Follow-up counseling for victim and her family should be provided.

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Notes


GYNECOLOGICAL EMERGENCIES

PEARLS

1. Ovarian torsion and ruptured ovarian cyst should be considered in a

patient with sudden onset of severe lower abdominal pain, a tender

adnexal mass, and a negative pregnancy test. The ruptured cyst will

have fluid in the cul de sac and both are diagnosed by laparoscopy.

2. Follicular cysts occur during the first 2 weeks of the menstrual cycle

while corpus luteum cysts occur during the last 2 weeks of the cycle.

3. Mittlesmertz is midcycle pain due to the ovum extruding from the

ovary.

4. Endometriosis most commonly involves the ovaries.

5. Risk factors for ectopic pregnancy include previous tubal infection, IUD

use, tubal surgery, congenital abnormality of the tube, and prior ectopic.

6. A dry tap from culdocentesis is nondiagnostic for ectopic pregnancy.

Clear/straw colored fluid is negative while nonclotting blood is positive. 7. Cases of trichomonas vaginalis in females should not be treated in

pregnant first trimester patients unless patients are symptomatic.

Treatment of asymptomatic cases of bacterial vaginosis is thought to

lower the complication rate in pregnancy. In either disease, when

treatment is warranted in pregnant patients, only the oral forms of

antibiotics should be used.

8. Clue cells are seen with bacterial vaginitis whereas multinucleated giant

cells on Tzanck smear are seen with Herpes Simplex.

9. Chlamydia is the most common sexually transmitted disease.

10. Fitz-Hugh-Curtis syndrome is bacterial perihepatitis with RUQ

tenderness associated with PID.

11. Indications for admission for PID include uncertain diagnosis

particularly if surgical diagnoses (e.g., appendicitis) cannot be ruled out,

suspected pelvic abscess, pregnancy, severe illness, lack of response to

outpatient therapy, inability to tolerate oral medicine, prepubertal age,

lack of follow-up or IUD presence.

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Notes


REFERENCES

1. Bukata WR. HIV prophylaxis after sexual exposure. Emerg Med and

Acute Care Essays, 1998: 21(8).

2. Centers for Disease Control and Prevention. Sexually Transmitted

Diseases Treatment Guidelines, 2010. MMWR 2010: 59 (No. RR-12):1-

95.

3. Centers for Disease Control and Prevention. Update to CDC’s

Sexually Transmitted Diseases Treatment Guidelines, 2006:

Fluoroquinolones No Longer Recommended for Treatment of

Gonococcal Infection. MMWR 2007: 56(14); 332-336.

4. Centers for Disease Control and Prevention. 2007. Web-based Injury

Statistics Query and Reporting Systems (online), National Center for

Injury Prevention and Control, Centers for Disease Control and

Prevention. www.cdc.gov/ncipe/wisqars/default.httm.

5. Centers for Disease Control and Prevention. 2010. Press Release: “CDC

Study Finds U.S. Herpes Rates Remain High” (online). NCHHSTP

Newsroom, Centers for Disease Control and Prevention.

www.cdc.gov/nchhstp/newsroom/hsv2pressrelease.html

6. Chomvarin C, Chantarsuk Y, Thongkrajai P, et al. An assessment

and evaluation of methods for diagnosis of chlamydia and

gonococcal infections. Southeast Asian J Trop Med Public Health

1997 Dec; 28 (4): 791-800.

7. Dicker LW, Mosure DJ, Steece R, Stone KM. Testing for sexually

transmitted diseases in U.S. public health laboratories in 2004. Sex

Transm Dis 2007;34:41-6.

8. Hurd WW. Criteria that indicate endometriosis is the cause of chronic

pelvic pain. Obstet Gynecol, 1998 Dec: 92(6):1029-32.

9. Jackson SL, Soper DE. Sexually transmitted diseases in pregnancy.

Obstet Gynecol Clin North Am 1997 Sep:24(3):631-44.

10. Kaplan B, Rabinerson D, Gibor Y. Single-dose systemic oral

fluconazole for the treatment of vaginal candidiasis. Int J Gynaecol

Obstet 1997 Jun:57(3):281-6.

11. Livengood CH, Soper DE, Sheehan KL, et al. Comparison of once-daily

and twice-daily dosing of 0.75% metronidazole gel in the treatment of

bacterial vaginosis. Sex Transm Dis 1999 Mar:26(3):137-42.

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12. Nadel E, Talbot-Stern J. Obstetric and gynecologic emergencies. Emerg

Med Clin North Am 1997 May:15(2):137-42.

13. Newman L, Moran JS, Workowski KA. Update on the management

of gonorrhea in adults in the United States. Clin Infect Dis 2007;

44:S84-S101.

14. Seamens C, Slovis C. Abnormal vaginal bleeding in the nonpregnant

patient. Emergency Medicine Reports 1996:17(22):219-228.

15. Tjaden P, Thoennes N. 2006. Extent, nature, and consequences of rape

victimization. Findings from the National Violence Against Women

Survey. Washington: US Department of Justice; Publication No

NCJ210346.

08/13

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Notes

Obstetrical Emergencies

OBSTETRICAL EMERGENCIES

Diagnosis of Pregnancy

I. DATING PARAMETERS

A. Gestational age:

1. Estimates pregnancy duration from the first day of the LMP.

2. @ two weeks before ovulation and fertilization.

3. @ three weeks before implantation.

B. Fetal heart tones:

1. Doppler:

a. Detectable as early as ten weeks gestational age (GA).

b. Consistently heard by twelve weeks GA.

2. Normal range: 120-160 beats per minute.

C. Uterine enlargement:

1. 12-13 weeks (3rd month) GA.

a. Fundus palpable abdominally just above the symphysis.

b. Uterus changes from pelvic to abdominal organ.

2. 16 weeks GA - fundus midway between umbilicus and

symphysis.

3. 20 weeks GA - fundus at the level of the umbilicus.

4. 28 weeks GA - fundus @ 28 cm above the symphysis pubis.

II. LABORATORY DIAGNOSIS

A. Pregnancy tests:

1. Human chorionic gonadotropin (hCG):

a. First detectable in the serum within 24 hours of

implantation.

b. The concentration of hCG doubles every 1.4 to 2.1 days.

c. Plateaus at a peak concentration of approximately 100,000

mIU/mL at 8-11 weeks GA.

d. Remains at this level and is detectable until approximately

two weeks after pregnancy termination.

2. Radioimmunoassay (RIA):

a. Specific for the beta subunit of hCG.

b. Most specific and sensitive test for the past 30 years.

c. False-negative rates <1% (5 mIU/mL hCG 2nd IS).

d. False-positive rates are also infrequent.

3. Urine two site ELISA tests:

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Notes


a. Sensitive to 10 mIU/mL to 75 mIU/mL.

b. 99+% specific for the B-hCG molecule.

c. Detect pregnancy at 2-3 weeks GA.

d. Simple, inexpensive and timely.

e. Cannot be quantified.

4. Serum two site ELISA test:

a. Sensitive to 5 mIU/mL hCG (IRP).

b. Can be quantified.

c. False negative rates <1% with ELISA or RIA.

d. Sensitivity of 20 mIU/mL (IRP).

e. Causes of false negativity:

i. Dilute urine samples.

ii. “Chronic” ectopic gestations.

5. Quantitative B-hCG:

a. RIA or 2-site ELISA.

b. Both single and serial levels are useful.

c. Single levels:

i. Tend to be lower in ectopic pg, but not diagnostic.

ii. In combination with ultrasound - very helpful.

d. Serial levels:

i. In normal early IUP, B-hCG doubles q 1.4 - 2.1

days. ii. Failure to double q 48 hrs suggests abnormal

pregnancy.

iii. <20% rise or a fall in the level is 100% predictive of

nonviable IUP, aborted IUP, or ectopic pregnancy.

iv. Need consistency in measuring serial levels - same

laboratory and international standard.

Hypertension Disorders in Pregnancy

I. GENERAL

A. Classification:

1. Pregnancy-induced hypertension (acute hypertension of

pregnancy):

a. Hypertension develops after 20 weeks GA (earlier if

trophoblastic disease) or within 24 hours postpartum.

b. AND hypertension resolves within 10 days postpartum.

c. 3 entities (pathophysiologic continuum):

i. Without proteinuria - gestational HTN.

ii. With proteinuria – preeclampsia.

iii. With seizures in nonepileptic woman – eclampsia.

2. Chronic (coincidental) hypertension:

a. Persistent hypertension antedating pregnancy or prior to 20

weeks GA (without trophoblastic disease).

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b. Or persistent hypertension beyond 6 weeks postpartum.

3. Pregnancy-aggravated hypertension:

a. Superimposed preeclampsia or eclampsia in a patient with

chronic hypertension.

B. Hypertension defined as any one of the following:

1. DBP of 90 mmHg or greater.

2. Rise in DBP of 15 mmHg.

3. SBP of 140 mmHg or greater.

4. Rise in SBP of 30 mmHg.

5. This rise must be present on two or more reading which are at

least six hours apart.

6. Diastolic pressure is more prognostic.

II. PREECLAMPSIA

A. Clinical presentation:

1. Except in molar pregnancies, signs and symptoms develop

after the 20th week of pregnancy.

2. Hypertension - see I.B. (although definitions changing – see

ACOG).

3. Proteinuria:

a. + screen - urine dipstick reading of 1+ or greater protein.

b. Diagnostic criteria:

i. Greater than 0.3 gm/L in a 24 hour urine collection.

ii. 1 gm/L or greater protein concentration of 2 separate

urine collections 6 hours apart.

c. Proteinuria is a late sign.

d. Degree of proteinuria in a 24-hour specimen correlates

with disease severity and maternal morbidity.

4. Edema - can be seen with preeclampsia, but no longer part of

the definition:

a. >1+ pitting edema after 12 hours of bed rest.

b. Pedal edema accompanied by edema of hands and face.

c. Rapid weight gain may be an early sign: > 6 lbs/month.

5. Severe preeclampsia:

a. DBP > 110 mmHg.

b. Marked proteinuria:

i. >2+ on several occasions or >5 gm/24 hours.

c. Clinical indications of severe disease:

i. Visual disturbances:

Secondary to retinal arteriolar spasm.

Blurred vision, "floaters or spots".

Funduscopic exam:

•• Segmental arteriolar spasm.

•• No hemorrhage or exudates.

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Notes


ii. Severe, unrelenting headache.

iii. Hyperreflexia.

iv. Right upper quadrant pain:

Secondary to stretching of the liver capsule.

Suggestive of impending seizure.

v. Thrombocytopenia.

vi. Liver or renal dysfunction.

B. Work-up:

1. Type and cross for 2-3 units packed red blood cell.

2. Hgb, Hct, WBC, urinalysis, electrolytes, BUN, uric acid,

creatinine, plasma estriol.

3. 12 or 24 hr urine for quantitative protein and Cr clearance.

C. Management:

1. General:

a. Safety of the mother is the first priority.

b. Hospitalization is indicated in the majority of patients.

c. Definitive treatment of toxemia is delivery of the infant:

i. Removal of inciting trophoblastic tissue.

ii. Indications for urgent delivery:

Immature infant and severe preeclampsia.

Mature infant and any degree of preeclampsia.

d. Expectant therapy:

i. Hospitalization with frequent evaluations.

ii. Enforced bed rest.

iii. Salt restriction.

iv. Seizure precautions.

e. Outpatient management, while infrequent, may be tried if:

i. SBP < 135 mmHg, DBP < 85 and no proteinuria.

ii. Patient reliable for follow-up and strict bed rest.

f. Goals of preeclamptic management:

i. Prevention of seizures.

ii. Blood pressure control.

iii. Stabilize and deliver if greater than 34 wks GA.

iv. If less than 34 wks, stabilize and carry to 34 weeks IF

THE MOTHER REMAINS STABLE. Otherwise

deliver.

2. Prevention of seizures:

a. Magnesium sulfate (MgSO4):

i. Drug of choice.

ii. Controls and prevents seizures due to toxemia.

iii. Dosage:

Loading dose - 4-6 grams in 10% solution IV

over 5-10 minutes.

Maintenance dose:

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Notes


•• 1-2 grams IV/hour.

•• Hold maintenance doses if:

••• Patellar reflex absent.

••• Depressed respirations.

••• Urine output < 100 ml/4 hr.

iv. Toxicity:

Dose dependent.

< 7 mEq/L - negligible toxicity.

7-10 mEq/L - loss of patellar reflexes.

> 10 mEq/L - respiratory depression.

10-15 mEq/L - prolonged cardiac conduction.

•• Prolonged P-R and QRS intervals.

>15 mEq/L - cardiac arrest in diastole.

Antidote:

•• Calcium gluconate 10% solution-10-20-ml

over 3 min.

•• Calcium chloride for cardiac arrest.

b. Anti-convulsants other than MgSO4:

i. Benzodiazepines:

Examples: Diazepam, lorazepam.

Indicated if high dose magnesium ineffective.

Side effects:

•• Maternal respiratory depression.

•• Maternal hypotension.

•• Crosses placenta:

••• Neonatal apnea.

••• Low Apgar scores.

ii. Phenytoin (Dilantin) or barbiturates.

iii. Second line therapy.

3. Antihypertensive therapy:

a. General:

i. All antihypertensive agents have a risk of lowering

placental perfusion.

ii. Antihypertensive agent indicated if DBP > 110

mmHg. iii. Attempt to maintain DBP of 90-100 mmHg.

b. Hydralazine (Apresoline):

i. Drug of choice in pregnancy.

ii. Thought to lower placental perfusion the least.

iii. Dosage:

Initial dose: 5 mg IV.

Repeat 5-10 mg IV every 10-20 minutes prn.

c. Labetalol:

i. Alpha and beta adrenergic blockade (ratio = 1:5).

ii. Also considered as a safe, first line drug in pregnancy.

iii. 20 mg IV bolus followed by 40mg IV if not effective

in 10 minutes to max total dose of 220 mg.

d. Nitroprusside (Nipride):

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Notes


i. Arterial and venous vasodilator.

ii. Benefit: most rapid onset and shortest half-life.

iii. Risk: Placental transfer may lead to neonatal cyanide

toxicity.

iv. Reserved for hypertension refractory to Hydralazine

or Labetalol (last line of defense).

e. Diazoxide:

i. Arteriolar vasodilator.

ii. 2nd or even 3rd line drug.

f. Nimodipine:

i. Relatively safe.

ii. Nifedipine SL not safe.

D. Prognosis:

1. Maternal:

a. Better prognosis in preeclampsia than eclampsia:

i. Mortality – negligible.

ii. Morbidity - higher; secondary to complications:

DIC.

Abruptio placenta.

Renal failure.

Intracerebral hemorrhage.

Pulmonary edema.

b. Signs and symptoms resolve swiftly following delivery.

2. Neonatal:

a. Prognosis is guarded in both preeclampsia and eclampsia.

b. Prognosis dependent on onset of disease process.

c. Mortality:

i. 15% perinatal mortality.

ii. Primarily due to prematurity.

d. Morbidity:

i. Fetal growth retardation.

ii. Prematurity.

3. Prognosis is worse when toxemia is superimposed on chronic

hypertensive disease.

III. ECLAMPSIA

A. Pathophysiology and clinical presentation:

1. Same as with preeclampsia.

2. Eclampsia is said to occur when patient develops seizures:

a. Generalized tonic-clonic seizure activity.

b. Seizures are more frequent the closer to term.

i. ≈ 50% develop seizures prior to labor.

ii. ≈ 25% develop seizures prior to delivery.

iii. ≈ 25% develop seizures within 48 hours postpartum.

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Notes


3. If seizure develops after 48 hours postpartum:

a. Potentially could be eclampsia (up to 1 week postpartum).

b. Must rule out CNS lesion, however.

4. RUQ tenderness (stretching of liver capsule) in the setting of

preeclampsia - may warn of impending seizure activity.

B. Treatment:

1. Delivery is curative:

a. Must deliver even in face of known fetal prematurity.

b. Mother’s health is physician’s first priority.

2. Treat seizures and prevent further seizure activity:

a. High dose magnesium sulfate.

b. Benzodiazepines, Phenytoin, barbiturates:

i. All second line drugs in eclampsia.

ii. All may lead to neonatal apnea and low Apgar scores.

c. Supportive care - including seizure precautions.

3. Treat hypertension - same therapy as used for preeclampsia.

C. Prognosis:

1. Maternal:

a. Mortality approaches 5%.

b. Morbidity also increased from that seen in preeclampsia.

c. Complications (same as with preeclampsia):

i. DIC.

ii. Abruptio placenta.

iii. Renal failure.

iv. Intracerebral hemorrhage.

v. Pulmonary edema.

d. Complications (secondary to seizure activity):

i. Apnea.

ii. Aspiration.

iii. Trauma.

iv. Acidosis.

v. Rhabdomyolysis with resultant renal failure.

2. Neonatal:

a. Mortality primarily related to infant prematurity as

delivery is mandatory regardless of degree of prematurity.

b. Maternal and neonatal morbidity and mortality increased

when eclampsia is superimposed on chronic hypertension.

IV. HELLP SYNDROME

A. Pathophysiology:

1. Hemolysis, elevated liver enzymes, low platelet count:

a. First described in 1954.

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Notes


b. Occurs on its own or in association with preeclampsia.

c. Multi-system disease with abnormal vascular tone,

vasospasm and coagulation defects.

d. Causes microvascular endothelial damage and

intravascular platelet activation, which releases

thromboxane A and serotonin, leading to a cascade of

platelet aggregation and further endothelial damage.

e. Occurs in ≈ 0.4% of pregnancies (less common than

preeclampsia).

f. Superimposed HELLP syndrome develops in 4-12% of

patients with preeclamptic symptoms.

g. Unlike preeclampsia, it occurs more often in multiparous

women.

2. Develops antepartum in 70% and postpartum in 30%:

a. Most commonly develops in the third trimester.

b. Postpartum presentation of HELLP usually develops

within 48 hours of delivery but may develop up to one

week later.


1. Patients may present with a variety of symptoms:

a. General malaise- 90%.

b. Right upper quadrant pain- 65%.

c. Headache- 31%.

d. Nausea and vomiting- 30%.

e. Blurred vision and jaundice.

2. Hypertension may be absent or mild; thus this disorder is often

initially misdiagnosed.

3. Proteinuria may also be absent or mild.

4. RUQ tenderness is present in ≈ 90%.

5. Often initially misdiagnosed as cholecystitis, gastritis,

hepatitis, ITP, TTP, hemolytic uremic syndrome and acute

fatty liver of pregnancy.

C. Work-up:

1. CBC:

a. Hematocrit may be low; however, this is often preceded by

laboratory evidence of thrombocytopenia and liver enzyme

abnormalities.

b. Decreased serum haptoglobin level is a more sensitive

indicator of hemolysis.

c. Elevated liver enzyme levels (AST, ALT, LDH, bilirubin).

2. Thrombocytopenia:

a. Most reliable indicator of HELLP syndrome.

b. Used to classify risk of maternal morbidity and mortality:

i. Class I <50,000 platelets B highest risk for

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Notes


complications.

ii. Class II 50,000-100,000 platelets.

iii. Class III 100,000-150,000 platelets – no longer meets

criteria for HELLP syndrome.

c. PT, PTT and fibrinogen levels are normal, unless DIC is

also present.

d. Patients with preeclampsia who have a positive D-dimer

are thought to be at increased risk of also developing

HELLP.

e. Best lab markers to guide therapy are the maternal

platelets count and LDH.

3. Subscapular hematoma or rupture can occur and are not

always reflected by laboratory abnormalities, so any woman

with HELLP syndrome who complains of right upper quadrant,

neck or shoulder pain should undergo hepatic imaging.

4. Lab abnormalities usually worsen after delivery, peak at 24-48

hours, and begin resolving 3-4 days postpartum.

D. Management:

1. Delivery of the infant if the mother is unstable or infant is 34

wks GA:

a. IV fluids- judiciously to avoid fluid overload.

b. Strict bed rest.

c. IV corticosteroids (Dexamethasone 10mg IV q 12 h).

d. Magnesium sulfate prophylaxis (prevent seizures or

coma) 4-6g IV bolus over 1 hour, followed by 2g/hr

infusion.

e. Treat hypertension if BP > 160/110.

f. Maintain diastolic pressure 90-100.

g. Reduces the risk of maternal cerebral hemorrhage and

seizure and possible placental abruption.

h. Hydralazine 5mg IV, then 2.5-5mg IV q 15-20 minutes.

i. Labetolol.

j. Blood products:

i. Platelet transfusion.

ii. For platelet counts <20,000.

iii. Or <50,000 who undergo cesarean section.

iv. Fresh frozen plasma and PRBC in those who develop

DIC.

v. Consider plasmapheresis in severe cases.

2. Prognosis:

a. 1% maternal mortality rate .

b. Higher morbidity secondary to complications- DIC,

placenta abruption, ARDS, hepatorenal failure, pulmonary

edema, subscapular hematoma and hepatic rupture.

c. Infant mortality range from 10-60% depending on fetal

GA at delivery and severity of maternal disease.

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Notes


d. High reoccurrence rate of developing HELLP

syndrome (19-27%) or preeclampsia (43%) in subsequent

pregnancies.

Ectopic Pregnancy

I. DEFINITION

A. Pregnancy that implants and develops outside of the intrauterine

cavity.

II. SITE

A. Tubal - 95%:

1. Ampulla:

a. 80%.

b. Rupture at 8-10 weeks gestational age.

c. Tubal abortion is common.

2. Isthmus:

a. 15%.

b. Rupture at 6-8 weeks gestational age.

c. Rupture is common.

3. Interstitial or cornual:

a. 2.5%.

b. Can rupture late (2nd - 4th month).

c. Physical exam may reveal asymmetry of uterus with no

adnexal mass.

d. Often produces fatal hemorrhage due to involvement of

both ovarian and uterine vessels.

4. Fimbrial.

III. COURSE

A. Death of ovum in tube and resorption:

1. 10-50%.

2. Under diagnosed.

3. Few days of lower abdominal pain, then asymptomatic.

B. Tubal abortion (NONRUPTURED ECTOPIC PREGNANCY):

1. Extrusion of the products of conception (POC) through the

fimbriae.

2. More frequent than rupture.

3. Especially frequent in ampullary pregnancies.

4. Less dramatic and with a more prolonged clinical course.

5. Symptoms increase as the mass increases.

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Notes


6. Incomplete extrusion - leakage of blood from the fimbriae

cause gradual intraperitoneal hemorrhage.

7. In complete extrusion, early tubal abortion symptoms are

similar to late painful menses.

C. Abortion into the uterine cavity.

D. Rupture through the tubal wall (RUPTURED ECTOPIC

PREGNANCY):

1. Sudden, intense pain.

2. Often preceded by vigorous exam, intercourse or trauma.

IV. PATHOPHYSIOLOGY

A. Implantation:

1. Tubal implantation is very similar to intrauterine implantation.

2. Exception: no decidua is formed.

3. Trophoblastic cells erode through the mucosa and muscularis

as they proliferate.

4. This destroys tissues and opens blood vessels, producing an

intratubal hemorrhage.

5. Increasing size of the tubal mass is due to this hemorrhage.

6. Slow leakage of blood may occur through the fimbriated ends

of the fallopian tube.

a. This may result in accumulation of blood in the posterior

cul-de-sac in the absence of tubal rupture.

b. This occurs in 65% of unruptured ectopic pregnancies.

B. Uterine changes:

1. Also very similar to normal pregnancy.

2. The uterine endometrium is converted to decidua in response to

maternal hormones.

3. Unlike normal pregnancy, there are no chorionic villi present.

4. When the fetus dies, gestational hormones are no longer

produced, and decidual growth ceases.

5. This endometrial decidua then degenerates and is shed:

a. Producing external bleeding when shed in pieces.

b. Less commonly, it is shed in one piece:

i. Decidual cast.

ii. 5% of ectopic pregnancies.

iii. May be mistaken for a complete abortion.

6. Pathologic analysis of "fetal tissue" to search for chorionic villi

or fetal parts.

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Notes


V. INCIDENCE

A. 2% of all pregnancies.

B. Incidence of ectopic pregnancy is increasing:

1. In the 1970s, the incidence was 0.5%.

2. Proposed etiology of this increase:

a. Increased usage of intrauterine device (IUD)

contraception.

b. Increased incidence of pelvic inflammatory disease (PID).

c. Antibiotic usage to treat PID.

d. Increased diagnosis of resorbed and tubal abortion.

C. Incidence of maternal mortality is decreasing:

1. Four-fold decrease from 1965 to 1980.

2. 4/100,000 live births.

3. Increased awareness leading to earlier diagnosis.

4. Sensitive hCG determinations and sonography.

D. Still remains the leading cause of first trimester maternal death.

E. Is the largest single cause of maternal death in non-Caucasians.

F. Ectopic pregnancy is responsible for 6% of maternal deaths.

VI. HISTORY

A. Risk factors:

1. Anything that impedes ovum transport.

2. PID (endosalpingitis):

a. Largely responsible for increasing incidence.

b. 30% of patients with ectopic give history of PID in past.

c. Up to 50% with histopathologic evidence of PID.

3. Exosalpingitis or peritubal adhesions:

a. Prior history of appendicitis, diverticulitis or abortions.

b. Prior generalized peritonitis.

c. 30% give history of previous abdominal surgery.

4. Current adjacent tumors - ovarian cysts, fibroids,

endometriosis.

5. Failed tubal ligation:

a. 16% risk.

b. 0.4% chance of pregnancy, but 50% of these are ectopic.

6. Failed intrauterine device:

a. 14% risk.

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Notes


b. Increased risk of PID.

c. Decreased receptivity of uterus.

d. Patient still ovulates, but has difficulty with intrauterine

implantation.

7. Previous ectopic pregnancy:

a. Especially if prior salpingotomy.

b. 8 times the risk.

8. History of infertility:

a. Particularly if taking ovulation-inducing agents.

b. Also increases the risk of combination pregnancy.

9. Prior salpingoplasty.

10. Increased maternal age.

11. Repeat visits, not responding to therapy for presumed

diagnosis.

B. Symptoms:

1. Signs and symptoms dependent on:

a. Extent of intraperitoneal hemorrhage:

i. Slow leakage.

ii. Actual rupture.

b. Site of implantation.

c. Duration of the pregnancy.

2. Symptoms of unruptured ectopic pregnancy:

a. Usually vague.

b. Less frequently diagnosed (15%) vs ruptured (85%).

3. Classic triad:

a. Abdominal pain, vaginal bleeding, amenorrhea.

b. 15% sensitive; 14% specific.

4. Abdominal pain:

a. Occurs in 95% of patients with ectopic pregnancy.

b. Poorly localized to the lower abdomen.

c. Dull and aching secondary to tubal distension.

d. Sudden sharp pain often occurs at the time of rupture.

e. After rupture, pain becomes generalized (peritonitis).

f. Pain typically unilateral, but not always.

g. Pain may radiate to the back, shoulder (10%) or rectum.

5. Vaginal bleeding:

a. Incidence is 50-84%.

b. Rarely profuse:

i. May occur with cornual pregnancy.

ii. More often seen with spontaneous abortion.

c. Slight spotting is much more typical.

d. Abdominal pain without abnormal vaginal bleeding occurs

in up to 1/3 of patients with ectopic pregnancy.

6. Amenorrhea:


b. Inquire if LMP was normal.

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Notes


7. Miscellaneous symptoms:

a. Symptoms of pregnancy (23%).

b. Tenesmus.

c. Three S's:

i. Less frequent but quite significant:

Shock 8-18%.

Syncope 15%.

Shoulder pain 10%.

•• Danforth's sign.

•• Hemoperitoneal diaphragm irritation.

VII. PHYSICAL EXAMINATION

A. Orthostatic vital signs:

1. Frank shock is rare; usually occurs after cornual rupture.

2. Shock:


b. Out of proportion to the amount of vaginal bleeding.

3. Lack of tachycardic response in face of hypotension:

a. Reported in 55% of patients in one study.

b. Parasympathetic response to hemoperitoneum.

c. All patients tested had significant orthostatic changes.

B. Abdominal exam:

1. Abdominal tenderness present in 70%.

2. Unilateral tenderness in 37-72%.

3. Rebound tenderness in 25-50%.

4. Signs dependent on status of tube integrity:

a. Ruptured - peritoneal findings expected.

b. Unruptured - abdominal exam may be unremarkable.

C. Pelvic examination:

1. Chadwick’s sign - bluish cervix.

2. Less cervical softening than a normal pregnancy.

3. Uterus is enlarged, but small for dates in 25%.

4. Cervical motion tenderness present in 50%.

5. Unilateral adnexal tenderness (but may be bilateral) in 95%.

6. Adnexal mass is absent in 70% of patients with ectopic.

7. Bulging, tender cul-de-sac suggests hemoperitoneum.

D. High index of suspicion for ectopic pregnancy necessary:

1. In any patient with lower abdominal pain or vaginal bleeding

with a positive pregnancy test in the first trimester.

Any female of reproductive age presenting in shock without

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Notes


history or evidence of trauma.

VIII. DIFFERENTIAL DIAGNOSIS

A. Positive B-hCG:

1. Intrauterine pregnancy:

a. Round ligament pain.

b. Persistent or ruptured corpus luteum cyst.

2. Spontaneous abortion:

a. Threatened, complete or incomplete abortion.

b. Usually cause more bleeding, less pain.

c. Pain usually described as midline cramping.

d. Adnexal mass could be corpus luteum cyst.

e. "Tissue" could be decidual cast:

i. Decidual cast shed intact in 5% of ectopic pregnancy.

ii. Send all tissue to pathology lab to assure presence of

chorionic villi or fetal tissue.

3. Normal intrauterine pregnancy with any surgical emergency:

a. Appendicitis.

b. Ovarian torsion.

c. All need operative intervention.

4. Molar pregnancy:

a. More vaginal bleeding.

b. Uterus large for dates.

c. Ultrasound diagnostic.

IX. DIAGNOSTIC MODALITIES

A. High index of suspicion for ectopic pregnancy is critical.

1. Difficult to diagnose:

a. History and physical exam alone correctly establish the

diagnosis in 50% of patients.

b. 50% of patients with ectopic pregnancy have been

previously seen by a least one physician prior to diagnosis.

2. Recognizing the pregnant patient is the most important step.

B. Quantitative B-hCG:

1. Single levels:

a. Serum B-hCG levels tend to be lower in patients with

ectopic pregnancy but this is variable.

b. Discriminatory zone (DZ) (see Table 1):

i. Minimum hCG level at which a uterine gestational sac

is seen by ultrasound in every viable IUP.

ii. DZ vary at different institutions.

iii. DZ value dependent upon:

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Notes


Type of probe - vaginal vs. abdominal.

Resolution of sonography.

Sonographer's experience level.

Specificity, sensitivity and reference standard of

the hCG determination used.

c. The combination of ultrasound with B-hCG level

within the DZ has a predictive value of 93% to 99%. 2. Serial quantitative hCG levels:

a. Useful if the quantitative hCG level is unavailable or

below the DZ at the time of presentation.

b. May be performed on an outpatient basis if:

i. < 5 weeks gestational age by dates.

ii. Vital signs are stable.

iii. There is no evidence of peritoneal irritation on exam.

c. Failure of hCG to double every 48 hours suggests an

abnormal pregnancy.

d. Ectopic rupture can occur despite low or declining levels.

e. Lack of chorionic villi or fetal tissue following a D & C

for a nonviable pregnancy strongly suggests ectopic

pregnancy.

f. 10% of patients with ectopic pregnancy have normal

doubling times initially.

C. Pelvic ultrasound:

1. Ultrasound results consistent with definitive ectopic

pregnancy: a. Detection of extrauterine fetal cardiac activity.

b. Uncommon with either TAS of TVS approach:

i. Occurs in 10%-24% of patients with ectopic gestation.

ii. More often seen with TVS than with TAS.

c. Late finding:

i. Cardiac activity detected at 6-7 weeks GA with TVS.

ii. Cardiac activity detected at 7-8 weeks GA with TAS.

2. Ultrasound results consistent with definitive intrauterine

pregnancy:

a. Visualization of cardiac activity, a fetal pole or a yolk

sac within the uterine cavity.

b. Seen approximately 1 week earlier with TVS versus TAS.

c. False negative rate of ectopic when IUP is identified is

rare:

i. Simultaneous ectopic and intrauterine gestation:

1/30,000 - calculated in 1948.

Current figure is 1/4,000 - 1/15,000.

Incidence may be as high as 1/100 in fertility

patients on ovulation stimulation therapy.

Check for cul-de-sac fluid or complex adnexal

mass.

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Notes


ii. Cornual (interstitial) ectopic pregnancy:

May be misidentified as IUP with TAS.

Potentially fatal hemorrhage if ruptures.

3. Ultrasound results suggestive of intrauterine pregnancy:

a. Intrauterine gestational sac noted.

b. True gestational sac - present in IUP:

i. Located eccentric to the endometrial stripe.

ii. Double decidual sac sign (DDSS):

Decidua vera - present in IUP and ectopic.

Decidua capsularis - present in IUP only.

IUP has double ring surrounding the sac.

Ectopic has one ring surrounding the intrauterine

pseudogestational sac.

c. Pseudogestational sac - present in ectopic pregnancy:

i. Located centrally along the endometrial stripe.

ii. Surrounded by a single echogenic ring.

iii. Present in 10-20% of patients with ectopic pregnancy.

4. Ultrasound findings suggestive of ectopic pregnancy:

a. “Empty uterus” in patients with hCG above the DZ:

i. DZ = minimum hCG value at which an intrauterine

gestational sac is seen sonographically in all IUPs.

ii. The DZ is lower for TVS versus TAS.

iii. Diagnose 1 week earlier with TVS vs TAS (Table 1).

iv. Only 10-40% of women with ectopic have B-hCG >

6500 at the time of presentation - so TVS preferred.

v. Differential of empty uterus at an hCG value > DZ:

Ectopic pregnancy.

Blighted ovum.

Spontaneous abortion.

b. Complex adnexal mass. c. Adnexal gestational sac may be visualized.

d. Internal echoes within this adnexal ring strongly suggests

ectopic gestation.

e. Moderate to large amount of posterior cul-de-sac fluid. 5. Inconclusive ultrasound findings:

a. 2-3 week window where ultrasound is nondiagnostic:

i. hCG detectable at ≈ 3 weeks GA.

ii. TVS detects IUP at ≈ 5 weeks GA.

iii. TAS detects IUP at ≈ 6 weeks GA.

b. In some emergency departments, quantitative B-hCG

levels are unavailable at the time of presentation.

c. Consider alternative diagnostic modalities:

i. Repeat quantitative B-hCG level in 48 hours.

ii. Culdocentesis.

iii. Admit for observation.

iv. Laparoscopy.

d. If pelvic pain/bleeding and low B-hCG (<1000), still do

ultrasound, checking for free cul-de-sac fluid or complex

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Notes


adnexal mass.

TABLE 1 Discriminatory hCG Levels

Finding TAS TVS

Gestational sac 5-6 weeks* 4-5 weeks

1800 IRP 1300 IRP

Fetal pole 7-8 weeks 6-7 weeks

6500 IRP 1800 IRP

Fetal heart beat 7-8 weeks 6-7 weeks

21,000 IRP 12,000 IRP

*Gestational age (weeks from onset of LMP)

from Wyte, C: Diagnostic Modalities in Pregnancy. In: Doan-

Wiggins, L(ed): Emerg Med Clin N Amer, WB Saunders,

1994:12(1):9-43.

