Page 1 of 217

THESE CARDS WAS PREPARED BY

DR.MAZEN AL SOHAIBANI.

King Fahad Medical City –Ryadh - Saudi Arabia

He was kind enough to share them with his residents. They describe the important

points-anesthetic concerns- in most common anesthesia topics, to help you prepare for

the vaiva/case scenario exam.I hope that you will find them helpful in your exam as well

as in your clinical works as it was for me.

A:airway.

B:breathing/respiaratory system

C:circulation/heart condition.

D:drugs.

M:metabolic concerns..lytes/glucose/ABG..etc.

G:gastrointestinal system.

Page 2 of 217

THA

Usually elderly Pt

If a revision blood loss and it takes longer Epidural or GA

Look for the cause of arthritis # due to CV disease (syncope) avascular necrosis

due steroids, infarction (sickle cell disease)

Spinal Vs GA less risk of PE with spinal and blood loss

A, B, C look under elderly, and other co-existing diseases

Consider Autologus blood donation

Lab: ECG, CBC….. depend on the co-existing diseases

If suspect a difficult A/W GA, due to position

Intra-op: risk of PE (cement, BM, fat) consider art-line in Pt with CV disease

Post-op: need to anticoagulated, pain epidural or PCA

DDx of circulatory collapse intra-op: PE, MI, total spinal, anaphylaxis

Page 3 of 217

Thalassemia

Ethnic: Mediterranean, African-American, middle east and Asian

-thalassemia o major (homozygote) (Cooley’s anemia) severe, need treatment

o intermediate (hetro)

o minor (hetro)

o manifest after 1st year of life, when Hb F disappears.

-thalassemia

o 4 genes for the -chain synthesis

o 1 gene deletion silent carrier.

o 2 genes deletion mild microcytic anemia.

o 3 genes deletion severe hemolytic anemia.

o 4 genes deletion hydrps fetalis

GI absorption of iron and with multi-Tx iron overload

hemochromatosis .

treatment :

o Tx and folate in mild form

o Multi Tx and iron chelating agent in the severe form

o Splenectomy

Page 4 of 217

The Myotonias

delayed relaxation of skeletal muscle after voluntary contraction,

myotonic contracture is not relieved by regional, NDMR, or deep GA.

Relaxation may be induced by infiltration of the muscle with local anesthetic.

caused by genetic abnormalities that produce defects in sodium or chloride

channels or proteins which alter ion channel function in muscle cells

giving drugs that Na influx into the cell and delay return of membrane

excitability,like quinine, tocainide, or mexilitene, may relax myotonic

contracture.

Myotonic Dystrophy (Steinert's Disease)

is the most common form of the myotonias and the most severe.

AD inherited disorder (1 in 8000), S/S during the 2nd

and 3rd

decades of life.

clinical features associated with myotonic dystrophy: muscle degeneration,

cataracts, premature balding, DM, thyroid dysfunction, adrenal insufficiency,

gonadal atrophy, cardiac conduction abnormalities.

Cardiac abnormalities LV diastolic dysfunction, cardiac failure is rare.

o AV block , A.fib, or flutter, ventricular dysrhythmias.

o 1st -degree AV block may actually precede the onset of clinical symptoms

o Sudden death may be a result of the abrupt onset of 3rd

-degree AV block.

Page 5 of 217

Thoracic trauma:

ACLS, and in addition to other injuries

Heart and major vessels

Chest wall flail chest > 3 ribs# need intubation with PEEP

Esophageal

Diaphragm initially no S/S then CXR diagnostic

Lung parenchyma contusion

Tracheal, bronchial injury with blunt trauma Pt may have stridor,

wheezing, dyspnea S: subQ emphysema, pneumomediastinum, air leak, loss

of expiratory volume

Due to association with other injury, mainly c-spine DLT is difficult to insert

so consider other option

If chest tube drain >1L initially or >200ml/h open

When putting a C-line have it in the same side of the chest injury

Always be careful with PPV which can worse the hemodynamic with

tamponade, and convert a pneumo to a tension pneumo

Complication of chest injury empyema, recurrent pneumo, persistence air

leak, BPF

Page 6 of 217

TOF

Most common cyanotic CHD, F=M

VSD, RVH, overriding aorta, RVOTO(sub, valvular, supra)

70% have bicuspid aortic valve, 10% LAD from RCA

CXR: pul vascular marking, Rt aortic arch, ECG: RAD, RVH

Tet spells: hypercyanotic attaches peak 2-6 m, by age 6y ferq & severity

Initiated by feeding, crying, defecation

Any thing that PVR or SVR tet spells (PO2, PCO2, acidosis) Rt

to Lt shunt

S/S: clubbing, cyanosis, polycythemia

Pre-op: avoid dehydration, and don’t upset them

Hemodynamic goals:

o Preload

o R/R slow and sinus

o cont

o SVR

o PVR

A N/A

Page 7 of 217

TOF, obst

Corrected TOF, not risk, and no special precautions

May have a residual or recur VSD, or pul outflow tract obstruction

All TOF need Echo for that reason

12-ECG may have arrhythmias, or conduction abnormality after the repair

So for residual defect manage as TOF

hemodynamic Goals:

o preload

o R/R slightly maintain sinus

o Cont maintain, or slightly

o Afterload maintain, avoid sudden in SVR

No spinal

early epidural is desirable, may PVR

Consider art-line

Page 8 of 217

Tonsillectomy and Adenoidectomy

Peds considerations

Indication: recurrent tonsillitis, OSA, abscess

A tonsils size(0-+4(75%)), A/W obstruction wheezing , stridor

B OSA with snoring, O2 sat, cor pulmonale, chest retraction and RR

C CHD need Abx prophylaxis, Rt heart failure ECG, CXR, Echo

D over counter meds may contain ASA

Induction normal

Intra-op avoid NSAID’s , give zofran and decadron

Post-op:

o N&V, dehydration, pain, bleeding see other card

o Pul edema due to relief of the obstruction frothy pink secretion in

the ETT, sat, wheezing, RR

o DDx anaphylaxis , CHF, volume overload, ARDS, aspiration

o Mx supportive ETT, PPV with PEEP, O2 , diuretics

o Usually subsided with in 24 hrs

Page 9 of 217

Transplanted heart

High risk of infection mainly cholecystitis

The efferent denervation is permanent, while some may retain afferent

innervations

The response to exercise in normal heart is by HR, in a transplanted heart it’s

by SV, with little and delayed in HR

They are preload dependent

ECG may shows both donor and recipient P waves

No vagal input No bradycardia

But they response to stress(hypoxia, PCO2) by HR but it’s delayed

Premature CAD, with in 3 yrs, mainly without angina, if they have Aff pain

The main symptom is dyspnea

C altered response to stress, and drugs, CAD, maintain preload

D atropine and pancuronium No effect, Neostgmine may slow HR,

Norepi -effect, Adenosine effect, in addition to the side effect of

immunosuppressant drugs, may need stress dose steroids, and Abx coverage

M adrenal suppression, glucose intolerance

Heme anemia, thrombocytopenia

Page 10 of 217

Trauma in pregnancy

Blunt

Closed head injury is the major cause of death

Other risks:

o Uterine rupture

o Placenta Abruption

o Fetal injury

o Spleen and liver rupture

Penetrating

GSW, stabbing

Burn

Same rule of nines apply to pregnant Pt

With inhalation injury CO poisoning the fetus has a higher affinity to CO

than the mother

Apply the same ATLS, maintain LUD

Have fetal US done, and continue FHR monitor

Page 11 of 217

TURP-TURB:

Distilled H2O hemolysis not used any more

Sorbitol converted to fructose hyperglycemia, and to lactate acidosis, also

well cause osmotic diuresis and dehydration

Glycine(inhibitory neurotransmitter) transit blindness ammonia

encephalopathy

TURP Syndrome:( water intoxication syndrome)

S/S mild (restlessness, nausea, SOB, or dizziness) to severe (seizures, coma, HTN,

bradycardia, or CV collapse).

In the awake patient: a classic triad of symptoms in both SBP and DBP

associated with an in pulse pressure, HR, and mental status changes.

Volume overload Lt heart failure pul edema

CNS S/S due to both the type of irrigation and the severity of in serum Na

Management:

o ABC, 100% O2, intubate

o Notify the surgeon to terminate the procedure

o Consider DDx: over-sedation hypercarbia, hypoxia,

Anaphylactic reaction if CV collapse, diabetic coma

o 12 leads ECG, and invasive monitoring art line, CVP

Page 12 of 217

Tylenol overdose

A single dose of 10-15g can produce liver injury, 25g fulminant hepatic failure

Ingestion even a lower dose with alcohol the chance of hepatic failure

Tylenol normally detoxified by conjugation to glutathione, but with overdose

glutathione depleted metabolized by P-450 to a toxic compound

First few hr after N&V, RUQ pain with or without obtundation

After 24h symptom disappear and Pt looks well

24-72h liver failure appear, with possible ATN, and cardiotoxicity

Poor prognosis with Phos, coaglupathy, encephalopathy and acidosis

bilirubin correlate with survival

Management:

o ABC

o Mucomyst, with best result if given 12-20h after ingestion

o Roughly 150mg/kg over 15min, then 50mg/kg over 4h then 100mg/kg

over 16h

o Look at the nomogram

Page 13 of 217

Ulcerative Colitis

A may have Ankylosing spondylitis difficult A/W, with S/S bowel

obstruction RSI

B possible restrictive lung disease with ank-spond

C AR, hypovolemia

D steroids (stress dose)

M electrolytes imbalance, K , metabolic acidosis, albumin, adrenal

insufficiency

G obstruction, perforation

Page 14 of 217

Upper Ext nerve injury:

Ulnar:

sensation over the 4th

and 5th

fingers

Muscle wasting, unable to grip a paper between fingers

Median:

Loss of skin sensation over the lateral 3 ½ of the palm of the hand

Weakness of wrist flexion, when making a fist the index and middle

finger remain straight, also loss of thumb flexion

Radial:

If the injury at the axilla unable to extend the forearm (triceps)

If in the spiral groove wrist drop

MCN:

Loss of arm flexion (biceps), loss of sensation over the lateral aspect of the

forearm

Axillary N

Loss of skin sensation over the lower ½ of the deltoid muscle, with

weakness of arm abduction

Page 15 of 217

URTI

Need to distinguish from allergic rhinitis

incidence of croup, bronchospasm, and laryngospasm

If emergency or urgent surgery proceed, and anticipate the above problems

If elective, and < 1yr postponed

If elective, >1 yr temp postponed

Elective > 1yr normal temp P/E purulent secretion, LRTI postponed

= = = = clear proceed to surgery

How long to postponed for, if too long, the child may end up with another episode

of URTI, So 2-4 wks is reasonable

Page 16 of 217

Uterine Rupture

Risk see box 37-1 chestnut

Mainly fetal distress and bleeding

A & B onst

C hypovolemic shock, hypotension

Heme bleeding, anemia

Mx

See abruption card

Basically same management they come for stat C/S due fetal distress

Page 17 of 217

VAE:

When the surgical field > 5cm above the Rt atrium.