D. Laparoscopy:

1. A definitive test in equivocal cases.

2. Unlike other diagnostic modalities, it permits definitive

treatment.

X. TREATMENT

A. Hemodynamically unstable patient – to OR.

B. Hemodynamically stable pregnant patient – urgent Gynecology

consult.

C. Removal of the ectopic gestation:

1. The earlier the diagnosis:

a. The more conservative approach may be attempted.

b. The greater the chance of subsequent fertility.

2. Methotrexate:

a. Halts thymine and purine, and thus DNA, production.

b. Inclusion criteria:

i. Hematosalpinx < 3.5 cm (3 cm) diameter.

ii. B-hCG < 3500 mIU/mL.

iii. No significant hemoperitoneum exists.

iv. The tubal serosa must be intact (nonruptured).

v. No intratubal cardiac activity noted.

c. Given in four doses of 1 mg/kg of methotrexate IM or IV

on alternating days, with 0.1 mg/kg of leucovorin given on

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Notes


the intervening days.

d. Alternative dosing is a single dose regimen (50 mg/m2).

e. Using proper inclusion criteria, early studies show a 95%

success rate; side effects have been minimal and minor.

3. Operative management - salpingostomy, salpingectomy.

4. Observation:

a. Avoids surgery in patients in whom spontaneous tubal

abortion or reabsorption may occur.

b. Natural course of an ectopic, however, is difficult to

predict.

c. Confers no advantage to conservative surgery in terms of

subsequent fertility or repeat ectopic pregnancy rate.

d. Reasonable option in an asymptomatic patient with low,

declining levels of serum hCG.

e. Patients who present to the ED are rarely

asymptomatic.

5. Persistent ectopic pregnancy:

a. 5% risk in patients treated by conservative methods.

b. Patient may present with recurring symptoms, and tubal

rupture is also possible.

c. Patients undergoing conservative surgical or chemical

therapy need to be monitored for this complication.

XI. PROGNOSIS

A. Mortality - up to 60% in undiagnosed, ruptured ectopic

pregnancies.

B. Morbidity:

1. Increased risk of subsequent ectopic pregnancies.

2. Subsequent fertility and pregnancy difficulties:

a. 40% will not conceive again.

b. Of the 60% who do become pregnant:

i. 12% have repeat ectopic pregnancies.

ii. 15-20% will have a spontaneous abortion.

c. 60% of a particular subset eventually have a term

pregnancy:

i. This is the most optimistic scenario.

ii. These women have no underlying tubal pathology.

iii. They were treated conservatively for their prior

ectopic.

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Notes


Hemorrhage in Early Pregnancy

I. ABORTION

A. Terminology:

Table 2. Clinical Classification of Spontaneous Abortion

Type of Abortion Internal Cervical Os Products of Conception

Threatened Closed Not Passed

Inevitable Open Not Passed

Imminent Open Within Dilated Cervix

Incomplete Usually Open Partially Passed

Complete Closed Completely Passed

from: Wyte CD: Hemorrhage in early pregnancy. In: Harwood-Nuss et al

(eds):The Clinical Practice of Emergency Medicine, 2nd

ed. In press.

B. Epidemiology:

1. Up to 25% of first trimester pregnancies complicated by

bleeding.

2. ≈ Half of all women with first trimester bleeding go on to

abort.

3. Abortion rate markedly decreased if positive fetal heart tones at

time of presentation to @10%, and < 5% if normal fetal

heart tones.

4. History of prior spontaneous abortion is best predictor of

subsequent abortion.

a. Probability increases with the number of previous losses:

i. @15% - no prior spontaneous abortions.

ii. 19% to 24% - following one spontaneous abortion.

iii. 25% - following two spontaneous abortions.

iv. 30-40% - in women with habitual abortion (3 or more

consecutive spontaneous abortions).

C. Natural history:

1. First trimester intrauterine bleeding outcome:

a. Half proceed to actual abortion.

b. 40% have a viable intrauterine pregnancy.

c. ≈ 10% have an ectopic pregnancy.

d. Rarely, have a molar pregnancy.

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Notes


D. Clinical presentation:

1. Threatened abortion:

a. Spotting or brownish vaginal discharge.

b. Mild, crampy suprapubic pain (may radiate to lower back).

c. Less bleeding and pain than seen with incomplete

abortion.

d. No passage of fetal tissue; however, clots may be mistaken

for fetal tissue.

e. Internal cervical os will be closed.

2. Complete abortion:

a. History of severe bleeding and cramping which rapidly

subsided after passing fetal tissue or "clots".

b. Cervical os closed.

c. Minimal vaginal bleeding and abdominal pain.

3. Incomplete, inevitable or imminent abortion:

a. Moderate to severe crampy lower midline abdominal

pain.

b. Significant vaginal bleeding:

i. May be quite severe.

ii. Continues until all POC are expelled.

c. Continued dilatation of the internal cervical os.

d. With only a slight amount of retained tissue, it may be

difficult to differentiate complete from incomplete

abortion on clinical grounds alone - ultrasound may be

helpful.

e. Distinction between incomplete, imminent and inevitable

abortion not clinically necessary - management is the

same.

4. Emergent problems:

a. Major complications are hemorrhage and infection.

b. Other less common but potentially fatal complications:

i. DIC.

ii. Septic shock.

iii. Pelvic thrombophlebitis with possible embolization.

iv. Endotoxic shock.

v. Peritonitis.

vi. Uterine rupture.

c. All complications more common in late first trimester

incomplete or missed abortion.

E. Differential diagnosis:

1. Non-gynecologic:

a. Urethral hemorrhage.

b. Rectal hemorrhage.

2. Careful history and pelvic and rectal examination.

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Notes


3. Gynecologic - non pregnancy-related:

a. Cervicitis or vaginitis.

b. Lacerations or abrasions - cervical or vaginal trauma.

c. Cervical polyps.

d. Cervical carcinoma.

e. Careful history and speculum examination.

4. Gynecologic – pregnancy-related:

a. Ectopic pregnancy:

i. Most important to rule out - see ECTOPIC section.

ii. Usually less bleeding and more pain than abortion.

iii. Difficult to differentiate by physical exam alone.

iv. Sonography may be diagnostic.

b. Ruptured hemorrhagic corpus luteal cyst:

i. If peritoneal signs or hypovolemia - diagnose in OR.

ii. In the stable patient, ultrasound may be useful.

c. Trophoblastic disease - see below.

F. Emergency department evaluation:

1. Physical examination:

a. Assessment and resuscitation of hemodynamic instability.

b. Frank shock :

i. Ruptured ectopic pregnancy.

ii. Ruptured hemorrhagic corpus luteal cyst.

iii. Incomplete abortion.

c. Narrowed pulse pressure or orthostatic changes.

d. Lower abdominal tenderness - NO peritoneal signs.

e. Speculum examination:

i. Briskness of external hemorrhage.

ii. Evidence of vaginitis, cervicitis, lacerations or polyps.

iii. Patency of the internal os.

iv. POC within the dilated cervix - imminent abortion.

f. Clots disintegrate easily when pulled apart - tissue does

not.

g. Bimanual exam:

i. Patency of the internal cervical os:

Multiparous with normal laxity of external os.

Incomplete abortion - internal os patent.

ii. Uterine tenderness, consistency, shape and size:

Size larger than expected for dates- mole.

Size smaller than dates:

•• Missed abortion.

•• Ectopic pregnancy.

iii. Posterior cul-de-sac fullness – hemoperitoneum.

iv. Unilateral adnexal tenderness and enlargement:

Nonspecific.

Ectopic pregnancy.

Hemorrhagic corpus luteal cysts.

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Notes


Multiple cysts seen with molar gestation.

Corpus luteal cyst in normal pregnancy.

v. Fetal heart tones:

Hand-held Doppler.

Worrisome if absent after 12 weeks GA.

2. Pregnancy testing:

a. Should be done in all women of child-bearing age who

present with abnormal vaginal bleeding or abdominal pain.

b. Patient interview alone is often unreliable.

c. Quantitative serum B-hCG level:

i. Used with ultrasound to exclude ectopic pregnancy.

ii. Marked elevation:

Molar pregnancy.

Multiple gestation.

d. Serial quantitative B-hCG levels:

i. B-hCG doubles q 1.4 - 2.1 days in early viable IUP.

ii. Failure B-hCG to double every 48 hours suggests:

Ectopic pregnancy.

Nonviable IUP.

Recent spontaneous abortion.

3. Other laboratory studies:

a. CBC if bleeding is either severe or prolonged.

b. Rho(D) blood typing.

c. Type and cross-match if potential hemorrhagic shock.

4. Ultrasound:

a. Use in first trimester hemorrhage:

i. Exclusion of ectopic pregnancy.

ii. Assessment of fetal viability.

iii. Identification of retained products of conception.

iv. Diagnose molar pregnancy.

b. Not needed if clinical evidence of incomplete or septic Ab.

c. Use in predicting outcome of pregnancy:

i. Risk of eventual abortion decreased to 5% when

normal fetal cardiac activity present.

ii. Fetal bradycardia predicts a high risk of fetal demise.

d. Subchorionic fluid and hemorrhage:

i. Both very common - occur in half of all pregnancies.

ii. Unrelated to fetal death in the absence of bleeding.

iii. Minimal increased risk if present with overt bleeding:

16% - 22% risk.

Expectant management indicated.

e. Blighted ovum:

i. Sac size > 2 cm TAS or 0.9 cm TVS without yolk sac.

ii. Sac 0.9 cm (TVS) or greater without cardiac activity.

f. Missed abortion - 5 mm fetal pole (TVS) without

heartbeat.

g. Hydatidiform mole - classic snowstorm pattern.

h. Retained POC:

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Notes


i. Ultrasound not indicated if presumptive diagnosis of

incomplete or septic abortion is made clinically (i.e.,

severe abdominal pain, hemorrhage, dilated os).

ii. 15% of patients thought to have a complete abortion

had retained POC on curettage analysis.

iii. Sonography had a 98% negative predictive value.

iv. Sonography had a 69% positive predictive value.

v. If unclear diagnosis, sonography is indicated.

vi. If results of Rubin's study are confirmed, sonography

may be indicated in presumed complete abortion.

5. Send all tissue to pathology lab for analysis:

a. Chorionic villi or fetal parts should be present if abortion.

b. If absent, must rethink diagnosis (ectopic, ectopic,

ectopic).

c. Molar "pregnancy" with classic pathology findings.

G. Emergency department management:

1. Definitive care:

a. Threatened abortion:

i. Expectant management.

ii. Quantitative hCG.

iii. Rho(D) testing.

iv. Anti-D immunoglobulin (RhoGAM) indicated if:

Rho(D) negative.

AND a negative indirect Coomb's test.

v. Discharge to home with 48 hr. gynecology follow-up:

Re-evaluation.

Repeat quantitative hCG testing.

vi. Avoid strenuous activity, intercourse, tampon usage.

vii. Intercourse may resume when bleeding has ceased.

viii. Return to ED promptly if increased bleeding or pain,

develop fever or pass tissue.

ix. Expelled tissue should be brought in for analysis.

b. Complete abortion:

i. Administer RhoGAM if indicated.

ii. Send specimens to path lab for analysis.

iii. If any doubt as to retained POC, further evaluation

with ultrasound or dilation and curettage is indicated.

iv. Discharge instructions - return to ED promptly if

fever, increased pain or bleeding or if pass further

tissue.

c. Incomplete abortion:

i. Requires urgent D & C by Gynecologist.

ii. Oxytocin (Pitocin) or the ergot alkaloids:

May be used to temporize hemorrhage while

awaiting curettage.

10 to 20 IU Oxytocin added to 1L isotonic IVF.

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Notes


Administer at a rate of 200 to 500 ml/hour.

0.2 mg methylergonovine (Methergine) IM.

iii. RhoGAM if indicated.

2. Indications for admission:

a. Hemodynamic instability

b. Coagulopathy

c. Trophoblastic disease

d. Severe anemia

e. Ectopic pregnancy

f. Septic abortion

II. TROPHOBLASTIC DISEASE (MOLAR PREGNANCY)

A. Pathophysiology:

1. Rare cause of late first trimester hemorrhage.

2. Chorionic villi of normal pregnancy are converted to a mass of

clear vesicles which hang from pedicles in a cluster, like

grapes.

3. Both the fetus and amnion fail to develop.

4. Etiology is fertilization which results in a pair of paternal

chromosomes (absent maternal genetic material):

a. Fertilization by two sperm of a chromosome-devoid ovum.

b. Fertilization of an ovum by a haploid sperm with

duplication of the paternal chromosomes after meiosis.

5. Infrequently, the trophoblast of a molar "pregnancy" will

progress:

a. Invasive mole which invades the myometrium.

b. Malignant transformation to choriocarcinoma (rare).

6. Incidence of hydatidiform mole:

a. One in 1,500 to 2,000 pregnancies.

b. Higher in Mexico and in native Alaskans.

c. Highest incidence (1 in 150 to 200) in Asian race.

d. Also very high incidence in women 45 years and older.


1. Typically develop symptoms in the second trimester.

2. Problems may arise in late first trimester.

3. Abdominal cramping.

4. Vaginal bleeding - scant spotting or profuse hemorrhage.

5. Often with persistent vaginal bleeding and resultant anemia.

6. Uterine size is large for dates in half of the cases.

7. Fetal heart tones and quickening are absent.

8. Severe and prolonged hyperemesis.

9. Grape-like clusters of tissue may be passed.

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Notes


10. Preeclampsia prior to 24 weeks GA is almost

pathognomonic.

C. Diagnosis:

1. Marked elevation in quantitative B-hCG levels.

2. Ultrasound typically reveals a classic “snowstorm”

appearance.

D. Treatment:

1. IV Oxytocin to control hemorrhage temporarily.

2. Dilation and curettage.

3. Must be carefully followed by a gynecologist.

Third Trimester Hemorrhage

I. INCIDENCE

A. Occurs in 4% of pregnancies.

B. Approximately 50% are significant.

II. DIFFERENTIAL DIAGNOSIS

A. Abruptio placenta – 1% incidence - see Section V.

B. Placenta previa – 0.5% incidence - see Sectopm VI.

C. Vasa previa:

1. Abnormal velamentous insertion of the fetal umbilical vessels

into the amniotic membranes.

2. Membrane rupture or fetal descent may thus cause fetal blood

loss.

3. Patient presents with painless vaginal bleeding.

4. Fetal distress is common.

5. Diagnosis possible with APT test:

a. Mix 1 part vaginal blood to 1 part 25% NaOH.

b. With fetal hemorrhage, no color reaction forms.

c. With maternal hemorrhage, light brown color forms.

D. Uterine rupture:

1. Incidence is 0.07%.

2. Significant, however, since responsible for 5% of maternal

deaths.

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Notes


3. Possible in any trimester.

4. Patient presents with massive painful hemorrhage, shock,

easily palpable fetal parts and regressive cervical dilation and

station.

5. Predisposing factors:

a. Uterine scars.

b. Cephalic-pelvic disproportion.

c. Oxytocin usage.

d. Grand multiparity.

e. Trauma.

E. Miscellaneous - @ 50% of third trimester hemorrhage:

1. Cervical effacement:

a. "Bloody show":

i. Small amount of blood-tinged mucous.

ii. Cervical canal mucous plug expulsion.

iii. Precedes labor by up to 72 hours.

2. Cervicitis or vaginitis - minimal blood.

3. Erosions or tumors or trauma to the birth canal.

III. INITIAL MANAGEMENT

A. ABCs:

1. Supplemental oxygen.

2. 2 or more large bore intravenous lines:

a. Consider blood transfusion for maternal shock.

b. Consider fresh frozen plasma if DIC exists.

c. Ensure early volume resuscitation:

i. Maternal blood volume increased up to 50% at term.

ii. Clinical evidence of hypovolemia may not be evident

until 30% of maternal blood volume is lost.

iii. Maternal physiology is maintained at the expense of

fetal circulation.

iv. Thus fetal distress (i.e., bradycardia) is often the

first detectable sign of impending maternal shock. 3. Place patient in the left lateral decubitus position:

a. Relieves venal caval compression.

b. May increase maternal cardiac output up to 30%.

4. Continuous cardiac monitoring of the mother.

5. Monitor fetal heart tones:

a. Normal range 120-160.

b. Fetal bradycardia is evidence of impending maternal

shock.

6. Consider pneumatic antishock garment:

a. Leg compartments inflated .

b. Contraindicated to inflate abdominal portion.

Page 363

Notes


7. Obtain rapid obstetrical consultation:

a. All patients with third trimester hemorrhage need

admission to an obstetrical unit for further evaluation and

monitoring.

b. Maternal instability and fetal distress may necessitate

emergency caesarean section.

IV. DIAGNOSIS

A. History:

1. Estimated date of confinement (EDC).

2. Gestational history:

a. Multiparous women with increased incidence of:

i. Placenta previa.

ii. Placenta abruption.

iii. Uterine rupture.

b. History of C-section? Increases risk of:

i. Uterine rupture.

ii. Placenta previa.

3. Previous history of placenta abruptio is a major risk factor for

recurrent placenta abruption.

4. Past medical history - hypertension, diabetes, renal failure, etc.

5. Complications during this pregnancy:

a. Preeclampsia.

b. Abdominal trauma.

c. Hypertension.

d. Prior bleeding episodes.

6. Amount and duration of bleeding.

7. Is the patient experiencing abdominal pain?

a. Placenta previa is a painless hemorrhage.

b. Placenta abruptio is usually painful hemorrhage.

c. Uterine rupture can be painful or relatively painless.

B. Physical examination:

1. Vital signs:

a. Narrowed pulse pressure.

b. Tilt test.

2. Fetal heart tones.

3. Abdominal examination:

a. Assess for tenderness:

i. Nontender - consider placenta previa.

ii. Tenderness noted:

Placenta abruptio.

Uterine rupture.

b. Assess fundal height.

c. Assess for uterine firmness and tenderness.

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Notes


d. Assess for uterine contraction.

4. Pelvic or rectal examination:

a. May dislodge the placenta, resulting in catastrophic

hemorrhage.

b. Thus a vaginal or rectal examination should NOT be

done on any patient with third trimester hemorrhage

unless:

i. Placenta previa has been definitively ruled out.

ii. The exam is performed by an obstetrician in an

operating suite with "double setup," in the event that

immediate caesarean delivery becomes necessary.

C. Diagnostic studies:

1. CBC.

2. DIC panel - PT, PTT, platelets, fibrinogen, fibrin split products

(FSP).

3. Baseline renal function studies.

4. Type and cross-match:

a. Consider transfusion if evidence of maternal shock.

b. Consider fresh frozen plasma transfusion if DIC ensues.

c. Rh status.

5. Pelvic ultrasound:

a. Only perform if mother is hemodynamically stable.

i. In the unstable patient, diagnosis should be made in

the operating suite with "double setup" by an

obstetrician.

b. Transabdominal approach only.

c. Useful to diagnose placenta previa:

i. TAS can reliably diagnose placenta previa in 93% to

98% of cases.

ii. False positive results:

Urinary bladder over distension.

Migrating placenta:

•• 5-30% incidence in second trimester.

•• Decreases drastically by term.

d. In placenta abruption:

i. Ultrasound able to definitively diagnose placenta

abruptio in less than 1% of cases.

ii. Retroplacental hemorrhage is difficult to distinguish

by current sonographic evaluation.

iii. Ultrasound's only role in abruption is in excluding

placenta previa.

V. ABRUPTIO PLACENTA

A. Premature separation of the placenta from the uterine myometrium:

Page 365

Notes


1. Separation may be partial or complete.

B. Painful hemorrhage:

1. 80% of present with painful dark red vaginal bleeding.

2. 20% of patients with abruptio have no apparent vaginal

bleeding.

3. Those with concealed retroplacental hemorrhage may present

with pelvic pain and rigidity, preterm labor, coagulopathy or

fetal distress.

4. Abdominal pain is usually present to some degrees.

5. The uterus is usually tender and hypertonic.

6. Shock is often out of proportion to the apparent blood loss.

C. Risk factors:

1. Previous history of abruptio:

a. 10 - 25% reoccurrence rate.

b. Probably secondary to underlying disease.

2. Underlying disease processes that predispose to placental

circulatory insufficiency:

a. Chronic hypertension.

b. Preeclampsia.

c. Diabetes mellitus.

d. Chronic renal disease.

3. States leading to vasoconstriction:

a. Maternal shock.

b. Abdominal trauma during last half of pregnancy.

c. Abrupt hypertension.

d. Venal caval compression.

D. Associated complications:

1. Preeclampsia.

2. DIC - Coagulopathy laboratory abnormalities seen in up to 1/3

of patients with abruption.

3. Acute renal failure:

a. 1-4 % of cases.

b. Incidence and severity directly correlated to the severity of

the abruption.

E. Definitive care:

1. Expectant in-patient management:

a. Immature fetus, mild hemorrhage.

b. Requires close maternal and fetal monitoring.

2. Vaginal delivery in selected cases.

3. Emergency caesarean section necessary if vaginal delivery is

Page 366

Notes


not imminent in the presence of any of the following:

a. Severe hemorrhage.

b. Fetal distress.

c. Maternal hemodynamic instability.

d. Tetonic uterine contractions.

e. Coagulopathy.

F. Mortality:

1. Maternal mortality rate is <1%.

2. Perinatal mortality rate approaches 35% - 50%.

VI. PLACENTA PREVIA

A. The covering of all or part of the internal cervical os by the placenta

- total, partial, marginal or low-lying.

B. Painless hemorrhage:

1. Classically presents as painless, bright red vaginal bleeding.

2. Bleeding tends to occur in late pregnancy due to mechanical

shearing of the placenta as lower uterine segment undergoes

effacement and dilatation.

3. Bleeding tends to reoccur and often worsens with each

episode. 4. Abdominal pain is generally absent.

5. The uterus is usually soft and nontender.

6. Shock is usually in proportion to the degree of hemorrhage.

C. Risk factors and associated complication:

1. Unlike abruptio, placenta previa occurs in the previously

healthy.

2. Risk factors for placenta previa include:

a. Multiple gestation.

b. Multiparity.

c. Previous scarring:

i. Prior caesarean section.

ii. Multiple elective abortions.

d. Previous placenta previa.

3. Placenta previa is associated with abnormal lie of the fetus.

D. Definitive care:

1. Diagnosis should be done by sonography if the patient is stable

and there is no evidence of impending fetal distress.

2. Otherwise, the diagnosis should be made by an obstetrician in

the operating suite.

Page 367

Notes


3. Expectant management if immature fetus and minor

hemorrhage.

4. Delivery by caesarean section if:

a. Severe hemorrhage.

b. Maternal instability.

c. Fetal distress.

d. Active labor develops.

E. Mortality:

1. Maternal mortality rate is <1%.

2. Perinatal mortality rate is 15% - 30%.

TABLE 1: Differentiating Placenta Abruptio from Placenta Previa in

Third Trimester Hemorrhage

PLACENTA ABRUPTIO PLACENTA PREVIA

INCIDENCE 1/100 1/200

28 wks to term 28 wks to term

multiparous multiparous

upper uterus lower uterus

prior history abnormal lie - 15%

low C-section (3x)

PAIN + none

BLEEDING +/- + bleeding

dark, like menses bright red blood

UTERUS hypertonic, tender soft, nontender

GIRTH may increase no change

FETUS +/- FHT +FHT

+/- palpable + palpable

PLACENTA not palpable palpable

SHOCK out of proportion if in proportion to

concealed blood loss

TOXEMIA + -

DIC + -

UA proteinuria, anuria normal

LABS decreased Hg/Hct decreased Hg/Hct

Page 368

Notes


increased WBC normal

decreased Fibrinogen normal

US +/- (1% accuracy) + (98% accuracy)

TREATMENT delivery expectant

VAG DELIVERY + -

MORTALITY fetal-up to 50% fetal-15%

maternal - very low maternal - 1/2 - 1%

Drugs and Radiation in Pregnancy

I. IONIZING RADIATION EXPOSURE IN PREGNANCY

A. Generally, a cumulative dosage of less than 5 rads has not been

associated with congenital anomalies or fetal growth retardation. It

is considered the upper limit of safe ionizing radiation exposure in

pregnancy.

TABLE 2

FETAL RADIATION DOSAGE IN

COMMON RADIOGRAPHIC STUDIES

X-RAY DOSAGE TO FETUS*

Skull series 4 millirads

Cervical spine series 1-10 millirads

Chest 8 millirads

Thoracic spine 9 millirads

Extremity series 2-3 millirads

Abdomen (KUB) 300 millirads

Pelvis 350 millirads

Hip 300 millirads

Lumbosacral spine 350 millirads

IVP 500 millirads

CT scan**

Pelvis 2000 millirads

2 inches from fetus 670 millirads



Annual environmental exposure*** 140 millirads

*with maternal abdomen and pelvis shielded when possible

Page 369

Notes


**fetal dose decreases by a factor of 3 (from the maximal dose of

2000) for every 2 inches the fetus is away from the nearest maternal

section scanned

***average annual individual exposure from cosmic irradiation and

other natural sources, for comparison

from Wyte, C: Diagnostic Modalities in Pregnancy. In: Doan-Wiggins,

L(ed): Emerg Med Clin N Amer, WB Saunders, 1994:12(1):9-43.

TABLE 3

GUIDELINES FOR X-RAY EVALUATION IN THE

PREGNANT PATIENT

* All fertile women should be considered to be possibly pregnant.

* A negative RIA or ELISA pregnancy test does not rule out pregnancy

< 3 weeks GA.

* Pregnant patients with negative pregnancy tests sensitive to 50

mIU/mL hCG or less, are at lower risk for teratogenic effects, than

later in the first trimester.

* Teratogenicity is more likely during the period of organogenesis (4

to 12 weeks GA).

* Radiation exposure should be limited when possible.

* The abdomen and pelvis of all fertile and pregnant patients should be

shielded.

* Filtration, collimation and avoidance of low-yield views.

* Elective x-rays should be postponed until after the first trimester.

* Necessary radiologic studies should never be withheld.

* Patients should be informed of the radiation risks involved whenever

possible.

* In pregnant patients who require extensive x-ray or CT scan studies,

radiation dosimetry calculations for subsequent genetic counseling may

be appropriate.

from Wyte, C: Diagnostic Modalities in Pregnancy. In: Doan-Wiggins,


II. MAGNETIC RESONANCE IMAGING (MRI) IN PREGNANCY

A. Uses in pregnancy:

1. Evaluate pelvic mass when ultrasound is nondiagnostic.

2. Real-time MRI:

a. Visualize fetal lung and kidneys.

b. Assess myelinization of the fetal brain.

c. Detect impaired placental perfusion.

3. Alternative to CT scan in studying non-pelvic pathology:

a. Lack of ionizing radiation.

b. Iodinated contrast agents not required.

Page 370

Notes


B. Safety issues of MRI:

1. No evidence to suggest MRI will have any harmful effect on

exposed fetus at the magnetic field strength and radio

frequency currently used for clinical diagnostic studies.

2. Local heating of tissue is a theoretical concern.

3. Gadolineum (Class C) should be avoided in all trimesters,

because of the long half life for the fetus

III. SONOGRAPHY

A. Ultrasound:

1. No ionizing radiation.

2. Potential adverse effects:

a. Heating of tissues.

b. Acoustic cavitation.

3. Usage in pregnancy considered safe if FDA guidelines

followed.

B. Color flow imaging:

1. Exposure virtually identical to that seen in gray-scale

sonography.

2. Poses no additional risk.

C. Pulsed Doppler:

1. Has potential to surpass maximum fetal energy exposure.

2. Additional guidelines are being proposed.

IV. DRUGS IN PREGNANCY

A. General:

1. Drugs should only be prescribed during pregnancy when there

is a clear medical need, as all drugs have the potential to affect

the developing fetus.

2. Untoward effects of neonatal drug exposure:

a. Teratogenicity - risk is greatest during the period of

organogenesis (4 to 12 weeks GA).

b. Toxicity.

3. FDA classification:

a. Class A - controlled studies have not demonstrated fetal

risk.

b. Class B:

i. Animal studies indicate no fetal risk, but no human

Page 371

Notes


studies to date.

ii. Animal studies show adverse effects, but human

studies do not.

c. Class C:

i. Animal studies indicate teratogenic effects; no human

studies to date.

ii. Or, no human or animal studies to date.

d. Class D - human studies show fetal risk, but benefits may

outweigh the risks.

e. Class X - fetal risk clearly outweighs any benefit.

B. Analgesics:

1. Acetaminophen – Class B:

a. Drug of choice during pregnancy:

i. Antipyretic.

ii. Analgesic.

b. Crosses placenta and secreted in breast milk but no

adverse effect known to fetus or infant.

2. Narcotics:

a. Meperidine (Demerol) and morphine relatively safe.

b. May cause CNS and respiratory depression in the newborn

if given to the mother in labor.

c. Chronic use during pregnancy may lead to withdrawal

symptoms in the newborn.

3. Nitrous oxide:

a. Not recommended in the first trimester of pregnancy.

b. Blocks folate and Vitamin B-12 metabolism.

c. Feto-toxic in long-term exposure in pregnant rats.

4. Salicylates and other nonsteroidal anti-inflammatory agents:

a. Not recommended in any trimester of pregnancy.

b. Increased incidence of abortions.

c. Platelet inhibitors.

d. Prostaglandin inhibitors:

i. Inhibit uterine contractions.

ii. Prolong labor.

iii. Associated with post-mature deliveries.

iv. May cause premature closure of the ductus arteriosus

in the fetus.

C. Antibiotics:

1. Aminoglycosides - Class C:

a. Not routinely recommended in pregnancy.

i. Crosses placenta poorly.

ii. BUT may cause fetal ototoxicity and nephrotoxicity.

b. Reserved for life-threatening gram negative infections.

2. Cephalosporins - Class B:

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Notes


a. Considered safe during all trimesters of pregnancy.

3. Chloramphenicol - Class C:

a. Contraindicated in third trimester pregnancy:

i. Newborns with suppressed metabolism.

ii. Gray baby syndrome is rate and dose-dependent.

4. Clindamycin - Class B:

a. No known adverse effects except do not use topical

vaginal cream formulations in pregnancy.

5. Erythromycin - Class B:

a. Erythromycin itself is safe during all trimesters of

pregnancy.

b. Estolate form (i.e., EES) should NOT be used –

hepatotoxicity.

c. Crosses placenta poorly - does not offer fetal therapy.

6. Nitroimidazoles:

a. Metronidazole:

i. Class B.

ii. Recommended in pregnancy for the treatment of

bacterial vaginosis or symptomatic Trichomonas.

b. Tinidazole:

i. Class C.

ii. Not recommended in pregnancy.

7. Nitrofurantoin:

a. Class B.

b. Safe to use in 2nd trimester (American College of

Obstetricians and Gynecologists, 2011).

c. Contraindicated in known G6PD deficiency and

controversial in 3rd

trimester:

i. Hemolytic anemia.

ii. Hyperbilirubinemia.

8. Penicillins - all Class B:

a. Natural penicillins and semisynthetics.

b. Considered safe in all trimesters of pregnancy.

c. Crosses placenta, therefore offers treatment of fetus also.

9. Quinolones - Class C:

a. Contraindicated in pregnancy.

b. Produce arthropathy in fetus.

10. Sulfonamides:

a. Dual classification:

i. Class B in first and second trimester.

ii. Class D - contraindicated in third trimester:

Competes with bilirubin for albumin binding

sites.

May cause kernicterus in neonates.

11. Tetracyclines - Class D:

a. Contraindicated in all trimesters of pregnancy.

b. Readily crosses the placenta.

c. Binds to developing fetal teeth and bone:

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Notes


i. Causes permanent discoloration of teeth.

ii. Causes long bone growth retardation.

d. Causes maternal hepatocellular necrosis.

12. Trimethoprim - Class C:

a. Contraindicated in first trimester - folate antagonist.

D. Anticoagulants:

1. Heparin:

a. Does not cross placenta due to its high molecular weight.

b. Negligible fetal effects.

c. May be reversed by protamine sulfate during labor.

2. Lovenox - Class B.

3. Warfarin (Coumadin) - Class X:

a. Contraindicated in 1st and 3rd trimester of pregnancy.

b. Readily crosses placenta.

c. Associated with congenital malformations in first

trimester.

d. Associated with third trimester maternal and fetal

hemorrhage.

E. Anticonvulsants:

1. The possible benefits of seizure control are thought to

outweigh potential teratogenic risks.

2. Acidosis and hypoxia during seizure are detrimental to fetus.

3. Epilepsy is associated with a two- to three-fold increase in

malformation rate:

a. Facial clefts are most common malformation.

b. Probably multifactorial.

c. Difficult to determine teratogenicity of anticonvulsants

since epilepsy itself produces adverse effects.

4. Usual anticonvulsant regimen maintained in patients.

5. Anticonvulsants considered RELATIVELY SAFE during

pregnancy:

a. Phenytoin (Dilantin) - unsure how much phenytoin versus

epilepsy is responsible for the fetal hydantoin syndrome.

b. Phenobarbital:

i. Newborn withdrawal has been described.

ii. Newborn withdrawal not associated with seizures.

c. Carbamazepine (Tegretol).

d. Neurontin – Class C.

e. Infants born to mothers taking anticonvulsants are at

increased risk of clotting abnormalities:

i. Clotting studies should be performed.

ii. Vitamin K injection recommended.

6. Anticonvulsants generally contraindicated during pregnancy:

a. Trimethadione (Tridione) - fetal malformations and mental

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retardation.

b. Valproic acid (Depakene) - neural tube defects.

c. Topamax – Class D

7. Status epilepticus should be treated early and aggressively:

a. Diazepam (Valium), phenytoin and phenobarbital.

b. Consider lidocaine, magnesium sulfate.

c. Poor fetal prognosis.

F. Antiemetics:

1. 5-HT3 receptor antagonists:

a. Ondansetron (Zofran).

b. Class B.

2. Antihistamines:

a. Trimethobenzamide (Tigan).

b. No known teratogenicity.

3. Phenothiazines:

a. Prochlorperazine (Compazine) – Class C.

b. Slight risk of hypotension and lower placental perfusion.

c. Effective and probably safe.

G. Asthma medications:

1. Adrenergic agents:

a. Albuterol - Class C:

i. No adverse fetal effects to date.

ii. Probably safer than fetal risk due to maternal hypoxia.

iii. Aerosolized form preferred.

b. Epinephrine:

i. Associated with increased risk of fetal malformations.

ii. May still be safer than maternal hypoxia in a patient

unresponsive to inhaled Beta agonists.

c. Isoproterenol and Ephedrine - Class D - not generally

indicated.

d. Metaproterenol - Class C:

i. No adverse fetal effects in 25 years of clinical years.

ii. Teratogenic in high doses in rabbits.

iii. Aerosolized form preferred.

e. Terbutaline - Class B-Tocolytic agent - therefore avoid in

term pregnancy.

2. Cromolyn sodium - Class B - No known adverse effects to

date.

3. Steroids:

a. No adverse fetal effects known in humans.

b. Maternal side-effects unchanged by pregnancy.

c. Inhalation route may be preferred: Beclomethasone -

Class C.

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H. Cardiac drugs:

1. Antiarrhythmic agents:

a. Agents considered safe in pregnancy:

i. Atropine.

ii. Lidocaine - Class B.

iii. Procainamide - Class C.

iv. Quinidine - Class C.

b. Agents to avoid in pregnancy:

i. Phenytoin.

ii. Amiodarone - Class C/D.

2. Antihypertensive agents:

a. Hydralazine and Labetolol - drugs of first choice.

b. Drugs to be avoided if possible in pregnancy:

i. ACE inhibitors - Class D.

ii. Diuretic agents - Class C/D.

iii. Nitrates - Class C.

iv. Nitroprusside - Class C/D.

3. Digoxin - considered safe in pregnancy - Class C.

I. Psychotropic drugs:

1. Avoid whenever possible in first trimester pregnancy.

2. Lithium known to cause cardiac defects in first trimester

pregnancy.

J. Vaccinations:

1. Inactivated vaccines safe:

a. Rabies.

b. Tetanus.

c. Hepatitis B.

d. Polio.

e. HPV – Class B

2. Live attenuated virus NOT recommended in pregnancy:

a. MMR (mumps, measles, rubella).

b. Varicella.

c. Influenza (LAVE).

d. Smallpox.

K. Immunoglobulins considered safe:

1. Rabies.

2. Tetanus.

3. Hepatitis B.

4. Varicella zoster - should be given to a pregnant woman

exposed to chicken pox if serology titer is negative.

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Acute Appendicitis in Pregnancy

I. INCIDENCE

A. Occurs in 1/550 to 1/3000 pregnancies.

B. Gestation does not predispose to appendicitis.

C. Occurs at same rate as general population, but diagnosis more

difficult.

II. DIAGNOSIS

A. Increasingly difficult as pregnancy progresses.

B. Location of abdominal tenderness:

1. First trimester:

a. Begins as poorly defined pain in the periumbilical region.

b. Migrates to the right lower quadrant.

c. May be superior to McBurney's point in late 1st trimester.

2. Third trimester:

a. May remain more diffusely localized.

b. Or may be localized to right upper quadrant.

c. Appendix moves upward and outward toward the flank in

later pregnancy.

C. Anorexia:

1. Sensitive sign in normal appendicitis.

2. May be lacking in appendicitis in pregnancy.

D. Nausea and vomiting - may be less specific, because commonly

seen in first 14-16 weeks of normal pregnancy.

E. Leukocytosis - may be less specific, because commonly seen in

normal pregnancy also.

III. COMPLICATIONS

A. Increased rate of abortion and premature labor.

B. Rate increased even further if peritonitis develops.

C. As appendix moves upward and outward, there is an increased risk

of rupture as "walling off" the area of inflammation is less possible.

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D. Risk of complications is highest in third trimester of pregnancy.

IV. DIFFERENTIAL DIAGNOSIS

A. Acute pyelonephritis:

1. Most common misdiagnosis during late pregnancy.

2. Both pyelonephritis and appendicitis:

a. Fever and chills - fever tends to be higher in

pyelonephritis.

b. Flank pain - in later pregnancy.

c. Absence of peritoneal signs - in later pregnancy.

3. The diagnosis of pyelonephritis should be strongly doubted in

the absence of bacteriuria or significant pyuria (over 10 WBC

per HPF).

4. Ureteral irritation from appendiceal inflammation may lead to

mild degrees of pyuria (i.e., 5-10 WBC per HPF or less), but no

bacteriuria.

5. Pregnant women with pyelonephritis should be admitted for

intravenous antibiotic therapy. Lack of response over 24 to 48

hours demands consideration of possible appendicitis or other

disease process (pelvic or abdominal or renal abscess, etc.).

B. Cholecystitis and cholelithiasis:

1. Second most common cause of acute abdomen during

pregnancy.

2. Incidence is slightly elevated during pregnancy.

3. Presents with right upper quadrant abdominal pain,

exacerbation with meals, possible Murphy’s sign.

4. Although presents very similar as in non-pregnant patient,

appendicitis and pyelonephritis must be considered.

5. Diagnosis may be made by sonography and liver function

studies.

6. HIDA scan is usually not necessary.

7. Treatment is bed rest, bowel rest and analgesia.

8. Surgery when indicated, is preferably performed in the second

trimester, and avoided in the first and third trimesters.

V. TREATMENT OF APPENDICITIS IN PREGNANCY

A. Immediate surgical laparotomy in all three trimesters.

B. Delay can worsen the prognosis, due to increased risk of rupture.

C. Caesarean section is rarely ever indicated at the time of

appendectomy.

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1. Recent abdominal incision poses no increased risk during labor

and vaginal delivery.

2. Risk of prematurity is of concern.

Trauma in Pregnancy

I. GENERAL

A. Diagnosis:

1. 7% of pregnancies are complicated by trauma.

2. More common in the third trimester.

3. Trauma is the leading cause of non-obstetrical maternal deaths.

4. Motor vehicle collisions, falls, and assaults are most common

causes:

a. 31.5% of hospitalized, injured pregnant patients are

secondary to domestic violence.

b. Most common cause of fetal death is maternal death,

followed by placental abruption, severe maternal injury

and less commonly by direct fetal injury.

B. Pathophysiology:

1. Metabolic demands and oxygen consumption increases.

2. Tidal volume and minute ventilatory volume increase, causing

a physiologic respiratory alkalosis.

3. Decreased gastric motility and increased laxity of the

gastroesophageal junction increases the risk of aspiration.

4. The bladder becomes intra-abdominal after 12 wks GA,

increasing the risk of injury.

5. Maternal blood volume increases:

a. Produces a physiologic anemia.

b. Hemorrhagic shock can be masked until 30-35% of

blood volume is depleted.

6. Normal cardiovascular changes:

a. Cardiac output is increased by 40%.

b. Pulse is increased by 20-30%.

c. Mild decrease in blood pressure.

7. Enlarged uterus may obstruct the inferior vena cava when the

patient is supine, reducing venous return to the heart by up to

30%, therefore decreasing cardiac output by up to 28%.

C. Treatment:

1. Primary survey should be no different than the non-pregnant

patient:

a. Appropriate maternal resuscitation will help achieve best

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Notes


fetal outcome.

b. Airway/breathing.

c. Protect patent airway.

d. Supplemental oxygen.

2. Circulation:

a. Establish two large bore intravenous catheters.

b. Pulse and blood pressure may be unreliable.

c. Because of increased blood volume, may lose 1500 cc of

blood prior to signs of maternal shock.

d. Fetal bradycardia is the earliest sign of impending

maternal shock.

e. Decreased capillary refill, decreased urine output and

decreased pulse pressure also are useful in detecting

hypoperfusion.

f. Place in left lateral decubitus position (wedge under

right side if on a backboard)-may increase venous return

by up to 30%.

g. Mast trousers - controversial - do NOT inflate

intraabdominal compartment.

h. Consider transfusion of PRBC for maternal shock (O

negative).

i. Consider transfusion of FFP for DIC (abruption).

j. Continuous cardiac monitoring of mother.

k. Monitor fetal heart tones:

i. Normal = 120-160.

ii. Fetal bradycardia is the earliest sign of impending

maternal shock.

iii. If fetus is viable, continue monitoring as fetal demise

can occur later.

3. Nasogastric tube insertion to prevent aspiration.

4. Foley catheter insertion to monitor urinary output.

5. Secondary survey including vaginal speculum exam and

assessment for amniotic fluid:

a. Vaginal bleeding - seen in 80% of patients with placenta

abruption. May lose up to 2 liters of blood in the uterine

cavity in the 20% of patients with concealed hemorrhage.

b. Nitrazine pH paper B vaginal secretions have a pH of 5;

amniotic fluid has a pH of 7.

6. Abdominal exam is less reliable in later pregnancy due to the

blunted response to peritoneal irritation.

7. Uterine tenderness is often present in placenta abruption

and uterine rupture.

8. Tetanus toxoid and tetanus immune globulin as indicated.

9. RhoGAM B 300 ugh given to Rh negative women with < 30 cc

vaginal bleeding.

10. Kleihauer-Betke testing used to quantify amount of fetal-

maternal hemorrhage. An additional 300 ug RhoGAM is given

for each additional 30 ml of fetal blood detected.

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11. Necessary X-rays should not be withheld:

a. Shield fetus when possible.

b. Cervical spine, chest X-ray and pelvis films are all < 1 rad.

c. Low teratogenic risk when exposed to < 10 rads.

12. Ultrasound is safe and preferred to assess for intraperitoneal

hemorrhage during first half of pregnancy in a stable patient.

a. Used to rule out placenta previa in third trimester

hemorrhage.

13. CT scan of the abdomen/pelvis is 3-10 rads.

a. Preferred in second half of pregnancy to assess for

intraperitoneal and retroperitoneal hemorrhage in the

stable patient.

14. Diagnostic peritoneal lavage (DPL):

a. Open supraumbilical approach in the first half of

pregnancy.

b. Rarely if ever performed in second half of pregnancy.

15. Chest tubes should be placed 1-2 interspaces higher in the

pregnant patient secondary to diaphragmatic elevation.

16. Order basic lab studies as indicated:

a. Trauma panel.

b. Indirect Coombs test and Rh typing.

c. DIC panel.

d. Indication of fetal injury.

e. Suggests placental abruption, amniotic fluid embolization

or in utero fetal demise.

17. Cardiogenic (myocardial contusion) and neurogenic shock

(spinal injury) are the only indications for vasopressors as they

decrease uterine blood flow.

18. Tocolysis is indicated only after oxygen, hydration, left lateral

position in the absence of placental abruption, hemorrhage, and

hypoperfusion.

19. Obstetric and trauma surgery consults.

D. Disposition:

1. Transfer patient when appropriate: trauma ICU, neonatal ICU,

and burn units all improve outcomes.

2. All patients with significant trauma in pregnancy need to

transfer to L & D for a minimum of 4 hours of fetal

monitoring prior to discharge.

3. If discharged, patients must return for abdominal pain, leaking

fluid, vaginal bleeding, more than six uterine contractions per

hour, or less than three fetal movements in a 12-hour period.

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II. BLUNT TRAUMA

A. Diagnosis:

1. Maternal death most often due to head injury or hemorrhagic

shock.

2. Risk of splenic injury and retroperitoneal hematoma is

greater due to increased vascularity.

3. Incidence of bowel injury is decreased because of uterine

displacement.

4. Placental abruption occurs in 1-5% of minor trauma and

20-50% of major trauma:

a. Up to 2 liters of blood may be lost.

b. Signs include vaginal bleeding, uterine rigidity and

tenderness, cramping, hypoperfusion, and fetal

bradycardia.

c. <25% of placental separation associated with premature

labor.

d. >50% of placental separation results in nearly inevitable

fetal demise.

5. Uterine rupture occurs <1% of all injuries:

a. Fetal mortality @ 100% in uterine rupture caused by

trauma.

B. Pathophysiology:

1. Hemodynamic changes and organ displacement change the

presenting signs and symptom.

2. Uterine rupture and placental abruption are unique to

pregnancy trauma.

C. Treatment:

1. Maternal resuscitation.

2. Fetal monitoring.

D. Disposition:

1. Fetal monitoring even for minor trauma.

2. Referral as in non-pregnant patients.

III. PENETRATING TRAUMA

A. Pathophysiology:

1. Gunshot wounds are more common than knife wounds.

2. Penetrating trauma inflicted in the first half of pregnancy are

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Notes


more likely to cause maternal gastrointestinal and vascular

injuries.

3. Penetrating trauma inflicted in the second half of pregnancy

are more like to cause uterine and fetal injuries.

4. The fetus is injured in 60-70% of gunshot wounds.

5. Stab wounds have a better prognosis.

B. Diagnosis:

1. Surgical exploration in most cases. Diagnostic peritoneal

lavage, ultrasound, and CT scan can offer non-surgical options.

C. Treatment and disposition:

1. Most require exploratory laparotomy.

IV. DOMESTIC VIOLENCE

A. 0.9% to 20.1% of pregnant women are victims of abuse.

B. Worsens as the pregnancy progresses.

C. Associated with low birth weights and drug/alcohol abuse.

Perimortem Cesarean Section

I. GENERAL

A. C-section indications:

1. Mother is in a state of cardiac arrest and does not respond

within four minutes to resuscitative measures.

2. Identify fetal heart tones.

3. Identify potential fetal viability - gestational age estimated >23

weeks .

4. Survival at 22 weeks is 0%, 26 weeks is 54.7%, and 98.7% at

34 weeks.

B. Procedure:

1. Midline vertical incision from the upper uterine segment to the

symphysis pubis.

2. Retract abdominal wall and bladder.

3. Vertical incision through lower uterine segment.

4. Extend incision vertically with scissors, using second hand as a

shield for the fetus.

5. Deliver infant through the incision.

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6. Vigorous resuscitation of the infant should be anticipated.

7. Resume maternal resuscitative efforts post delivery.

C. Prognosis:

1. Infant survival is 10-40%.

2. Survival dependent on gestational age, birth weight, time from

maternal death to delivery and presence of maternal CPR.

3. Good prognosis if time from maternal death to deliver < 5

minutes.

4. No reported survival if >25 min from maternal death to

delivery.

5. Rare maternal survival reported after delivery.

Emergency Delivery

I. METHODS FOR EMERGENCY DELIVERY

A. Mechanism of vertex delivery:

1. Follows 7 cardinal movements:

a. Engagement - biparietal diameter of fetal head passes

through pelvic inlet:

i. Occurs during labor – multiparous.

ii. Occurs in last two weeks of pregnancy – nulliparous.

b. Flexion of infant’s head.

c. Descent.

d. Internal rotation.

e. Extension of head:

i. Occurs when head reaches the vulva.

ii. Head is delivered when full extension occurs.

f. External rotation:

i. Brings shoulders into anterior-posterior plane.

g. Expulsion:

i. Delivery of shoulders and then remainder of body.

2. Controlled technique is essential.

B. Technique for vertex delivery:

1. Modified Ritgin maneuver after crowning:

a. Exert gentle upward pressure to the fetal head with gloved

hand covered by a sterile towel.

b. Simultaneously exert pressure superiorly on the infant’s

occiput.

c. This allows more control of the delivery of the head, thus

reducing maternal injury.

2. Assess for loops of cord around infant’s neck.

3. Free such loops if found after delivery of the head and prior to

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Notes


delivery of the shoulders.

4. Bulb suction infant’s nares and oropharynx at the perineum.

5. If meconium present, intubation and tracheal suction

indicated post delivery.

6. Delivery of shoulders.

7. Usually occurs spontaneously:

a. May exert gentle downward traction on infant’s head to

ease delivery of the anterior shoulder.

b. Then gentle upward traction on head to aid delivery of

posterior shoulder.

8. Remainder of delivery follows rapidly.

9. Double clamp cord and cut in between clamps.

10. Infants are slippery until cleansed:

a. Rest infant’s head in your antecubital fossa.

b. While hooking hand around one of the infant’s legs.

11. Dry off infant and warm:

a. Isolette when possible.

b. Warm blankets, maternal heat until incubator available.

12. Delivery of placenta:

a. Separation of placenta occurs within 1-5 minutes:

i. Uterus changes from discoid to globular and firmer.

ii. Often see a gush of blood.

iii. Umbilical cord protrudes out of the vagina further.

b. Gentle, steady umbilical traction while lifting uterus

cephalad with the abdominal hand until placenta at

introitus.

c. Remove placenta from the vagina by lifting the cord up.

d. Examine placenta for completeness and send to path lab.

13. Post-delivery:

a. Gentle fundal massage.

b. Oxytocin 20 IU in 1 liter crystalloid:

i. Infuse at rate of 10 ml/minute until uterus

contracted.

ii. Then reduce rate to 1-2 ml/min.

c. 5-10 IU Oxytocin may be given IM if no venous access.

d. Methylergonovine maleate (Methergine) - 0.2 mg IM.

II. DYSTOCIA (DIFFICULT LABOR)

A. Precipitous labor:

1. Extremely rapid, tumultuous labor and delivery.

2. Complications include:

a. Uterine rupture.

b. Lacerations of the cervix, vagina, vulva or perineum.

c. Amniotic fluid embolism – rare.

d. Postpartum hemorrhage.

e. Fetal distress - tumultuous uterine contractions prevent

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Notes


adequate uterine blood flow.

f. Fetal intracranial trauma.

3. Management:

a. Try to keep as controlled as possible:

i. Modified Ritgin maneuver for delivery of head.

ii. Check for nuchal chord.

iii. Attempt to suction nares and mouth at perineum.

b. Do NOT attempt to delay delivery by holding the baby's

head back or other physical maneuvers.

B. Shoulder dystocia:

1. Impaction of the shoulder in the pelvic canal, halting the

progression of infant delivery after delivery of the head.

2. Incidence is 0.15%.

3. Incidence increases in post-term or >4000 gram infants (1.7%).

4. Suspect shoulder dystocia if fetal head "retracts" during

delivery.

5. Treatment:

a. Large mediolateral episiotomy.

b. Adequate anesthesia.

c. Suction the infant's mouth and nose.

d. Woods "screw" maneuver - apply pressure to the infant's

posterior scapula to rotate upward. The posterior shoulder

then passes beneath the symphysis and is delivered as an

anterior shoulder.

e. If unsuccessful, sweep the posterior arm across the infant's

chest and deliver it. This rotates the shoulder girdle.

C. Breech presentation:

1. Incidence is 3% to 4%.

2. Incidence increased in prematurity, grand multiparity, multiple

gestations, uterine and congenital abnormalities.

3. Complications:

a. Increased perinatal morbidity and mortality:

i. 12-fold increase in mortality rate (versus vertex birth).

ii. Intracranial hemorrhage is most common cause of

infant death. Also spinal cord, liver, adrenal glands

and spleen.

b. Prematurity.

c. Prolapsed cord - especially in footling breaches (11%).

d. Placenta previa.

4. Types:

a. Frank breech - feet lie in close proximity to head - most

common (legs flexed at the hips and extended at the

knees).

b. Complete breech - one or both knees are flexed.

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Notes


c. Footling (incomplete) breech - a foot or knee is lowest in

the birth canal.

5. In breech delivery, successive infant parts become harder to

deliver (opposite of that seen with vertex deliveries).

6. Management:

a. Caesarean section preferred - decreased morbidity and

mortality.

b. Partial or total breech extraction usually necessary in

vaginal deliveries.

III. FETAL DISTRESS IN ACTIVE LABOR

A. Evaluate:

1. Fetal heart rate:

a. Hand-held Doppler.

b. Normal baseline at term is 120-160 beats per minute.

2. Fetal heart rate response to palpable maternal contractions -

uses principles used in formal cardiotopography.

3. Evidence of fetal distress:

a. Baseline fetal bradycardia (heart rate of 110 bpm or

less).

b. Late or variable decelerations:

i. Late decelerations:

Represents uteroplacental insufficiency.

Fetal heart rate drops as contraction intensity

peaks. Recovery to baseline heart rate does not

occur until after the contraction is over.

ii. Variable decelerations:

Represents cord compression.

Deceleration of fetal heart rate occurs but without

correlation to the timing of contractions.

4. Early decelerations occur early during the contraction and are

merely in response to fetal head compression during

contractions. Occasionally they represent compression of the

umbilical cord.

B. Management:


2. Place mother in left lateral decubitus position.

a. Displaces uterus away from the inferior vena cava.

b. This increases maternal venous return, which will then

increase placental perfusion.

3. Rule out prolapsed umbilical cord by vaginal exam.

4. Emergency obstetrical consultation.

5. Definitive therapy is delivery, possibly by caesarean section.

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Notes


IV. PROLAPSED UMBILICAL CORD

A. Definition:

1. Rupture of membranes with obvious prolapse of cord through

the cervix.

2. Concealed prolapse - cord lies along side or in front of

presenting fetal part with or without ruptured membranes.

B. Pathophysiology:

1. Incidence is 3-6 per 1000 deliveries.

2. Associated with prematurity, abnormal presentation, multiple

gestation, hydramnios and grand multiparity.

C. Clinical presentation:

1. Usually membranes rupture first.

2. Patient reports feeling something in or coming out of their

vagina.

3. Patient may or may not be in active labor.

4. Umbilical cord may be visualized at the introitus.

5. Umbilical cord may be palpable on digital exam.

6. If any doubt, do speculum exam.

D. Treatment:

1. Place mother in left lateral knee-chest or deep

Trendelenburg position.


3. Manually displace uterus to left using abdominal hand.

4. Apply continuous upward digital pressure through the vagina

on the presenting fetal part while rushing patient up to the

OR.

5. Definitive treatment is delivery, usually by caesarean section.

V. PREMATURE RUPTURE OF MEMBRANES

A. General:

1. Definition - leakage of amniotic fluid prior to the onset of

labor.

2. Incidence:

a. Normally rupture of membranes occurs during active

labor.

b. In 10% of cases it occurs prior to the onset of labor.

3. Etiology – unknown.

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Notes


B. Complications:

1. Intrauterine infection - risk increases if greater than 24 hours

elapse between membrane rupture and delivery.

2. Precipitation of labor.

3. Increased incidence of cord prolapse, if presenting part is not

engaged in pelvis.

4. The closer to term the membranes rupture, the less serious the

complications are.

C. Diagnosis:

1. Patient may complain of a sudden gush of clear fluid.

2. Amniotic fluid may be present at the cervical os or vaginal

fornix.

3. Nitrazine paper:

a. Vaginal secretions with pH of 4.5 to 5.5 - paper stays

yellow.

b. Amniotic fluid with pH of 7 to 7.5 - turns paper blue.

c. Blood gives false positive result (pH 7.4) - turns paper

blue.

4. Ferning:

a. Amniotic fluid with high sodium chloride content.

b. Blood may interfere with ferning (false negative).

5. Heating:

a. Amniotic fluid turns white.

b. Cervical mucous turns brown.

6. Differentiate from "bloody show":

a. Extrusion of mucous plug which precedes labor.

b. Small amount of blood-tinged mucous.

c. Differentiate from third trimester hemorrhage.

D. Management:

1. Admit.

2. Minimize vaginal examinations:

a. Single sterile speculum exam to diagnose fluid.

b. Single sterile-gloved digital exam to rule out cord

prolapse.

3. Definitive care - dependent on gestational age:

a. >36 weeks - induction of labor within 12-24 hours.

b. <36 weeks:

i. Dependent on fetal maturity and evidence of infection.

ii. Conservative approach:

Admission with bedrest.

Glucocorticoids to promote fetal lung maturity

iii. Delivery - if infection occurs.

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Notes


OBSTETRICAL EMERGENCIES

PEARLS

1. Patients with history of tubal ligation or recent elective or spontaneous

abortion are at increased risk of death, because of failure to consider

ectopic pregnancy.

2. Patients who present with a "complete Ab" should have all tissue sent to

pathology to ensure presence of chorionic villi or fetal parts. 5% of

patients with ectopic pregnancy shed a decidual cast, which may be

misinterpreted for fetal tissue on gross inspection.

3. Cornual pregnancies may rupture later (14-16 weeks), while isthmic

pregnancies may rupture earlier (6-8 weeks) than the classic 8-10

weeks.

4. The physical examination, including pelvic exam, is quite unreliable in

the diagnosis of ectopic pregnancy. The absence of an adnexal mass in

particular should not lessen one's suspicion for ectopic pregnancy.

5. Clinical findings consistent with ectopic pregnancy should outweigh

any single negative test result.

6. Clinical distinction between complete and incomplete abortion may be

insufficient.

7. Any cause of first trimester hemorrhage may result in Rho(D)

sensitization in the Rho(D) negative woman.

8. Unrelenting abdominal pain or hemorrhage after passage of tissue is

indicative of incomplete abortion, and further therapy or observation is

required.

9. Fetal heart tones are often detected at ten weeks by hand-held Doppler

10. Beta-HCG may be detected in the maternal serum as early as 8-9 days

after fertilization.

11. HCG levels peak approximately 65 days after conception at about

50,000 mIU/ml.

12. Toxemia is most likely due to arteriolar vasospasm secondary to an

imbalance between prostaglandin (PG'2) and thromboxane (TxA2).

13. Preeclampsia is diagnosed usually after 20 weeks gestation and should

include hypertension (acute) with proteinuria.

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14. Eclampsia criteria include preeclampsia plus convulsions and/or coma.

15. The two types of therapy for preeclampsia are delivery (the only definite

form) and expectant (may be justified if immature fetus).

16. The two most common complications with expectant management of a

severely preeclamptic patient are abruption (22%) and

thrombocytopenia (20%).

17. MgSO4 is the pharmacologic mainstay for seizure prophylaxis in

preeclampsia.

18. All antihypertensive agents also lower placental perfusion.

19. Hydralazine (5 mg IVP increments) is still the antihypertensive of

choice since it probably lowers placental perfusion the least.

20. Pelvic exam stimulation can induce convulsions in a preeclamptic

patient.

21. Ectopic pregnancy may occur even in absence of history of amenorrhea.

22. Some degree of abdominal and vaginal/cervical tenderness is present in

75% of ectopic pregnancies.

23. Abruption placenta and placenta previa are the major causes of third

trimester bleeding.

24. Abruptions often present with vaginal bleeding, a board-like uterus,

uterine tenderness, and varying levels of shock.

25. Advancing age and multiparity are associated with increased incidence

of a placenta previa.

26. Placenta previa typically presents with painless vaginal bleeding after

the seventh month.

27. A speculum exam during third trimester bleeding may be indicated but

avoid bimanual and rectal exams especially with placenta previa.

Page 391

Notes


REFERENCES

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6. Burgher SW, Tandy TK, Dawdy MR. Transvaginal ultrasonography

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7. Chang J, Elam-Evans LD, Berg CJ, et al. Pregnancy-related mortality

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9. Dart RG, Kaplan B, Varaklis K. Predictive value of history and

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11. Duff P. Antibiotic selection in obstetric patients. Infect dis Clin

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13. Estroff JA. Emergency obstetric and gynecologic ultrasound. Radiol

clin North Am 1997 Jul:35(4):921-57.

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14. Goldman S, Wagner L. Radiologic management of abdominal trauma

in pregnancy. Am J Radiol 1996;166:763-7.

15. Hartwell EA. Use of Rh immune globulin: ASCP practice parameter.

American Society of Clinical Pathologists. Am J Clin Pathol 1998

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16. Haughey M, Calderon Y. Trauma in pregnancy: Optimizing maternal

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17. Henderson S, Mallon WK. Trauma in pregnancy. Emerg Med Clin

North Am 1998;16:209-28.

18. Hoxsey R, Rinehart JS. Infertility and subsequent pregnancy. Clin

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19. Lanoix R, Akkapeddi V, Goldfedder B. Perimortem Cesarean

section: Case reports and recommendations. Acad Emerg Med

1995;2:1063-7.

20. Lavery JP, Staten-McCormick M. Management of moderate to

severe trauma in pregnancy. Obstet Gynecol Clin North Am

1995;22:69-90.

21. Li TC. Recurrent miscarriage: principles of management. Hum

Reprod 1998 Feb:13(2):478-82.

22. Mason E, Rosene-Montella K, Powrie R. Medical problems during

pregnancy. Med Clin North Am 1998 Mar:82(2):249-69.

23. Mercer BM. Management of preterm premature rupture of the

membranes. Clin Obstet Gynecol 1998 Dec:41(4):870-82.

24. Morris JA, Rosenbower TJ, et al. Infant survival after Cesarean

section for trauma. Ann Surg 1996;223:481-91.

25. Morrison EH. Common peripartum emergencies. Am Fam Physician

1998 Nov 1:58(7):1593-604.

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obstetric tragedy. Obstet Gynecol Surv 1999 Feb:54(2):138-45.

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29. Peterson R, Gazmarian JA, et al. Violence and adverse pregnancy

outcomes: A review of the literature and directions for future

research. Am J Prev Med 1997;13:366-73.

30. Platt LD, Santulli T, Carlson DE, et al. Three-dimensional

ultrasonography in obstetrics and gynecology: preliminary

experience. Am J Obstet Gynecol 1998 June:178(6):1199-206.

31. Poole G, Martin J, Perry K, et al. Trauma in pregnancy: The role of

interpersonal violence. Am J Obstet Gynecol 1996;174:1873-6.

32. Portis R, Jacobs MA, Skerman JH, et al. HELLP syndrome

(hemolysis, elevated liver enzymes, and low platelets)

pathophysiology and anesthetic considerations. AANA J 1997

Feb:65(1):37-47.

33. Rai R, Regan L. Obstetric complications of antiphospholipid

antibodies. Curr Opin Obstet Gynecol 1997 Dec:9(6):387-90.

34. Rantala M, Makinen J. Tubal patency and fertility outcome after

expectant management of ectopic pregnancy. Fertil Steril 1997

Dec:68(6):1043-6.

35. Shalev E, Yarom I, Bustan M, et al. Transvaginal sonography as the

ultimate diagnostic tool for the management of ectopic pregnancy:

experience with 840 cases. Fertil Steril 1998 Jan:69(1):62-5.

36. Shih CH. Effect of emergency physician-performed pelvic

sonography on length of stay in the emergency department. Ann

Emerg Med 1997 March:29(3):348-51.

37. Tarraza HM, Moore RD. Gynecologic causes of the acute abdomen

and the acute abdomen in pregnancy. Surg Clin North Am 1997

Dec:77(6):1371-94.

38. Torry DS, Labarrere CA, McIntyre JA. Uteroplacental vascular

involvement in recurrent spontaneous abortion. Curr Opin Obstet

Gynecol 1998 Oct:10(5):379-82.

39. Walsh SW. Maternal-placental interactions of oxidative stress and

antioxidants in preeclampsia. Semin Reprod Endocrinol

1998:16(1):93-104.

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Obstetric concerns and treatment. Rheum Dis Clin North Am 1997

Feb:23(1):71-84.

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41. Wyte C: Hemorrhage in early pregnancy. In: Harwood-Nuss AL, et

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08/13

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Page 396

EENT/Ophthalmologic Emergencies

Marc Dorfman, MD, FACEP, MACP

Residency Director, Emergency Medicine Residency, Presence Resurrection Medical Center; Assistant

Clinical Professor, University of Illinois at Chicago

Page 397

Page 398

Notes


EENT/OPHTHALMOLOGIC EMERGENCIES

EENT Emergencies

I. THE EAR

A. Auricle:

1. Auricular hematoma:

a. Blunt trauma (classically in wrestlers and boxers).

b. Collection of blood between the perichondrium and the

cartilage.

c. Untreated may result in cartilage necrosis ("cauliflower" ear).

d. Diagnosis is clinical: pain, tenderness, swelling.

e. Treatment: drainage (I & D or needle aspiration), possible

anti-staphylococcus oral antibiotics, and a compressive

dressing. Should be reassessed in 24 hrs (re-accumulation).

2. Perichondritis and chondritis:

a. Infection of the auricular soft tissues.

b. Causes include uncontrolled otitis externa, auricular

hematoma, and auricular abrasions or lacerations.

c. TREATMENT IS ADMISSION FOR IV ANTIBIOTICS

broad coverage.

d. Pseudomonas aeruginosa - often causative agent.

3. Relapsing polychondritis:

a. Disease of unknown etiology which may mimic

perichondritis.

b. Characterized by inflammation and destruction of

cartilaginous tissues throughout the body.

c. Ears and nose are affected in 80-90% of patients, resulting in

floppy ears and a collapsed nose.

d. Labs - elevated erythrocyte sedimentation rate (ESR).

e. Diagnosis - auricle is inflamed but the lobe (i.e., no cartilage)

is spared. Confirmed by biopsy.

f. Treatment: steroids.

B. External auditory canal:

1. Otitis externa:

a. Infection of the auditory canal usually preceded by excessive

moisture, abrasions, or lacerations.

b. Presentation is pain and otorrhea.

c. The auditory canal is inflamed, swollen with tenderness in

auricular motion or tragal pressure.

d. Pseudomonas aeruginosa is common pathogen and less

commonly Staph. aureus.

e. Treatment is antibiotic/steroid combination ear drops

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Notes


(Cortisporin otic suspension) or an acetic acid solution

(Vosol).

f. If the canal is too swollen to allow penetration of antibiotics,

insert a compressed cellulose wick (i.e., “Pope” ear wick).

g. If cellulitis or periauricular adenopathy is present, the patient

should be started on an oral antibiotic.

2. Malignant otitis externa:

a. Immunocompromised patients (i.e., elderly, diabetic,

chemotherapy, high dose oral steroids) are at risk.

b. Most commonly pseudomonas aeruginosa.

c. Classical finding is granulation tissue on the floor of the

auditory canal at the bony-cartilage junction.

d. Facial nerve paralysis ensues as the disease reaches the

stylomastoid foramen. The disease can progress to multiple

cranial nerve involvement and meningitis.

e. Treatment may include immediate referral to an

otolaryngologist for surgical debridement and IV antibiotics.

3. Herpes zoster (Ramsay-Hunt Syndrome):

a. Infection of the geniculate ganglion resulting in painful

vesicular rash of the external auditory canal, auricle, and

surrounding area.

b. Usually an associated sensorineural hearing loss and facial

nerve paralysis.

c. Treatment is admission for IV antivirals.

4. Foreign body:

a. Most common source of unilateral hearing loss is cerumen

impaction.

b. Tools for removal include irrigation (e.g., partially

obstructing FB), alligator forceps, suction, hook, or cerumen

loop.

c. Do not irrigate vegetable matter because it may expand.

d. Live insects should be stupefied by either lidocaine or

mineral oil prior to removal.

e. Removal can be complicated by traumatic tympanic

membrane perforation and ossicular disruption; therefore,

proximal foreign bodies or those in uncooperative patients

should be removed under anesthesia by an otolaryngologist.

C. Tympanic membrane:

1. Perforation:

a. Caused by sharp instrumentation, blunt trauma, or change in

pressure.

b. Most injuries occur to the anterior inferior portion of the TM

(pars tensa).

c. Findings include bloody otorrhea and partial conductive

hearing loss. Weber tuning fork test will lateralize to the side

of injury.

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Notes


d. Clean injury - no antibiotic is required and 95% will heal

spontaneously.

e. Contaminated injuries require antibiotics (e.g., injury

sustained while water skiing).

f. Ossicular disruption is much more likely if the perforation is

in the posterior superior quadrant (pars flaccida). Associated

with pronounced hearing loss and possibly vertigo. They do

not require immediate repair.

g. Treatment is the same as above but otolaryngology referral is

mandatory.

h. With profound hearing loss (i.e., sensorineural) and vertigo, a

perilymph fistula should be suspected. This results from

displacement of the stapes from the oval window. This

condition requires immediate otolaryngology referral and

hospital admission.

2. Bullous myringitis:

a. Characterized by clear or hemorrhagic blebs on the TM.

b. Present with otalgia and usually have an associated URI.

c. Etiologies are viral (most common) and mycoplasma.

d. Treatment consists of systemic analgesics, macrolides.