40-50% in the sitting position, if known PFO, avoid sitting position

Dx. By TEE the most sensitive then pericardial doppler, placed in the Rt

sternal border 3rd

to 6th

intercostal space, which detect 0.25ml of air

Miller all Pt going for N.surgery in sitting position need to have CVP

Mx: 100% O2

Notify the surgeon, flood the surgical field with saline gauze

Wax the bone edges

Compress the jugular vein

Head down

Aspirate through the CVP

D/C N2O, and PEEP which may cause paradoxical embolism

Page 18 of 217

von Willebrand's Disease

AD, 3types I, II, III(very rare), group O blood have 20-30% less vWF

Prolonged bleeding time, N PT and PTT

I (70-80%) vWF, IIA also function abnormal, IIB they have

thrombocytopenia which aggravated by giving DDAVP (C/I).

Pregnancy vWF

Rx DDAVP 0.3ug/kg 1hr prior to surgery.

DDAVP may cause fibrinolysis by releasing t-PA so consider giving TXA

Cryo have vWF , recombinant Vwf.

Hematology consult, Possible HIV +

Do gentle intubation, avoid blind suctioning, avoid Regional anesthesia

Page 19 of 217

VSD

Rare in adult , with S/S depend on the size, and PVR, the larger, and the lower

PVR more severe symptom

small asymptomatic, load pansystolic murmur Lt sternal border, with normal

ECG and CXR

mod also asymptomatic, with biventricular enlargement on CXR

large when pul blood flow > systemic, S/S early as 4 wks, Lt Rt change to

Rt Lt cyanosis

hemodynamic goals:

o Preload

o R/R N and sinus

o Cont slight

o Afterload

o PVR

Pre-op Abx prophylaxis

A N/A

B pul edema

C shunt, CHF, low forward CO

Page 20 of 217

White Cell–Related Transfusion Reactions

Febrile Reactions:

antibodies to the HLAs after multiple Tx, 1% of all RBC transfusions.

the patient experiences a temp of more than 1°C within 4 hrs of a blood Tx and

defervesces within 48 hours.may also develop chills, respiratory distress, anxiety,

headache, myalgias, nausea, and a nonproductive cough.

Febrile reactions can be treated with acetaminophen

should be distinguished from a hemolytic transfusion reaction (direct Coombs test)

Graft-versus-Host Disease (GVHD)

the donor lymphocytes may become engrafted, proliferate, and establish an

immune response against the recipient.

Patients at risk for GVHD include organ transplant recipients, neonates who have

undergone a blood-exchange Tx, and patients immunocompromised by many other

disease processes. GVHD typically progresses rapidly to pancytopenia, and the

fatality rate is very high

Also when a genetic relationship exists between the donor and the recipient

GVHD has been reported with the transfusion of whole blood, packed RBCs,

granulocytes, platelets, and fresh, not frozen, plasma. It has not occurred following

transfusion of FFP, cryoprecipitate, or frozen RBCs

Page 21 of 217

Wilms tumor

A delayed G. emptying RSI

B lung mets, chemo, and radiotherapy effect

C HTN, severe if both kidneys involved CHF, renin secretion

D chemo

R hyperaldosternism(2nd

) K

H severe anemia, low PLT, acquired vWD possible need F VIII concentrate

M art,and central line

Lab X-match, Lytes CBC

other upper body IV access

Potential intra-op problem IVC obstruction CO

Tumor in the IVC embolic phenomena

Post-op ICU backup �mazen � m a z e n |N�

h o m e o f f i c e , � �

Page 22 of 217

AAA Elective

Long procedure, large fluid shift, and high risk of blood loss

A N/A

B potential COPD

C CAD, HTN,

Renal border line function

In the pre-op evaluation: concentrate on cardiac function with detailed H/P and

work up

Lab: CBC-D, BUN, creat, Lytes, Mg, ECG, CXR, PFT, ABG, Echo if available

Consider optimizing any medical condition pre-op by meds, consultation, and

further evaluation.

X-match for at least 6 U of blood, have FFP ready

Consider Epidural to do it as a combined technique

Have the cell saver in the room, IV worming device, with blood set

Lines: Big 14G peripheral IV, Art line, CVP/PAC, bear hugger

Monitors: standard + 5 leads ECG, Foley, temp, art-line, CVP/PAC, TEE

Induction: routine, modify on cardiac status

Before induction have inotrops and vasodilators ready to go

Page 23 of 217

Abruptio placenta

Risk with cocaine abuse, smoking, trauma, previous abruption, age

Most common cause of DIC, risk ante-postpartum hemorrhage, fetal hypoxia

The bleeding could be concealed, and can have 2500ml of blood

DDx placenta previa, uterine rupture

A obst

B obst

C hypovolemic shock,

Heme anemia, coaglupathy DIC

R ARF from both shock, and DIC

Fetus Demise, hypoxia,

Mx:

Depend on the severity, usually partial managed conservative with bed rest

ABC, RSI, GI prophylaxis, induction with Ketamine, LUD

Lab CBC, Lytes, BUN, creat, PT, PTT, fibrinogen, D-dimer , X-match

Monitor Art line, CVP/PAC, fetal monitoring , large IV

Synto may not work atony consider ergot, hemoabt(PGF2), may end up

need hysterectomy

Page 24 of 217

Achondroplasia:

A potential difficult A/W, foramen Magnum Stenosis Avoid neck

extension , OSA

B Kyphoscoliosis Restrictive lung disease

C Cor-pulmonale, pul HTN

CNS hydrocephalus, possible ICP, central sleep apnea

Lab CXR, C-spine, CT, MRI base of the skull, PFT, ECG, Echo, in

addition to the regular blood work

Page 25 of 217

Acromegaly

99% from pituitary adenoma

A large tongue , epiglottis, large nose difficult intubation and mask fitting

Need FOI, possible vocal cord paralysis, and subglottic stenosis smaller

ETT, and potential post-op A/W obstruction

B OSA

C HTN, Cardiomegaly, cardiomyopathy, arrhythmias, CHF, hemodynamic

instability (ECG, CXR, Echo)

D steroids for other pituitary problems

N neuropathy (document), adenoma effect ? pressure vision

M DM, hyperthyroid,

Position nerve compression

Monitors art line

Page 26 of 217

ACT

Mainly for depression, possible difficult to obtain an accurate medical history

C/I: Pheo, pregnancy, recent CVA and MI, SOL with ICP, and long bone #

The main effect is on the CVS:

o Initial PSN effect with hypotension and bradycardia, even arrest

o Followed by intense SNS activation with HTN, tachycardia, arrhythmias

and ICP and IOP

Review the old anesthetic record for the dose, and any problems may had

happened

Also review all Pt med (TCA, MAOI) avoid indirect sympathomimetics, also

be careful when direct acting drugs exaggerated response

Monitors standard CAS monitors, consider invasive monitoring in sick Pt

Pt with pacemaker or AICD not C/I have the magnet in the room, know what is

the program

Page 27 of 217

Acute liver dysfunction

M&M

Postponed if not an emergency

History of alcohol, drugs, exposure to toxins at work

A LOC

B hypoxia, hyperventilation, V/Q mismatch

D altered drug metabolism

M lytes abnormalities

Renal impairment

CNS encephalopathy

Heme coags abnormalities

Avoid sedation pre-op

Correct coags pre-op

Intra-op avoid hypoxemia, and hypotension both hepatic blood flow

Page 28 of 217

Acute pericarditis, and effusion

Most common cause is viral infection

Post-MI Dressler Syndrome

S/S diffuse chest pain, with diffuse ST-elevation in ECG pericardial leads,

with sinus tachy, chest exam friction rub.

Consider Echo, if suspected effusion or tamponade

Normal pericardial fluid 20-30 ml,

o In chronic effusion the pericardium can accommodate up to 1000

ml, without S/S of tamponade

o But in acute effusion as low as 200 ml can give symptoms

Page 29 of 217

Adrenal Insufficiency (Addison disease):

Need 90% destruction of the adrenal gland to produce symptoms

primary (Addison's disease) is idiopathic adrenal insufficiency due to

autoimmune destruction. causes both a gluco and a mineralocorticoid

deficiency.

Hashimoto's thyroiditis in association with autoimmune adrenal insufficiency

is termed Schmidt's syndrome.

Other: bacterial or fungal infections, metastatic cancer, sepsis and

hemorrhage.

Secondary: anterior pituitary fails to secrete sufficient quantities of ACTH.

from tumor, infection, surgical ablation, or radiation therapy.( less severe S/S,

aldosterone is maintained

S/S Wt loss, muscle weakness, BP, abd/back pain due bleeding, N&V,

hyperpigmenation in primary only

Dx by ACTH stim test

Page 30 of 217

Adult with repaired CHD

Type of CHD,

When, What, and Where, (Repair)

Understand the physiology of the repair

Residue, Sequelae, and the complication of the repair.

Follow up with cardiologist, recent Echo, if not ask for one

Discuss the case with a college who knows more about CHD(peds cardiac

anesthetist)

The Need for SBE prophylaxis

High risk for arrhythmia (pads on) for pacing, cardioversion, or shock

Have inotrops support ready.

In case of shunt be meticulous about air in the IV, use saline instead of

air for epidurals.