D. Middle ear:

1. Acute suppurative otitis media:

a. Most common between 6-36 months of age.

b. Most common organisms in the pediatric age group are

Streptococcus pneumoniae (29%), Haemophilus influenzae-

nontypeable (23%), and Branhamella catarrhalis (13%).

c. Treatment – antibiotics (amoxicillin).

d. Most common complication is TM perforation, which usually

heals spontaneously.

e. Most serious complication is mastoiditis. Symptoms include

purulent otorrhea with TM perforation, sagging of the

posterior-superior external auditory canal, tenderness over the

mastoid prominence, and post-auricular fluctuance.

Radiography of the mastoid will reveal loss of normal air

cells and a “ground glass” appearance. Treatment is

admission for IV antibiotics and possible mastoidectomy.

Complications include extension to the inner ear, meningitis,

intracranial abscess, and lateral sinus thrombophlebitis.

2. Otitis media with effusion:

a. Presents with a dull, often retracted, poorly mobile tympanic

membrane. Bubbles or an air-fluid level may be visualized.

b. Pneumatic otoscopy confirms decreased TM mobility.

c. In children, it is usually associated with a URI, but allergy,

immunologic disorder, and submucosal cleft palate can also

be etiologies.

d. Antihistamines and decongestants have been demonstrated to

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Notes


be ineffective.

e. Although as many as 80% will spontaneously resolve within

2 months, most clinicians will treat with oral antibiotics. This

is supported by a 48-66% positive culture rate of middle ear

aspirates.

f. In adults, antihistamines and decongestants may be useful,

especially when associated with upper respiratory allergies.

g. Unilateral effusion may be the presenting sign of a

nasopharyngeal tumor.

3. Barotrauma:

a. Caused by rapid changes in atmospheric pressure such as in

flying or scuba diving.

b. Complains of a plugged feeling, pain, and decreased hearing.

c. Treatment consists of analgesics, oral decongestants, and

topical nasal spray decongestants.

d. Antibiotics are not helpful unless secondary infection is

suspected.

e. Severe cases may require myringotomy for symptomatic

relief.

E. Inner ear:

1. Presents with painless hearing loss developing over minutes to

hours.

a. Tinnitus and/or vertigo may be present.

b. The etiology for unilateral loss is viral neuritis, acoustic

neuroma, and Ménière’s disease.

c. The etiology of bilateral loss is ototoxic drugs

(aminoglycosides, erythromycin, vancomycin, antimalarials,

ASA, NSAIDs, furosemide, ethacrynic acid, cisplatin) and

loud noise.

d. Refer to an otolaryngologist.

2. Perilymph fistula:

a. Sudden onset hearing loss with tinnitus and severe vertigo is

indicative of a perilymph fistula.

b. The oval or round window is disrupted. This often occurs

while straining (i.e., heavy lifting, coughing, barotrauma

valsalva).

c. Pressure applied with a pneumatic otoscope will induce

vertigo, nystagmus, and sensorineural hearing loss. Straining

(coughing, sneezing, and lifting) exacerbates symptoms.

d. Treatment is usually conservative but surgical intervention

may be necessary.

3. Acoustic neuroma:

a. A rare cause of sensorineural hearing loss, the

cerebellopontine angle tumor (i.e., acoustic neuroma).

b. Symptoms include tinnitus followed by a gradual unilateral

hearing loss over many months to years.

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Notes


c. Late symptoms include a constant, mild vertigo and finally,

facial paralysis as the eighth and seventh cranial nerves,

respectively, are compressed in the internal auditory canal.

d. It should be suspected in an elderly patient with unilateral

sensorineural hearing loss.

4. Weber and Rinne tests:

a. Weber test:

i. 512 Hz tuning fork on the patient's forehead. With a

unilateral conductive hearing loss, the tone is perceived as

louder in the ear with the hearing loss.

ii. In a unilateral sensorineural hearing loss, the patient hears

the tone louder in the better ear.

b. Rinne test:

i. 256 Hz tuning fork placed on the patient’s mastoid and

then near the ear. The purpose is to compare loudness

between the fork placed on the skin over the mastoid

cortex (i.e., bone conduction) and the same fork held in

the air near the patient's ear canal (i.e., air conduction).

Normal is for air conduction to be louder than bone

conduction.

ii. Air conduction (AC) is louder than bone conduction

(BC). This is because the tympanic membrane and

ossicles amplify sound to the inner ear.

iii. With a conductive hearing loss (i.e., disruption of the TM

or ossicles), it will be heard louder over the mastoid

cortex.

iv. Sensorineural hearing loss - the Weber test lateralizes to

the better ear. The Rinne test will be louder in the air than

on the mastoid cortex.

EXAMPLES:

RIGHT SIDED UNILATERAL RIGHT SIDE UNILATERAL

CONDUCTIVE HEARING LOSS SENSORINEURAL

HEARING LOSS

Weber lateralizes to right Weber lateralizes to left

Rinne BC > AC Rinne AC > BC

II. NOSE AND PARANASAL SINUSES

A. Epistaxis:

1. Anterior most common due to erosion of superficial blood

vessels near the anterior end of the nasal septum (i.e., Little's

Area or Kiesselbach's Plexus).

2. Etiologies are as follows:

a. Local: i. Excessive dryness (mostly seen in winter months when

Page 403

Notes


there is low humidity).

ii. Digital trauma (i.e., nose picking) or nose blowing.

iii. Upper respiratory infection.

iv. Nasal trauma.

v. Nasal tumors.

vi. Nasal foreign bodies.

b. Systemic:

i. Hypertension.

ii. Arteriosclerosis.

iii. Blood dyscrasia.

iv. Coagulation disorder.

v. Drugs (i.e., aspirin, Coumadin).

vi. Hereditary hemorrhagic telangiectasia (Osler-Weber-

Rendu Syndrome).

Autosomal dominant trait characterized by multiple

mucosal (i.e., nose, oral cavity, stomach, colon, lungs)

and cutaneous telangiectasias.

3. If significant bleeding or a clotting disorder is suspected, then

laboratory studies (i.e., CBC, PT< PTT) are indicated.

4. Management of anterior nasal bleeds:

a. Patient in upright position and pinch nose for 10-15 minutes.

b. If continued bleeding, inspect nose and cauterize bleeding site

with silver nitrate or electrocautery.

c. If bleeding continues, pack the nose with Vaseline strip gauze

or a commercially available device.

5. Complications of anterior nasal packings include sinusitis, toxic

shock syndrome. Applying antibiotic ointment may prevent the

latter. Any patient with a packing for greater than 24 hours

should be put on oral antibiotics.

6. Posterior nasal bleeds are usually seen in the elderly, diagnosed

by failure of anterior nasal packs to control the hemorrhage.

Management is as follows:

a. Posterior nasal packing/intranasal balloon device or a Foley

catheter.

b. Admitted for humidified oxygen, analgesics, and antibiotics.

Posterior packing may lead to hypoxemia.

c. For uncontrollable hemorrhage, patients may require arterial

ligation or arteriography with embolization.

B. Nasal foreign bodies:

1. Most common in children and the mentally ill.

2. Patients present with a malodorous, purulent, unilateral

rhinorrhea.

3. Diagnosis is by inspection.

4. Treatment is removal with a nasal speculum, suction, forceps,

and/or ear curette or right-angled hook.

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Notes


C. SINUSITIS

1. Acute sinusitis (less than 3 weeks duration) most commonly

caused by Haemophilus influenzae, Streptococcus pneumoniae,

Group A Streptococcus, Staph. aureus, and Moraxella catarrhalis.

2. Chronic sinusitis (greater than 3 weeks) is more likely caused by

anaerobic bacteria, fungi, and mixed flora.

3. Complications of acute sinusitis result from extension of

infection into contiguous structures- bone, CNS, eye, or vascular

system.

4. Acute maxillary sinusitis - facial pain below the eyes, fever,

purulent nasal discharge, and upper dental pain. Pain is often

accentuated by leaning forward.

5. Acute ethmoid sinusitis is a disease of children, has a propensity

to spread into the orbit or CNS. Complications include

periorbital cellulitis, orbital abscess, meningitis, and cavernous

sinus thrombosis.

6. Cavernous sinus thrombosis: high fevers and appear toxic. There

is eyelid edema, proptosis, and chemosis third and sixth nerve

palsies, pupillary dysfunction, and papillary edema occur. CNS

symptoms include lethargy, coma, or seizures. Diagnosis may be

confirmed by CT scan or MRI.

7. Acute frontal sinusitis presents with frontal headache, fever,

purulent rhinorrhea. The frontal sinus begins to develop at ages

6-8 and may never develop in a small proportion of the

population. Therefore, frontal sinusitis is not seen in young

children. The infection may cause an osteitis of the anterior sinus

wall (Pott's puffy tumor).

8. Acute sphenoid sinusitis is an uncommon disease. Pain is poorly

localized to the vertex, occiput, or mastoid area of the skull.

9. CT of sinuses most sensitive for diagnosing sinus disease.

10. Treatment of acute sinusitis is topical nasal decongestants for 2-3

days, analgesics and oral decongestants. Antibiotics are indicated

for severe or persistent symptoms > 1 week.

11. Immunocompromised patients are prone to a highly invasive

rhinocerebral fungal sinusitis caused by the Phycomycetes class

of fungi (e.g., Mucormycosis).

a. Exam reveals nasopharyngeal necrosis, dark nasal discharge,

ocular findings, and cranial nerve palsies.

b. X-rays may show bony destruction.

III. SALIVARY GLANDS, OROPHARYNX, AND HYPOPHARYNX

A. Sialadenitis and sialolithiasis:

1. Sialadenitis refers to an infection of the salivary glands. It is

most commonly seen in debilitated patients (i.e., elderly,

dehydrated, diabetic).

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Notes


2. Presents as a painful swelling of either the submandibular gland

(most common), parotid.

3. Purulent discharge can often be seen from Stenson's or Wharton's

duct.

4. Staph. aureus is the most common pathogen.

5. Treatment is hydration and anti-staphylococcus oral antibiotics.

6. Mumps (paramyxovirus-most common viral pathogen) is usually

seen in children ages 5-15 but may be seen at any age.

a. Typically a prodrome of low grade fever, anorexia, malaise,

and headache, followed by bilateral diffuse, tender parotid

swelling.

b. The disease is usually mild, self-limited and treatment is

symptomatic.

c. Orchitis is a common complication in postpubertal men and

occurs with a 25% incidence.

d. Unilateral hearing loss may occur at all ages with a 4%

incidence. It is usually temporary.

e. Encephalitis is a rare complication.

7. Sialolithiasis - obstruction of a salivary duct by a stone.

a. 90% are located in Wharton’s duct, and 10% in Stenson’s.

b. X-ray may be diagnostic since the majority of stones are

radiopaque.

c. Most pass spontaneously and treatment is sialogogues (i.e.,

lemon drops) to induce salivation.

d. Antibiotics are reserved for secondary infection.

B. Pharyngitis:

1. Group A streptococci (i.e., Streptococcus pyogenes) accounts

for 20-30% of all cases of acute pharyngitis.

a. Treat because of risk of acute rheumatic fever.

b. Rapid strep detection tests have a false negative rate of up to

20%.

c. Antibiotic treatment is advocated for the following reasons:

i. Shortens the course of illness.

ii. Prevents suppurative complications (i.e., peritonsillar

abscess and cellulitis, retropharyngeal abscess).

iii. Prevents acute rheumatic fever (antibiotic treatment

within 9 days of symptomatic pharyngitis has been proven

effective).

iv. Acute glomerulonephritis is not prevented by treatment

with antibiotics.

2. Mononucleosis usually presents with exudative pharyngitis and

fever.

a. Splenomegaly occurs in approximately 50% of patients and

predisposes to splenic rupture.

b. Severe tonsillar swelling and exudate may rarely cause upper

airway obstruction.

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Notes


c. Diagnosis is confirmed by a positive monospot test.

d. Avoidance of contact sports is recommended when

splenomegaly is present.

3. Gonococcal pharyngitis occurs from orogenital contact.

a. It is usually asymptomatic but may present with tonsillar

swelling, erythema, and exudate with cervical lympenopathy.

b. Treatment – antibiotics.

4. Diphtheria caused by Corynebacterium diphtheriae.

a. An exudative pharyngitis with production of an exotoxin

affecting the myocardium and peripheral nervous system.

b. Characteristically, there is a blue-white membrane in the

pharynx composed of bacteria, fibrin, and necrotic debris.

c. Sudden airway obstruction may ensue from pharyngeal

swelling and copious exudate.

d. Mortality is directly related to delay in treatment with an

antitoxin.

e. Additional management includes antibiotics (i.e., penicillin or

erythromycin), and admission for cardiac monitoring.

C. Deep tissue infections:

1. Peritonsillar abscess is usually a complication of acute

suppurative tonsillitis.

a. Present with severe sore throat, fever, odynophagia and

drooling, "hot potato" voice, and variable degrees of trismus.

b. Treatment is IV antibiotics (i.e., penicillin) and drainage.

2. Ludwig's angina is a bilateral cellulitis of the floor of the mouth

involving the sublingual and submandibular spaces.

a. True emergency because rapidly progressive pharyngeal

swelling and displacement of the tongue leads to upper

airway obstruction.

b. Most common in elderly, debilitated men.

c. Usually caused by dental infections (lower molars) and

bacterial cultures grow mixed anaerobic and aerobic flora.

d. Diagnosis is made clinically by verifying brawny edema of

the submandibular area in a febrile patient with a protruding

elevated tongue and respiratory distress.

e. Treatment is IV antibiotics (clindamycin or cefoxitin or pen +

metronidazole) and the airway must be secured to prevent

pending obstruction.

3. Retropharyngeal abscess is most common in children under 3

years of age (6 months – 3 years).

a. Present with fever, neck pain, muffled voice, dysphagia and

snoring or stridorous breathing.

b. Patients prefer to lie supine; forced sitting can increase

airway compromise.

c. Diagnosis is confirmed by soft tissue X-ray of lateral neck.

d. CT scan may be helpful to assess the extent of involvement.

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Notes


e. Treatment is IV antibiotics, admission, and ENT referral for

surgical drainage.

IV. SUPRAGLOTTIC LARYNX

A. Adult epiglottitis (pediatric epiglottitis is discussed elsewhere):

1. In contrast to children, complete upper airway obstruction is

infrequent probably because of a larger, more rigid airway. Peak

incidences: age 20-40.

a. Should be suspected in cases where symptoms of sore throat

and dysphagia are out of proportion to findings on pharyngeal

examination.

b. Adults will often have prodrome of 1-2 day URI symptoms

c. H. influenzae is the most common pathogen, but adults have a

greater incidence of gram positive and Branhamella

catarrhalis infections.

d. Lateral soft tissue neck X-rays reveal classic finding of

“thumbprint-like” epiglottis

e. Airway equipment at bedside, ICU, immediate ENT consult,

antibiotics.

B. Croup:

1. Inflammation of the larynx and subglottic airway.

2. Parainfluenza virus most common. Also RSV, adenovirus.

3. Children ages 3 to 36 months. Rare after age six.

4. Treatment - steroids, humidified oxygen (warm vs. cool), racemic

epinephrine.

5. A randomized trial of a single dose of oral dexamethasone for

mild croup

6. For children with “mild” croup, use of a single dose of

dexamethasone (0.6mg/kg) results in significant benefits,

including being less likely to return for croup problems within

seven days.

V. DENTAL EMERGENCIES

A. Nontraumatic:

1. Dental caries:

a. Most common cause of odontogenic pain.

b. Tooth decay should be evident on examination.

c. Treatment: analgesics (or nerve block), antibiotics and

referral to a dentist.

2. Alveolar osteitis (dry socket):

a. Severe pain associated with a foul order and taste in the

mouth two to three days after an extraction.

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Notes


b. Cause is loss of the healing blood clot and localized

osteomyelitis.

c. Treatment - saline irrigation of the socket and application of a

medicated dental packing or iodoform gauze slightly

dampened with eugenol (oil of cloves).

d. Dental referral.

3. Periodontal abscess:

a. Swelling of the gingiva secondary to entrapment of plaque

and debris between the tooth and the gingiva.

b. Treatment consists of warm saline irrigation and antibiotics

(i.e., penicillin or tetracycline).

4. Acute necrotizing ulcerative gingivitis (ANUG or trench mouth,

Vincent angina - extension to the pharynx and tonsils):

a. An acute destructive disease in which bacteria invade non-

necrotic tissue.

b. Etiology is fusobacteria and spirochetes.

c. Gingiva appears edematous and fiery red; interdental papillae

are swollen and covered with a grayish pseudomembrane.

d. Accompanied by systemic illness including fever, malaise

and regional lymphadenopathy.

e. Treatment is antibiotics, warm saline rinses, systemic

analgesics, and application of topical local anesthetics such as

viscous lidocaine.

B. Traumatic:

1. Tooth fractures:

a. Ellis Class I fractures - only involve the enamel portion of the

tooth. This requires no treatment in the emergency

department.

b. Ellis Class II fractures - involve the enamel and the

underlying dentin. There may be sensitivity to heat, cold or

even air.

i. Under the age of 12, place dressing of a calcium

hydroxide paste on the exposed dentin, which is then

covered by dry gauze, aluminum foil or dental dry foil.

ii. > 12 years of age patients are advised to avoid extremes

in temperature and to seek dental care the following day.

c. Ellis Class III fractures - involve the enamel, dentin and pulp.

This is a true dental emergency and requires immediate

attention from a general dentist or endodontist. If a dentist is

not immediately available, cover the tooth with aluminum foil

or seal with “cavet,” a temporary root canal sealer.

2. Tooth avulsion:

a. Avulsed primary teeth in the pediatric population (i.e., ages 6

months to 5 years) are not replaced into their sockets.

b. One percentage point for successful replantation is lost each

minute that tooth is absent from the oral cavity.

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Notes


c. Do not handle any portion of the tooth other than the crown -

disrupts periodontal ligament need for reimplantation.

d. The tooth should be transported either in the patient’s mouth

or in a cold glass of milk.

e. Successful reimplantation is associated with survival of the

periodontal ligament fibers on the root.

f. Hank’s solution has been shown to maintain viability of the

periodontal ligaments for four to six hours or longer. If a

tooth has been avulsed for longer than 30 minutes, there is

evidence that soaking in Hank’s solution for 20 to 30 minutes

prior to replantation may improve survival.

g. The avulsed tooth should be replaced in the socket in the

emergency department and seen by dentist within 24 hours

for stabilization.

3. Temporomandibular joint dislocation:

a. Occur secondary to yawning, laughter, or trauma.

b. If unilateral, the jaw deviates to the opposite side.

c. To reduce, operator must overcome masseter contraction.

d. Post reduction, avoid extreme opening of mandible, laughing

or yawning. Soft diet for 1 week, warm backs, NSAIDs.

e. Patients with chronic dislocations maybe helped with a

Barton bandage.

VI. VERTIGO

A. Vertigo is characterized by an illusion of motion where no motion

exists (i.e., spinning sensation, imbalance or sensation of being

pulled to one side or the other). Once it has been determined that the

“dizzy” patient has vertigo, the history and physical should focus on

differentiating central from peripheral etiologies.

Differentiating factors are as follows:

CENTRAL

PERIPHERAL

Vertigo

Mild/constant

Severe/intermittent

Nausea &

vomiting

Intermittent

Frequent

Hearing loss &

tinnitus

Absent

May be present

Nystagmus

Multidirectional, nonfatigable,

not positional, not inhibited by

ocular fixation, may be vertical

Unidirectional, fatigable,

horizontal or rotary vertical,

positional, inhibited by ocular

fixation, never vertical Neurological

symptoms

May be associated with ataxia,

diplopia, cranial nerve findings,

hemiparesis

None

Onset

Slow Sudden

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Notes


Etiologies Brainstem infarct or tumor

Cerebellar infarct or bleed

Vestibular neuronitis

Labyrinthitis

Perilymph fistula

Ménière’s disease

Benign positional vertigo

Drug effects

Posttraumatic vertigo

Acoustic neuroma

B. If the history and physical do not clearly differentiate a peripheral

etiology: CT scan.

C. Several features to remember are as follows:

1. Ménière’s disease or endolymphatic hydrops is characterized by

recurrent attacks of vertigo with a progressive, fluctuating

hearing loss. Tinnitus is usually present during attacks. ED

treatment consists of medications shown to inhibit vertigo (i.e.,

meclizine, Valium, droperidol).

2. Acute labyrinthitis is presumed viral but the etiology is often

unknown. The illness is self limited.

3. A perilymph fistula presents with severe vertigo and

sensorineural hearing loss. Straining (i.e., coughing, sneezing,

and lifting) exacerbates symptoms. Diagnosis can be presumed if

symptoms worsen with pneumatic otoscopy.

4. Posttraumatic vertigo is common following closed head trauma.

It is due to concussion of the labyrinth.

5. Benign positional vertigo is a self limited disease (i.e., few

weeks) seen most commonly in the elderly. Patients have brief,

repeated attacks of vertigo associated with movement or changes

in head position. There is no hearing loss or tinnitus. Treatment

is symptomatic and an exercise program designed to repetitively

induce symptoms may be helpful.

6. Central-Wallenberg Syndrome - infarct of brain stem (lateral

medullary). Symptoms include numbness, Horner’s, contralateral

loss of pain, temp.

7. Other central-vertebral basilar insufficiency - multiple sclerosis.

Ophthalmologic Emergencies

I. PHYSICAL EXAM

A. Visual acuity - best corrected response:

1. Pinhole can approximate prescriptive eyewear (object is centered

over visual axis through mid lens and to fovea) – squinting.

2. Snellen at 20 feet/Rosenbaum at 14 inches.

3. If necessary, document counting fingers (CF), hand motion

Page 411

Notes


(HM), or light perception (LP).

B. Pupils recall Marcus-Gunn pupil (afferent pupil defect) and Adies

pupil (syphilis pupil - one that "accommodates but does not react").

II. EYELID DISEASE

A. Blepharitis:

1. Inflammation of eyelids may be chronic.

a. Scaly, erythematous, greasy lid margins.

b. S. aureus most common agent.

c. Symptoms - pruritus, redness, irritation, AM crustiness.

2. Treatment:

a. Warm soaks/lid scrubs frequently (baby shampoo ideal).

b. May consider sulfacetamide drops or antibiotic ointment to

eyelid margins (erythromycin or bacitracin).

B. Hordeolum (sty):

1. Acute inflammation of lid margin. S. aureus most common.

a. Internal:

i. Infection meibomian gland.

b. External:

i. Eyelash follicle or lid margin tear gland.

2. Symptoms - redness, focal swelling with a tender nodule or

pustule on the eyelid usually close to the margin, pain.

3. Treatment:

a. Warm compresses.

b. Soaps.

c. Topical sulfa/erythromycin 7 days.

d. May need incision and drainage if no improvement.

C. Chalazion:

1. Chronic granulomatous inflammation of Zeis or Meibomian tear

gland.

2. Inflamed, nontender, lesion.

3. Commonly seen in patients with:

a. Blepharitis.

b. Rosacea.

4. Treatment:

a. Warm compresses and massage.

b. Incision and Curettage/ steroid injection by ophthalmologist.

c. If recurrent:

i. Sebaceous cell, basal cell or meibomian gland carcinoma.

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Notes


D. Dacryocystitis - acute infection of lacrimal sac, in infants and adults

> 40 years of age:

1. Painful, red, swollen below medial canthus.

2. Most commonly Staph. aureus, then staph. epidermidis, strep, H.

flu.

3. Referral to ophthalmology, warm soaks, and systemic broad

spectrum antibiotics (Augmentin), topical antibiotics.

E. Preseptal cellulitis:

1. Lid erythema, warmth, tenderness.

2. Absence of proptosis, restricted eye movement, pain with eye

movement - if any of these, think orbital cellulitis.

III. THE RED EYE

A. Painless:

1. Conjunctivitis - most common cause of red eye.

a. Definition - conjunctival inflammation which typically spares

the cornea.

b. Symptoms - itching, burning, tearing, F.B. sensation, gritty.

c. Signs - redness, exudate, chemosis, follicular hyperplasia

(cobblestoning), normal cornea, normal visual acuity.

d. Viral - most common of all conjunctivitis:

i. Initially unilateral (bilateral within 24-48 hours).

ii. Copious clear secretions.

iii. Contagious, viral prodrome, preauricular

lymphadenopathy.

iv. Agents – adenovirus is most common, Coxsackie,

Enterovirus.

Epidemic keratoconjunctivitis (EKC) differs in that

this may present with photophobia and corneal

involvement.

v. Treatment - cool compresses, antihistamine for pruritus.

e. Bacterial:

i. Similar to viral, discharge can be purulent, AM crust.

ii. Different from Blepharitis in discharge is continuous

through the day.

iii. Agents - Staph, Strep, H. flu, pneumococcus, Moraxella,

or mixed.

iv. Treatment:

Broad spectrum antibiotics drops every 2 hours;

ointment every 6 hours.

Local hygiene.

No steroids, no patching.

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Notes


v. Neisseria gonorrhoeae - real potential for vision loss:

Can ulcerate or perforate cornea; true ocular

emergency.

Adults - parenteral ceftriaxone and topical antibiotics.

Treat for concomitant Chlamydia infection; ocular

irrigation; consult ophthalmology; admit all but

mildest cases. Concurrent urethritis common.

vi. Neonatal (ophthalmia neonatorum) conjunctivitis within

first month of life. N. Gonorrhea first 2-4 days

(ceftriaxone). Chlamydia 5-13 days (topical

erythromycin).

vii. Chlamydial - not as serious as N. gon:

Erythromycin P.O. and topical for 14 days.

Maybe cause for refractory conjunctivitis, leading

cause of preventable blindness worldwide.

Must treat sexual contact(s).

viii. Allergic - chief complaint is itching:

Clear watery discharge with cobblestoning; bilateral.

Typically seasonal, environmental.

May see chemosis.

ix. Treatment:

Cold compresses.

Topical decongestant (naphazoline) and/or

antihistamine (pheniramine) - Naphcon A.

B. Painful:

1. Iritis - (AKA uveitis, iridocyclitis):

a. Definition - internal inflammation without infection.

b. Etiology - allergic, infectious, post-traumatic, foreign body,

most commonly idiopathic.

c. Symptoms - dull ocular pain, may or may not have blurred

vision, reddened eye, photophobia.

d. Signs - pupil constricted (secondary to spasm), injected

bulbar conjunctiva, perilimbal/ciliary flush, anterior amber

with flare and cell (F/C).

e. Clues – will have consensual photophobia, pain not relieved

with topical anesthetic.

f. Differentiate from acute glaucoma in that iritis has "normal"

cornea, constricted to mid-range pupil, and normal intraocular

pressure.

g. Treatment – cycloplegics such as homatropine, may use

steroids after consulting ophthalmology, referral.

2. Acute narrow angle glaucoma (ANAG):

a. Leading cause of blindness in the U.S.

b. Definition - acute flow obstruction at canal of Schlemm in

patients with congenital defect of angle or predisposed with

shallow anterior chamber.

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Notes


c. Symptoms - severe unilateral ocular pain, red eye, blurry

vision, photophobia, halos around lights, headache,

nausea/emesis, cephalgia, abdominal pain (systemic

symptoms often "cloud" syndrome).

d. Signs - corneal edema, ciliary flush, increased IOP (>40

mmHg), rock hard globe, mid-range pupil, sluggish or

nonreactive pupil, injected bulbar conjunctiva, decreased

visual acuity.

e. Treatment – EMERGENT consultation during treatment:

i. Constrict pupil (remove iris from meshwork) pilocarpine

2% 1 drop every 15 minutes for 2 hours.

ii. Decreased aqueous humor production:

Beta blockers – Timolol 0.5% 1 drop and repeat in

10 minutes (beware of cardiac and pulmonary

contraindications).

Acetazolamide (CAI - carbonic anhydrase inhibitor) -

Diamox – 500 mg IVPB.

Adrenergic-imodipine 0.1% drop.

iii. Hyperosmotics:

Glycerol 50% 1-1.5 mg/kg P.O. (dilute with juice and

remember diabetics), or

Mannitol 20% 1-2 gm/kg IV over 30 minutes

(beware of osmolarity).

iv. Antiemetics.

v. Consult ophthalmology for surgery - peripheral

iridectomy, laser iridotomy.

C. Corneal disorders:

1. Foreign body (FB):

a. Symptoms - history usually guides; burning, redness, tearing,

irritation.

b. Signs - may visualize in upper/lower lids, embedded within

cornea, or positive fluorescein staining; if none of the above,

visualize all eyelashes.

c. Removal – irrigation, spud, blade, needle, swab.

d. Rust ring – iron containing FB, can cause chronic irritation,

visual acuity disturbance, corneal staining, remove after 24

hours.

e. Refer deeply embedded FB, old FB, and large FBs over the

visual axis.

f. Antibiotics, analgesics, tetanus immunization and referral.

2. Corneal abrasion:

a. Symptoms similar to foreign body.

b. Normal exam unless abrasion over visual axis, positive

fluorescein.

c. Antibiotic, cycloplegics, topical anti-inflammatories,

analgesics, tetanus immunization, potential referral (“dirty”

Page 415

Notes


abrasions from human or animal causes may require more

aggressive therapy and referral).

d. Avoid eye patching.

3. Contact lens syndrome:

a. Very common.

b. Painful, red eye; may have iritis.

c. Usually not infected.

d. Injected conjunctiva with fluorescein positive keratopathy.

e. Stop lens usage, antibiotics and may need cycloplegic;

referral.

f. Ulcers almost invariably pseudomonas a. and require

ophthalmologic consultation and frequent antibiotics

(ciprofloxacin a good choice).

4. UV keratitis (welders, sunbathers, skiers, tanning booths, high

altitude):

a. Typically bilateral, painful, red eyes; usually presents 6-8

hours after incident.

b. Injected conjunctiva; decreased visual acuity, diffuse,

punctate keratopathy with fluorescein; possible iritis.

c. Antibiotics, analgesics, topical cycloplegic agent referral if

iritis.

d. Topical anesthetics unjustifiable - falsely protects and known

cellular toxin.

e. Oral pain management may be needed.

5. Viral corneal infection:

a. Herpes simplex infection:

i. May be primary outbreak or reactivation.

ii. Symptoms - foreign body sensation, tearing, photophobia,

pain.

iii. Signs - may have typical vesicles on lids, conjunctiva;

cornea may have dendritic or ulcerative process with

fluorescein uptake; decreased visual acuity if over visual

axis.

iv. Treatment – referral to ophthalmologist, topical antiviral

agents such as trifluridine or vidarabine, cycloplegics.

6. Herpes zoster ophthalmia - varicella virus:

a. Symptoms - paraesthesia, burning, pain, rash; most common

form of recurrent zoster.

b. Signs - vesicular eruptions along CN V1, unilateral

involvement, keratitis, scleritis, conjunctivitis, dendritic

defect, lesions to the tip of the nose (Hutchinson’s sign)

signal nasociliary nerve involvement and high likelihood of

ocular lesions.

c. Treatment:

i. Oral acyclovir or famciclovir.

ii. Topical steroids may decrease neuralgia but consult

ophthalmologist.

iii. Referral.

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Notes


7. Pterygium:

a. Fibrovascular tissue, usually wedged shaped.

b. Extends onto cornea.

c. Treatment - artificial tears, non-emergent referral.

D. Pupillary syndromes:

1. Horner’s Syndrome:

a. Ptosis.

b. Miosis.

c. Anhyrdosis.

d. Opiates, brain stem stoke.

2. Argyll Robertson:

a. Small irregular pupil.

b. Neurosyphilis.

c. Accommodates but doesn’t react.

3. Marcus Gunn:

a. Afferent pupillary defect.

i. Inadequate response to light in affected eye.

b. MS, optic neuritis, retinal artery/vein occlusion, globe retina

disease.

IV. OCULAR TRAUMA

A. Orbital fracture:

1. Blunt more common than penetrating trauma.

2. 10-25% have associated globe injury.

3. Blow-out fracture:

a. Floor and medial wall most susceptible.

b. Entrapment (fat, inferior rectus, and inferior oblique

muscles).

c. Hypesthesia ipsilateral cheek and lip, diplopia and limited

upward gaze.

d. Antibiotics only if fracture involves infected sinus.

e. Surgical repair if persistent diplopia, cosmetic.

f. Usually delayed 7-10 days.

4. Medial wall fractures-subcutaneous emphysema, ethmoid sinus,

epistaxis.

B. Retrobulbar hemorrhage:

1. Orbital hemorrhage in potential space surrounding globe:

a. May occlude central retinal artery (pressure phenomenon).

b. Clinically - proptosis, visual loss, increased IOP.

c. Diagnosis - CT scan.

d. Treatment - CAI, beta blockers, mannitol, lateral canthotomy,

immediate optho consult.

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Notes


C. Lids/conjunctival injury:

1. Lid injuries typically from penetrating trauma; most primarily

repaired but refer following:

a. Lid margin injuries - require multilayer closure and often

cosmetically poor result.

b. Canalicular involvement - medial 1/3 of lid (upper or lower)

can involve lacrimal system and may need stenting.

c. Levator/canthal tendon involvement - ptosis often results with

poor repair.

d. Puncture/laceration through orbital septum (fat protrusion in

wound) - risk of infection.

e. Rule out penetrating globe injury/ foreign body.

f. Laceration/avulsion - those with significant skin loss.

2. Conjunctival injuries:

a. Less than 1 cm left alone.

b. Repair those greater than 1 cm.

c. More important not to miss a foreign body or associated

globe injury.

D. Anterior segment injury:

1. Corneal laceration:

a. Symptoms - decreased vision, pain.

b. May have shallow anterior chamber, tear drop iris, leaky

aqueous humor, or prolapsed iris.

c. Treatment - stop further exam, rigid metal eye shield and

referral.

2. Scleral laceration/perforated globe:

a. True ocular emergency.

b. Blunt or penetrating trauma with significant force, commonly

located in inferior aspect.

c. Up to 20% of globe ruptures have no signs of perforation.

d. Tear drop pupil, bloody chemosis, decreased visual acuity,

flattening of anterior chamber, small fragments of iris at

wound edges on exam.

i. Seidel test – positive if fluorescein stain reveals efflux of

aqueous humor in “river like” pattern from laceration on

slit lamp exam.

e. Treatment:

i. Halt exam, no pressure to eye, metal eye shield, tetanus

immunization, parenteral antibiotics, immediate referral,

nothing topically.

f. Sympathetic ophthalmia:

i. Seen with severe injuries.

ii. Occurs in unaffected eye.

iii. Mechanism - autoimmune granulomatous reaction

Page 418

Notes


affecting contralateral eye forcing enucleation of injured

eye if vision is to be preserved.

3. Hyphema - anterior chamber hemorrhage:

a. Patient sitting up, blood layers and form meniscus.

b. Blunt much more common than penetrating.

c. 25-35% have an associated eye injury.

d. Symptoms - pain, photophobia, blurry vision best examined

in sitting/upright position.

e. Complications:

i. Rebleed in 2 to 5 days with worse prognosis.

ii. Corneal staining.

iii. Secondary glaucoma.

iv. Anterior and posterior synechia.

f. Treatment:

i. Small size, reliable patient outpatient, all others admitted.

ii. Analgesics but avoid salicylates/NSAIDs, platelet

inhibitors.

iii. Referral; may or may not hospitalize.

iv. Rest with head elevated 45º.

v. Cycloplegics, miotics, mydriatics, antifibrinolytics,

steroids.

vi. Sickle cell – beta blockers, alpha agonist, CAI.

4. Lens injury:

a. Dislocated/subluxed.

b. Invariably visual disturbance - monocular diplopia.

c. Iridodonesis - trembling of iris after rapid eye movements.

d. Blunt trauma, Marfans, syphilis.

e. Funduscopic exam different from contralateral eye, may be

anterior or posterior dislocation.

f. Immediate ophthalmology consult.

5. Pupil injury:

a. Traumatic mydriasis.

b. Often associated with blunt injury with selective neurapraxia

of parasympathetic fibers of CN III affecting constrictors

(hence dilated) and accommodation (hence visual

disturbance).

i. Note that mydriasis can imply:

Significant intracranial pathology - "blown pupil".

Atropine administration.

Accidental Neo-Synephrine administration when

vasoconstricting nasal mucosa prior to nasotracheal

intubation.

Can reverse mydriasis caused by intracranial mass

with pilocarpine; the same will not work initially for

a. and b. above.

Treatment - referral; typically spontaneously resolves

c. Traumatic miosis:

i. Selective neurapraxia to sympathetic fibers to pupil

Page 419

Notes


dilators (hence unopposed constriction); may see with

Horner's syndrome.

ii. Treatment - referral; typically spontaneously resolves.

6. Subconjunctival hemorrhage:

a. Very common - typically asymptomatic.

b. Can occur with minor (sneezing, screaming, Valsalva,

coughing) or major (globe rupture) trauma.

c. If history and physical examination dictate benign process,

then reassure that this entity will spontaneously resolve

within 10-14 days.

d. May have associated facial/lid petechia.

E. Posterior segment injury:

1. Intraocular foreign body:

a. History more helpful than physical examination.

b. Search for entry wound, i.e., grinding wheel, working with

metal.

c. X-rays, sonography, CT, MRI, dictated by suspicion, exam,

and type of FB.

d. Treatment, immediate referral, tetanus immunization, metal

shield, antibiotics.

2. Vitreous hemorrhage:

a. Blunt injury, diabetic retinopathy.

b. Symptoms – sudden painless unilateral loss of vision,

floaters, visual disturbance.

c. Signs - visual acuity deficit, may see hemorrhage.

d. Treatment - rest, head elevation, immediate referral.

3. Preretinal, superficial retinal, and/or chorioretinal injury:

a. Shaken baby syndrome.

b. Retinal - tear/detachment.

c. Treatment - rest, referral.

4. Complications:

a. Infection.

b. Ulcerations.

c. Endopthalmitis - infection of deep eye structure, pain,

decreased visual acuity.

i. Treatment - intraocular and systemic antibiotic.

d. Sympathetic opthalmia.

V. SUDDEN VISION LOSS

A. Trauma (see IX A-D).

B. Vascular:

1. Central retinal artery occlusion (CRAO):

a. Symptoms - sudden, painless, unilateral vision loss.

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Notes


b. Risks - carotid artery disease, sickle cell, acute glaucoma,

retrobulbar hemorrhage, exophthalmos.

c. Signs:

i. Severe decreased visual acuity.

ii. Afferent pupil defect.

iii. Optic disk pallor, macular edema, bloodless arterioles,

dark veins, "cherry-red spot" (choroidal vessels supply

macula).

iv. Treatment - (ischemic time 30-60 minutes) goal is to

restore retinal artery blood flow by dislodging clot,

dilating the artery and lowering IOP.

Immediate referral:

•• Vigorous massage (5 second intervals).

•• Enhance vasodilation – carbogen or paper bag

breathing (beware of hypoxemia with latter).

•• Acetazolamide and a topical β blocker.

Surgical paracentesis of anterior chamber.

2. Central retinal vein occlusion (CRVO):

a. Symptoms – sudden, painless, unilateral vision loss typically

less severe than CRAO.

b. Etiology – thrombosis of the central retinal vein.

c. Signs:

i. Decreased visual acuity:

"Blood and thunder" retina, engorged veins, retinal

hemorrhage.

Differential diagnosis includes pseudotumor cerebri

and papilledema.

d. Treatment - referral, treat underlying cause, poor prognosis.

3. Miscellaneous - TIAs, ocular migraine, vitreous hemorrhage.

C. Idiopathic:

1. Retinal detachment:

a. Symptoms - painless "veil over eyes" or "drawn curtain”; can

have prodrome of floaters, cloudy vision, flashing lights,

spider webs; typically >50 year old patients.

b. Etiology - unknown cause for separation between sensory and

pigmented retina.

c. Signs:

i. Decreased visual acuity if macula involved.

ii. Detached undulating gray retina.

iii. Tear, hole, bulla, fold.

d. Treatment – immediate referral, rest; spontaneous

reattachment rare.

2. Hysterical blindness:

a. Normal exam except for complaint.

b. Occipital CVA only confounder but differentiate with

optokinetic reflex.

Page 421

Notes


c. A normal pupillary reaction, funduscopic exam, and lack of

afferent pupillary defect is very suggestive of hysteria/

conversion disorder or malingering.

D. Inflammatory:

1. Optic neuritis:

a. Symptoms - sudden, unilateral vision loss, can have pain with

EOM.

b. Signs - loss of central retinal vision with intact peripheral

vision (central scotomata); decreased color vision; normal

exam - "the patient sees nothing and the doctor sees

nothing."

c. An association with multiple sclerosis; 25-65% will develop

MS.

d. Treatment – emergent referral, systemic and/or retrobulbar

steroids.

2. Temporal (giant cell) arteritis:

a. Vasculitis of medium and large arteries that can cause optic

nerve infarction and permanent vision loss, female

predominance, most > age 50.

b. Symptoms - unilateral, boring pain; tenderness; may have

sudden onset; may have flu-like prodrome consistent with

polymyalgia rheumatic; visual disturbance that progresses.

c. Signs - erythema, swelling, tenderness, and nodularity of

artery involved; funduscopic exam can reveal pallor,

hemorrhage, exudates; iritis; ESR > 70; temporal artery

biopsy for diagnosis.

d. Treatment - referral; high dose systemic steroids.

VI. OCULAR BURNS

A. Acid (the only eye emergency requiring treatment prior to visual

acuity evaluation):

1. Coagulation necrosis of epithelium and usually self limiting.

2. Less devastating than alkaline burns.

3. Treatment - "irrigation, irrigation, irrigation;" fluorescein

staining, cycloplegics, +/- antibiotics, +/- referral, reassess pH

(Nitrazine paper), no neutralization.

B. Alkaline:

1. Drain cleaners, chemical detergents, fertilizers, ammonia

derivatives.

2. Initially conjunctivitis but liquefaction necrosis continues burn

process until alkali removed.

3. Signs - perilimbal blanching and corneal edema are poor

Page 422

Notes


prognostic indicators.

4. Treatment - copious irrigation; referral mandatory if any signs if

injury from alkaline burn; reassess pH; no neutralization.

5. Long term complications-perforation, adhesions, glaucoma,

cataracts.

C. Thermal:

1. Rare due to Bell's phenomenon - in response to stimulus, eyes

blink and roll up. Assess lid closure - if cornea is exposed, it must

be kept moist.

Page 423

Notes


EENT/OPHTHALMOLOGIC EMERGENCIES

PEARLS

EENT Emergencies

1. An auricular hematoma must be emergently drained and a compressive

dressing applied to avoid the complication of “cauliflower ear.”

2. The most common pathogen in otitis externa is Pseudomonas aeruginosa

followed by Staphylococcus aureus.

3. Relapsing polychondritis is an autoimmune inflammatory disease of

cartilage. When the auricle is affected, the ear lobe is spared since it

does not have cartilage.

4. The classic physical finding in malignant otitis externa is granulation

tissue on the floor of the auditory canal at the bone-cartilage junction.

5. Malignant otitis externa is an osteomyelitis seen in immunocompromised

patients requiring surgical debridement and IV antibiotics covering

Pseudomonas.

6. Herpes zoster of the geniculate ganglion (Ramsay-Hunt Syndrome) may

present with painful rash, hearing loss, and facial nerve paralysis.

7. Traumatic perforation of the tympanic membrane will heal

spontaneously in 95% of patients within 3 months. Profound hearing

loss or vertigo should raise suspicion of ossicular disruption and should

be referred to ENT.

8. The most common pathogen in otitis media of children is Strep.

pneumoniae followed by H. influenzae.

9. The most common site of nosebleeds is the anterior nasal septum

(Kiesselbach's plexus or Little's area).

10. Patients with posterior nasal packings are at risk for hypoxemia and

must be admitted to a monitored setting.

11. The most common pathogen in acute sinusitis is H. influenzae and Strep.

pneumoniae. (Chronic sinusitis is caused by allergic, then infectious

mixed flora, anaerobes and fungi.)

Page 424

Notes


12. Cavernous sinus thrombosis is a complication of ethmoid sinusitis and

presents with eyelid edema, proptosis, chemosis, 3rd & 6th cranial nerve

palsies, pupillary dysfunction, and papillary edema. Diagnosis is

confirmed by CT scan or MRI and treatment is IV antibiotics, not

surgical.

13. Frontal sinuses develop at ages 6-8; therefore, frontal sinusitis is not

seen in children.

14. Ludwig's angina is a cellulitis of the floor of the mouth. It is most

common in older males with bad teeth. Treatment is IV antibiotics,

possible intubation, possible surgery.

15. Retropharyngeal abscess is commonly seen in children less than 3 years

of age due to atrophy of the retropharyngeal nodes with aging.

16. Antibiotic treatment of strep pharyngitis within 9 days of the onset of

symptoms will prevent acute rheumatic fever, but not acute

glomerulonephritis.

17. A permanent tooth avulsed intact should be replaced into the socket as

soon as possible. The chance of survival drops approximately 1% every

minute the tooth remains out of socket. Do not replace primary teeth in

children.

18. Avulsed teeth should be transported to the ED in milk or the patient's

mouth.

19. Bullous myringitis is most commonly caused by viruses but also may be

caused by Mycoplasma pneumoniae.

20. The most reliable sign of AOM is decreased mobility of the tympanic

membrane on pneumatic otoscopy.

21. The most common source of posterior nosebleeds is the sphenopalatine

artery.


1. The only indication for the emergent use of a miotic agent (green caps)

is for acute angle closure glaucoma (pilocarpine 2%).

2. Topical corticosteroids can cause HSV reactivation.

3. S. aureus is the most common agent causing blepharitis and hordeolum

(sty).

Page 425

Notes


4. The most common cause of a painless red eye is viral conjunctivitis and

the most common etiology is adenovirus.

5. Neisseria gonorrhea ophthalmic infection can cause loss of vision and

perforate an intact cornea and is considered an ocular emergency. In

general should be admitted for parenteral ceftriaxone and topical

antibiotics.

6. The most common cause of a painful red eye is iritis (AKA

uveitis/iridocyclitis).

7. Classic iritis presents with the following signs: constricted pupil,

injected conjunctiva (bulbar), flushed perilimbus and inflamed anterior

chamber (flare/cell).

8. Differentiate iritis from acute angle closure glaucoma by iritis having a

normal cornea, small pupil, and normal tonometry.

9. Typical signs of acute narrow angle glaucoma (ANAG) include: corneal

edema, ciliary flush, decreased visual acuity, mid-range and sluggish

pupil, and increased IOP (>50 mmHg).

10. Treatment for ANAG includes: consultation, pupillary constriction,

decrease aqueous humor production, hyperosmotics, antiemetics, and

surgery.

11. Most common form of recurrent zoster is herpes zoster ophthalmia

(varicella virus). Lesions on the tip of the nose (Hutchinson’s sign)

from nasociliary nerve involvement indicate high likelihood of ocular

lesions.

12. Ten to twenty percent of orbital fractures have an associated globe

injury.

13. Complications of hyphema are re-bleed (2 to 5 days), corneal staining,

and glaucoma.

14. Subconjunctival hemorrhage is very common, typically asymptomatic,

and resolves without sequelae.

15. Central retinal artery and vein occlusions can present as sudden painless

unilateral loss of vision.

16. Central retinal vein occlusion presents with decreased visual acuity and

a blood and thunder appearance on fundoscopic exam

17. Of all eye exposure injuries, alkaline injuries carry poorest prognosis

due to the mechanism of liquefaction necrosis.

Page 426

Notes


REFERENCES

EENT Emergencies

1. “Acute Pharyngitis: How Effective is Therapy?” Emergency Medicine

News, pg. 7-9, October, 1995.

2. Diseases of the Nose, Throat, Ear, Head, and Neck, Ballenger, John,

Lea and Febiger, 1991.

3. “ENT Emergencies,” Emergency Medicine Clinics of North America,

May, 1997.

4. Emergency Medicine, A Comprehensive Study Guide 6th

ed, Tintinalli,

Judith, McGraw-Hill, 2004.

5. Rosen’s Emergency Medicine, Concepts and Clinical, 6th

Ed Rosen, P

et al, 2006.

6. “Evaluation and Management of Acute Uvular Edema,” Annals of

Emergency Medicine, 22(2):251-5, Feb., 1993.

7. “Removing Cockroaches from the Auditory Canal: Controlled Trial,”

NEJM, 312(18), May, 1985.

8. “Pharyngitis: The Value of Laboratory Testing,” Emergency Medicine

News, pg. 4-11, September, 1995.


1. Rosen’s Emergency Medicine, Concepts and Clinical, 6th

Ed Rosen, P

etal, 2006.

2. Bienfang DC, et al: Medical progress: Ophthalmology NEJM 1990;

323:958-959.

3. Janda RM: Ocular Emergencies, in Tintinalli; J (eds): Emergency

Medicine, ed 6 2004. St. Louis, McGraw-Hill, Inc., 2004.

4. Drugs for viral infections. Medical Letter 1992; 34:31-36.

5. Brunette DD, et al: Ophthalmology, in Rosen P (eds): Emergency

Medicine, ed 5. St. Louis, Mosby, 2002, Vol 2, pp.908-927.

6. Shingleton BJ: Eye injuries. NEJM 1991; 325:408-413.

Page 427

Notes


7. Rhee D, Pyfer, M. The Wills Eye Manual. Office and Emergency

Room Diagnosis and Treatment of Eye Disease. 3rd

Ed 1999

Lippincott Williams & Wilkins.

08/13

Page 428

GI Emergencies

Brian Donahue, MD, FACEP

Clinical Assistant Professor, University of Illinois at Chicago; Attending Physician, Department of Emergency Medicine,

Presence Resurrection Medical Center, Chicago

Page 429

Page 430

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GI Emergencies

GI EMERGENCIES

I. ABDOMINAL PAIN

A. General:

1. Very common causes for ED visits (10%); (8-11% of test):

a. Nonspecific abdominal pain:

i. (Most common) young-middle age, women of child-

bearing age, low socioeconomic status, psychiatric

disorders.

b. Elderly: more likely to have a life-threatening process.

2. Presentations extremely variable, KNOW THE CLASSICS!

3. Always consider extra-abdominal causes.

4. High index of suspicion for children, elderly, and

immunocompromised patients.

II. DISORDERS OF THE GALLBLADDER / BILIARY TREE

A. Cholelithiasis (gallstones):

1. Etiology:

a. 20% females, 8% males have asymptomatic gallstones.

2. Risk factors:

a. Female, as high as 4:1.

b. Age.

c. Family history.

d. High estrogen state: female, fertile, forty, fat,

contraceptives, clofibrate.

e. IBD: Crohn’s, ulcerative colitis.

f. Cystic fibrosis.

g. Hemoglobinopathies.

h. Sickle cell disease, thalassemia.

i. Rapid weight loss/starvation.

j. Elevated lipids/triglycerides.

k. TPN.

l. Post-op.

3. Types of stones:

a. Cholesterol (pure or mixed):

i. Most common! (> 75%)

ii. Radiolucent (not visible) on X-ray.

iii. Due to delayed GB emptying and bile stasis (increasing

cholesterol concentration).

b. Pigmented (black or brown):

i. Unconjugated bilirubin + calcium salts.

ii. Radiopaque (due to calcium).

iii. Black stones.

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Advanced liver disease.

Hemolytic disorders.

Found exclusively in the GB.

iv. Brown stones:

Associated with infection.

Found throughout biliary system.

4. History:

a. RUQ/epigastric pain – constant or intermittent.

b. Radiation to scapula or shoulder.

c. N/V.

d. Similar episodes in past.

5. Physical exam:

a. RUQ/epigastric tenderness.

6. Diagnosis:

a. Labs often within normal.

b. X-ray – only 10% of GB stones visualized.

c. US – test of choice:

i. Highly sensitive for GB stones.

7. Treatment:

a. For asymptomatic patients:

i. No acute treatment needed.

ii. 15-20% becomes symptomatic.

iii. Outpatient elective surgery if:

Frequent or severe attacks.

Diabetic.

Large biliary calculi.

b. For symptomatic patients:

i. Pain control.

ii. Antiemetics.

iii. Outpatient elective surgery.

iv. 90% have recurrent symptoms within 2 years.

v. 50% will develop acute cholecystitis.

B. Acute cholecystitis:

1. Etiology:

a. Sudden inflammation of GB.

b. Bacterial infection in 50-75%.

c. E. Coli, Klebsiella, Enterococci predominant. 2. History:

a. RUQ or epigastric pain; radiation to tip of (scapula).

b. Pain becomes constant!

c. Nausea / vomiting.

d. +/- fever.

3. Physical exam:

a. RUQ tenderness.

b. Murphy’s sign (stops inspiratory breath upon deep

palpation).

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i. Much lower sensitivity in elderly.

4. Diagnosis:

a. CBC.

b. Often elevated WBC with left shift.

c. Alk Phos, Bilirubin, AST/ALT:

i. Mildly elevated or normal.

ii. Large elevations of Alk Phos, Bilirubin suggests stone in

common bile duct (CBD).

d. KUB:

i. Poor sensitivity, stones seen ~ 10%.

ii. Air in biliary tree … rare, but serious! (Gangrenous infx)

e. Ultrasound: modality of choice: i. Gallstones.

ii. Thickened GB wall.

iii. Pericholecystic fluid.

iv. Sensitivity 90-95%; specificity 75-85%.

US can miss stones in cystic duct.

f. CT scan:

i. Sensitivity 92%, specificity 99%.

ii. Especially helpful in emphysematous and hemorrhagic

cholecystitis.

iii. Excellent for diagnosing other intraabdominal disorders.

g. HIDA scan – gold standard for this disease: i. Positive = no visualization of GB.

ii. Identifies stones in cystic duct.

iii. Very sensitive; neg scan essentially rules out diagnosis.

5. Treatment:

a. Admit, NPO, IVFL.

b. Pain, emesis control (NGT if multiple emesis).

c. Antibiotics recommended:

i. Bugs = gram negatives, anaerobes and Enterococcus.

ii. Coverage with single broad-spectrum antibiotic (2-3rd

generation Cephalosporin) adequate if not septic.

iii. Triple coverage if septic.

d. Surgical consultation: i. Surgery typically 24-72 hr after symptoms resolve.

ii. Immediate surgery if toxic/gangrene/perforation.

6. Complications:

a. Perforation (3-5%).

b. Emphysematous cholecystitis (1%): i. Gangrene due to gas forming bacteria.

E. Coli, Clostridium perfringens, Klebsiella.

ii. Increased risk in diabetics, elderly.

iii. High mortality.

iv. Acalculous in 30% cases.

c. Gallstone ileus.

d. Pancreatitis (15-20%).

e. Ascending cholangitis.

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f. GB empyema:

i. Complete obstruction of cystic duct with bacteria.

ii. Abscess formation within GB wall.

C. Acute acalculous cholecystitis:

1. No stones present in GB.

2. 2-12% of acute cholecystitis.

3. Rapid, malignant course, up to 41% mortality. 4. Bile stasis equivalent to common duct obstruction.

5. Risk factors:

a. Elderly.

b. Post-surgery.

c. Diabetics. d. Trauma, burns.

e. Sepsis.

f. AIDS (due to CMV or Cryptosporidium Infx).

g. Systemic vasculitic states.

6. Presentation:

a. Similar to acute calculous cholecystitis EXCEPT:

i. Gravely ill on presentation.

ii. Frequently a complication of another process.

7. Diagnosis:

a. HIDA scan: i. Poor filling of gallbladder without gallstones.

b. Ultrasound: i. No gallstone.

ii. Thickened GB wall, pericholecystic fluid.

8. Treatment:

a. NPO, IVFL.

b. Emergent surgical consultation for cholecystectomy vs.

drain if unstable.

c. Broad spectrum antibiotics.

D. Ascending cholangitis:

1. Obstructed bile flow causes retrograde infection up biliary tree

(gram negatives, enterococci, anaerobic).

2. Causes/risk factors:

a. Choledocholithiasis (CBD stone): #1 cause. b. Diabetes.

c. Malignant strictures.

d. Sclerosing cholangitis.

3. Presentation:

a. Charcot’s triad: i. RUQ pain.

ii. Fever/chills.

iii. Jaundice.

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b. Reynolds’s pentad = Charcot’s triad plus:

i. Sepsis.

ii. Mental status change.

4. Diagnosis:

a. Labs:

i. Elevated WBC.

ii. Hyperbilirubinemia.

iii. Elevated alkaline phosphatase.

b. ERCP. c. Transhepatic cholangiography.

d. Ultrasound: i. Shows common and intrahepatic ductal dilatation.

ii. Often non-diagnostic.

5. Treatment:

a. NPO, IVFL.

b. Broad spectrum antibiotics.

c. ERCP: i. Removal of stones, tract decompression.

d. Emergency surgical consultation.

e. Mortality nears 100% if untreated.

III. HEPATITIS

A. General:

1. Definition: general inflammation of liver.

2. Etiology: viral (Hep A, B, C or D, EBV), bacterial, alcoholic,

immune, medications.

B. Hepatitis A virus:

1. RNA virus.

2. Fecal-oral transmission. 3. 33% of US with immunity secondary to exposure.

4. Greatest infectivity before onset of symptoms of disease.

5. Usually self-limited.

6. Acute disease, no chronic carrier state.

C. Hepatitis B:

1. DNA virus (3 major antigens):

a. HepBsAg – surface antigen.

b. HepCcAg – core antigen.

c. HepBeAg – e antigen. 2. Effective vaccination has decreased prevalence.

3. Spread through parenteral/intimate exposure.

4. Highest among IVDA and homosexual males.

5. Onset of symptoms 60-90 days after exposure.

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6. 10% infected adults (90% neonates) develop chronic hepatitis or

carrier stage.

D. Hepatitis C virus:

1. RNA virus.

2. Previously called non-A non-B.

3. Most common of blood borne infections in U.S.: a. Occupational exposure (i.e., needle sticks).

b. IVDA.

c. Transfusions:

i. Prior to screening, risk was 0.45% / unit.

ii. With screening, risk now 0.03% / unit.

4. Chronic HCV infection occurs in 85% of infected patients. a. 50% develop chronic hepatitis.

b. Cirrhosis develops in 20% of this group within 10 years.

E. Hepatitis D virus:

1. Defective RNA virus.

2. Only co-infects patients with chronic or current Hep B.

3. High incidence in IVDA, homosexual males.

4. Increased risk of fulminant disease.

F. History (hepatitis in general):

1. Variable, many cases asymptomatic.

2. Malaise, low-grade fever, anorexia (most common complaints).

3. Other complaints: N/V, abdominal pain, diarrhea.

4. Jaundice most often reason for 1st physician visit.

5. If fulminant hepatitis:

a. Acute onset (days) of liver failure and encephalopathy.

b. Seen mostly in Hep B + Hep D.

c. Hallmarks = altered mental status, mucosal bleeding.

G. Physical exam:

1. Low-grade temperature.

2. Icterus (yellowing of sclera when bili >2.5 mg/dl). 3. RUQ abdominal tenderness.

4. Often tachycardic when vomiting is present.

5. Hepatomegaly.

H. Diagnosis:

1. ALT > AST (Both 10 – 100 x normal!):

a. AST > ALT seen in alcoholic hepatitis!

2. Bilirubin elevated (mild/severe).

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3. Protime (PT):

a. Elevated PT is a sign of significant hepatic disfunction and

the first sign of a complicated course.

4. Hepatitis A:

a. Acute infection = presence of HAV-Ab (IgM antibody). 5. Hepatitis B:

a. Acute HBV infection = presence of HBsAg + HBcAb

(IgM).

b. High infectivity = presence of HBeAg.

c. Past infection or immunization = presence of HBsAb.

I. Treatment:

1. Treatment of viral hepatitis is primarily symptomatic.

2. Correct fluid / electrolyte imbalances.

3. Stop nonessential medications with potential hepatotoxicity.

4. Abstinence from alcohol.

5. Admit if altered sensorium or PT 5 seconds above normal.

J. Complications:

1. Fluid and electrolyte imbalances (acute disease).

2. GI bleed from multiple emesis.

3. Liver failure.

4. Hepatic encephalopathy.

5. Cirrhosis.

6. Death.

K. Prophylaxis:

1. Hepatitis A – provide to household or daycare contacts:

a. Serum Globulin (if serologic testing negative for prior

immunity). b. Minimal risk of contacting to health care workers if universal

precautions are followed (handwashing/hygiene).

2. Hepatitis B – provide to percutaneous or sexual contacts if

previously unvaccinated:

a. HBIG + start HB vaccine.

IV. SPONTANEOUS BACTERIAL PERITONITIS

A. Definition: Acute bacterial infection of cirrhotic ascitic fluid.

B. Pathophysiology:

1. Migration of enteric organisms through edematous bowel:

a. E. coli (47-55% of cases). b. Streptococcus species (18-26%).

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c. Klebsiella species (11%).

d. Streptococcus pneumoniae (8-20%).

e. Polymicrobic/anaerobes NOT common (<1%)

C. History:

1. Variable presentations.

2. Abdominal pain (insidious or acute, mild or severe).

3. Fever/chills.

4. If septic: Hepatic encephalopathy and hemodynamic instability.

D. Physical exam:

1. Variable: a. Ranges from mild abdominal tenderness to rigidity and

guarding with rebound.

E. Diagnosis:

1. Paracentesis:

a. WBCs > 500 cells/mm3.

b. Treat if neutrophil count > 250 cells/mm3.

i. Even if paracentesis culture negative! c. If coagulopathic (high PT), give FFP prior to procedure.

F. Treatment:

1. IV antibiotics:

a. 3rd

generation cephalosporin treatment or choice.

b. OR ampicillin-sulbactam.

V. PANCREATITIS

A. Pathophysiology:

1. Release of activated digestive enzymes.

2. Autodigestion of pancreatic / parapancreatic tissues.

3. Edema and inflammatory cell infiltration.

B. Etiology in the U.S.:

1. Gallstone – most common cause.

a. Women > men.

b. Together account for 80% of cases in U.S.

2. Alcoholic – second most common cause.

a. Men > women

3. Gallstones and ETOH together account for 80-90% of cases in

U.S.

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4. Idiopathic.

5. Infectious:

a. Viral:

i. Mumps; coxsackie B (most common viruses). ii. EBV/ CMV.

iii. Hep A, B, C.

iv. HIV.

b. Bacterial:

i. Mycoplasma.

ii. Legionella.

iii. M. avium complex.

6. Trauma.

7. S/p ERCP.

8. Pregnancy.

9. Scorpion stings. 10. Hyperlipidemia (>500).

11. Hypercalcemia (often from hyperparathyroidism).

12. Drugs: a. Lasix.

b. Tetracycline.

c. Thiazides.

d. HIV medications.

C. History:

1. Abdominal pain (classically “a boring pain”):

a. Epigastric/LUQ.

b. Constant (colicky pain suggests alternate diagnosis).

c. Radiation to midback. d. May find pain improved with sitting forward.

2. Nausea / vomiting.

D. Physical exam:

1. Vital signs:

a. Tachycardia common.

b. Shock/hypotension in serious disease.

2. Epigastric/LUQ tenderness:

a. Guarding common.

b. Rebound tenderness uncommon because the pancreas is a

retroperitoneal organ.

c. Pain often out of proportion to exam.

3. Palpable mass (phlegmon, pseudocyst).

4. Jaundice possible.

5. Grey-Turner sign: a. Ecchymosis at flank.

b. Indicates severe hemorrhagic pancreatitis.

6. Cullen sign:

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a. Ecchymosis at umbilicus.

b. Indicates severe hemorrhagic pancreatitis.

E. Diagnosis:

1. Amylase:

a. Elevated in majority of acute pancreatitis.

b. May be normal in chronic pancreatitis.

c. Sensitivity 79-95%.

d. Poor specificity; differential includes: i. Pancreatic/lung cancer.

ii. Bowel obstruction/perforation/infarction.

iii. Renal failure.

iv. Parotid disease.

v. Hepatitis.

vi. Ruptured ectopic pregnancy.

e. Specificity increased if 5x normal level used.

f. Elevates within 6-24 hr, peak 48 hr, normal 5-7 days.

2. Lipase:

a. Found mostly in pancreas.

b. More specific than amylase (80-90%). c. Sensitivity equal to or better than amylase.

d. Remains elevated 8-14 days. 3. Very high amylase/lipase suggests gallstone pancreatitis.

a. Amylase/lipase levels do not correlate with

prognosis/severity.

F. Ranson’s criteria – predicts outcome in acute alcoholic pancreatitis:

1. Criteria on admission: a. Age over 55 yo.

b. Blood glucose > 200mg/dl.

c. WBC > 16,000.

d. SGOT (AST) > 250.

e. LDH > 350.

2. Criteria after 48 hours:

a. HCT decreases >10%.

b. BUN rises > 5 mg/dl.

c. Calcium < 8 mg/dl.

d. pO2 < 60 mmHg.

e. Fluid sequestration > 6L.

f. Base deficit > 4 mEq/L.

3. Mortality criteria:

a. 0 – 2 criteria = 1% mortality.

b. 3 – 4 criteria = 15% mortality.

c. 5 – 6 criteria = 40% mortality.

d. 7 -8 criteria = 100% mortality.

***Ranson’s criteria was developed at a time when we did not

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have the aggressive resuscitation measures that we do today.

Mortality scores, therefore, are not as directly applicable to

today’s practices. There are more recent scoring systems but their

use in the ED is not very applicable.

G. Imaging tests:

1. Abdomen plain films: little utility:

a. Pancreatic calcifications = chronic disease. b. “Sentinel loop” seen if local ileus.

c. Left pleural effusion/atelectasis possible.

2. Ultrasound:

a. Pancreas poorly imaged: i. Retroperitoneal organ.

ii. Seen in only 60% scans.

b. Test of choice to evaluate if gallstone etiology.

c. Good for pseudocyst, phlegmon, abscess.

d. Overall inferior to CT for acute pancreatitis.

3. CT scan: contrast enhanced very useful: a. Can diagnose enlarged pancreas, necrosis/hemorrhage,

pseudocyst or abscess formation.

b. Rule out other diseases in abdomen.

H. Treatment:

1. IV hydration (fluids, fluids, fluids!):

a. Consider CVP line if serious disease.

b. Electrolyte replacement as needed.

2. NPO, pain control.

3. Antiemetics; NGT if persistent emesis.

4. Antibiotics if gallstone etiology, septic, or severe disease.

5. Surgical consultation for:

a. Gallstone etiology.

b. Severe disease.

c. Abscess/hemorrhage/pseudocyst.

6. ERCP if common duct stone.

I. Complications:

1. Pancreatic pseudocyst or phlegmon:

a. 1-8% of patients.

b. Approx. 2-4 wks after initial attack.

2. Hemorrhagic pancreatitis.

3. Pancreatic abscess, infected pseudocyst.

4. Pulmonary effusions (usually left-sided).

5. ARDS (mortality 60%).

6. Cardiovascular collapse.

7. Renal failure (ATN).

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8. Acute GI bleeding, DIC.

9. Hypocalcemia, hyperglycemia.

10. Pancreatic insufficiency – exocrine and endocrine:

a. Most commonly with chronic pancreatitis.

b. Fat malabsorption when 90% of pancreas is destroyed.

VI. DISORDERS OF THE ESOPHAGUS

A. Esophageal dysphagia:

1. Obstructive disease (85%):

a. Foreign body / food impaction:

i. Main areas of obstruction:

Cricopharyngeus muscle (at C6) near upper

esophageal sphincter.

Aortic arch.

Left mainstem bronchus.

Lower esophageal sphincter.

Most impactions occur at the mid-distal third of the

esophagus.

b. Carcinoma:

i. Squamous cell - 95% .

ii. Risks factors:

Alcohol.

Smoking.

Achalasia.

Caustic lye ingestion.

c. Webs:

i. Mid – proximal esophagus.

ii. Plummer-Vinson syndrome.

Chronic iron deficient anemia.

d. Schatzki’s ring:

i. Distal esophagus.

ii. Food impaction common.

e. Strictures:

i. Scarring from GERD or chronic inflammation.

f. Thyroid enlargement / goiter.

g. Diverticulum:

i. Can occur anywhere along esophagus.

ii. Zenker’s diverticulum:

Proximal to upper esophageal sphincter (UES).

After age 50.

2. Neuromuscular disorders (15%):

a. Achalasia:

i. Impaired relaxation of LES.

ii. Odynophagia, CP, regurge, wt loss.

b. Peristaltic dysfunction:

i. “Nutcracker esophagus”.

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ii. Strong, prolonged peristaltic contractions.

c. Scleroderma, myasthenia gravis, MS, dermatomyositis.

d. Infectious: i. Polio.

ii. Diphtheria.

iii. Botulism.

iv. Rabies.

v. Tetanus.

e. ALS.

f. CVA.

g. Diabetic neuropathy.

3. History / physical exam:

a. Determine if acute, subacute or chronic.

b. Determine if obstructed to solids, liquids or both:

i. Solids only = obstructive. ii. Solids and liquids = neuromuscular.

c. If complete obstruction:

i. Inability to swallow.

ii. Drooling.

iii. Induced retching.

iv. Pain from neck to epigastric region.

4. Diagnosis:

a. X-rays of neck/chest:

i. Visualize FB.

ii. Mediastinal air if perforated.

b. EGD – gold standard: i. Diagnosis and treatment.

c. Gastrografin / barium contrast studies:

i. Used if EGD unavailable.

ii. Use Gastrografin if suspected perforation!

Gastrografin is water soluble; barium is not.

Gastrografin is a pulmonary irritant…don’t use if

aspiration risk.

iii. Barium may interfere with later EGD visualization.

5. Treatment:

a. Food impaction:

i. Glucagon 1 mg IV (up to 2 mg):

Relaxes lower esophageal smooth muscle.

Do NOT use if history of pheochromocytoma, may

precipitate hypertensive crisis.

ii. Carbonated beverages:

Avoid if complete obstruction or obstruction of > 24

hrs due to possible perforation.

iii. Nifedipine 10 mg SL:

Relaxes smooth muscle.

iv. Nitroglycerin:

Relaxes smooth muscle.

Avoid if hypotensive.