In case of pulmonary HTN have NO in the room

Page 31 of 217

AI

Well tolerated in pregnancy

hemodynamic Goals:

o preload maintain, LUD

o R/R slightly maintain sinus

o Cont maintain, avoid cardiodepressant

o Afterlaod

Epidural is good

Page 32 of 217

Airway foreign body

Emergency and potential life threatening

In addition to peds consideration

Brief H/P AMPLE, depend on the Severity of the symptoms and

hypoxemia may consider CXR( most are radiolucent), but may see

atelectasis

Do inhalation induction with Sevo, Avoid PPV, minimal support if needed

Assess the eye for depth (see later)

The dilemma Full stomach Vs need of maintaining spontaneous

Ventilation

Once the eye in stage III do direct laryngoscopy Lidocaine spray

May give IV bolus of propofol upon the removal of the foreign body

Consider a dose of decadron , and racemic Epi

Page 33 of 217

Airway laser surgery:

Risk for both the patient and OR personal

Knew what is the indication papiloma, stenosis, neoplasm PFT, flow volume

loop, CT

The airway is shared with the surgeon close communication

Eyeglasses and laser mask, Pt eyes closed, covered with wet gauzes, and metal

shields, cover the exposed skin with wet towels

Consider glyco pre-med

Use laser-metal ETT, and fill the cuff with NS with methylene blue

Avoid N2O, use the lowest FiO2 possible < 40%, other Jet ventilation

Pt need to be completely paralyzed

In case of airway fire remove ETT, have 60 cc syringe filled with NS ready,

after controlling the fire asses the airway damage, and ongoing fire, avoid high

Fi02 initially till you make sure that there is no ongoing fire direct

laryngoscope, bronchoscope with possible lavage and CXR, reintubate with new

ETT, keep intubated, Abx, and steroids ICU post-op

CO2 laser only 0.01 mm penetration less bleeding and edema post-op

With Nd-YAG laser deeper penetration, and risk of air embolism

The metal-ETT are bigger than the PVC tubes so use one size smaller

Page 34 of 217

Equations

alveolar gas equation:

Shunt equation

ventilation–perfusion ratio (VQI),is determined as follows:

Page 35 of 217

Amniotic fluid embolism

Catastrophic event with high mortality rate 86%

A LOC, obst

B hypoxia, pul edema

C cardiopul collapse, RV failure

D D/C synto

Heme DIC, hemorrhage

R ARF

CNS seizure

Mx:

ABC, 100% O2, Large IV,LUD, Lab as abruption, last thing to do CPB (case

report)

If Pt survive ICU

Page 36 of 217

Amphetamines

For management same as cocaine

A&B obst

C HTN arrhythmias, tachycardia

D MAC with acute intoxication, while chronic MAC

CNS seizure

Obst risk of abruption

R. anesthesia severe hypotension, with possible arrest

Ecstasy:

serotonin and dopamine level

C HTN arrhythmia

H DIC,

MSK rhabdomyolysis

M+R lytes abnormality, ARF

Fetus toxicity

Mx

Page 37 of 217

Amyloidosis:

Extracellular deposition of amyloid type protein

A macrogolssia, tracheal stenosis (smaller ETT)

B pul edema from CHF

C arrhythmias, restrictive myopathy, CHF, autonomic dysfunction

Renal CRF, nephritic syndrome

Heme Factor X deficiency

Lab/DI: CBC, lytes, BUN, Creat, CXR, PFT/ flow volume loop, ABG,

ECG, ECHO, coags

Monitoring: CAS, Art-line, CVP/PAC, TEE

Avoid Regional if coagulopathic

The main goal intra-op is to maintain U/O, avoid any nephro-toxic drugs

Have an ICU backup

Page 38 of 217

Amyotrophic Lateral Sclerosis (ALS)

Degenerative disease of the CNS with involvement of both UMN and LMN

S/S Asymmetric weakness, reflex, fasciculation and muscle atrophy

A bulbar involvement Aspiration mod RSI

B respiratory failure

C

D Sux C/I, sensitivity to NDMR,

M abnormal glucose and Ca metabolism, with thyroid dysfunction

Do Regional technique better

If GA: Mod RSI, ICU post-op

Page 39 of 217

Anesthesia for organ donation:

COMMON PHYSIOLOGIC DERANGEMENTS AFTER BRAIN DEATH

Condition Cause

Hypotension Hypovolemia (DI; hemorrhage) Neurogenic shock

Hypoxemia Neurogenic pul edema, Pul contusion, Pneumonia

Gastric aspiration, Fluid overload

Hypothermia Hypothalamic infarction, Exposure

Dysrhythmia Intracranial injury or herniation, Hypothermia

(especially bradycardia) Hypoxia, Electrolyte abnormality

Myocardial contusion, ischemia

Avoid vasopressors may cause visceral ischemia

Consider using low dose Dopamine if needed

They are atropine resistance

Consider use NDMR due to somatic spinal reflex

No need for GA, for BP consider use vasodilators

Page 40 of 217

Anesthesia For The Geriatric Patient

physiological reserve of all organs

Common diseases with aging are Sleep apnea, COPD, CAD, HTN,

arrhythmias, DM, arthritis, Alzheimer

A stiff neck

B CC, CV, V/Q mismatch, response to hypoxia and hypercarbia

C diastolic dysfunction, HTN, CAD, arrhythmias, CHF

D Vd, with both hepatic and renal clearance, MAC, sensitivity to

narcotics and sedatives

M DM, Na, heat production with more prone to hypothermia

GI/hep gastric empting, hepatic mass and blood flow

Renal GFR, Na losing , drugs clearance, risk of volume overload

CNS Alzheimer, dementia, stiff ligament difficult epidural/spinal

heme anemia

Always IV wormer, bear hugger, and consider invasive monitoring

Page 41 of 217

Aneurysm

F>M, usually present with SAH

Aneurismal SAH classification by Hunt & Hess and WFNS to estimate the

surgical risk and outcome

WFNS Grade GCS Scale* Motor Deficit

I 15 Absent

II 13–14 Absent

III 13–14 Present

IV 7–12 Present or absent

V 3–6 Present or absent

A LOC

B pul edema

C HTN, ECG changes ST, T, QT, U role out IHD

M lytes disturbance, SIADH, DI, pituitary dysfunction

Classic S/S: headache, N&V, photophobia, LOC

Lab: CBC, Lytes, BUN, Creat, CXR, ECG, review CT/MRI, X-match

Induction as Supratentorial

May need controlled hypotension, unless they do temporary clipping

Page 42 of 217

Ankylosing spondylitis

M>F, 20-30 y.o, -ve rheumatoid factor, HLA-B27 is +ve in 90% of Pts

S/S: back pain and stiffness improve with exercise, lumber disc

degeneration, sacroilitis

A; Spines: limitation in the movement of all the spines, with risk of C5-C7 #,

possible difficult intubation , TMJ involvement, Cricoarytenoid involvement

(rare)

B: restrictive lung disease, chest wall compliance and VC, consider PFT

C: Aortitis with AI, CHF due to cardiomyopathy, dysrhythmias secondary to

cardiac conduction system involvement.

Renal risk of RF

Drugs: anti-inflammatory drugs

Better to extubate awake

Intervertebral ligament calcification, difficult to perform neuraxial block by

midline approach, ? C/I if pt have peripheral neuropathy.

Page 43 of 217

Aortic Regurgitation

Chronic: rheumatic disease, hypertensive and atherosclerotic diseases, cystic medial

necrosis with or without other features of Marfan's syndrome, connective tissue diseases

including Reiter's syndrome and ankylosing spondylitis, luetic (syphilitic) aortitis,

Acute: infective endocarditis, nonpenetrating trauma, ascending aortic aneurysm dissection

Pathogenesis

Chronic: LV volume overload LV dilationLVH eccentric hypertrophy

LVEDV but LVEDP still normal over time LVEDP

Acute: severe AR LV volume overload, but without time for LV dilation,HR is the only

comp mechanism to maintain forward CO, LVEDP and LAP rapidly, with pul congestion.

History: chronic AR usually remain asymptomatic for years. Early symptoms include a

sensation pounding in the chest, palpitations, or head pounding. Exertional dyspnea may be the

first manifestation of LV decompensation, with later development of orthopnea and PND.

Symptoms of more advanced disease include angina pectoris, which may be nocturnal, and

eventually symptoms of right-sided CHF with ascites and peripheral edema.

Prognosis worsens with the onset of symptoms; mortality rate is estimated to be more than

10% per year among patients with severe AR and angina pectoris and more than 20% per

year among patients with symptoms of CHF.

Acute severe AR Patients typically exhibit symptoms referable to the underlying disease,

including fever with infective endocarditis, and chest or back pain with aortic dissection.

Page 44 of 217

Aortic Stenosis

Valvular AS should be distinguished from nonvalvular forms of LV outflow obstruction, including

congenital supravalvular stenosis and subvalvular membrane, ridge or tunnel stenosis, and dynamic

subvalvular LV outflow obstruction in HOCM

The normal AVA is 2.5-3.5 cm2. AS is not usually of hemodynamic significance until the valve

area is to 25% of normal. mild 1.5 to 3.0 cm2, moderate 1.0 to 1.5 cm

2, severe <1.0 cm

2. With

normal CO, severe AS mean transvalvular pressure gradient 50 mm Hg.

Transvalvular gradients are affected by flow, so patients may have low gradients despite severe AS

if there is LV systolic dysfunction.

therapeutic decisions typically are based on the presence of symptoms in the setting of significant

aortic stenosis, categorization of disease as mild, moderate, or severe is of lesser clinical

importance.

Etiology congenital (bicuspid), rheumatic, or senile degenerative (calcific) in origin.

History long latent period >30 yrs

The three classic symptoms associated with aortic stenosis are dyspnea, angina pectoris, and

syncope. (life expectancy < 5 yrs)

Dyspnea due to in LVDP, LA, and pulmonary venous pressures.

Angina occurs without CAD resulting from O2 demand from LV mass and intracavitary

pressures in the setting of a fixed blood supply and from coronary flow due to progressive

outflow obstruction.

Syncope may be caused by peripheral vasodilation with exertion, with in peripheral oxygen

requirement in the setting of a fixed CO.

Page 45 of 217

Appendectomy

In older Pt consider other and possible catastrophic problem (AAA)

A full stomach (RSI)

C dehydration, with intravascular volume

GI Vomiting, full stomach

M Lytes abnormalities, acid base disturbance

Other could be septic

Lab CBC-D, lytes, BUN, Creat, ABG

Pain PCA

APR

For rectal Ca, with possible bowel obstruction

Usually in elderly with other co morbidities

With bowel prep fluid deficit hypotension upon induction

A RSI (b. obstruction)

C hypovolemia, elderly

Position lithotomy, jackknife

Monitors CAS, art line, temp, foley

Pain PCA, epidural

Page 46 of 217

Arnold chiari malformation

It’s one of the chiari malformation it’s type II

associated with myelomeningocele

present for posterior fossa decompression and repair of myelomeningocele and

insertion of shunt

on of the main issue is position during induction due to myelomeningocele,

may put a donut where the defect is in the hall, if big may have to the induction

in lateral position then turn prone

A potential difficult airway, due to hydrocephalus awake intubation

B vocal cords paralysis trach, resp depression due to post fossa compression

C bradycardia

CNS the defects, and CN palsy

position as above

Page 47 of 217

AS

Mild well tolerated

Mod/severe not well tolerated

hemodynamic Goals:

o preload maintain, LUD, treat hypovolemia aggressively

o R/R slightly maintain sinus treat arrhythmia aggressively

o Cont maintain, avoid cardiodepressant

o Afterlaod , avoid sudden in SVR

Need are-line, CVP/PAC risk of arrhythmia with insertion, to maintain

PCWP =18

GA opioids, mix kitamine/STP

Have the crash cart in the room, pads on the Pt

ASD:

3 types: ostium secundum @ foramen ovale

Page 48 of 217

Asthma:

H/P: how bad is the asthma? Severity? Frequency? Any hospital or ICU admission

in the past, if yes when was the last one, how he/she manage the asthma at home,

or need ER visit, Exam: V/S, A/E , wheezing

Review PFT results pre-post bronchodilators, and optimize pre-op

If Pt is steroids (PO) dependent asthma consider steroids coverage peri-op

Pre-med -agonist, Anticholenergics,

Induction: IV Lidocaine, avoid STP, intubate deep, may consider LMA

Maintenance: avoid any histamine releasing drugs,

Emergence: consider extubate deep, IV Lidocaine pre-extubation

Consider regional anesthesia to avoid intubation

Page 49 of 217

Autonomic hyperreflexia:

Post spinal cord injury above T-7 70-75%, following the resolution of

spinal shock, 2-3 weeks after injury

Stimulation below the level of transection Severe HTN with bradycardia

A potential difficult A/W, unstable C-spine, aspiration risk (FOI), (RSI)

B respiratory reserve and volumes, risk of aspiration, pneumonia, PE,

respiratory failure PFT, ABG, post-op vent (ICU)

C hyperreflexia, orthostatic hypotension, assess the volume status. ECG,

D (Sux C/I), have anti-HTN ready (Niprid) N. stimulator show resistance

N deficit

Neuraxial best is a good choice but may be difficult to assess the level of

the block too high, or too low

Hyper-reflexia may happen post-op due to bladder or rectal distension.

Sequelae CV collapse, arrhythmias, pul edema, stroke, seizure, death

Page 50 of 217

AVM:

M>F, 10-40yrs

S/S parenchymal hemorrhage, SAH, Sz, motor/sens deficit

In Peds Vein of Galen AVM hydrocephalus + high output cardiac failure

A LOC

B aspiration during Sz

C CHF

CNS Sz, LOC, ICP

Pt may have (NPPB) normal perfusion pressure breakthrough cerebral

hyperperfusion with normal CPP

o Rx: diuretics, hypervent, mild hypothermia, N-low MAP, high dose STP

The rest of management like Aneurysm

High risk of bleeding blood in the room

Page 51 of 217

Airway laser surgery:

Risk for both the patient and OR personal

Knew what is the indication papiloma, stenosis, neoplasm PFT, flow

volume loop, CT

The airway is shared with the surgeon close communication

Eyeglasses, Pt eyes closed, covered with wet gauzes, and metal shields

Consider glyco pre-med

Use laser-metal ETT, and fill the cuff with NS with methylene blue

Avoid N2O, use the lowest FiO2 possible, other Jet ventilation

Pt need to be completely paralyzed

In case of airway fire remove ETT, have 60 cc syringe filled with NS

ready, after controlling the fire asses the airway damage direct

laryngoscope, bronchoscope with possible lavage and CXR, reintubate with

new ETT consider ICU post-op

Page 52 of 217

EEG FREQUENCY RANGES

Delta rhythm (0–3 Hz) Deep sleep, deep anesthesia, or pathologic states (e.g.,

brain tumors, hypoxia, metabolic encephalopathy)

Theta rhythm (4–7 Hz) Sleep and anesthesia in adults, hyperventilation in

awake children and young adults

Alpha rhythm (8–13 Hz) Resting, awake adult with eyes closed; predominantly

seen in occipital leads

Beta rhythm (>13 Hz) Mental activity, light anesthesia

Page 53 of 217

Hyponatremia < 130

or in serum Na & in ECV & PV, so it’s result from excess or deficit of water

total body Na regulated by aldosterone and ANP, where serum [Na] by ADH

S/S depend on the rate and severity of of Na: loss of apatite, N&V, cramps, weakness,

LOC, coma and seizure

Acute CNS S/S is due to cerebral edema

What is the serum osmolality see figure

Cerebral salt wasting syndrome, mediated by BNP, independent of SIADH, risk head

trauma, tumor, SAH, and infection

SIADH see other card

Rx < 120 with 3% NS @ 1-2 ml/kg/hr to serum Na 1-2 mEq/l/hr only for few hrs, not

more than 25 mEq/l/48 hrs

Rapid correction abrupt brain dehydration central pontine myelinolysis mild (transient

behavioral disturbances or seizures) to severe (including pseudobulbar palsy and

quadriparesis).Within 3 to 4 weeks of the clinical onset of the syndrome, areas of

demyelination are apparent on MRI, risk factors (alcoholism, poor nutritional status, liver

disease, burns, and hypokalemia) , cerebral hemorrhage and CHF

Once serum Na > 120 fluid restriction is enough , Also treat the underlying causes

To calculate the net water loss necessary to [Na+] in hyponatremia, use the following equation:

Current [Na+] × current TBW = desired [Na

+] × desired TBW TBW= 0.6x wt

Page 54 of 217

INDICATIONS FOR ONE-LUNG VENTILATION

ABSOLUTE 1. Isolation of each lung to prevent contamination of a healthy lung

a. Infection (abscess, infected cyst) b. Massive hemorrhage

2. Control of distribution of ventilation to only one lung

a. Bronchopleural fistula b. Bronchopleural cutaneous fistula

c. Unilateral cyst or bullae d. Major bronchial disruption or trauma

3. Unilateral lung lavage

4. Video-assisted thoracoscopic surgery

RELATIVE 1. Surgical exposure—high priority

a. Thoracic aortic aneurysm

b. Pneumonectomy

c. Upper lobectomy

2. Surgical exposure—low priority

a. Esophageal surgery

b. Middle and lower lobectomy

c. Thoracoscopy under general anesthesia

Page 55 of 217

Omphalocele and Gastroschisis

o Impaired blood supply to the herniated organs, and intestinal obstruction

o Major intravascular fluid shift and dehydration full-strength balanced salt

solution

o Hypothermia and hypoglycemia

A possible difficult airway Beckwith-Wiedemann syndrome consists of

mental retardation, hypoglycemia, congenital heart disease, a large tongue, and

an omphalocele.

B respiratory failure

C CHD in 20% of infants with omphalocele.

Induction: NG aspirate gastric content then RSI , need large IV , possible

central, and arterial line

Post-op keep intubated

Page 56 of 217

Stroke & TIA:

Hemorrhagic or ischemic

Etiology: Atherosclerosis, embolic MI, A.fib, VHD, post-op CEA,

trauma, severe HTN

A LOC, loss of A/W reflux (RSI)

B hypoventilation

C HTN, CAD, VHD, A.fib, arrhythmias ECG, Echo

D anti-PLT, ASA, coumadin

N LOC

Peri-op

Avoid swinging in BP, and hyperglycemia

With chronic HTN the cerebral autoregulation curve shifted to the Rt

Page 57 of 217

Bioterrorism

Use of nerve gases which are a potent Ach.esterase inhibitor and cause a

cholinergic crisis

A mass casualty with both physical trauma and gas intoxication

Healthy soldiers Vs civilian with different age groups and other co-

morbidities

The amount, duration and the rout of exposure are the major determine of

the clinical course of intoxication

Exposure to vapor gives respiratory symptoms (SOB, wheezing,

bronchorrhea) with rapid cardiopulmonary collapse (muscarinic effect)

Where dermal exposure slow, and gradual S/S local muscle twitches

and fasciculation (nicotinic effect) then resp failure, also carry more risk

to the health care personal with direct contact

All the nerve gases causes irreversible inhibition to AchE in both central

and peripheral NS

The key point in the management is to give the antidote ASAP, and protect

the health care personal

Page 58 of 217

BKA

For PVD, DM, gangrene, trauma, tumor

Most of the Pt with major co-morbidities e.g. CAD, PVD, DM, COPD,

CVA, Sepsis, CRF,

H/P standard + depend on the co-morbidities

Lab also as above

Options: GA Vs spinal/epidural may the incidence of phantom limb

pain, but look for C/I

monitors standard + depend on the above co-morbidities

Position risk of ischemic necrosis (pads)

EBL 250 ml

The use of tourniquet bleeding, but be aware of risk thrombus

embolization PE

Post-op pain(epidural, nerve block, PCA), DVT (S/C heparin), MI, CVA,

infection, bleeding

Page 59 of 217

BPF and Empyema

Causes: after pulmonary resection for carcinoma, traumatic rupture of a

bronchus or bulla ( barotrauma or PEEP), penetrating chest wound, or

spontaneous drainage into the bronchial tree of an empyema cavity or lung

cyst

PPV contamination of the healthy lung, loss of air with alveolar

ventilation and CO2 retention, and potential tension Pneumothorax

In case of empyema with BPF drain the empyema under LA with chest tube

under suction, then do a CXR, then may fix the BPF under GA

GA options ( the main target is to avoid PPV)

o Awake intubation with DLT

o Gas induction and maintaining spontaneous ventilation

o RSI

Keep FiO2 always 1, and avoid N2O

For non-surgical management: DLT and resting the affected lung, or use of

HFJV

Keep a high index of suspicion for tension Pneumothorax

Page 60 of 217

Brain death

―irreversible cessation of all function of the entire brain, including the cortex

and brain stem, determined in accordance with accepted medical standards‖

CRITERIA FOR THE DIAGNOSIS OF BRAIN DEATH:

LOSS OF CEREBRAL CORTICAL FUNCTION

o No spontaneous movement

o Unresponsive to external stimuli

LOSS OF BRAIN STEM FUNCTION

o Absent respiratory reflex (apnea test)

o Absent cranial nerve reflexes (Gag or cough reflex to suction)

o Pupillary light reflex ( no pupil constriction)

o Corneal reflex ( no blinking with corneal touch)

o Oculocephalic reflex ( doll’s eyes)

o Oculovestibular reflex (cold caloric test)

o Atropine resistance

SUPPORTING STUDIES

o Electroencephalography

Page 61 of 217

Brain metabolism and physiology:

In adult:O2 3.5 ml/100g/min& 5.5 mg/100g/min of glucose, peds 5.5 ml O2

the autoregulation is abolished by trauma and hypoxia

CSF from the choroids plexus and absorbed by the arachnoid villi, volume

100-150 ml, rate of production and absorption 0.3-0.4 ml/min, with

production by Lasix and acetazolamide

Enf production and resistance to absorption, Iso 0/ resistance

ICP N= 10 mmHg, ICP CPP, and herniation

All volatile agents CBF with return to baseline in 3 hrs, with CMRO2

All volatile agents and kitamine cause cerebral vasodilation, except N2O

N2O cause CBF w/out dilation, and no change in CMRO2

All IV drugs cause CBF and CMRO2

Page 62 of 217

Bronchiectasis:

Localized irreversible dilation of bronchus

May have COPD, and restrictive component

And may associated with other condition so look of other underlying disease:

aspergillosis, HIV, R. arthritis

If Pt present to OR with active pul infection postponed Sx, and give Abx therapy

Lab: PFT, ABG, CXR pneumonia

Pt may present with hymoptysis required arterial embolization, or resection of

the affected segment

Consider DLT to isolate the affect lung

Need pre-op Abx

Page 63 of 217

Carcinoid Tumors

GI is the most common source, 50% appendix, 25% in the ileum(the source of

metastatic tumors), also from the lung,

hormones secreted by nonmetastatic tumors reach the liver by portal vein and are

usually inactivated there. once metastases to the liver, the hormones secreted by

the hepatic metastases may have direct access to the systemic circulation, to

produce the S/S of the carcinoid syndrome

Could be a manifestation of MEN I,

Release Serotonin, Histamine, Kinins

Symptoms: cutaneous flushing, abd pain, V, diarrhea, HTN, hypotension,

bronchospasm, and hyperglycemia

A N/A, Gentle induction, avoid sux, STP

B bronchospasm, endobronchial tumor obstruction

C Rt side disease myocardial fibrosis TR, PR, consider CVP, art line

sympathomimetic drugs can trigger mediator release from carcinoid tumors

D Give antihistamines, avoid drugs that can cause histamine release

octreotide 10-100 ug IV

M Dehydration due to diarrhea, and vasoconstriction , hyperglycemia

Intra-op

Page 64 of 217

Cardiac herniation

An emergency and life threatening with mortality 50%

With pneumonectomy, in the 1st few hrs or few days later

Pathophysiology:

o twisting of the SVC (SVC syndrome),

o twisting IVC (cardiovascular collapse),

o twisting distal trachea (wheezing),

o twisting pulmonary veins (pulmonary edema),

o pericardial constriction of the heart (myocardial ischemia and

ventricular arrhythmia)

Risks:

o Events that intrapleural pressure in the (ventilated) hemithorax or

that intrapleural pressure in the surgical (empty) hemithorax may

predispose the patient to cardiac herniation.

o Placing the patient with the empty hemithorax in a dependent

o Use of high levels of pressure and volume during mechanical

ventilation of the remaining lung can push the heart into the empty

hemithorax. And coughing

Page 65 of 217

Cardiac Risk* Stratification for Noncardiac Surgical Procedures

High (Reported cardiac risk often greater than 5%)

· Emergent major operations, particularly in the elderly

· Aortic and other major vascular surgery

· Peripheral vascular surgery

· Anticipated prolonged surgical procedures associated with large fluid

shifts and/or blood loss

Intermediate (Reported cardiac risk generally less than 5%)

· Carotid endarterectomy

· Head and neck surgery

· Intraperitoneal and intrathoracic surgery

· Orthopedic surgery

· Prostate surgery

Low† (Reported cardiac risk generally less than 1%)

· Endoscopic procedures · Superficial procedure

· Cataract surgery · Breast surgery

*Combined incidence of cardiac death and nonfatal myocardial infarction.

†Do not generally require further preoperative cardiac testing.

Page 66 of 217

CAROTID ENDARTERECTOMY

Pre-op: H/P

Lab: CBC, Lytes, BUN, creat, Glucose, ECG, PFT if needed

A N/A

B possible smoker COPD

C CAD, HTN (need to well controlled pre-op)

M DM

CNS neurological deficit

Regional (deep, superficial cervical plexus) Vs GA same out come

Induction: anticipate fluctuation of BP

Maintenance: Iso neuro-protection, Keep BP 20% higher, monitor blood

glucose, LA infiltration over the carotid sinus, give heparin 100u/kg

Monitors: standard+ 5leads ECG, Art-line, in cardiac Pt consider TEE,

Emergence: early to assess for nay neuro deficit

Post-op potential problems: new neuro deficit back to OR or Angio,

hemodynamic instability mainly HTN, bleeding with hematoma formation which

may compromise the Airway Back to the OR, 100% O2 have difficult airway

Page 67 of 217

Canadian Cardiovascular Society Functional Classification of Angina Pectoris

Class Definition Specific Activity Scale

I Ordinary physical activity, (eg, walking and climbing stairs) does not cause

angina; angina occurs with strenuous, rapid, or prolonged exertion at work or

recreation. Ability to ski, play basketball, light jog (5 mph), or shovel snow

without angina

II Slight limitation of ordinary activity; angina occurs on walking or climbing

stairs rapidly; walking uphill; walking or stair climbing after meals, in cold, in wind,

or under emotional stress; or only during the few hours after awakening; when

walking > 2 blocks on level ground; or when climbing more than 1 flight of stairs at a

normal pace and in normal conditions. Ability to garden, rake, roller skate, walk

at 4 mph on level ground, and have sexual intercourse without stopping

III Marked limitation of ordinary physical activity; angina occurs on walking 1 to

2 blocks on level ground or climbing 1 flight of stairs at a normal pace in normal

conditions. Ability to shower or dress without stopping, walk 2.5 mph, bowl, make

a bed, and play golf

IV Inability to perform any physical activity without discomfort; anginal

symptoms may be present at rest. Inability to perform activities requiring 2 or

fewer metabolic equivalents (METs) without angina

Page 68 of 217

Cesarean Section

Depend if elective/urgent Vs stat

Always have the room ready: Anesthesia machine checked, A/W equipment

ready, Emergency drugs ready

Always ask for blood for any bleeding case

Elective/urgent:

Enough time to evaluate Pt, H/P as routine obstetric Hx, and anesthetic Hx with

physical exam mainly the A/W, chest, edema …..+ review lab, obstetric

consideration

Obtain informed consent from the Pt for neuroaxial block, with risk/benefit

discussion, if not C/I for the block.

Pre-meds GI, other if indicated e.g. asthma, anxiety, endocarditis, steroids

IV at least 1.5 -2.0 L of fluids

O2, Pre-block V/S

If using hyperbaric L.A lie the Pt down very quickly + LUD, repeat BP

Inform the Pt that if she feel sick to tell me right way (BP)

Examine the block by asking the surgeon to use a teeth forceps

As soon as the baby out give synto 5 U then 20 U in the bag

For spinal: 10.5 mg marcaine hyperbaric, 20 ug fentanyl, 150 ug epimorph

Page 69 of 217

CHF:

Causes: IHD, VHD, CHD, Cardiomyopathy, HTN, pul HTN

Hallmark: CO, VEDP, SVR, metabolic acidosis

Could be Sys Vs Dias, Rt or Lt

S/S: SOBOE, orthopnea, PND, exercise tolerance

P/E: crackles,S3 gallop, JVP, hepatosplenomegaly, ascites, peripheral edema

Rx that proven to improve outcome: ACEI, -blocker, spironlactone

Rx that improve symptom: Dig, and loop diuretics

Other antiarrhythmics, anticoag, vasodilators

Other modality: biventricular pacing, AICD

Assess using NYHA functional capacity

I no limitation with normal activity, and no symptom

II slight limitation with normal activity, symptomatic

III marked limitation with normal activity, comfortable at rest, les the normal

activity produce symptom

VI severe limitation, symptomatic at rest

Pre-op: postponed if decompensated, Cardiology consult to optimize

Workup: CBC, Lytes, Chem, 12-ECG, CXR, review Echo

Page 70 of 217

Lab and Clinical Criteria for Estimating Hepatic Reserve (Child-Pugh

Classification)

CRITERIA CLASS A CLASS B CLASS C Serum bilirubin

mg/100 mL <2.0 2.0–3.0 >3.0

Serum albumin

g/100 mL >3.5 3.0–3.5 <3.0

Ascites None Easily controlled Not easily controlled

Encephalopathy None Minimal Advanced

Nutrition Excellent Good Poor

Prothrombin time

(sec > control) 1–4 4–6 >6

Surgical risk mortality rate 5% 10% 50%

Page 71 of 217

Chronic constrictive pericarditis

It resemble tamponade in impede diasolic pressure, venous pressure, and

stroke volume

Causes: idiopathic, CRF, radiation, R. arthritis, and post-heart

S/S: arrhythmias A.fib and flutter, kussmaul sign exaggerationin CVP with

inspiration, pulsus paradoxes but less than tamponade

CXR: calcification over the pericardium.

ECG: voltage of QRS, inverted T-waves

Rx surgical pericardiotomy

Anesthesia Mx

o Preload maintain, and avoid , since they’re preload dependent

o Cont maintain, avoid cardio-depressant drugs

o Rate: avoid sudden HR

o Afterload maintain, avoid sudden drop in SVR, since limited CO

o Avoid all histamine releasing drugs

o Art-line, PAC, CVP at least

Page 72 of 217

Clinical Predictors of Increased Perioperative Cardiovascular Risk (Myocardial

Infarction, Heart Failure, Death)

Major

Unstable coronary syndromes

· Acute or recent myocardial infarction* with evidence of important

ischemic risk by clinical symptoms or noninvasive study

· Unstable or severe† angina (Canadian class III or IV)‡

Decompensated heart failure

Significant arrhythmias

· High-grade atrioventricular block

· Symptomatic ventricular arrhythmias in the presence of underlying heart disease

· Supraventricular arrhythmias with uncontrolled ventricular rate

Severe valvular disease

Intermediate

Mild angina pectoris (Canadian class I or II)

Previous myocardial infarction by history or pathological Q waves

Compensated or prior heart failure

Diabetes mellitus (particularly insulin-dependent)

Renal insufficiency

Page 73 of 217

Coarctation of the Aorta

If corrected no special precautions

Arm-leg different < 20mmHg good outcome

Uncorrected high risk of LV failure, aortic rupture or dissection, endocarditis

High mortality rate, risk of offspring CHD

Risk of having bicuspid aortic valve, aneurysm of circle of Willis

Measure Rt Vs Lt side BP, and upper Vs lower BP

Need Echo and 12-ECG

hemodynamic Goals:

o preload

o R/R slightly maintain sinus

o Cont maintain, avoid cardiodepressant

o Afterload maintain, avoid sudden in SVR

Avoid Regional GA is better tolerated for C/S

Monitors Art-line, CVP,

Ephedrine and dopamine are the best choice since they have choronotropic

effect

Page 74 of 217

Cocaine abuse

Affect three main neurotransmitters Norepi, Serotonin and dopamine

Can present like PIH with HTN, edema, proteinuria

A

B aspiration, bronchspasm, pneumothorax, pneumomediasinum

C MI, HTN, arrhythmias

Renal ARF

Heme thrombocytopenia, DIC, anemia

Hepatic failure, rupture

CNS seizure, ICH, SAH, CVA

fetus UP blood flow, cross placenta

The main problem is severe HTN with induction, So consider NTG, hydralazin

with induction, avoid pure -blockers alone may get unopposed -effect, with

risk of coronary vasospasm

Regional OK, be aware of severe hypotension with spinal,and ephedrine is not

a good choice(not work) Neo better

Page 75 of 217

Coma/LOC

Management:

o ABC

o Monitors

o Give thiamine 100 mg IV, Dextrose 50g IV

o Lab: ABG, ECG, chemostrip, lytes, BUN, creat, CBC-D, LFT,

coagulation profile, urine analysis, blood/urine for toxicology and

drugs level

DDx:

o CNS pathology: tumor, trauma, seizure disorder, aneurysm, AVM

o Infection: meningitis, encephalitis, sepsis

o Metabolic: hypoglycemia, DKA, HONKC, uremia, hepatic

encephalopathy , acidosis

o Respiratory: hypoxia, hypercarbia

o Overdose: EtOH, drugs(opioids, TCA, Cocaine, Tylenol,…..)