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v. Meat tenderizers:

Not recommended!!

vi. EGD if readily available or all else fails:

Gold standard.

b. Foreign bodies:

i. If able to visualize, remove with forceps.

ii. Esophageal FBs need EGD.

iii. FBs passed into stomach can follow-up as outpatient (if

not sharp/long).

c. Strictures/webs/rings:

i. Dilatation by gastroenterologist.

B. Esophagitis:

1. Etiology (many!):

a. Infectious:

i. Usually immunocompromised:

Chemotherapy patients.

HIV.

Transplant.

DM.

ETOH.

ii. Organisms:

Candida (most common).

HSV.

CMV.

b. Inflammatory.

c. GERD:

i. May lead to ulcers, strictures, Barrett’s esophagus.

d. Medications – pills stick to esophagus:

i. Doxycycline (most common). ii. NSAIDs.

iii. KCl supplements.

iv. Ferrous sulfate.

2. History:

a. Odynophagia.

b. Dysphagia (liquids and solids).

c. CP, heartburn.

d. Fever/bleeding in some immunocompromised patients.

3. Physical exam:

a. Oropharynx may appear normal.

4. Diagnosis:

a. EGD:

i. White plaques seen in Candida. ii. Ulcerative lesions seen in HSV.

iii. Definitive diagnosis is with biopsy.

b. Air-contrast barium swallow:

i. Reveals ulcerations/plaques.

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ii. Not definitive.

iii. Bad idea if any perforations.

c. X-rays not helpful.

5. Treatment:

a. Candida infection:

i. Oral fluconazole (other –azoles) 3-4 wks.

b. HSV:

i. Acyclovir (Fam/Valacyclovir) 1-2wks.

c. CMV:

i. Ganciclovir or Foscarnet for 2-3 wks.

d. Admit for severe disease, dehydration.

e. Topical anesthetics, antacids, sucralfate.

C. Boerhaave’s syndrome:

1. Spontaneous rupture of esophagus:

a. Most commonly during forceful emesis.

b. Classically seen in alcoholic patients. c. Also seen in severe coughing, straining during childbirth

and weightlifting.

d. **(Endoscopy now most common cause of overall

esophageal perforation). 2. Esophageal perforation generally has highest mortality of all

perforated GI viscus.

3. History:

a. Episode of severe, violent emesis.

b. Chest pain.

4. Physical:

a. Hamman’s sign: i. “Crunching” on auscultation of heart due to mediastinal

emphysema.

b. Neck crepitans, subcutaneous emphysema.

c. Septic shock (late presentation).

5. Diagnosis:

a. CXR:

i. Mediastinal air, subcutaneous emphysema,

pneumothorax, air-fluid levels, pleural effusion (Rt > Lt).

b. Gastrografin swallow study: i. Shows extravasation through perforation.

ii. Do not use if risk for aspiration (causes pneumonitis).

iii. **Barium may be used with caution (can incite

inflammatory response to tissues) if high suspicion and

negative Gastrografin study.

6. Treatment:

a. Broad spectrum antibiotics.

b. Fluid resuscitation.

c. Emergent surgical repair.

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D. GERD (Gastroesophageal Reflux Disease):

1. Affects up to 25% adult population; higher in elderly.

2. Pathophysiology:

a. Intermittent decrease in LES pressure.

b. Decreased esophageal motility.

c. Prolonged gastric emptying time.

3. History:

a. Burning sensation / discomfort / pressure in chest, neck.

b. May radiate to arms, shoulders, back.

c. Regurgitation (bitter or acid material in mouth).

d. Symptoms worse after meals.

e. Relief with antacids (often brief).

f. Worse when lying down.

g. May be aggravated with activity, better at rest.

h. Asthma (reflux gastric contents into lungs).

4. Physical exam:

a. Not very helpful.

b. History is key.

5. Diagnosis:

a. Clinical diagnosis (history) in ED.

b. R/O cardiac cause of pain.

c. EGD for definitive diagnosis.

6. Treatment:

a. Lifestyle modifications:

i. Sleep at angle (30°), not recumbent.

ii. Do not eat within 3 hrs of bedtime.

iii. Avoidance of:

Smoking / nicotine.

Alcohol, caffeine, fatty foods, citrus.

Tomato based foods, chocolate.

b. Antacids.

c. H2 blockers, PPIs.

d. Surgery last resort.

7. Complications:

a. Changes in esophageal mucosa lead to inflammation, ulcers,

erosions and strictures.

b. Barrett’s esophagus: i. Metaplasia from normal stratified squamous epithelium to

metaplastic columnar epithelium.

ii. Strong correlation with adenocarcinoma of esophagus.

c. Asthma exacerbations.

d. Dental erosions. e. Chronic cough.

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VII. DISORDERS OF THE STOMACH

A. Acute gastritis:

1. Pathophysiology:

a. Superficial gastric erosions (not into submucosa).

b. Localized or generalized.

2. Causes:

a. Helicobacter pylori.

b. Drugs:

i. ASA/NSAIDs.

ii. Iron.

iii. Potassium.

iv. ETOH.

c. Infectious (viral, bacterial, parasitic).

d. Corrosive agents:

i. Acids.

ii. Alkali.

e. Ischemia from severe illness:

i. Shock, trauma, severe burns, organ failure.

f. Crohn’s.

g. Sarcoidosis.

3. Presentation:

a. Epigastric pain – burning, midline.

b. Pain increases with eating in 50%.

c. Vomiting often relieves pain that occurs after eating.

4. Diagnosis:

a. Usually clinical diagnosis in ED.

b. Endoscopy is test of choice.

c. Rule out other diseases.

5. Treatment:

a. Antibiotics for H. pylori:

i. Not usually started in ED.

b. H2 receptor antagonists.

c. Antacids, sucralfate.

d. Discontinue contributing factors:

i. NSAIDs, ETOH.

ii. Stress.

6. Complications:

a. Pernicious anemia: i. Macrocytic anemia, memory loss, peripheral neuropathy.

ii. Pathophysiology:

Destruction of gastric parietal cells, leads to…

Loss of intrinsic factor production, which leads to…

Malabsorption of vitamin B12 (pernicious anemia).

b. Bleeding.

c. Gastric outlet obstruction.

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d. Perforation.

B. Peptic Ulcer Disease (PUD):

1. Erosions into submucosal layer of stomach or duodenum.

2. Duodenal 80%; gastric ulcers 20%. 3. Risk factors:

a. H. pylori – most common.

b. NSAIDs – second most common.

c. Zollinger-Ellison syndrome: i. Gastrin secreting tumor.

ii. Causes up to 1% of PUD cases.

d. Smoking.

e. Alcohol.

f. Family history of PUD.

g. Male > female.

h. Stress, e.g., ICU, trauma, and neurosurgery.

4. Duodenal ulcers:

a. Common, seen in up to 10% of population.

b. Recurs in up to 90% within 2 years.

c. H. pylori present in 70-80% of patients. d. H. pylori eradication reduces the recurrence rate to 15%.

5. Gastric ulcers:

a. 95% are within 2 cm of pylorus.

b. Up to 20% also have duodenal ulcer disease.

c. H. pylori present in 60-70% of patients. 6. Presentation:

a. Epigastric pain seen in both types of ulcers:

i. Duodenal: food relieves pain.

ii. Gastric: classically worse with food.

b. Constant, gnawing or aching pain:

i. Pain may awaken the patient at night (increased gastric

output).

ii. Pain may radiate to the back.

iii. Relief often with antacids.

c. Weight loss.

7. Physical exam:

a. Vague epigastric tenderness.

b. Heme positive stools (not sensitive).

8. Diagnosis:

a. Labs (primarily to rule out other diseases).

b. Test for H. pylori:

i. Not usually done in ED.

ii. Biopsy, CLO test during EGD.

iii. Urea breath test.

iv. Antibody testing.

Antibodies remain positive for years after eradication.

c. EGD: gold standard.

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d. Radiographic studies (upper GI).

9. Treatment:

a. General measures:

i. Stop smoking. ii. Frequent small, bland meals.

iii. Avoid alcohol, NSAIDs.

iv. Decrease stress.

b. Medications:

i. Antibiotics for H. pylori:

Not usually started in ED.

Pylori antibiotic regimens often changing.

ii. Antacids:

May decrease absorption of warfarin, digoxin, some

anticonvulsants/antibiotics.

iii. PPI (preferred for NSAID related ulcers).

iv. H2-receptor antagonists.

v. Sucralfate.

vi. Misoprostol (Prostaglandin E analog).

c. Surgery indicated in medical failures.

10. Complications:

a. Hemorrhage:

i. Occurs in up to 15% patients.

ii. Accounts for 60% of UGI bleeds. iii. Factors predicting higher risk of death:

Older age.

Comorbid illnesses.

Large initial bleed.

Hemodynamic instability.

Continued or recurrent bleeding.

Failure to clear NG with lavage.

iv. Emergency treatment:

IV (2 large bore).

Resuscitate with isotonic fluid/PRBCs.

Transfuse with screened whole blood if patient

deteriorating (don’t wait for cross-matched).

NG lavage.

IV H2 blockers.

Emergent EGD if uncontrolled bleeding for

sclerotherapy, coagulation, or laser therapy.

b. Perforation:

i. Less common (7% patients).

ii. Most often on anterior surface of the duodenum/pylorus

or lesser curve of stomach.

iii. Abrupt onset of severe pain!

Localized pain, quickly spreads to entire abdomen.

Elderly with less pain, less impressive exam.

iv. Duodenal ulcers:

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Perforate posteriorly into pancreas, retroperitoneum.

v. Gastric ulcers:

Perforate anteriorly into abdomen.

vi. Upright Abd X-ray in anterior perforation shows

subdiaphragmatic air.

May insufflate 200-400 cc air through NG tube to

accentuate – this is controversial.

vii. Treatment of perforation with antibiotics, NGT, surgery.

c. Gastric outlet obstruction: i. 2% patients.

ii. Edema and scarring near gastroduodenal ulcers.

iii. Presents as weight loss, reflux, pain, vomiting, early

satiety.

iv. Physical exam: abdominal distention, succussion splash.

v. Treatment: IVFL, NGT, admit.

Some obstructions will open as edema subsides.

Others need surgical procedure.

VIII. PERFORATED VISCUS

A. Pathophysiology:

1. Results from acutely or chronically diseased viscus:

a. Rare to occur in normal bowel (except trauma).

b. Small bowel perforation:

i. Mid-gut perforations are rare.

c. Large bowel perforation:

i. Usually due to:

Diverticulitis.

Carcinoma.

Trauma.

Colitis.

Foreign bodies.

ii. Rapid onset due to bacterial contamination.

2. Most perforations occur freely into peritoneum.

3. High mortality rate.

B. Presentation:

1. Abrupt onset of abdominal pain.

a. Elderly may have little or no pain.

2. Frank peritoneal signs (mild to severe).

3. Vomiting.

4. +/- fever.

5. Hypovolemic, toxic late in course.

6. Severity depends on:

a. Site of perforation:

i. Gastric = chemical peritonitis.

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ii. Intestinal = bacterial peritonitis.

b. Time from onset of perforation.

c. Age.

d. Comorbid diseases, immunocompetency.

C. Physical exam:

1. Decreased bowel sounds.

2. Tympany.

3. Rigid abdomen. 4. Tachycardia.

D. Diagnosis:

1. X-ray:

a. Upright chest:

i. Air under diaphragm.

Can increase yield by adding 200-400 ml of air into

NGT and retaking film – this is controversial.

b. Left lateral decubitus abdominal film.

i. Air over liver.

c. Abdominal flat plate.

i. Air around bowel wall.

2. CT scan - very sensitive for air!

3. Causes of pneumoperitoneum seen on X-ray or CT scan NOT

from perforated viscus:

a. Tracheostomy.

b. S/p DPL, abdominal surgery.

c. Pneumothorax.

d. Infection from gas forming organisms.

e. Urogenital insufflation during sex.

E. Treatment:

1. Fluid resuscitation.

2. IV antibiotics.

3. NGT.

4. Emergent surgical consultation / immediate surgery.

IX. DISORDERS OF THE SMALL AND LARGE INTESTINE

A. Intestinal obstruction (general):

1. Common cause of abdominal pain in ED:

a. SBO represents 20% of hospital admissions for acute

abdominal pain.

2. Overall mortality:

a. 3-5 % for SBO.

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b. 20% for LBO.

B. Mechanical small bowel obstruction (SBO):

1. Etiology:

a. Adhesions – post surgical:

i. Most common cause! (more than 50%).

ii. Typically months to years after surgery; however, may

occur within the first few weeks.

b. Incarcerated hernias (15% of cases):

c. Neoplasms (15% of cases):

i. Adenocarcinoma.

ii. Polyps.

iii. Lymphoma.

d. Intussusception:

i. Often lymphoma at the lead point in adults.

e. Bezoars:

i. In patients s/p pyloroplasty or pyloric resection.

f. Crohn’s disease.

g. Infection/abscess.

h. Radiation enteritis.

2. Pathophysiology, H&P, diagnosis and treatment: included below

under Large Bowel Obstruction.

C. Functional small bowel obstruction (adynamic ileus):

1. Etiology: No structural abnormality:

a. Abdominal trauma, s/p laparotomy.

b. Infection with local inflammation.

c. Metabolic (hypokalemia!).

d. Drugs (opiates).

e. Others: MI, scleroderma, hypothyroidism.

2. Pathophysiology, H&P, diagnosis and treatment: included below

under Large Bowel Obstruction.

D. Large bowel obstruction:

1. Etiology:

a. Colorectal cancer 53% (most common cause!):

i. Tumors on left = obstruct.

ii. Tumors on right = bleed.

b. Volvulus 17% (see next section for more detail):

i. Sigmoid: 80 – 85% of cases.

ii. Cecal: 10 – 15% of cases.

c. Diverticulitis 12%.

d. Fecal impaction:

i. Elderly, nursing home patients.

ii. Narcotic and laxative abusers.

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iii. Mentally delayed.

e. FB.

f. Crohn’s.

g. Radiation or ischemic colitis.

2. Pathophysiology:

a. Proximal bowel distends.

b. Lymphatic and venous compromise with edema and stasis.

c. Third spacing of fluids in distended loops of bowel.

d. Bacteria propagate in distended loop.

e. Increasing intra-luminal pressure impairs vascular supply.

f. Bowel wall becomes ischemic, develops gangrene, perforates.

g. Peritonitis, sepsis, shock.

3. History:

a. Crampy, colicky abdominal pain.

b. Vomiting.

c. Obstipation suggests complete obstruction (late finding).

4. Physical exam:

a. Abdominal distention.

b. High pitched bowel sounds, “rushes”.

c. Tenderness (variable): minimal / diffuse or severe / localized.

d. Peritoneal signs seen in gangrenous or perforated bowel.

e. Fever, hypotension, tachycardia suggest sepsis.

5. Diagnosis:

a. Obstructive series: flat and upright Abd, upright CXR, lateral

decubitus film.

i. SBO confirmed by XRY in 50-60% cases:

“Step ladder” air fluid levels.

Absence of large bowel gas.

ii. Dilated loops of bowel:

Large bowel >10 cm = imminent perforation.

Small bowel >3 cm = distention.

b. Laboratory (very nonspecific).

6. Treatment:

a. IV fluids!!

b. Correct electrolyte abnormalities.

c. NG suctioning.

d. Broad spectrum antibiotics if strangulation, perforation or

peritonitis.

e. Emergent surgical consultation.

E. Sigmoid volvulus – most common volvulus (80 – 85%):

1. Epidemiology:

a. Elderly, bedridden. b. Psychiatric patients on anticholinergics.

c. Neurologic disorders.

d. History of constipation. 2. Pathophysiology:

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a. Lengthening of chronically distended colon.

b. Leads to redundant sigmoid loop which twists on itself.

3. History:

a. Crampy abdominal pain.

b. N/V/dehydration.

c. Constipation.

d. SOB due to abdominal distention.

e. Similar episodes in past that resolved with passage of flatus

and stool.

4. Physical exam:

a. Diffuse abdominal tenderness.

b. Distention.

c. Fever suggests possible peritonitis due to bowel strangulation

or perforation in older patients.

5. Diagnosis:

a. Must have high index of suspicion in incapacitated patients

with abdominal pain.

b. KUB confirms diagnosis in 80% of cases: i. Dilated loop of colon on left.

ii. “Bent inner tube”. c. Barium enema = “Bird’s beak”.

i. Use Gastrografin if perforation suspected.

d. WBC > 20,000 suggests strangulation present.

e. CT scan often useful.

6. Treatment:

a. IV fluids.

b. Antibiotics if peritonitis / strangulation.

c. Surgery consult:

i. Decompression with sigmoidoscopy and rectal tube

50-95% success rate:

Recurrence rate 60%.

Mortality = 20% overall (>50% if gangrene present).

ii. Surgery:

If unable to decompress.

If signs of peritonitis.

Elective surgical resection often after decompression.

F. Cecal volvulus:

1. Most common in ages 25-35.

2. NO history of chronic constipation. 3. Pathophysiology:

a. Hypofixation of bowel to the posterior abdominal wall.

i. Often congenital.

b. Previous abdominal surgery, disrupting the fixation of cecum

to posterior abdominal wall.

c. Rotation of bowel leads to closed loop obstruction.

4. History:

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a. Severe, colicky abdominal pain.

b. N/V/dehydration.

5. Physical exam:

a. Diffusely tender abdomen with large distention.

6. Diagnosis:

a. KUB: Large dilated loop of colon in midabdomen.

i. Empty distal bowel.

ii. “Coffee bean” deformity. iii. Free air indicates bowel perforation.

7. Treatment:

a. Surgery is treatment of choice!

b. Non-operative decompression is unavailable.

c. Mortality rate is high if gangrene! i. 10% if bowel viable.

ii. 30-40% if bowel gangrenous.

G. Hernias:

1. Types:

a. Inguinal (most common): i. 75% of all U.S. hernia operations are inguinal.

ii. Indirect (50%) = through inguinal ring, failure of

obliteration of processus vaginalis.

iii. Direct (25%) = through Hesselbach’s triangle, weakness

of transversalis fascia.

iv. Men > women.

v. High risk of incarceration in kids.

b. Femoral (5%):

i. Women > men.

c. Incisional (10%).

d. Umbilical.

i. Common in newborns:

Incarceration very rare.

80% spontaneously close by 3-4 yo.

ii. In adults, women > men.

iii. Higher risk in obese, pregnant, ascites.

e. Other: epigastric, spigelian, obturator.

2. Definitions:

a. Incarcerated = unable to reduce.

b. Strangulated = incarcerated with vascular compromise.

3. Clinical presentation:

a. Vast majority asymptomatic.

b. Pain at site if incarceration.

c. Infants may just be irritable.

d. Leads to SBO symptoms.

e. Strangulation and necrosis may present as peritonitis and

shock.

4. Treatment:

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a. Reduce if recent, non-tender incarceration:

i. Trendelenburg, sedation, warm compresses.

ii. Do NOT reduce if prolonged incarceration or possible

dead bowel present!

b. IV, NGT, labs, supportive care.

c. Antibiotics if perforation or dead bowel suspected.

d. All non-reducible, acutely incarcerated hernias or

strangulated hernias need emergent surgical repair.

H. Mesenteric vascular disease:

1. Rare, but catastrophic; high mortality rate! (>50%)

2. Occurs primarily in elderly (>50 years old).

3. Etiology:

a. Arterial embolus 50%. b. Arterial thrombus 25%.

c. Non-occlusive disease 20%:

i. CHF, hypovolemia, sepsis, shock.

d. Venous occlusion 5%.

4. Risk factors:

a. Increased age.

b. CAD, vascular disease, valvular heart disease.

c. Dysrhythmias (Afib!).

d. Drugs: vasopressors, diuretics, digitalis, cocaine.

e. Bleeding, dehydration, low cardiac output.

f. Hypercoagulable states.

5. Pathophysiology:

a. Impaired blood supply from SMA, IMA, and celiac trunk.

b. Adynamic Ileus due to lack of blood supply.

c. Mucosal infarction/sloughing (occult or gross bleeding).

d. Third-spacing of fluid in affected bowel.

e. Bacterial invasion of bowel wall/ blood supply.

6. Presentation:

a. Acute, severe colicky pain, poorly localized in pt > 50 yo

with significant underlying vascular disease (i.e., Afib).

b. Recent h/o postprandial pain (intestinal angina), weight loss,

altered bowel habits in non-occlusive or arterial thrombus

disease.

c. N/V/D.

d. 25% with predominant complaint of abdominal distention

with rectal bleed (without abdominal pain).

7. Physical exam:

a. Pain out of proportion to exam (classic!). b. Nonspecific exam.

c. Abdominal distention.

d. Heme positive stools (more than half of all cases).

e. Tenderness progresses with time.

f. Late findings = peritonitis, shock, hypothermia.

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8. Diagnosis:

a. Clinical suspicion is most useful!

b. Tachycardia.

c. WBC often > 15,000 (nonspecific).

d. Metabolic acidosis (lactic acidosis).

i. High sensitivity (but nonspecific).

e. Elevated amylase, phosphate, LDH (nonspecific).

f. Angiography is gold standard! i. Diagnostic and therapeutic.

ii. Contraindicated if patient in shock or receiving

vasopressor therapy – each mimics disease.

g. CT scan of abdomen:

i. Edema of bowel wall and mesentery.

ii. Demonstrates abnormal gas patterns.

iii. Occasionally see mesenteric thrombus.

iv. Normal CT scan does not rule out ischemia. h. Plain X-rays:

i. Nonspecific.

ii. Only late findings may be seen:

Ileus.

Bowel wall edema.

Gas in portal venous system.

Gas in bowel wall - “pneumatosis intestinalis”

(classic).

i. Barium studies:

i. Thumb printing (thick mucosal folds).

ii. Contraindicated because barium can limit visualization

during angiography.

9. Treatment:

a. Aggressive IV fluid hydration.

b. Correct precipitating causes.

c. NG tube.

d. IV antibiotics – broad spectrum.

e. Interarterial papaverine (reduces arterial spasms).

f. Emergent surgical and radiographic consult:

i. Laparotomy should be avoided in nonocclusive

mesenteric ischemia. Anesthesia and operative

manipulation can cause ischemia to progress to necrosis.

ii. Angioplasty (especially for thrombosis of SMA, poor

surgical candidates).

iii. Surgical resection of necrotic bowel.

I. Acute appendicitis:

1. General:

a. Common cause of abdominal pain.

b. 250 – 300,000 new cases yearly in U.S.

c. Approximately 7% of people in their lifetime will develop

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appendicitis.

d. Low mortality:

i. 0.1% in simple appendicitis.

ii. 2-6% with perforation (general public).

iii. 9% with perforation + elderly + comorbidities.

e. Can affect all ages (peaks at 10 – 30 yo).

f. Difficult to diagnose in young, old, pregnant and

immunocompromised.

i. Spontaneous fetal abortion = 5-15% in simple

appendicitis; up to 37% if complicated.

ii. Premature labor = 15-45%.

2. Pathophysiology:

a. Appendiceal luminal obstruction leads to inflammation,

bacterial invasion, infection, vascular compromise,

appendiceal edema.

b. May progress to gangrene, perforation, sepsis, and death.

3. History:

a. Abdominal pain (98% of cases). i. “Classic” presentation (much less often):

Vague epigastric, periumbilical pain later migrating to

RLQ.

Occurs in 20 – 60% young adults, 30% elderly.

< 48 hrs to localize to RLQ.

b. Anorexia (70%).

c. Nausea, vomiting (67%).

d. Kids, elderly and pregnant perforate more often: i. Delay in diagnosis is greatest risk.

ii. Nonspecific complaints and exam.

iii. Elderly perforate up to 60% of cases.

iv. Children < 3 years old perforate as high as 80%.

v. 50% of kids diagnosed with appendicitis previously seen

by physician with misdiagnosis:

Gastroenteritis, UTI most common misdiagnoses.

e. Pregnant patients often with RUQ tenderness: i. Appendix rises as uterus grows.

4. Physical exam:

a. RLQ to right mid tenderness seen in nearly 95%.

b. Rovsing sign: RLQ pain on palpating LLQ.

c. Psoas sign: pain on elevation and extension of right hip.

d. Obturator sign: flexion and internal rotation causes pain.

e. Palpable mass felt in <5%.

f. Rebound tenderness is late finding.

g. Pelvic appendix may lead to rectal / vaginal tenderness.

5. Diagnosis:

a. Laboratory:

i. WBC > 10K (80-90% of patients):

Normal value does NOT rule out diagnosis.

Left shift common.

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ii. Urinalysis:

Sterile pyuria common, especially if pelvic appendix.

> 20 WBCs/hpf more likely to have genitourinary

tract infection.

b. X-ray:

i. KUB not helpful, may help to r/o other diseases.

c. Ultrasound:

i. Sensitivity 75-90%, specificity 85-95%.

ii. Best for kids, pregnant women.

iii. Visualization of immobile, non-compressible appendix of

greater than 6 mm diameter.

iv. Drawbacks: results are operator dependent, difficult to

visualize if retrocecal, obese, has strictures.

v. Absence of abnormality does not rule out appendicitis

unless appendix well visualized.

d. CT scan:

i. Test of choice! ii. Oral and IV contrast best.

iii. Sensitivity 87-100%, specificity 89-98%.

iv. Large appendix > 6 mm diameter.

v. Pericecal inflammation.

vi. Appendicolith.

6. Treatment:

a. IV fluids.

b. Antibiotics to cover abdominal flora.

c. Surgery is definitive treatment.

7. Complications:

a. Perforation, abscess.

b. Localized wound infection, especially if perforated.

c. Low complication rate if not perforated.

d. SBO.

J. Irritable Bowel Syndrome:

1. Approx. 15% population with symptoms consistent with IBS.

2. Young to middle-aged adults.

3. Female: male = 2: 1. 4. Pathophysiology:

a. Precipitating cause unknown.

b. Alteration in intestinal motility and sensation.

c. Thought to be neurophysiologic disorder.

5. History:

a. Abdominal pain:

i. Often relieved with passage of stools/flatus.

b. Altered defecation: i. Constipation, diarrhea, or both.

ii. Incomplete evacuation.

iii. Mucus in stools.

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c. Many extracolonic symptoms:

i. Bloating, belching, nausea, weakness.

ii. Significant weight loss is UNUSUAL. 6. Physical exam:

a. Nonspecific.

b. Anxiety.

c. Mild, diffuse, vague lower abdominal tenderness.

d. No stool on rectal exam.

7. Diagnosis:

a. No specific tests.

b. Diagnosis of exclusion. c. Outpatient work-up often includes:

i. Sigmoidoscopy.

ii. Stool examination:

Occult blood.

Bacteria, parasites (Giardia).

iii. Food allergies.

iv. Testing for lactose intolerance.

8. Treatment:

a. Dietary:

i. Increase stool bulk.

ii. Avoid milk products.

iii. Avoid caffeine.

b. Anti-diarrheals prn.

c. Reassurance.

i. Avoid implying that problem is all psychological!

d. Consider anticholinergics.

e. Consider anxiolytics, antidepressants. Usually reserved for

primary physician.

f. Avoid narcotic analgesics! g. Regular appointments and therapeutic relationship with

primary physician most helpful.

K. Diverticular disease:

1. Pathophysiology (general):

a. Herniation of mucosa/submucosa through defects in muscular

wall of bowel.

b. Most common in sigmoid colon (not exclusively).

c. Diverticulosis:

i. Presence of one or more diverticulum.

d. Diverticulitis:

i. Inflammation of a diverticulum which is almost always

symptomatic.

ii. Develop in 10-30% with diverticulosis.

2. Acute diverticulitis:

a. Inflamed diverticulum with microperforation:

i. Left > right.

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ii. Incidence increases with age (2-4% under 40 yo).

b. History:

i. Pain, often in LLQ, worsened with bowel movements. ii. Change in bowel habits, often constipation.

iii. N/V.

c. Physical exam:

i. Low grade fever.

ii. Abdominal distention.

iii. Heme positive stools >50%.

iv. LLQ abdominal tenderness:

May have localized peritoneal finding.

d. Diagnosis:

i. Often clinical.

ii. KUB nonspecific.

iii. Sigmoidoscopy may show diverticula:

Not done with acute diverticulitis for fear of

perforation.

iv. Barium enema often shows diverticula:

Not done with acute diverticulitis for fear of

perforation.

v. CT scan:

Test of choice.

Show inflamed diverticula and local irritation to

bowel/fat.

Abscess.

Evaluates for other disease processes.

e. Treatment:

i. If pain only:

Clear liquid diet.

Stool softeners.

Pain meds.

Oral antibiotics.

Can manage as outpatient if no comorbidities.

ii. If systemic symptoms, significant inflammation or

abscess:

Admit.

Bowel rest (NPO, NG).

IV antibiotics.

Surgical consultation.

After 2 episodes of acute diverticulitis, consider

elective surgery for resection.

f. Complications:

i. Fistula.

ii. Abscess.

iii. Obstruction.

iv. Perforation.

3. Painful diverticular disease:

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a. Pathophysiology:

i. Increased muscular contraction leads to increased

intraluminal pressure and stretching of bowel wall and

pain.

b. History:

i. Recurrent, intermittent LLQ pain:

Pain often post meals.

Often relieved with defecation or flatus.

ii. Diarrhea or constipation.

May be increased with emotional stimuli.

c. Physical exam:

i. Mild LLQ tenderness:

No rebound.

No guarding.

ii. No fevers.

d. Diagnosis:

i. Suspect if > 40 years old with above symptoms.

ii. WBC wnl.

iii. Barium enema.

iv. Colonoscopy.

e. Treatment – goal is to decrease bowel spasm:

i. Anticholinergics.

ii. Local heat.

iii. High fiber diet.

iv. Anxiolytics.

v. Laxatives/stool softeners.

vi. No antibiotics.

4. Diverticular bleeding:

a. Most common cause of significant LGI bleed. b. Most patients asymptomatic until bleed.

c. Prevalence increases with age.

d. Diverticula cause stretching of vasa recta vessels:

i. Bleeding occurs when the vasa recta rupture into the

diverticulum.

e. Presentation:

i. Mild hematochezia to massive lower GI bleeding.

ii. Most bleeds are painless (classic).

iii. Many with previous episodes of diverticulitis / pain.

f. Diagnosis:

i. Sigmoidoscopy/colonoscopy:

Proctosigmoidoscopy can r/o hemorrhoidal bleeding.

ii. Tagged red blood cell studies:

Need bleeding of 0.1-0.2 ml/min.

iii. Selective arteriography:

Need bleeding of 0.5 ml/min.

g. Treatment:

i. Resuscitation:

2 large bore IVs.

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Isotonic fluid.

ii. Transfuse PRBCs if needed.

iii. Surgical consultation.

iv. Sigmoidoscopy/colonoscopy.

Sclerotherapy.

v. Arterial catheterization at bleeding site.

Inject vasopressor to slow bleed.

L. Colonic tumors:

1. Presentation:

a. Weight loss.

b. Change in stool character.

c. Rectal bleeding.

d. Obstructive symptoms.

2. Adenocarcinoma most common tumor.

3. Lower GI:

a. Apple core lesion (typically left sided).

4. Colonoscopy for definitive diagnosis.

M. Crohn’s disease:

1. Pathophysiology:

a. Chronic inflammatory disease of the GI tract that can involve

any part from mouth to anus.

b. Segmental granulomatous inflammation “skip lesions”:

i. Transmural inflammation.

ii. Ileum is most common site.

c. “Cobblestoning” by criss-crossing longitudinal ulcers.

d. Confined to colon in 20%.

e. Perianal complications 90%.

2. General:

a. Peak incidence 15-22 yo.

b. Secondary peak 55-60 yo.

c. Prevalence: 10 cases / 100,000.

d. Increasing in U.S. over 20 years.

e. Women increased risk by 20-30%.

f. More common in Caucasians; 4x more prevalent in Jewish.

g. Family history in 10-15%.

h. Diagnosed by upper GI, air-contrast barium enema and

colonoscopy.

i. Recurrence rate 25-50% in 1 year for those that have

responded to medical management.

j. 75% require surgery within 20 years of onset.

k. Presentation (Crohn’s exacerbation):

i. Abdominal pain/cramps.

ii. Diarrhea:

May be bloody, but less common than ulcerative

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colitis.

iii. Anorexia, weight loss.

iv. Low grade fever.

v. Anemia, malabsorption.

vi. Approximately ½ patients c/o perianal disease.

3. Treatment:

a. IV fluids, NPO.

b. Symptomatic care (analgesics, antipyretics, antiemetics).

c. Steroids.

d. Sulfasalazine. e. Nutritional support.

f. Broad-spectrum antibiotics if fulminant colitis.

g. Evaluate for possible complications (below).

h. Surgery may be needed for complications.

4. Complications (lifetime):

a. Perianal abscess / fissure / fistula seen in 1/3 of patients.

b. Internal abscess / fissure formation in 30%.

c. Toxic megacolon – 6%.

d. Extraintestinal manifestations in 25-30%:

i. Gastrointestinal:

Perforation.

Peritonitis.

Obstruction.

Reason for surgery in 33% cases.

ii. Rheumatologic:

Arthritis.

Ankylosing spondylitis.

Sacroiliitis.

iii. Dermatologic:

Erythema nodosum.

Pyoderma gangrenosum.

iv. Hepatobiliary:

Gallstones.

Pericholangitis, cholangiocarcinoma.

Pancreatitis.

v. Ophthalmologic:

Uveitis.

Episcleritis.

vi. Vascular:

Vasculitis.

Thromboembolic disease.

vii. Cancer:

Risk increased 3-5x as compared to the general

population.

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N. Ulcerative colitis:

1. Epidemiology (similar to Crohn’s):

a. All age groups; peak in 2nd

- 3rd

decades of life.

b. Industrialized nations; increasing in U.S.

c. Family history in 10-15% cases.

d. Caucasians 4x higher risk.

e. Males slightly more prevalent.

2. Pathophysiology:

a. Chronic inflammatory disease of colon and rectum.

b. Continuous from rectum proximally.

c. Limited to mucosa and submucosa, shallow ulcers.

d. Bloody diarrhea with mucoid stools due to friable, ulcerated

mucosa -“crypt abscesses”.

3. Presentation:

a. Broken into mild, moderate, severe disease:

i. Mild (60%), < 4 BMs per day, few extraintestinal

manifestations.

ii. Moderate (25%).

iii. Severe (15%), > 6 BMs per day, anemia, fever, wt. loss,

low albumin, multiple extraintestinal manifestations.

b. 10% usually present with:

i. Low grade fever.

ii. Crampy abdominal pain.

iii. Tenesmus.

iv. Bloody, mucopurulent stool.

c. Remainder with:

i. Insidious onset.

ii. Recurrent fevers.

iii. Abdominal pain.

iv. Anorexia.

v. Mild diarrhea.

4. Diagnosis:

a. Sigmoidoscopy / colonoscopy and biopsy.

5. Treatment:

a. IV fluids, correct electrolyte abnormalities.

b. Steroids or ACTH.

c. Sulfasalazine. d. Enemas:

i. Topical glucocorticoid.

ii. 5-aminosalicylic.

e. Antibiotics controversial, used primarily in severe dz.

f. If mild disease: discharge on low residue diet, close medical

F/U, possible medication adjustments.

g. Admission if severe symptoms or toxic megacolon.