H/P AMPLE, VS, Neuro GCS, lateralization, pupils,

Page 76 of 217

COMPARISON OF MYASTHENIC SYNDROME ANDMYASTHENIA

GRAVIS

Myasthenic Syndrome Myasthenia Gravis

Manifestations Proximal limb weakness Extraocular, bulbar and

(arms > legs) facial muscle weakness

Exercise improves with strength Fatigue with exercise

Muscle pain common Muscle pain uncommon

Reflexes absent or Reflexes normal

Gender Male > female Female > male

pathology Small cell carcinoma of the lung Thymoma

Response to Sensitive to Sux and NDMR Resistant to Sux

muscle relaxants Sensitive to NDMR

Poor response to Good response to

anticholinesterases anticholinesterases

Page 77 of 217

Congenital Diaphragmatic Hernia

95% Lt side

neonatal and premature consideration

A insert NGT , keep suction

B hypoplastic lung RDS, risk of pneumothorax with PPV, keep Airway

pressure < 20-30 cmH2O, and avoid lung expansion after hernia repair, neonate

could be on NO or ECMO, N2O is C/I, keep 100% O2

C 15% CHD

R renal abnormality

N neuro abnormality

Congenital lobar emphysema

o LUL most common

o Emergency and potential life threatening

A ?

B resp failure, ball valve avoid PPV, cyanosis, N2O C/I, 100% O2

C mediastinal shift hemodynamic instability , 20% CHD

Lab X-match

Induction gas induction, with spontaneous breathing

Page 78 of 217

COPD

A airway reactivity bronchospasm

B risk of hypoxia, hypercarbia, bronchospasm, and PPC: atelectasis, pneumonia,

respiratory failure, smoking

C cor pulmonale, RV failure, pul HTN

D avoid STP, sensitivity to resp depressant drugs

Heme polycythemia

Lytes

PPC with: FEV1/FVC < 70%, FEF25-75 <50%, FVC< 75%, with respiratory

failure more likely if FEV1 <50%, PaCO2 > 50

H/P: smoking, wheezing, coughing, sputum amount and color, exercise tolerance,

home O2, A/E bilaterally, wheezing, crackles, JVP, peripheral edema, cyanosis

With smoking risk of CAD

Lab: CXR, ABG, PFT, ECG, CBC-D, lytes, BUN, creat

For PFT do pre and post bronchodilators

Optimize the Pt pre-op: smoking cessation, bronchodilators(-agonist, steroids,

anticholenergic) , consider Abx therapy

Pt may need O2 supplement pre-op if PaO2<60, cor pulmonale, Hct >55

Page 79 of 217

Coronary Artery Disease— Myocardial Infarction

Anatomic Site Leads ECG Changes Coronary Artery

Inferior II, III, aVF Q, ST, T Right

Lateral I, aVL, V5–V6 Q, ST, T Left circumflex

Anterior I, aVL, V1–V4 Q, ST, T Left

Anteroseptal V1–V4 Q, ST, T LAD

Electrolyte Disturbances

Ca2+ Ca2+ K+ K+

Rate <100 <100 <100 <100

Rhythm Regular Regular Regular Regular

PR interval Normal Normal/ Normal Normal

QT interval T flat/U wave T peaked QT

Page 80 of 217

Craniosynostosis:

May associated with other syndrome Crouzon’s syndrome (MH)

Main issues: difficult A/W, massive blood loss, VAE, ICP

A possible difficult A/W maxillary hypoplasia, large tongue, micrognethia

Awake FOI, multi masks and blads

B tracheal stenosis, tracheomalacia, OSA

C CHD ASD, TOF, PDA

D Avoid ketamine and sux

M lytes abnormality

N ICP, seizure disorder, mental retardation

Have a big IV access, blood in the OR

If only one suture short procedure, if > 1 , long with risk of bleeding

so need art line, CVP, IV wormer , bear hugger, Foley cath

If involve below the orbit A/W swelling keep intubated post-op (ICU)

till the swelling subsided

Page 81 of 217

Creutzfeldt - Jakob disease

human spongiform encephalopathies.

The other two diseases in this group are kuru and Gerstmann-Straussler syndrome.

Pathologically, these disorders are characterized by vacuolation of brain tissue and neuronal

loss. caused by an unusual infectious agent—a prion. A prion is a small proteinaceous

infectious agent. Prions are resistant to alcohol, formalin, ionizing radiation, proteases, and

nucleases, but can be inactivated by heat (autoclaving), phenol, detergents, and extremes of

pH.

incubation time is long (years)

The typical clinical characteristics include subacute dementia, myoclonus, and EEG

changes.

Management of Anesthesia

Because of the transmissibility of the disease, appropriate precautions should be taken to

protect other patients and health care providers.

A prone to aspirate gastric impaired swallowing function and decreased activity of laryngeal

reflexes.

C autonomic dysfunction abnormal CV responses to anesthesia and vasoactive drugs.

DBecause lower motor neuron dysfunction succinylcholine should be avoided.

Page 82 of 217

Crohn's Disease

A RSI for S/S of bowel obstruction

B N/A

C hypovolemia

D Steroids (stress dose), immunosuppressant

G obstruction, fatty liver, cirrhosis, perforation

R amyloidosis

Heme chronic anemia, iron def, vit B12, folate

M hypovolemia, K, 3rd

space loss, albumin free fraction of drugs

MSK arthritis with ROM

Page 83 of 217

Cushing Syndrome :( Glucocorticoid Excess)

Cortisol function: 1- maintain BP by converting Norepi epi, 2- anti-

inflammatory, 3- Na retention, and K excretion, 4- hyperglycemia by

gluconeogenesis, and glucose uptake by the cells

Exogenous therapy (most common) > 21 days

Bilateral adrenal hyperplasia due to ACTH from pituitary adenoma or non-

endocrine tumor (lung, kidney, pancreas)

A possible difficult A/W, mucosa easily traumatize

B OSA

C HTN, volume overload

D steroids (stress dose), avoid etomidate, titrate NDMR

N emotional, psycosis

M DM, K, met alk, Addison crisis

MSK osteopenia, muscle wasting

Immun infection

Post bilateral adrenalectomy may need mineralocorticoid replacement in day 5,

give 0.05–0.1 mg·day–1

of fludrocortisone

Page 84 of 217

CV diseases in pregnancy

Lt Rt shunt e.g. ASD, VSD, PDA are well tolerated in pregnancy

The main keys in management for anesthesia are

o Avoid air bubble in the IV

o For epidural insertion use saline instead of air both due to risk of

paradoxical air embolism

o Pain catecholamine SVR shunt RV failure

o So early epidural is desirable

o Slowly titrate the epidural, and avoid spinal sudden SVR convert

the shunt to Rt Lt

o Give O2 all the time

Page 85 of 217

CVP Waveform Components

WAVEFORM PHASE MECHANICAL EVENT

a wave End-diastole Atrial contraction

c wave Early systole Isovolumic ventricular contraction,

tricuspid motion toward right atrium

v wave Late systole Systolic filling of atrium

h wave Mid- to late diastole Diastolic plateau

x descent Mid-systole Atrial relaxation, descent of the

base, systolic collapse

y descent Early diastole Early ventricular filling, diastolic

collapse

Page 86 of 217

Cyanide toxicity

By preventing oxidative phosphorylation cellular hypoxia anaerobic

metabolism

S/S lactic acidosis, tachyphylaxis to SNP, SvO2, Sz

Management:

D/C SNP

100% O2

Thiosulfate 150 mg/kg IV administered over 15 minutes (acts as a sulfur

donor to convert cyanide to thiocyanate)

If severe, with deteriorating hemodynamics and metabolic acidosis slow

IV administration of sodium nitrate, 5 mg/kg. ( converts Hb to

methemoglobin, which acts as an antidote by converting cyanide to

cyanomethemoglobin

hydroxocobalamin (vitamin B12a) which binds cyanide to form

cyanocobalamin (vitamin B12) can be administered (25 mg/hour IV to a

maximum of 100 mg)

Page 87 of 217

Cystic fibrosis:

A disease of the exocrine glands: salivary, sweet, GI, pul

Rx: chest physio, Abx, bronchodilator, GI enzyme

A sinusitis avoid nasal intubation with active nasal infection.

B pneumonia, mixed obstructive/restrictive disease, bronchiectasis

C cor-pulmonale

GI cholelithiasis, pancreatic insufficiency, hepatic dysfunction

Heme bleeding disorder

Lab: CBC-D, lytes, BUN, creat, coags, CXR, PFT, ECG, Echo if needed

Monitors: CAS, art-line

Suction the airway before extubation

Consider regional block for post-op pain control

Encourage chest physio post-op

Page 88 of 217

Deliberate Hypotension:

Mainly used to blood loss: aneurysm, AVM, spine Sx, major head and neck

The main C/I are: uncontrolled HTN, severe anemia, TIA’s angina, heart failure,

resp failure, acidosis, hypoxia, Renal insuff

Ass intravascular volume pre-op, and expand it if necessary.

Have a target MAP based on awake MAP e.g. 70% of the awake MAP

Monitors: Art-line, CVP, SSEP or EEG in brain and spine Sx

Choices:

o SNP: rapid on/off, risks: pul shunt, ICP, cyanide and thiocyanate toxicity,

and rebound HTN, also it’s inhibit PLT aggregation, do not exceed

10ug/kg/min for 10 min, or > 1mg/kg in 2hrs, or 0.5mg/kg in 24hrs, Rx of

toxicity: IV thiosulfate, if abnormal renal functionhydroxocobalamin

o NTG: less potent, no cyanide problem, but shunt,

o Isoflurane: easy titration, CMRO2,

o Other: Trimethaphan, Esmolol and Labetalol, Prostaglandin E1, Nicardipine

Page 89 of 217

Diabetes Insipidus

from inadequate secretion of ADH (central DI)

or resistance on the part of the renal tubules to ADH (nephrogenic DI)

Failure to secrete adequate amounts of ADH results in polydipsia,

hypernatremia, and a high output of poorly concentrated urine.

Etiology

due to destruction of the pituitary gland by intracranial trauma, infiltrating

lesions, or surgery.

management

depends on the extent of the hormonal deficiency. During surgery, the

patient with complete DI receives an iv infusion of aqueous ADH (100–200

mU·h–1

) combined with administration of an isotonic crystalloid solution.

The serum sodium and plasma osmolality are measured on a regular basis,

and therapeutic changes are made accordingly.

ADH also may be given intramuscularly (as vasopressin tannate in oil).

DDAVP administered intranasally has prolonged antidiuretic activity (12–

24 hours) and is associated with a low incidence of pressor effects.

As a consequence of the large outpouring of ADH in response to surgical

stress, patients with a residually functioning gland usually do not need

Page 90 of 217

DIABETES MELLITUS

A stiff joint syndrome ―prayer sign,‖, mobility of the AO joint. difficult

intubation, FOI, RSI full stomach

B N/A

C CAD, PVD, cardiomyopathy , silent MI, autonomic neuropathy, risk of

post-op MI

D metformin associated with lactic acidosis in hypotension, hypoxia

GI delayed gastric emptying, full stomach

M hypo, hyperglycemia, lytes abnormalities, DKA, hyperosmolar coma

Renal renal function

CNS neuropathy (positioning), CVA

Pre-op: lab: ECG, Lytes, FBS, BUN, creat

D/C OHA in AM, consider insulin/D5% infusion peri-op for long cases

Document neuropathy pre-op for positioning and regional anesthesia

monitoring intra-op, includes 5-leads ECG, Art-line, frequent ABG, or

chemosrip for glucose, and in PARR

unless it’s an emergency Sx, postponed DKA, and hyperosmoalr coma

Page 91 of 217

Diabetic Ketoacidosis

Accumulation of acetoacetate and -hydroxybutyrate

ketone bodies are organic acids metabolic acidosis with an unmeasured AG.

Provoked by intercurrent illness, trauma, or cessation of insulin therapy.

the degree of hyperglycemia does not correlate with the severity of the acidosis.

Blood sugar levels are often in the 300–500 mg·dl–1

range.

leukocytosis, abdominal pain, GI ileus, and mildly amylase levels are all

common in DKA, Pt may Dx as acute abdomen.

Treatment

Regular insulin 10 units iv bolus followed by an insulin infusion nominally at

(blood glucose/150) units·h–1

Isotonic iv fluids as guided by V/S and urine OP; anticipate 4–10 l deficit

When urine >0.5 ml·kg–1

·h–1

, give KCl 10–40 mEq·h–1

(with continuous ECG)

When glucose to 250 mg·dl–1

, add dextrose 5% at 100 ml·h–1

Consider sodium bicarbonate to correct pH <7.1

When glucose levels below 250 mg·dl–1

, glucose should be added to the iv

fluid while insulin therapy continues.

K replacement is a key concern in patients with DKA, Because of the diuresis,

the total body potassium stores are reduced.

Page 92 of 217

DIC

Dilated Cardiomyopathy

myocardial contractility systolic dysfunction CO ventricular filling pressure

Dilatation of both ventricles MR, TR.

Causes: the most common is IHD and alcohol

Other causes:

o Direct:

Toxic :Alcohol, Anthracyclines, Catecholamines, Cobalt, Phenothiazines, Radiation,

Uremia, Adriamycin.

Infectious:Protozoan (Chagas' disease) Viral (coxsackievirus, other enteroviruses,

influenza)

Metabolic :Starvation, Thiamine deficiency (beriberi)

Genetic, Idiopathic

o Indirect

Ischemic

Large-vessel coronary disease (postinfarction cardiomyopathy)

Small-vessel coronary disease

Global ischemia (cardiac surgery)

Anemia, TTP, Hypersensitivity, Idiopathic myocarditis

Page 93 of 217

Down syndrome:

Highly associated with CHD 50%, cyanotic 8%(mainly TOF)

A C1-2 subluxation, subglottic stenosis, large tongue difficult intubation, avoid

neck extension

B

C CHD, TOF, CHF, Tet spells, Rt Lt shunt ( be meticulous about air in the IV)

M hypothyroidism, hypothermia

CNS MR

ECT during pregnancy

Obstetric consideration

Risk of abortion and premature labor, also risk of bleeding

Minimize the amount of drugs as much as possible

Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids,

Ketamine, Etomidate)

Have an obstetric consultation

Beyond the 1st trimester do GA with ETT, RSI, with maintaining LUD

Have FHR monitor

Page 94 of 217

EEG FREQUENCY RANGES

Delta rhythm (0–3 Hz) Deep sleep, deep anesthesia, or pathologic states (e.g.,

brain tumors, hypoxia, metabolic encephalopathy)

Theta rhythm (4–7 Hz) Sleep and anesthesia in adults, hyperventilation in

awake children and young adults

Alpha rhythm (8–13 Hz) Resting, awake adult with eyes closed;

predominantly seen in occipital leads

Beta rhythm (>13 Hz) Mental activity, light anesthesia

Effect of anesthesia is depend on the dose.

@ low dose frequency

@ moderate dose frequency and amplitude

@ high dose silent

compare to SEP, EEG records the spontaneous brain activity with higher

amplitude, while the SEP have a smaller amplitude in response to a specific

stimuli.

Page 95 of 217

Ehlers-danlos Syndrome:

CTD, abnormal metabolism of type III collagen

A avoid A/W traumatization

B spontaneous Pneumothorax, Avoid high airway pressure

C MR, Arrhythmias, consider SBE prophylaxis

Heme bleeding disorder with normal coags profile

Anticipated problem bleeding

Obstetric premature labor & bleeding

Avoid Regional Anesthesia

Page 96 of 217

Eisenmenger Syndrome

Chronic Lt Rt shunt changes to Rt Lt

Pregnancy S/S due to SVR

hypoxia IUGR, demise

high rish of thromboembolic event mainly post partum

Hemodynamic Goals:

o preload maintain, avoid AC compression LUD

o R/R maintain normal sinus

o Cont maintain, avoid cardiodepressant

o Afterload maintain, avoid sudden in SVR

o PVR avoid by hypoxia, acidosis, PCO2

Consider inhaled NO, O2 all the time, with pulse oxi

Monitors Art-line, PAC/CVP

For the 1st stage single shot spinal opioids

2nd

stage may consider slow titrating epidural

Be aware that they could be anticoagulated

For C/S crash cart in the room, with pads on the Pt

Epidural have better outcome than GA careful titrate LA

Page 97 of 217

Electric shock and lightning strike

Electric shock

o Direct effect of the current

o Conversion of electric to heat energy

Factors determine the nature and severity: magnitude of energy delivered,

resistance to current, type of current, current pathway, and duration of

contact

o Bone and skin have a high resistance

o Blood vessels, muscle, nerve have a low resistance

o The skin resistance can be by moist and convert a low voltage to a

life threatening shock

o Alternating current is more dangerous than a direct current

o Transthoracic (hand-hand) are more dangerous than vertical ones

o VF more common with alternating, while asystole more with direct

o Respiratory arrest due to CNS effect (medulla), tetanic contraction of

resp muscles, and prolonged paralysis

o Consider C-spine precaution, and other injuries

o Potential burn to the face early intubation

Page 98 of 217

Cardiac Conditions Associated With Endocarditis

Endocarditis prophylaxis recommended

High-risk category

Prosthetic cardiac valves, including bioprosthetic and homograft valves

Previous bacterial endocarditis

Complex cyanotic CHD (eg, single ventricle states, TGA, TOF)

Surgically constructed systemic pulmonary shunts or conduits

Moderate-risk category

Most other congenital cardiac malformations (other than above and below)

Acquired valvar dysfunction (eg, rheumatic heart disease)

Hypertrophic cardiomyopathy

Mitral valve prolapse with valvar regurgitation and/or thickened leaflets

Endocarditis prophylaxis not recommended

Negligible-risk category (no greater risk than the general population)

Isolated secundum atrial septal defect

Surgical repair of ASD, VSD, or PDA (without residua beyond 6 mo)

Previous coronary artery bypass graft surgery

Mitral valve prolapse without valvar regurgitation

Physiologic, functional, or innocent heart murmurs

Page 99 of 217

Endocarditis Prophylaxis

Dental, oral, esophageal, and respiratory

o Adult: Ampicillin 2g IV 30 min pre-op

o Peds: Ampicillin 50mg/kg within 30 min of starting

o Allergy to Amp Clindamycin 600 mg , Peds 20mg/kg

GU/GI

o High risk: Amp & Gent

Adult 2g/ 1.5/kg max 120mg

Peds 50mg/kg & 1.5 kg

Allergy to Amp Vanco and Gent, 1g for adult and

20mg/kg for peds

o Moderate risk: Amp alone

Same as above dose

Allergy to Amp Vanco also the same dose

Page 100 of 217

Epidermolysis Bullosa

inherited or acquired

loss of intercellular bridges and separation of the skin layers intradermal

fluids accumulation and bulla formation.

3 types

o simplex benign

o junctional rarely survive beyond early childhood

o dystrophic.