6. Complications:

a. Toxic megacolon:

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i. Seen in 5% cases.

ii. Etiology: Loss of neuromuscular tone leads to dilatation

of transverse colon.

iii. KUB = long segment of air-filled colon dilated more than

6 cm; possible thumbprinting.

iv. Risks:

Drugs that decrease bowel motility.

Cathartics.

Enemas.

v. Presentation:

Systemic toxicity.

Marked abdominal distention.

Peritonitis.

vi. Treatment:

IVFL, NG, steroids, antibiotics.

Surgery if not improved 24-48 hr.

b. Obstruction.

c. GI bleed.

d. Perforation (25%).

i. 50% mortality.

e. Perianal abscesses not as common as in Crohn’s.

f. Iron deficiency.

g. Stricture.

h. Extracolonic complications:

i. Same as those seen with Crohn’s.

X. ANORECTAL DISORDERS

A. Anal fissure:

1. General:

a. Most common cause of painful rectal bleeding. 2. Pathophysiology:

a. Tear in squamous epithelium of anal canal.

3. Presentation:

a. Pain on defecation! b. Hematochezia – not massive!

c. Often initiated by passage of a hard or sharp stool.

4. Physical exam:

a. “Fissure triad”:

i. Deep ulcer.

ii. Sentinel pile.

iii. Enlarged anal papillae.

b. Sentinel pile:

i. 90% posterior midline.

ii. Central linear ulcer.

iii. Hypertrophic papilla internally.

iv. Hypertrophied skin externally, chronic inflammation.

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c. Treatment:

i. Sitz baths.

ii. Stool softeners.

iii. Bulking agents.

iv. Non-narcotic pain medications.

v. Topical lidocaine.

vi. Antispasmodic agents – nitroglycerin or calcium-channel

blocker gel.

B. Hemorrhoids:

1. Pathophysiology:

a. Dilated venules of hemorrhoidal plexus.

b. Precipitating factors:

i. Low bulk diet.

ii. Erect posture.

iii. Increased abdominal pressure (straining).

iv. Chronic constipation.

v. Pregnant.

c. Can occur internally or externally.

d. Anoscopy to evaluate for internal hemorrhoids.

e. Dentate (pectinate) line:

i. Defines junction of squamous and columnar epithelium.

ii. Defines internal from external hemorrhoids.

f. External hemorrhoids:

i. Below dentate line.

ii. Covered with skin. iii. Painful.

g. Internal hemorrhoids:

i. Above dentate line.

ii. Covered with mucosa. iii. Painless.

2. External hemorrhoids:

a. Presentation:

i. Itching.

ii. Burning.

iii. Rectal bleeding with defecation.

iv. Thrombosis (pain!).

b. Treatment:

i. NSAIDs for pain.

ii. Sitz baths.

iii. Stool bulking agents/stool softening agents.

iv. Avoidance of straining.

v. Excision of thrombosed hemorrhoid. 3. Internal hemorrhoids:

a. Presentation:

i. Painless, bright-red rectal bleed with defecation.

Common cause of rectal bleeding.

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ii. Prolapse of internal hemorrhoid:

Often while straining.

May become permanent.

May appear like thrombosed external hemorrhoid.

Often painful.

b. Treatment:

i. Non-prolapsed:

Hot sitz baths TID.

Analgesics.

Prevent prolonged sitting / straining.

Bulk laxatives / stool softener.

High fiber/bran diet.

ii. Prolapsed:

Manual reduction!

No excision or I&D!

Surgery may be needed (band ligation) if continued

bleeding or irreducible prolapsed hemorrhoid.

C. Rectal foreign body:

1. Seen in assault, self-administration, psych patients.

2. Fever, abdominal pain suggest perforation.

3. Diagnosis:

a. Abdominal X-ray:

i. See foreign body, position, shape.

ii. Evaluate for free air / perforation.

4. Treatment:

a. Soft, low lying (< 10 cm from anal verge):

i. Remove safely in ED:

Sedation/muscle relaxant.

Local anesthesia.

Have patient bear down.

Forceps.

May try to pass a Foley beyond obstruction, then

inflate balloon and provide gentle traction.

b. Do not try to remove large, fragile, hard object, especially

if >10cm from verge.

c. Surgical consultation/general anesthesia often needed.

d. Do not use cathartics!

e. Indications for admission:

i. Signs of perforation.

ii. Rectal bleeding.

iii. Torn sphincter.

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D. Anorectal abscess:

1. Presentation:

a. Pain!

i. Worse with defecation, sitting.

b. Fever +/-.

c. Mucopurulent discharge.

2. Physical exam:

a. Localized external tenderness:

i. Painful swelling at anal verge = perianal.

ii. Lateral pain, swelling = perirectal abscess.

Perirectal abscesses may extend into surrounding

potential spaces.

Fluctuance.

Painful digital exam with tender mass / induration.

Anoscopy with pus and anal crypts.

3. Complications:

a. Fistulas.

b. Gas gangrene.

c. Necrotizing fasciitis.

d. Sepsis.

4. Treatment:

a. I & D necessary in virtually all cases:

i. Simple perianal abscess = in ED.

ii. Pilonidal cyst = in ED.

iii. Perirectal abscess = in OR.

b. Pack all drained abscesses.

c. Antibiotics only if:

i. Immunocompromised.

ii. Toxic appearing.

iii. Diabetic.

iv. Marked cellulitis.

d. Culture if antibiotics are given.

e. Surgical consultation often necessary.

E. Infectious proctitis:

1. Seen in patients who have had receptive anal intercourse.

2. Initially: itching, seepage, mild pain / irritation.

3. Untreated: significant pain, bleeding, discharge.

4. Organisms:

a. Gonococcus.

b. Chlamydia.

c. Syphilis.

d. Condylomata acuminate (papillomavirus).

e. Pinworms.

f. Herpes simplex virus.

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g. Atypical organisms seen in AIDS:

i. Mycobacterium avium.

ii. CMV.

5. Treatment:

a. Take cultures prior to treatment.

b. Gonorrhea:

i. Multiple choices of antibiotics.

ii. 50% concomitant Chlamydia infection.

c. Chlamydia:

i. Doxycycline first line.

d. Syphilis:

i. PCN.

e. Herpes:

i. Acyclovir.

F. Radiation proctitis:

1. Presentation:

a. Immediate or delayed after irradiation.

b. Diarrhea, tenesmus, urgency.

c. Mild to moderate rectal bleeding.

d. Constipation and obstruction.

i. Usually late, secondary to strictures.

e. Edematous, friable mucosa in anal canal.

f. Fistulas, abscesses.

2. Diagnosis:

a. Made clinically in one with diarrhea or rectal bleeding with

h/o pelvic irradiation.

3. Treatment:

a. Steroid enemas helpful in acute stages.

b. Bulk forming agents.

c. Antimotility agents.

d. Iron supplements.

XI. INFECTIOUS DISORDERS OF THE GASTROINTESTINAL TRACT

A. Diarrhea:

1. Leading cause of death worldwide due to dehydration.

2. Second to “common cold” for lost days from work/school in U.S.

3. Dysentery = diarrhea with blood, pus, mucous.

4. Etiology:

a. Infectious #1:

i. Viral (70%). ii. Bacterial (24%).

iii. Parasitic (6%).

b. Drugs.

c. Diet.

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d. Food allergies.

e. Inflammatory bowel disease.

f. Other:

i. Malabsorption.

ii. Malignancy.

iii. Laxatives.

iv. Obstruction.

5. Pathophysiology:

a. Invasive:

i. Alteration of GI mucosa.

b. Enterotoxin:

ii. Causes mucosal hypersecretion:

Isotonic diarrhea in adults.

Hypotonic diarrhea in children.

6. Presentation (variable):

a. History of ill contacts.

b. New meds or diet.

c. Diarrhea (qualitative, quantitative):

i. Watery.

ii. Bloody.

iii. Mucus.

d. Abdominal pain:

i. Generalized.

ii. Crampy.

e. Low grade fevers, myalgias, fatigue.

7. Diagnosis:

a. Stool WBC > 5/hpf suggests possible invasive infection. b. Stool cultures:

i. Who needs them?

Public health concerns.

Immunocompromised.

Travel history.

Prolonged symptoms.

ii. Fecal leukocytes:

Seen in invasive diarrhea; not seen with toxigenic

diarrhea.

iii. AM stool preferable.

c. Stool O & P and special strains.

8. Treatment:

a. Proper hydration without heavy osmotic loads (sugar).

b. Antiemetics.

c. Antidiarrheals – controversial!

d. Antibiotics:

i. High suspicion for invasive diarrhea.

ii. Toxic appearing.

iii. Positive culture.

iv. Ciprofloxacin or TMP-SMX most common.

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XII. BACTERIAL GASTROINTESTINAL DISEASE

A. Salmonella (invasive):

1. Second most common cause of bacterial enteritis in U.S.

2. Invasive bacteria.

3. Food and water borne, also transmitted by:

a. Domestic pets (10%).

b. Eggs.

c. Unpasteurized milk.

d. Pet turtles/reptiles.

e. Chickens/turkeys.

4. 8-48 hour incubation.

5. Presentation:

a. Bradycardic with fever.

b. Colicky abdominal pain.

c. Watery diarrhea, often with mucous/blood.

d. Mild nausea or vomiting.

e. Can cause osteomyelitis, especially in sickle cell patients.

f. Can cause septic arthritis in HIV and splenectomized patients.

6. Treatment:

a. Uncomplicated:

i. Rarely needs antibiotics.

ii. Increases carrier state and resistance with antibiotics.

b. Antibiotics (Ciprofloxin) in typhoid fever (serotype D).

B. Shigella (invasive):

1. Food and water borne.

2. Oral/fecal transmission.

3. As little as 50-100 bacilli can cause infection.

4. Invasive and exotoxin meditated disease:

a. Seen in confined population.

b. Nursing homes.

c. Penal institutions.

d. Indian reservations.

5. 24 – 48 hour incubation.

6. Presentation:

a. Severe abdominal cramping.

b. Mild watery and often bloody diarrhea.

c. Dysentery possible.

d. Fever.

e. Seizures/neurologic effects (rare).

7. Treatment:

a. No antibiotics needed unless severe disease or culture

positive for Shigella dysenteriae.

b. Consider Ciprofloxacin, TMP-SMX.

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C. Yersinia (invasive):

1. Food (milk, pork) and water borne.

2. Oral/fecal transmission.

3. Invasive bacteria.

4. Domesticated animals.

5. Presentation:

a. Fever.

b. Watery and sometimes bloody diarrhea.

c. Colicky abdominal pain.

d. Anorexia and vomiting.

e. Usually lasts 10-14 days.

f. Cause of mesenteric adenitis, “pseudoappendicitis”.

g. Can cause erythema nodosum.

6. Treatment:

a. Supportive care.

b. No antibiotics usually necessary.

i. Reserved for refractory disease or immunocompromised.

D. Campylobacter (invasive):

1. Overview:

a. Most common bacterial causing diarrhea. b. Frequent cause of “Backpacker’s Diarrhea”.

c. Water borne (streams).

d. Raw milk, chicken, pigeons.

e. Invasive bacteria.

f. 2-5 day incubation.

2. Presentation – symptoms of rapid onset!

a. Crampy abdominal pain.

b. Bloody/loose/watery diarrhea 8-10/day.

c. Constitutional symptoms are the rule:

i. Anorexia.

ii. HA.

iii. Myalgias, malaise.

iv. Fever.

3. Treatment:

a. Ciprofloxacin.

b. Erythromycin.

c. Resistance pattern to TMP-SMX.

E. Vibrio parahaemolyticus (invasive):

1. General:

a. Found in temperate coastal sea waters:

i. Very common in Japan, U.S.

b. Invasive bacteria.

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c. Raw fish/shellfish common source: i. Cruise ships!

2. Presentation:

a. Incubation often 8-12 hr (range 4 - 48 hr).

b. Diarrhea.

c. Moderately severe abdominal cramping.

d. Fever.

e. HA.

f. Vomiting not predominant.

3. Treatment:

a. Most are self-limited (usually lasts 24-48 hr).

b. Treatment with Cipro or TMP-SMX shortens duration.

F. E. coli serotype 0157:H7 (cytotoxin):

1. General:

a. Toxin mediated:

i. Cytotoxic to intestinal wall.

b. Contaminated food:

i. Undercooked meats. ii. Raw milk.

iii. Apple cider.

iv. Raspberries.

c. Person-to-person spread, especially:

i. Day care centers.

ii. Nursing homes.

2. Presentation:

a. Incubation 4-9 days.

b. Severe abdominal cramps.

c. Watery stools initially.

d. Becomes grossly bloody in 95% patients.

3. Treatment:

a. Avoid anti-motility agents.

b. Antibiotics often indicated.

4. Complications:

a. Hemolytic-uremic syndrome (HUS): i. Seen in 20-25 % patients.

b. Thrombotic thrombocytopenic purpura (TTP).

G. Traveler’s diarrhea (enterotoxin):

1. Enterotoxic E. coli most common cause (50-75%).

2. Seen throughout the world.

3. Contaminated food/water.

4. 18-72 hour incubation.

5. Presentation:

a. Watery diarrhea without fecal leukocytes (classic).

b. Vomiting seen in less than 50%.

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c. Mild abdominal pain.

d. Possible bloody stools.

6. Treatment:

a. Bismuth – large doses.

b. TMP-SMX or tetracycline.

c. Yogurt (natural “good” bacteria, i.e., lactobacillus).

H. Bacillus cereus (enterotoxin):

1. Aerobic, spore forming gram (+) rod.

2. Two forms:

a. Emetic form – contaminated fried rice < 6 hours prior.

b. Diarrheal – meats or vegetables.

3. Presentation:

a. Emetic form:

i. Incubation 2-3 hours.

ii. Abdominal cramps.

iii. Diarrhea in 25% patients.

iv. < 10 hours duration.

b. Diarrheal form:

i. Incubation 6-14 hours.

ii. Diarrhea 100%.

iii. Abdominal cramping 75%.

iv. Vomiting 20%.

v. Duration 20-36 hours.

4. Treatment:

a. Mild and self-limited.

b. No antibiotics.

c. Antiemetics as needed.

I. Staphylococcal (enterotoxin):

1. Grows in protein rich foods (picnic foods!):

a. Mayonnaise.

b. Potato salad.

c. Eggs.

d. Ham.

2. Only few hours needed for bacteria to grow / make enterotoxin.

3. Presentation:

a. Explosive onset within 6 hours. b. Crampy, abdominal pain.

c. Multiple vomiting.

d. Diarrhea mild.

e. Fever occasionally.

f. Lasts 6-8 hours, possibly as long as 24 hours.

4. Treatment:

a. Antiemetics.

b. IV fluids.

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c. No antibiotics.

d. Rapid uncomplicated recovery is rule.

J. Clostridium perfringens (enterotoxin):

1. Probably #1 cause of acute food poisoning in U.S.

2. Undercooked meat / poultry (esp. after sitting out > 24 hours).

3. Presentation:

a. Onset after 6-12 hr, possibly up to 24 hr.

b. Watery diarrhea.

c. Moderate – severe abdominal cramping.

d. Rarely fevers, N/V.

4. Treatment:

a. Self-limited.

b. Lasts < 24 hr.

K. Clostridium difficile (enterotoxin):

1. Pseudomembranous colitis.

2. Overgrowth of flora bacteria due to antibiotic use. 3. Toxin mediated – beware of toxin A.

4. All classes of antibiotics implicated, especially:

a. Clindamycin.

b. Ampicillin.

c. Cephalosporins.

5. Increased risk if using constipating agents.

6. Presentation:

a. During or up to 3 weeks after antibiotic use.

b. Watery, profuse diarrhea:

i. Occasionally bloody.

ii. Up to 30 stools/day.

c. Crampy abdominal pain.

d. Fecal WBC common.

e. High WBC counts. 7. Diagnosis:

a. Difficile toxin in stool.

i. Takes lab 48-72 hr.

8. Treatment:

a. Stop antibiotic!

b. Flagyl PO or IV first line.

c. Vancomycin PO only if second course needed.

d. 25% relapse after 7-14 days.

XIII. VIRAL GASTROINTESTINAL INFECTIONS

A. Rotavirus:

1. Most common cause of gastroenteritis in young children.

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2. Double stranded RNA virus.

3. Seasonal in winter.

4. Severe diarrhea and dehydration.

5. Vomiting early then subsides.

6. High fever may be seen.

7. Self-limited.

8. Immunity develops.

B. Norwalk agent:

1. Adults, older children.

2. Single stranded RNA virus.

3. Acute onset diarrhea and mild abdominal cramps.

4. Usually no vomiting.

5. Possible low-grade fever.

6. Myalgias common.

7. Self-limited, rarely severe.

8. No immunity.

XIV. PARASITIC GASTROINTESTINAL INFECTIONS

A. Giardia lamblia:

1. Most common parasitic cause of diarrhea. 2. Most common waterborne cause of diarrhea.

3. Water supplies infected with cystic-infected human or animal

feces:

a. Beavers.

b. Dogs.

c. Raccoons.

4. “Backpacker’s diarrhea”; foreign travel with bad water.

5. Giardia trophozoites infect small bowel.

6. Presentation:

a. Colicky abdominal pain.

b. Bloating and flatulence characteristic:

i. Often audible borborygmi sounds.

c. Explosive, foul smelling stool. 7. Treatment:

a. Metronidazole. b. Quinacrine.

B. Entamoeba histolytica:

1. In U.S., chronic disease more common than acute illness:

a. Incubation 1 week – 1 year.

2. Fecal/oral transmission.

3. Vague abdominal cramping.

4. Flatulence.

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5. Bloody diarrhea of gradual onset.

6. Can cause liver abscess.

7. O & P may take up to 6 stools to obtain cysts.

8. Treatment:

a. Metronidazole plus tetracycline, or metronidazole plus

iodoquinol for 5-10 days.

b. If carrier: Iodoquinol 650 mg TID for 20 days.

XV. GASTROINTESTINAL TOXINS

A. Scombroid:

1. Heat stable toxin:

a. Produced by bacterial action in certain types of dark-meat

fish (improperly refrigerated):

i Dark meat of tuna.

ii Bluefish (mackerel, swordfish).

iii Mahi-mahi.

2. Presentation:

a. Histamine-like reaction (key!):

i. Flushing (facial sunburn).

ii. Urticarial at times.

b. Diarrhea.

c. Headache.

d. Abdominal cramping.

e. Peppery, metallic taste may be noted.

f. Onset within 20-30 minutes of ingestion.

g. Resolves in 5-6 hours.

3. Treatment:

a. Self-limited.

b. Antihistamines (diphenhydramine).

c. H2 blockers.

B. Ciguatera:

1. Most common cause of fish-related poisoning in U.S.

2. Ciguatoxin:

a. Heat stable neurotoxin made by dinoflagellate (small

plankton that sit within algae).

b. Accumulates in tissue of fish (larger, older fish):

i. Red snapper.

ii. Grouper.

iii. Sea bass.

iv. Sturgeon.

v. Barracuda.

vi. Moray eels.

3. Presentation:

a. 2-6 hour incubation.

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b. Predominantly GI and neurologic findings.

c. GI:

i. N/V.

ii. Profuse diarrhea.

iii. Abdominal cramping seen early.

d. Neurologic:

i. Throat and perioral dysesthesias, paraesthesias.

ii. Distorted temperature sensation “hot–cold reversal”-

highly suggestive.

e. Worsened by alcohol. f. Lasts 1-2 weeks on average.

4. Treatment:

a. Supportive.

b. IV mannitol may be helpful.

i. 1g/kg of 20% solution over 30 minutes.

c. Abstain from alcohol until all symptoms resolve.

XVI. GI BLEED

A. Overview:

1. Overall mortality 10%.

2. Upper vs. lower/ligament of Treitz.

3. Causes upper GI bleed:

a. PUD (60%, most common etiology!).

b. Gastritis/esophagitis (15%).

c. Varices:

i. Portal hypertension, liver disease.

d. Mallory-Weiss tear:

i. Mucosal tear in lower esophageal region.

ii. Classic: repeated retching, followed by bright red

hematemesis.

e. Aortoenteric fissure:

i. History of aortic graft (AAA repair).

ii. Classic: small self-limited “herald” bleed, subsequent

massive hemorrhage. f. Others:

i. Stress ulcers.

ii. Malignancy.

iii. AV malformation.

g. ENT emergencies can masquerade as GI bleeds.

4. Causes of primary lower GI bleed:

a. Hemorrhoids:

i. Most common overall LGI bleed. b. Diverticulosis:

i. Most common severe LGI bleed. c. Angiodysplasia:

i. Usually of right colon.

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ii. Undiagnosed.

d. Polyps/cancer.

e. Rectal disease.

f. IBD.

B. History:

1. Hematemesis seen in approximately 50% UGI bleeds.

2. Melena:

a. 150 – 200 ml blood in GI tract for prolonged period.

b. Seen in 70% patients with UGI bleed.

c. Seen in 30% patients with LGI bleed.

d. Iron, Bismuth can simulate (stool guaiac = Neg).

3. Hematochezia:

a. Bright red/maroon stools.

b. Most likely LGI bleed.

c. Can be UGI bleed if rapid transit time.

4. Ask about NSAIDs, ASA, ETOH.

5. Weight loss, changes in bowel habits:

a. Malignancy.

6. May complain solely of:

a. Weakness.

b. SOB.

c. Dizziness.

d. ICP.

e. Abdominal pain.

C. Physical exam:

1. Vital signs, orthostatics.

2. Skin: warmth, diaphoresis, color, rashes:

a. Cool, clammy skin is sign of shock.

b. Spider angiomata, palmer erythema, jaundice, bruises suggest

underlying liver disease.

3. Abdomen.

4. Rectal.

D. Diagnosis:

1. Hemoccult:

a. Can have guaiac positive stool up to 14 days after UGI bleed.

b. False positives:

i. Certain fruits (cantaloupe, grapefruit, figs), uncooked

vegetables (broccoli, cauliflower, radish), or red meat.

ii. Iodide.

iii. Methylene blue.

2. Labs:

a. CBC:

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GI Emergencies

i. Hgb/Hct—traditionally transfuse acute bleed if Hgb < 8.

ii. Platelets.

b. PT/PTT:

i. Increased PT/INR may be from liver failure, vitamin K

deficiency, Coumadin.

c. Type & screen / type & cross:

i. Type specific blood in 10-15 minutes.

ii. Fully crossmatched blood in 45-60 minutes.

d. Electrolytes:

i. Decreased potassium; metabolic acidosis if vomiting.

ii. Pre-renal azotemia:

Reabsorption of blood from GI tract increases BUN.

Hypovolemia increases BUN.

3. EKG:

a. Obtain when:

i. >50 yo.

ii. Preexisting CAD.

iii. Patients with significant anemia.

iv. CP/SOB.

v. May have asymptomatic MI.

4. X-rays:

a. Not helpful.

b. Barium studies limit use of endoscopy or angiograms.

5. Treatment:

a. If unstable, initial resuscitation:

i. 2 large bore IVs, O2, monitor.

ii. Blood products.

iii. GI consult for UGI bleed, surgery consult for LGI bleed.

b. NGT and lavage:

i. May help identify UGI vs LGI bleed.

ii. Evaluate for active UGI bleed.

iii. Neg NG does not r/o UGI bleed.

iv. Note: 14% of bright red/maroon blood per rectum

unexpectedly from UGI.

v. OK with varices. vi. Done with room temperature water.

c. Anoscopy/proctosigmoidoscopy:

i. For mild rectal bleeding.

ii. Check for hemorrhoids.

iii. Check if stool above rectum with blood.

d. Colonoscopy:

i. Diagnose diverticulosis, AV malformations.

ii. Able to ligate or sclerose.

e. EGD:

i. Most accurate diagnostic tool for UGI bleeds. ii. Identifies lesions up to 95% patients.

iii. Emergently at bedside if unstable, otherwise if stable may

be done in 12-24 hours.

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iv. Band ligation or sclerotherapy for varices.

f. Octreotide / Somatostatin:

i. Patients with varices, peptic ulcer disease.

ii. IV infusion at 50 mcg/hr for 24 hours in ICU.

g. Vasopressin:

i. Patients with varices.

ii. Many catecholamine side effects.

iii. Consult with GI before using.

h. Balloon tamponade (Sengstaken-Blakemore tube):

i. Controls variceal hemorrhage in 40-80%.

ii. Many serious side effects.

iii. Use has decreased significantly.

i. Surgery indications:

i. Hemodynamically unstable. ii. Unresponsive to volume resuscitation, endoscopy and

correction of coagulopathy.

iii. Transfused > 5 units within 4-6 hours, OR 2 units every 4

hours after replacing initial loss.

iv. Mortality approaches 23% when taken emergently to

operating room.

j. May discharge home if:

i. Currently asymptomatic.

ii. No comorbidities.

iii. Normal vital signs, normal hgb/hct.

iv. NG aspirate negative.

v. Heme negative or trace heme positive stools.

vi. Patient with understanding of disease with good follow-

up within 24 hours and ability to return if worse.

vii. Admit all others.

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GI Emergencies

GI EMERGENCIES

PEARLS

1. Appendicitis is the most common cause of acute abdominal pain

requiring emergency surgery (37%).

2. Elderly patients are more prone to perforation from appendicitis (44-

70% compared to 10-17% for adults under 60 years) due to the poor

blood supply to the appendix and the thin appendix wall. Children

under 6 years also have a high appendix perforation rate (65%) due to

atypical presentation and inability to communicate.

3. Intermittent abdominal pain and vomiting with a prior surgery or trauma

- think obstruction.

4. The most common causes of small bowel obstruction are postoperative

adhesions (50%), hernia (15%) and malignancy (15%).

5. The most common causes of large bowel obstruction (excluding fecal

impaction) are carcinoma (50-69%), volvulus (10-25%) and diverticular

disease (10-15%).

6. Adynamic (paralytic) ileus is the most common cause of ileus overall.

7. Acalculous cholecystitis due to biliary stasis and obstruction has an

atypical presentation with higher morbidity and mortality than calculous

cholecystitis.

8. Charcot’s triad for ascending cholangitis is fever, jaundice and RUQ

pain.

9. Air in the biliary tree is associated with emphysematous cholecystitis

and gallstone ileus.

10. There are many causes of pancreatitis but the most common by far are

alcoholism and biliary tract disease.

11. No clinical features are pathognomonic for pancreatitis.

12. Know Ranson’s criteria (on admission):

Age over 55

Blood sugar greater than 200 mg/dl

WBC greater than 16,000 mm3

SGOT greater than 250 SF units/L

LDH greater than 700 IU/L

(during initial 48 hours):

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GI Emergencies

HCT fall > 10%

BUN rise > 5 mg/dL

Serum calcium < 8 mg/dL

Base deficit > 4 mEq/L

Estimated fluid sequestration > 6L

Arterial pO2 < 60 mmHg

13. Risk factors for peptic ulcer disease include cigarettes, alcohol, coffee,

cola, aspirin, NSAIDs, family history, Helicobacter pylori infection.

Posterior duodenal ulcers penetrate into the pancreas while anterior

ulcers perforate into the peritoneum.

14. A normal viscus will not perforate.

15. The most common cause of visceral perforation overall is ulcers. The

most common cause of colonic perforations is diverticular disease.

16. The classic presentation for perforated ulcer is sudden onset of severe

pain with a predisposing cause for perforation. Pneumoperitoneum is

found in up to 50-80%.

17. Pain out of proportion to physical findings suggests mesenteric

ischemia, particularly in the elderly with an arrhythmia.

18. Weight loss, change in bowel habits and abdominal pain—think

mesenteric ischemia or cancer.

19. Avoid digoxin, beta blockers and vasopressors in a patient with

mesenteric ischemia as they all decrease splanchnic blood flow.

20. The sigmoid colon is involved in 90% of diverticular disease; 80% of

patients with diverticular disease are asymptomatic.

21. Bleeding diverticula are painless, usually from the right colon, and are

the most common cause of massive LGI bleed overall.

22. Crohn’s disease has segmental granulomatous lesions involving all

layers of the intestinal wall with skip areas of normal intestine in

between; 75% involve the ileum and perianal disease is common.

23. Ulcerative colitis and Crohn’s disease have similar systemic symptoms

and both can result in toxic megacolon.

24. Inguinal hernias are the most common hernias for both sexes.

25. Gastrointestinal “flags”:

Pet turtles, fever but bradycardic, osteomyelitis

- Salmonella

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GI Emergencies

Fever, diarrhea, seizure

- Shigella

Mesenteric adenitis, erythema nodosum

- Yersinia

Cruise ship, raw fish / shellfish

- Vibrio

Bad meat, crampy pain, H-U Syndrome

- E. coli 0157:H7

Contaminated fried rice

- Bacillus cereus

Picnic, potato salad, explosive diarrhea

- Staphylococcal

Antibiotic use, diarrhea

- C. diff

Child, winter, severe watery diarrhea

- Rotavirus

Backpacker, bloating/gas, foul-smelling diarrhea

- Giardia

Fish, flushing / urticaria

- Scombroid

Fish, paresthesias, hot / cold reversals

- Ciguatera

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GI Emergencies

REFERENCES

Abdominal Pain

1. Kelly E. King, John M. Wightman. Abdominal Pain. Rosen’s Emergency


Edition; 209 – 219.

2. Leslie S. Zun, Amardeep Singh. Nausea and Vomiting. Rosen’s

Emergency Medicine: Concepts and Clinical Practice, 6th

Edition; 200 –

208.

Acute Appendicitis

1. Jeannette M. Wolfe, Philip L. Henneman. Acute Appendicitis. Rosen’s


Edition; 1451 –

1459.

Anorectal Disease

1. Wendy C. Coates. Anorectum. Rosen’s Emergency Medicine: Concepts

and Clinical Practice, 6th

Edition; 1507 – 1523.

Colonic Disease

1. Michael A. Peterson. Large Intestine. Rosen’s Emergency Medicine:

Concepts and Clinical Practice, 6th

Edition; 1490 – 1506.

Gall Bladder Disease

1. David A. Guss. Liver and Biliary Tract. Rosen’s Emergency Medicine:


Edition; 1402 – 1425.

Gastroenteritis

1. Robert A. Bitterman, David K. Zich. Acute Gastroenteritis. Rosen’s


Edition; 1460 –

1489.

2. John E. Gough, Phillip A. Clement. Diarrhea. Rosen’s Emergency


Edition; 227 – 236.

Page 486

Notes

GI Emergencies

Gastrointestinal Bleeding

1. Philip L. Henneman. Gastrointestinal Bleeding. Rosen’s Emergency


Edition; 220 – 226.

2. Mark J. Lowell. Esophagus, Stomach, and Duodenum. Rosen’s


Edition; 1382 –

1401.

Hepatic Disease

1. David A. Guss. Liver and Biliary Tract. Rosen’s Emergency Medicine:


Edition; 1402 – 1425.

Inflammatory Bowel Disease



Edition; 1490 – 1506.

Ischemic Bowel Disease and Bowel Infarction

1. Susan P. Torrey, Philip L. Henneman. Disorders of the Small Intestine.

Rosen’s Emergency Medicine: Concepts and Clinical Practice, 6th

Edition;

1440 – 1450.



Edition; 1490 – 1506.

Intestinal Obstruction



Edition; 1490 – 1506.



Edition;

1440 – 1450.

Pancreatitis

1. Sally A. Santen, Robin R. Hemphill. Pancreas. Rosen’s Emergency


Edition; 1426 – 1439.

Page 487

Notes

GI Emergencies

Peptic Ulcer Disease / GERD

1. Mark J. Lowell. Esophagus, Stomach, and Duodenum. Rosen’s


Edition; 1382 –

1401.

Small Intestinal Disease



Edition;

1440 – 1450.

08/13

Page 488

Infectious Disease

Joseph Peters, DO, RDMS, FACEP, FACOEP

Clinical Assistant Professor of Surgery, University

of Illinois College of Medicine at Peoria; Attending Physician, Department of Emergency Medicine,

OSF Saint Francis Medical Center, Peoria

Page 489

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Notes

Infectious Disease

HIV/AIDS

I. DEFINITIONS

A. HIV – Human Immunodeficiency Virus:

1. Reverse transcriptase retrovirus.

2. Infects and kills CD4+ T-cells.

3. 2 main viruses with many different strains:

HIV-1: Majority of HIV infections worldwide. a.

HIV-2: West Africa. b.

II. PRIMARY HIV INFECTION: ACUTE RETROVIRAL SYNDROME

A. Develops in 50-90% patients.

B. Onset 2-4 wks post-exposure as a mono-like syndrome (fever,

malaise, lymphadenopathy, pharyngitis, rash) lasting 1-2 weeks,

but may last up to 6 wks.

C. Seroconversion: presence of anti-HIV antibodies, occurs 3-8 weeks

after initial infection.

III. EPIDEMIOLOGY

A. Worldwide: (as of 2010):

1. Estimated 34 million people living with HIV/AIDS.

2. New cases peaked in 1996 with the advent of HAART.

3. Number of new diagnoses and mortality are declining.

B. Risk factors:

1. Men having sex with men.

2. IV drug users.

3. Heterosexual exposure.

4. Maternal-fetal transmission.

5. Transfusions.

IV. HIV TESTING AND DISEASE MARKERS

A. ELISA: screening test, sensitivity > 99.9%.

B. Western Blot: confirmatory test, 100% sensitivity/specificity.

C. CD4 count: predictor of disease progression.

D. Viral load: most important predictor of disease progression; measures

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HIV RNA in blood.

V. AIDS – ACQUIRED IMMUNODEFICIENCY SYNDROME

A. Definition:

1. HIV infection with either presence of AIDS Indicator Condition

or CD4 count < 200.

2. AIDS Indicator Conditions:

Esophageal candidiasis. a.

Cryptococcosis. b. Cryptosporidiosis. c.

Cytomegalovirus retinitis. d.

Herpes simplex virus. e.

Kaposi sarcoma. f. Brain lymphoma. g.

Mycobacterium avium complex infection. h.

Pneumocystis jiroveci (P. carinii) pneumonia. i. Progressive multifocal leukoencephalopathy. j.

Brain toxoplasmosis. k. HIV encephalopathy. l.

HIV wasting syndrome. m.

Disseminated histoplasmosis. n.

Isosporiasis. o.

Disseminated Mycobacterium tuberculosis disease. p.

Recurrent Salmonella septicemia. q.

Pulmonary tuberculosis. r.

Recurrent bacterial pneumonia. s.

Invasive cervical cancer. t.

VI. CURRENT TREATMENT CONCEPTS

A. Treatment requires multi-drug therapy from 5 different classes of

anti-retrovirals. Monotherapy creates resistance.

B. Treatment should be initiated:

1. CD4 < 350cells/mm3, or:

2. Regardless of CD4 count with the following:

History of an AIDS-defining illness. a.

Pregnancy. b.

Other HIV-related conditions and certain co-infection. c.

CD4: d.

i. < 50 MAC, CMV.

ii. <100 Thrush, Esophagitis, Cryptococcus, Toxoplasmosis.

iii. <200 PJP (formerly PCP).

iv. <500 TB.

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3. Drug side effects:

Zidovudine (AZT) - marrow suppression, myopathy. a.

Ds—ddI, ddC, d4T - Pancreatitis, peripheral neuropathy. b.

Abacavir - Fatal hypersensitivity reaction. c.

Indivir - Kidney stones. d.

Efavirenz - Teratogenic. e.

3TC - Pancreatitis f.

C. Monitoring treatment:

1. Viral load: useful in determining response to therapy and

prognosis.

2. CD4 count: demonstrates immune reconstitution, guides

prophylaxis for opportunistic infections.

D. Treatment goals:

1. Non-detectable viral load.

2. Improved CD4+ count.

E. IRIS: Immune Reconstitution Inflammatory Syndrome:

1. Flu-like symptoms or worsening of previous infections due to

improving immune system.

2. Increasing CD4 count.

3. Usually within 60 days of starting HAART.

4. MAC.

VII. RESPIRATORY INFECTIONS

A. PCP: Pneumocystis jiroveci (carinii) pneumonia:

1. Most common opportunistic infection.

2. Gradual onset over weeks of fever, SOB, DOE, non-productive

cough, tachypnea, +/- rales.

3. Lab findings:

Increased LDH. a.

Decreased PaO2. b.

4. CXR:

Diffuse, bilateral infiltrates. a.

Mild disease—normal. b.

PTX and pneumatoceles are common. c.

High resolution CT—ground glass appearance. d.

5. PCP classification:

Mild: a.

i. PaO2 > 70, A-a gradient < 35.

ii. PO meds +/- output therapy.

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Severe: b.

i. PaO2 < 70, A-a gradient >35.

ii. IV antibiotics, steroids, admit.

6. Treatment:

All treatment— 21 days: a.

i. Trimethoprim/sulfamethoxazole (TMP/SMX).

ii. Alternatives: pentamidine IV (if Bactrim allergic).

Steroids: b.

Reduce risk of respiratory failure and death. i. Recommended if PaO2 < 70 mmHg, A-a gradient >35 (or ii.

pulse ox < 90% on room air).

Contraindicated for suspected TB or disseminated fungal iii.

infection.

7. PCP prophylaxis:

CD4 < 200. a.

Previous PCP. b. Oral TMP/SMX 1 double strength tab QD or 3 times/wk. c.

B. Mycobacterium tuberculosis:

1. Incidence 200-500x higher than general population.

2. Risk factors: prison, shelters, IVDU, inner city.

3. Fever, cough, hemoptysis.

4. Diagnosis:

Sputum AFB smear and cultures. a.

PPD: b.

i. PPD positive in early HIV.

ii. PPD often negative in late HIV.

iii. HIV patient with PPD > 5 mm is considered to have

clinical infection.

CXR: often atypical lower lobe, diffuse infiltrates or marked c.

adenopathy.

5. Extrapulmonary involvement common: lymph nodes, liver,

blood, bone marrow, meninges.

6. Treatment:

Triple-drug therapy; four-drug therapy in resistant areas. a.

INH, rifampin, pyrazinamide, ethambutol (or streptomycin). b.

C. Mycobacterium avium complex:

1. Persistent bacteremia with widespread systemic symptoms.

2. Disseminated MAI:

a. Most common opportunistic BACTERIAL infection.

b. CD4 < 50.

c. Treatment: clarithromycin + ethambutol or rifabutin.

d. Prophylaxis: clarithromycin or azithromycin +/- rifabutin.

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D. Bacterial pneumonia:

1. Occurs frequently in HIV.

2. Recurrent bacterial pneumonia is AIDS identifying condition.

3. Bacteremia very common.

4. Treatment same as in normal host.

VIII. CENTRAL NERVOUS SYSTEM INFECTIONS

A. AIDS dementia:

1. Secondary to long-term HIV infection.

2. Most common neurologic problem in patients with AIDS.

3. No treatment but antiretroviral therapy may delay onset.

B. Cryptococcus neoformans meningitis:

1. CD4 count usually < 100.

2. May be disseminated or isolated.

3. Subtle presentation:

a. HA.

b. Fever.

Slow changes in personality or mentation. c.

CNS often involved. d.

Photophobia, neck stiffness, seizures, focal deficits rare. e.4. Diagnosis:

CT scan: usually non-diagnostic; may see cryptococcomas. a.

CSF examination and culture: b.

i. India ink (CFS) smear positive 60%-80%.

ii. Opening pressure > 200 mm in 70%.

iii. Serum and CSF Cryptococcal antigen.

5. Treatment: Amphotericin B +/- flucytosine for 2 weeks, then

fluconazole or itraconazole po X 8-10 weeks.

6. Prophylaxis: life-time with fluconazole.

C. Toxoplasmosis:

1. Most common cause of FOCAL encephalitis.

2. Parasite transmitted by cats, flies, cockroaches and undercooked

meat.

3. Encephalitis seen with CD4 count < 100.

4. Fever, HA, confusion, lethargy, seizures, focal neuro deficit.

5. Diagnosis:

CT/MRI: single or multiple ring-enhancing lesions with a.

surrounding edema (CNS lymphoma usually single, large

lesion).

CSF: nonspecific and may be normal. b.

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Toxoplasmosis titers: very nonspecific. c.

Brain biopsy: definitive. d.

6. Treatment:

Treat for 8 weeks or until neg. CT. a.

Pyrimethamine plus folonic acid plus sulfadiazine. b.

Steroids - may be required to decrease edema. c.

Lifetime prophylaxis required. d.

D. CNS lymphoma:

1. HA, seizures, focal deficits, encephalopathy, CN polyneuropathy,

fever.

2. Diagnosis:

Requires brain bx to confirm. a.

CT - solitary lesion/s with peripheral enhancement. b.

3. Treatment:

Radiation or multiagent chemotherapy. a.

If edema, consider Decadron/mannitol. b.

4. Often mistaken for toxoplasmosis and then identified after no

improvement in 7-10 days of antibiotic therapy.

5. Prognosis poor.

E. CMV encephalitis:

1. CD4 count < 100.

2. Fever, +/- delirium, rapidly progressive confusion, apathy,

malaise and HA, no focal neuro deficits.

3. Diagnosis by CMV PCR or CMV antigen in CSF.

4. Treatment - Ganciclovir, Foscarnet.

F. HIV meningitis: aseptic encephalitis:

1. Direct consequence of HIV; may be self-limited.

2. HA, meningismus.

3. Diagnosis of exclusion.

4. Treatment - supportive with high-dose AZT.

G. Bacterial meningitis:

1. Uncommon in HIV.

2. Consider Listeria if suspicious.

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IX. OPHTHALMOLOGIC DISEASE IN HIV PATIENTS

A. Cotton wool spots are one of the earliest changes in HIV.

B. CMV retinitis:

1. Most frequent and serious ocular opportunistic infection.

2. Most common cause of blindness in AIDS patients.

3. CD4 < 50.

4. Cottage cheese and ketchup lesions on funduscopy.

5. Treatment - foscarnet or ganciclovir.

6. Blindness occurs in 10% despite therapy.

X. GI MANIFESTATIONS OF HIV

A. Oral candidiasis:

1. Most common infection of the GI tract of AIDS.

2. Usually asymptomatic but may cause odynophagia.

3. Rx with clotrimazole or nystatin.

B. Esophagitis - intraoral lesions may or may not be seen.

C. Diarrhea:

1. Most common symptom in HIV.

2. Significant factor contributing to morbidity and AIDS wasting

syndrome.

3. Medications are a frequent cause.

4. Specific agent not found in 30-50% of patients:

Salmonella. a.

Shigella. b.

Campylobacter. c.

E. coli. d.

C. diff. e.

Giardia. f.

Viruses. g.

MAC. h.

Cryptosporidium. i. Microsporida. j.

HIV itself. k.

D. CMV:

1. Diarrhea, bleeding or perforation.

2. Treatment: Ganciclovir IV or po, Foscarnet po.

3. All patients should have eye exam to exclude retinitis.

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E. Proctitis:

1. Etiology: Herpes simplex, gonorrhea, candida, syphilis,

Chlamydia trachomatis, HPV, Enterobius vermicularis, Phthirus

pubis, Sarcoptes scabiei, trauma.

2. Clinical: tenesmus, mucoid, suppurative discharge.

3. Treatment: as per cause; stool softeners prn; for HSV: oral

acyclovir.

F. Bowel obstruction: May be secondary to lymphadenopathy with TB,

CMV, HIV, lymphoma.

G. AIDS cholangiopathy:

1. Causes: Cryptosporidium, Microsporidia, CMV.

2. Clinical: RUQ abdominal pain without diarrhea, fever, elevated

alkaline phosphatase, normal bilirubin; acalculous cholecystitis;

may be result of portal lymphadenopathy from opportunistic

infections and neoplasm.

H. Pancreatitis:

1. Very common.

2. Causes: direct viral injury, secondary to gall bladder disease,

extrinsic compression due to retroperitoneal nodes or neoplasm

or side effect of medications.

XI. DERMATOLOGIC MANIFESTATIONS

A. Kaposi’s sarcoma (KS):

1. Most common malignancy in patients with AIDS.

2. Purple, non-blanching, painless patches on skin, MM and viscera.

3. Uncommon in heterosexual HIV patient.

4. Treatment: anti-retroviral therapy, radiation, alpha-interferon,

chemotherapy.

B. Mucocutaneous HSV:

1. Clinical: painful grouped vesicles or non-healing ulcers around

nose, mouth, perineum.

2. Diagnosis: viral culture.

3. Treatment: acyclovir po; if ocular involvement, may need IV.

C. Varicella zoster:

1. May herald the diagnosis of AIDS, especially if seen in a

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Infectious Disease

young patient or with diffuse, bilateral disease.

2. Treatment – PO or IV acyclovir.

D. Miscellaneous:

1. Molluscum Contagiosum.

2. Psoriasis.

3. Recurrent seborrheic dermatitis.

4. Recurrent vaginal candidiasis.

XII. HIV IN WOMEN AND CHILDREN

A. Incidence:

1. Fastest growing group is young women.

2. Nearly all children with HIV acquire it perinatally.

B. Frequent complications in women:

1. HPV and cervical neoplasia.

2. Severe recurrent PID.

3. Breast CA.

4. Recurrent or persistent vaginal fungal infections.

C. HIV transmission to infant:

1. AZT given during pregnancy, labor, delivery and

administration to newborn for first 6 weeks of life reduces

transmission to 8% compared with 25% in untreated

patients.

2. Breast-feeding increases risk of HIV from 10% to 19%.

XIII. POST-EXPOSURE PROPHYLAXIS

A. PEP reduces risk of seroconversion by 79%.

B. Non-occupational exposure:

1. Risk of HIV transmission from certain sexual activities and IV

drug use is similar to percutaneous occupational exposures.

2. Seroconversion is low in sexual assault, but there are several

factors associated with increased risk:

a. Trauma/bleeding with penetration.

b. High-ejaculate viral load.

c. Presence of STDs/genital lesions.

d. Multiple suspects/recently incarcerated suspect/use of

drugs by suspect.

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C. Risk of seroconversion following exposure to known HIV positive

source:

1. Needlestick or cut - 0.3%.

2. Eye, nose, mouth (splash) - 0.1%.

3. Intact skin exposure < 0.1%.

4. Unprotected anal intercourse - 0.008-0.032 infections/exposure.

5. Receptive vaginal intercourse - 0.0005-0.0015

infections/exposure.

D. General considerations:

1. Initiate as quickly as possible; no benefit after 36-72 hrs.

2. All wounds should be washed with soap and water immediately;

mucus membranes flushed with water.

3. Baseline testing of exposed patient for HIV, HBV, HCV:

a. Consider need for HBV vaccination or immune globulin.

b. Refer for follow-up testing 6 wks, 3 months and 6 months.

4. Determine risk of seroconversion:

a. Higher risk:

i. Deep injury.

ii. Visible blood on device.

iii. Hollow needle, large-bore.

iv. Needle was placed in vessel of source patient.

v. Source patient with high viral load, late-stage AIDS,

or acute seroconversion.

b. Lower risk:

i. Superficial injury or mucosal exposure.

ii. Solid needle (suture).

iii. Small amount of blood from source.

iv. Non-blood body fluid.

v. Low viral load.

5. All prophylaxis is given for 4 weeks:

a. Basic 2-drug regimen for low risk exposures.

b. Expanded 3-drug regimen for intermediate-to-high risk

exposures.

6. Give PEP?

a. Known HIV source.

b. Two questions:

i. Is fluid bloody?

ii. Is skin compromised?

c. If answer yes to both, give PEP.

d. If answer yes to one, no PEP.

e. If urine, no PEP.

Page 500

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Infectious Disease

HIV/AIDS

PEARLS

1. AIDS = HIV infection with either presence of AIDS Indicator Condition

or CD4 < 200.

2. Number of new HIV/AIDS diagnoses and mortality are declining.

3. ELISA screening test 99.9% sensitive; Western Blot confirmatory test is

100% sensitive/specific.

4. Acute Retroviral Syndrome is a mono-like syndrome that occurs 2-4 wks

post HIV exposure.

5. Treatment should be started:

CD4 count < 350 , or

Regardless of CD4 count with:

1. AIDS-defining illness.

2. Pregnancy.

6. PCP is the most common opportunistic infection. Prophylaxis should be

started if CD4 < 200 or patients has had previous PCP infection.

7. MAC is the most common opportunistic bacterial infection.

8. Recurrent bacterial pneumonia is an AIDS Identifying Condition.

9. Cryptococcus meningitis has a subtle presentation and is the most

common fungal opportunistic infection.

10. Toxoplasmosis has multiple ring-enhancing lesions on CT/MRI while

CNS lymphoma usually has a single, large lesion.

11. CNS lymphoma is often mistaken for toxoplasmosis and then identified

after no improvement on ABX therapy.

12. Diarrhea is the most common symptom in HIV/AIDS.

13. All patients with CMV diarrhea need an eye exam to exclude retinitis.

14. Diffuse zoster may herald the diagnosis of AIDS in a young patient.

15. Kaposi’s sarcoma is uncommon in heterosexual HIV patients.

16. Breast-feeding increases risk of HIV transmission from 10 to 19%.

17. PEP reduces risk of seroconversion by 79%. No benefit after 36-72 hours

post-exposure. Is blood present? Is skin compromised?

Page 501

Notes

Infectious Disease

REFERENCES

1. Simon V, Ho DD, Abdool Karim Q. HIV/AIDS epidemiology,

pathogenesis, prevention, and treatment. Lancet 2006; 368:489.

2. Marx J, et al. Rosen’s emergency medicine: concepts and clinical

practice 7th ed. Mosby Elsevier: 2010.

3. Tintinalli JE, et al. Tintinalli’s Emergency Medicine: A comprehensive

study guide, 7e. McGraw-Hill: 2010.

4. Quinn TC. Acute primary HIV infection. JAMA 1997; 278:58.

5. Brooks JT, Kaplan JE, Holmes KK, et al. HIV-associated opportunistic

infections--going, going, but not gone: the continued need for

prevention and treatment guidelines. Clin Infect Dis 2009; 48:609.

6. Rivers CS, et al. Preparing for the written board exam in emergency

medicine, 5e. Emergency medicine educational enterprises, Inc: 2006.

7. Shelburn SA, et al. Incidence and risk factors for immune reconstitution

inflammatory syndrome during highly active antiretroviral therapy.

AIDS 2005, Vol 19 No 4.

8. Greenwald JL, et al. A Rapid Review of HIV Antibody Tests. Current

Infectious Disease Reports 2006, 8: 125-131

9. Newell ML, Prevention of mother-to-child transmission of HIV:

challenges for the current decade. Bulletin of the World Health

Organization, 2001, 79(12)

10. CDC Website.

08/13

Page 502

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Infectious Disease

INFECTIOUS DISEASE

I. SEPSIS

A. Definitions:

1. SIRS-Systemic Inflammatory Response Syndrome. Must have

2/4:

Temp >38 or <36. a.

HR > 90/min. b.

RR > 20/min or PaCO2 < 32mmHg. c.

WBC > 12,000, <4000 or > 10% bands. d.

2. Sepsis = SIRS + documented infection.

3. Severe sepsis = sepsis + signs of hypoperfusion or organ

dysfunction (abnormal capillary permeability leads to

vasodilation and intravascular volume depletion).

4. Septic shock = severe sepsis + one or both of the following:

MAP < 60 mmHg (or < 80 mmHg if the patient has baseline a.

hypertension).

Vasopressors required to maintain MAP, despite adequate b.

fluid bolus (20-30ml/kg).

B. Epidemiology:

1. Gram positive sepsis:

Increased incidence with pneumonia/central lines. a.

More common than gram negative sepsis in the U.S. b.

2. Gram negative sepsis:

More lethal. a.

Usually endotoxin mediated. b.

3. High risk populations:

Elderly or very young. a.

Immunocompromised. b.

Diabetics. c.

C. Complications:

1. Renal failure.

2. ARDS.

3. DIC.

4. High output heart failure.

5. Liver failure.

6. Death.

D. Treatment:

1. Aggressive supportive care.

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2. Early goal-directed therapy:

CVP 8-12 cm. a.

Scvo2 > 70%. b.

Vasoactive medications to maintain MAP >65 mmHg. c.

Hematocrit > 30%. d.

Lactate clearance. e.

Intubation and mechanical ventilation with sedation. f.

3. Broad-spectrum antibiotic use.

4. Steroids are controversial.

5. Glucose control (ideal <150mg/dl).

II. VIRAL INFECTIONS

A. Influenza:

1. Acute respiratory illness caused by influenza A, B during winter

months.

2. Further classified by serotypes, e.g., H1N1, H5N1.

3. Respiratory large particle droplet transmission.

4. Incubation period 1-4 days.

5. Viral shedding starts 24-48 hours before illness onset and ends on

day 7-10.

6. Abrupt onset fever, HA, myalgias, malaise and respiratory

tract symptoms.

7. Complications:

Pneumonia most common: a.i. Primary influenza pneumonia.

ii. Secondary bacterial pneumonia – rapid decline after

initial improvement.

iii. Mixture of both.

Myositis and rhabdomyolysis. b.

Encephalitis, transverse myelitis, aseptic meningitis, Guillain-c.

Barre.

Myocarditis and pericarditis. d.

Toxic shock syndrome. e.

8. Treatment:

Oseltamivir or zanamivir – treats both influenza A and B. a.

Amantadine and rimantadine treat only influenza A and have b.

high rates of resistance.

Can shorten the duration of illness by 1-3 days (greatest c.

benefit if started within first 24-30 hours of illness).

Thought to also decrease severity of illness and viral d.

shedding.

Who should be treated: e.i. Residents of chronic care facilities.

ii. Adults > 65 years of age, kids < 2 years of age.

iii. Pregnant women and those who are less than 2 weeks

post-partum.

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iv. Patients with chronic medical conditions.

v. Highest risk = patients with underlying lung disease,

immunosuppression.

vi. Morbidly obese patients.

vii. Illness requiring hospitalization.

B. SARS (severe acute respiratory syndrome):

1. First reported in 2002 in China.

2. Novel coronavirus transmitted by droplet spread.

3. Clinical definition (all 4 required):

History of fever or documented fever. a.

Cough or SOB. b.

Radiographic evidence of pneumonia or ARDS. c.

No alternative diagnosis. d.4. Incubation period 2-10 days.

5. Tends to be mild in children < 12 years.


Prodrome 2-10 days - fever, HA, malaise, myalgias. a.

Respiratory phase begins after prodrome – nonproductive b.

cough, SOB, respiratory failure.

7. Treatment is supportive; early quarantine essential.

C. West Nile infections:

1. RNA virus discovered in Uganda in 1937.

2. Appeared in the U.S. in 1999 and is now widespread.

3. Human illness peaks in late summer and early fall.

4. Birds serve as the amplifying hosts: “Bird-Mosquito-Bird

Cycle”. 5. Transmitted via mosquito bites, but also via blood transfusions,

organ transplantation, transplacental, occupational exposure and

breast milk.

6. Virus replicates in the skin, liver and kidney - then spreads to

CNS.


Most persons asymptomatic; 20-40% show symptoms. a.

Incubation period of 2-14 days. b.

Life-long immunity develops after recovery. c.

West Nile fever: d.

i. Self-limited headache, fever, malaise, myalgias,

anorexia, rash (maculopapular on chest, arms, back).

ii. Persists 3-5 days but many patients report symptoms for

30 or more days.

Neuroinvasive disease: e.i. Can present as encephalitis, meningitis or flaccid

paralysis.

ii. Ranges from mild, self-limited to coma and death.

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iii. Cranial nerves palsies accompanied by flaccid paralysis

indicates a high probability of respiratory failure.

iv. Can also develop seizures, ataxia, optic neuritis.

8. Diagnosis:

Normal to elevated leukocyte count in peripheral blood. a.

CSF shows pleocytosis with lymphocytosis and elevated b.

protein concentration and normal glucose.

CT usually normal; MRI often shows widespread signal c.

intensity.

EEG shows generalized slowing. d.

ELISA IgM antibody testing of serum or CSF often times e.

confirms diagnosis.

9. Treatment is supportive; vaccines are being developed.

10. Prognosis:

Serious adverse outcomes are seen in patients with a.

neuroinvasive disease.

Older age and immunosuppressed patients at highest risk. b.

III. MALARIA

A. Epidemiology:

1. 41% of world’s population live in endemic areas:

Africa. a.

Asia. b.

Oceania. c.

Central and South America. d.

2. 300–500 million infections annually, 1.5–2.7 million deaths:

Mosquito bites. a.

Blood transfusions. b.

IVDU. c.

Perinatal transmission. d.

Organ transplantation. e.

“Airport” malaria. f.3. Mosquito-born protozoan infection of RBCs:

Plasmodium falciparum—most severe form. a.

i. Banana gamete.

ii. Multiple seen on one slide.

P. vivax. b.

P. ovale. c.

P. malariae. d.

i. Nephrotic syndrome.

B. Pathophysiology:

1. Female Anopheles mosquito ingests gameocytes from host.

2. Sexual reproduction occurs in mosquito gut.

3. Sporozoites released from salivary gland into human host.

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4. Penetrate and multiply in liver.

5. Hepatic cell lysis leads to erythrocyte invasion and lysis.

C. Clinical features:

1. Irregular fevers are the hallmark of disease:

Anemia. a.

Headache. b.

Nausea. c.

Chills. d.

Lethargy. e.

Abdominal pain. f.

Upper respiratory complaints. g.

2. P. falciparum can cause severe disease:

Cerebral malaria – seizures and coma. a.

Hypoglycemia (specifically in kids). b.

Metabolic acidosis. c.

Severe anemia. d.

Renal failure. e.

Pulmonary edema. f.

DIC. g.

Death. h.

3. Chronic malaria (P. vivax and ovale lies dormant in liver for

years): VO.

Increased cellularity from immune response causes a.

hepatosplenomegaly.

Parasitized RBCs adhere to spleen reducing its immunologic b.

response.

Anemia from acute and chronic hemolysis. c.

Hemoglobinuria caused by severe hemolysis. d.

D. Diagnosis:

1. Thin and thick blood smears are gold standard.

2. Several slides may be needed depending on parasite burden.

E. Management:

1. Chloroquine phosphate:

No longer treatment of choice secondary to resistance. a. Use only in sensitive areas for uncomplicated disease. b.

2. Quinine + doxycycline for P. falciparum. (Quinine can be given

parentally for severe disease.)

Page 507

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IV. HELMINTHIC (WORM) INFECTIONS

A. Round worms: Eosinophils:

1. Enterobiasis (pinworm):

Most common helminthic infection in U.S. a. Enterobius eggs ingested and develop into adult worms in b.

large intestine and gravid females migrate to anus at night to

deposit eggs.

Outbreaks occur in schools, day care centers, etc. c.

Clinical features: d.i. Nocturnal puritis ani.

ii. Skin changes, bacterial infection, UTI/vaginitis,

insomnia.

Diagnosis: e.

i. Identify adult worms migrating in perineal area or eggs on

a tape swab of the anus.

ii. Eosinophilia absent.

Treatment: single dose of Mebendazole that is repeated in 2 f.

weeks (treat all family members).

2. Hookworm (Necator Americanus):

Larvae penetrate through intact skin from feces-a.contaminated soil.

Found in warmer climates (tropics, southeastern U.S.). b.

Larvae enter bloodstream, ascend trachea, descend the c.

esophagus to differentiate into adult worms and migrate

to upper intestine where they attach to the mucosal wall to

feed on host blood.

Clinical features: d.

i. Diarrhea, abdominal pain, fever, cough, rash, weight loss.

ii. Anemia common in heavily infected kids.

Diagnosis: e.

i. Ova in stool.

ii. Anemia + eosinophilia.

Treatment: Mebendazole, Albendazole + iron supplement. f.

3. Ascarias (roundworm):

Large nematode normally found in ileum. a.

Fecal-oral transmission. b.

Rare in U.S. - modern sanitation/waste treatment (1900s). c. Most infections are asymptomatic. d.

Worms migrate from the GI tract through the bloodstream: e.

i. Gut - obstruction, volvulus, malnutrition.

ii. Biliary tree - cholecystitis, ascending cholangitis,

pancreatitis.

iii. Brain – impaired cognitive function in kids.

iv. Kidney.

v. Eye.

Page 508

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Infectious Disease

vi. Lungs - cough, SOB, fever, hemoptysis.

Diagnosis: visible worms and eggs in feces and/or vomit. f.

Treatment: Albendazole, Mebendazole or Pyrantel Pamoate. g.

4. Whipworm (Trichiura):

Colon inhabitant. a.

Multiple small worms. b.

Diagnosis: Blood and mucus in stool, rectal prolapse. c.

Treatment: Mebendazole or Albendazole. d.

5. Trichinosis:

Roundworm that burrows into striated muscle. a.

Acquired by eating undercooked pork. b.

Clinical features: c.

i. Early (1 week): diarrhea, N/V, crampy abdominal pain.

ii. Later (1-2 months): myalgias and periorbital edema.

Diagnosis: d.

i. Eosinophilia.

ii. Elevated CPK level.

iii. ELISA becomes positive 3 weeks after infection.

iv. Muscle biopsy.

Treatment: mebendazole + steroids (reduce the muscle e.

inflammatory response).

6. Strongyloides:

Threadworm endemic to tropical and subtropical regions. a.

Very rare in SE U.S., immigrants and military personnel. b.

Unlike all other helminthic parasites, Strongyliodes can c.

complete its entire life cycle within the human host.

Clinical features: d.

i. Usually asymptomatic.

Dermatitis, weight loss, nausea, coughing, hemoptysis.

“Hyperinfection Syndrome” flare-up during

diminished host defenses (steroids, chemo or

malnutrition) which can lead to disseminated disease

with septic shock. Occurrence in WWII vets.

Diagnosis: ova and parasites in stool sample. e.

Treatment: ivermectin or thiabendazole. f.

7. Wuchereria Bancrofti:

Mosquito. a.

Africa, S. America. b.

Elephantiasis. c.

B. Flatworms:

1. Tapeworms:

Acquired by eating undercooked food. a.

Attach to intestinal wall with hooks or suckers. b.

3 most common types: c.

i. Beef – Taenia Saginata.

ii. Fish – Diphyllobothrium Latum.

Page 509

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Infectious Disease

iii. Pork – Taenia Solium:

Long tapeworm or brain cyst.

Cysticercosis - eggs hatch in the GI tract, embryos

burrow through gut wall and travel to distant locations

(eye, brain).

Larvae in the brain causes Neurocysticercosis

(primary cause of new-onset seizures in many parts of

the world).

Diagnosis: Stool samples. d.

Treatment: Praziquantel. e.

2. Tremetodes—Flukes:

Schistosomiasis—predilection for veins. a.

i. Mansoni:

Liver disease.

ii. Haematobium:

Bladder disease.

iii. Japonicum:

SMV, bowel.

Chinese liver fluke: b.

i. Biliary obstruction.

ii. Raw fish.

Diagnosis: Eggs in stool. c.

Treatment: Praziquantel. d.

V. SOFT TISSUE INFECTIONS

A. Cellulitis:

1. Strep Pyogenes and MSSA most common.

2. Systemic symptoms rare.

3. Routine blood cultures NOT indicated.

4. Multiple areas indicate hematogenous spread.

5. Treatment:

Penicillinase penicillins, cephalosporins. a.

Always consider MRSA. b.

6. Purulence means Staph Aureus.

7. Staph means consider MRSA.

8. Staph Epi—line infections.

9. Staph Saprophitcus—UTIs young women.

B. Methicillin-Resistant Staphylcoccus Aureus (MRSA):

1. Ca-MRSA very prevalent – no longer a hospital problem.

2. Risk factors:

Healthcare-associated: a.

i. ABX in prior month.

ii. Long-term facility.

iii. DM.

Page 510

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Infectious Disease

iv. Previous hospitalization.

v. Indwelling catheters.

vi. Mechanical vent.

vii. TPN.

Community-acquired: b.

i. Daycare.

ii. Household contacts with ca-MRSA.

iii. Homeless.

iv. Athletes.

v. Prisoners.

vi. Military.


Patients often report “spider bite”. a.

Warm, red, indurated, possibly fluctuant and draining. b.

4. Treatment:

Healthcare MRSA and ca-MRSA have different a.

susceptibilities.

ca-MRSA: b.

i. Clindamycin.

ii. TMP/SMX:

Doesn’t cover strep.

Add 1st gen Cephalosporin.

Cutaneous abscesses: c.

i. <5 cm, drainage alone.

ii. >5 cm or comorbidities, drainage + ABX.

iii. Needle aspiration inadequate.

C. Necrotizing soft tissue infections:

1. Polymicrobial – gram positive, gram negative and anaerobes.

2. Presentation:

Initially red, swollen and exquisitely tender/painful. a.

Rapid progression to purple - blue - gray with bullae and b.

loss of sensation.

Subcutaneous gas, crepitus. c.

Systemic toxicity. d.

High mortality. e.

3. Treatment:

Supportive care. a.

Poly-microbial ABX coverage: b.i. Vancomycin for MRSA.

i. Extended-spectrum beta lactam or monobactam.

ii. Clindamycin – anaerobic coverage and inhibits toxin

production.

Early surgical debridement. c.

Page 511

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Infectious Disease

D. Tetanus:

1. Usually from soft tissue injuries.

2. High risk in elderly, diabetics, IVDU and immunosuppressed.

3. Tetanospasmin (exotoxin) causes muscle spasms (lockjaw) and

hypersympathetic state.

4. Treatment:

Tetanus immune globulin (TIG) – neutralizes toxin. a.

Metronidazole. b.

Muscle relaxants. c.

Neuromuscular blockade. d.

5. Vaccination:

Minor wounds: a.i. Td only if > 10 years since vaccination/last booster.

ii. Do not administer TIG for minor wounds.

All other wounds: b.i. Nothing if vaccinated/booster < 5 years.

ii. Td if >5 years since vaccination/booster.

iii. If no previous vaccination, administer Td and TIG.

Tdap—one dose between ages 11 and 65. c.

i. Now ok to give one dose over age 65.

E. Rabies:

1. Fatal viral encephalitis.

2. Infected saliva.

3. High incidence worldwide, 29 cases in US since 2001.

4. Common carriers in U.S.:

Raccoons. a.

Bats. b.

Skunks. c.

Foxes. d.

CATS most common domestic animal. e.5. Uncommon carriers in U.S.:

Squirrels. a.

Hamsters. b.

Rats. c.

Mice. d.

Birds. e.

Reptiles. f.

Rabbits. g.6. Average incubation period 1-2 months.

7. Can range from 10 days to 2 years.

8. Post-exposure prophylaxis is 100% effective if started before

symptoms begin:

Indicted with bite, scratch or mucus membrane contamination a.

from high-risk animal.

Page 512

Notes

Infectious Disease

i. Passive immunity achieved using human rabies immune

globulin.

ii. Active immunity achieved with human diploid cell

vaccine on days 0, 3, 7, 14 (and 28 for

immunosuppressed).

Page 513

Notes

Infectious Disease

INFECTIOUS DISEASES

PEARLS

1. Irregular fevers are the hallmark of malaria.

2. P. falciparum can cause severe disease.

3. Thin and thick blood smears are gold standard in diagnosing malaria.

4. Neurocysticercosis is one of the primary causes of new-onset

seizures in many parts of the world.

5. Enterobiasis (pinworm) is the most common helminthic infection in

U.S.

6. Trichinosis is a roundworm that burrows into striated muscle. It is

acquired by eating undercooked pork.

7. Strongyloidiasis “Hyperinfection Syndrome” is a flare-up during

diminished host defenses (steroids, chemo or malnutrition) which can

lead to disseminated disease with septic shock. WWII vet!

8. West Nile disease - CSF shows pleocytosis with lymphocytosis and

elevated protein concentration and normal glucose. Treatment is

supportive.

9. SARS clinical definition:

History of fever or documented fever –AND-

Cough or SOB –AND-

Radiographic evidence of pneumonia or ARDS –AND-

No alternative diagnosis.

10. Influenza: Abrupt onset fever, HA, myalgias, malaise and respiratory

tract symptoms. Pneumonia is the most common complication.

11. Sepsis treatment:

Aggressive supportive care.

Early Goal-Directed Therapy:

CVP 8-12 cm.

Scvo2 > 70%.

Vasoactive medications to maintain MAP >65 mmHg.

Hematocrit > 30%.

Lactate clearance.

Intubation and mechanical ventilation with sedation.

Broad-spectrum antibiotic use.

Page 514

Notes

Infectious Disease

Steroids are controversial.

Glucose control (ideal <150mg/dl).

12. Routine blood cultures not indicated in cellulitis.

13. Patients often report “spider bite” with ca-MRSA infections.

14. Treat necrotizing soft tissue infections with poly-microbial ABX

coverage and early surgical debridement.

15. Tetanospasmin (exotoxin) causes muscle spasms (lockjaw) and

hypersympathetic state in tetanus infections.

Tdap one time, then dT boosters.

16. Common rabies carriers in U.S.:

Raccoons.

Bats.

Skunks.

Foxes.

CATS most common domestic animal

Page 515

Notes

Infectious Disease

REFERENCES

1. American College of Chest Physicians/Society of Critical Care

Medicine Consensus Conference: Definitions of sepsis and organ failure

and guidelines for the use of innovative therapies in sepsis. Crit Care

Med 1992; 20:864.

2. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the

treatment of severe sepsis and septic shock. N Eng J Med 2001;

345:1368.

3. Glezen WP. Clinical Practice. Prevention and treatment of seasonal

influenza. N Engl J Med 2008; 359:2579.

4. Peiris, JS, Yeun KY, Osterhaus AD, Stohr K. The severe acute

respiratory syndrome. N Eng J Med 2003; 349:2431.

5. Greenwood BM et al. Malaria. Lancet 2005; 365:1487.

6. Marx J, et al. Rosen’s emergency medicine: concepts and clinical

practice 7th ed. Mosby Elsevier: 2010.

7. Tintinalli JE, et al. Tintinalli’s Emergency Medicine: A comprehensive

study guide, 7e. McGraw-Hill: 2010.

8. Rivers CS, et al. Preparing for the written board exam in emergency

medicine, 5e. Emergency medicine educational enterprises, Inc: 2006.

9. CDC Website.

10. Illinois Department of Public Health Website.

08/13

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