Systemic manifestations and Anesthetic considerations:

o A very fragile m.m bledding & bulla formation with fixation of

the tongue difficult intubation

use a lot of lubricant on the ETT, and avoid suctioning

o skin: very fragile avoid tapes for IV and ETT, avoid tourniquet, BP

cuff must be pad with cotton

o GI: esophageal stricture malnutrition anemia, cardiomyopathy

o CVS: cardiomyopathy and MVP

o Lytes: loss of albumin hypovolemia and electrolytes imbalance

o Associated diseases: D.M, hypercoagulation, porphyria cutanea tarda,

multiple myoloma

Page 101 of 217

Epiglottitis

an emergency and life threatening condition

1-7 y.o, most common pathogen is H. influenzae, with incidence due to vaccine

The main conflict is difficult airway with risk of aspiration

Other DDx is retropharyngeal abscess

Rapid onset within 24h, high grade fever, and the kid is sitting foreword, mouth

opening and drooling, inspiratory stridor, with toxic appearance

Need to managed in the OR, keep the kid with the parents, and do a gas induction

without starting an IV, in the presence of the ENT surgeon in the room, and the

difficult airway cart in the room

Do a gas induction with Sevo, and maintain spontaneous ventilation

Use a smaller ETT, and have different sizes ready

After Intubation keep sedated and transfer to ICU, and need to be kept intubated

for 24-72h, with Abx therapy

After intubation risk of pul edema

NO NO NO muscle relaxant

Give atropine

Page 102 of 217

Epilepsy:

H/P: why(pathology: head injury, tumor, CVA, bleeding), frequency, type, last

aepisode, S/S of ICP

Meds: what, dose, to be taken in AM

A N/A

B possible frequent aspiration

C tuberous sclerosis, drugs effect (cardiotoxicity)

D resistance to NDMR with phenytoin, enzyme induction with pentobarb,

hepatic toxicity with carbamazepine, other: aplastic anemia, avoid any drugs that

may seizure threshold.

Page 103 of 217

Epilepsy surgery

Hx type generalized, focal, absence, with, or without Aura

Review all meds, mainly anticonvulsant metabolism of NDMR

Discuss with the surgeon the anesthetic plan GA Vs sedation with LA

May need awake test with speech mapping

In case of sedation use a judicious amount of sedation, O2 by NP, and

keep communication with Pt all the time

In case of A/W obstruction D/C sedation gtt, 100% O2 LMA, ETT

In addition to the standard CAS monitoring, if an Art-line needed have in

the same side of the lesion e.g. Rt temporal Rt radial art line

Avoid any pre-med that may change the seizure threshold, also avoid any

long acting anticonvulsant

Page 104 of 217

Ethylene Glycol poisoning

Found in: detergent, antifreeze, polish

The toxic metabolite Glycolic acid is responsible for the metabolic acidosis

with anion gap, and osmolar gap

S/S depend on when they present and at which stage:

o Stage I (30min-12hr) CNS with hallucination, coma, Sz, tetany

o II (12-24hr) Cardioresp HTN, tachycardia, pul edema

o III (24-72hr) Renal flank pain, Ca oxalate in the urine

Management:

o ABC

o Lab: CBC-D, Lytes, BUN, creat, EG level, ABG, Osmolality, CXR,

ECG

o Monitors: ECG, art-line, pulse oxi, Foley cath

o ECG QT, Lytes Ca

o Gastric lavage

o Depend on the serum level of EG whether to give EtOH or not or to

start HD

Page 105 of 217

Familial Periodic Paralysis

Two forms: hyperkalemic, and hypokalemic, both AD inherited diseases.

intermittent, acute episodes of skeletal muscle weakness. Attach may last hours

or days.

Hyperkalemic Periodic Paralysis.

evidence of myotonia as well as episodes of muscle weakness.

caused by a sodium channel mutation.

Episodes of weakness lasting several hours can occur: during rest after exercise,

infusions of KCl, metabolic acidosis, or hypothermia.

The weakness may be so severe as to produce respiratory distress.

hyperkalemia is often transient, occurring only at the onset of weakness.

K levels measured during the episode of weakness may be N or even

Treatment consists of a low-K diet and the administration of thiazide diuretics.

Consider glucose containing solution pre-op during fasting.

Hypokalemic Periodic Paralysis. More common. caused by a calcium channel mutation.

Page 106 of 217

Fat Embolus Syndrome

associated with multiple traumatic injuries and surgery for long bone #

Risk factors include:male sex, age (20–30 years), hypovolemic shock,

intramedullary instrumentation, rheumatoid arthritis,

The incidence of FES in isolated long bone fractures is 3–4%, and the

mortality rate ranging from 10 to 20%.

CRITERIA FOR DIAGNOSIS OF FAT EMBOLUS SYNDROME

o MAJOR

Axillary/subconjunctival petechiae

Hypoxemia (PaO2 < 60 mm Hg; FIO2 < 0.4)

CNS depression (disproportionate to hypoxemia)

Pulmonary edema

o MINOR

Tachycardia (>110 beats·min–1)

Hyperthermia

Retinal fat emboli

Urinary fat globules

platelets/hematocrit (unexplained)

Page 107 of 217

Flow volume loop

Page 108 of 217

Fluids

Blood volume

o Preterm 100 ml/kg

o Newborn 85 ml/kg

o Up to 2y 75 ml/kg

o 2-puberty 70 ml/kg

Maintenance use the rule 4-2-1, add the deficit using the same rule from NPO

and replace it 50% in the first hr, and the rest in the nest 2 hrs

Glucose requirement for neonate 4-6 mg/kg/min

D10W 100mg/ml of glucose

Dehydration

o Based on body wt in infant 5% mild, 10% mod, 15% severe

o >15 kg 3% mild, 6% mod, 9% severe

Clinical signs

Mild mod severe

Urine anuria

Mucosa slight dry Dry parched

Fontanel N sunken marked sunken

Eye N sunken marked sunken

Page 109 of 217

Gestationl diabetes

maternal/fetal M/M, risk of C/S

In addition to obstetric consideration

A Stiff joint syndrome difficult A/W

B

C hypovolemia, ANS dysfunction hypotension with R.anesthesia

D insulin

M hypoglycemia, DKA, HNKC

CNS ANS dysfunction,

R renal dysfunction

Fetus/neonate hypoglycemia, hypothermia, bili, lethargy

Lab: CBC-D, Lytes, BUN, Creat, ECG, ABG (PRN)

Pre-med GI,

Review White classification for DM its according to the severity

Page 110 of 217

Guillian barre’ Syndrome

Widespread inflammatory demyelination of peripheral and ANS

It’s ascending in nature, LMN involvement ? caused by viral infection GI, flu

A full stomach, difficult intubation if TMJ involvement

B respiratory involvement

C arrhythmia, autonomic dysfunction

D NO Sux, (K), sensitivity to NDMR

GI bowel obstruction

CNS demyelination

Pre-op: PFT, ABG, CXR, ECG, CBC, Lytes

Before induction have an art-line in place, unpredictable response to intubation

and induction, consider CVP, have N. stimulator in place

Post-op: continue mech vent (ICU)

In Pt with previous disease assess for residual neuropathy, and do PFT

In pregnancy premature labor, epidural OK, avoid Spinal severe

hypotension

Page 111 of 217

Head and spinal cord injury

15% of CO to the brain, with CBF of 50ml/100g/min

Pathophysiology:

TBI primary injury is due to hematoma, contusion, or DAI, the secondary is

an exacerbation of neuronal damage from change in CBF, and systemic factors

e.g. BP, hypoxia, severe PCO2, anemia, temp, Sz

Hypotension is the most important factor poor prognosis

The effect of ICP CPP, and herniation

The Autorgulation of CBF is disrupted, but PCO2 reactivity is preserved with

in magnitude, it’s very important to maintain SBP > 90

ICP maintain O2, adequate cerebral drain head up, adequate pain/sedation,

PCO2 30, mannitol .25-1g/k, hypothermia

Anesthesia goals:

o Optimize CPP, avoid ischemia, avoid drugs/tech ICP, avoid CMRO2

Exam: GCS, pupils, brainstem reflex, focal/lateralization neuro signs

Lab: CT-head, CBC, Coags, Lytes, toxicology screen

Induction: RSI, use lido, sux , inline stabilization.

Monitors: routine, art line, CVP, ICP, temp

Page 112 of 217

Table 25-4. DERIVED HEMODYNAMIC VARIABLES

Name Calculation Units

CI CO/BSA l·min–1·m–2

SVR (MAP-CVP/CO) X 80 dyne-cm·s–5

PVR (MPAP-PCWP/CO) X 80 dyne-cm·s–5

Stroke index SI CI/heart rate cc·beat–1·m–2

Left ventricular stroke work index :LVSWI SI X (MAP-PCWP) X 0.0136

g-m·beat–1·m–2

Right ventricular stroke work index :RVSWI SI X (MPAP-CVP) X 0.0136

g-m·beat–1·m–2

Page 113 of 217

Hemophilia

A deficient or functionally defective Factor VIII:C. (85%)

B (Christmas disease) deficiency or abnormality of Factors IX(14%)

C deficiency or abnormality of Factor XI (1%)

Both hemophilia A and B are sex-linked recessive disorders, which therefore

occur almost exclusively in males. Hemophilia C is an AR disorder that

occurs almost exclusively in Ashkenazi Jews

Normal concentration of vWF, direct relation between the severity of

bleeding and the plasma concentration of the factors

CNS bleed is the major cause of death.

Lab: PTT, with N PT, with normal BT, Hematology consult

Rx factors concentrate VIII, IX and XI, may give Cryo if needed, VIII t1/2

is 12 hrs, IX is 24 hrs, also DDAVP factors release from the endothelium

With time type A may develop inhibitors to factor VIII:C , and the dose of

factor VIII:C need to be , Possible HIV +

Do gentle intubation, avoid blind suctioning, avoid Regional anesthesia

Page 114 of 217

Hepatitis B,C,

Depends on the activity and the stage, with Post-op M&M

Risk of transmission to OR personal (use needle-less system)

A RSI for GI bleeding,

B hypoxemia due to shunt, restrictive lung disease, Pul HTN

C hyperdynamic circulation, CHF

D altered drug pharmacokinetics

Heme anemia, PLT, coagulation defect

M albumin, lytes abnormality, hypoglycemia, acidosis

Renal hepatorenal syndrome

GI portal HTN, ascites, upper GI bleed

CNS encephalopathy

Correct coagulation pre-op (FFP, Cryo, PLT, Vit K)

Consider paracentesis pre-op if respiratory compromise

Have an ICU consult and back-up bed

Lab: CBC-D, BUN, creat, lytes, coags(PT, PTT, fibrinogen), CXR, PFT, ECG,

Echo, LFT, ABG

Page 115 of 217

HIV

The main considerations are the disease process, side effect of antiviral drugs,

and health care personal safety

A N/A

B PCP, TB, hypoxia, ARDS like,

C accelerated CAD, pericarditis, myocarditis, pul HTN, endocarditis, autonomic

neuropathy

D drugs related side effect neuropathy, pancreatitis, lactic acidosis, and the

protease inhibitor may interact with cytochrome P-450 either by induction or

inhibition which can sensitivity to BNZ

GI esophagitis, diarrhea

Heme leukopenia, anemia, ITP

Endo DM, adrenal insufficiency

CNS demyeliantion neropathy like gullian barre’ syndrome

R+ Lytes CRF from sepsis, dehydration, drugs

Possible substance abuse cocaine, heroin, opioids , other infection HCV,

HBV

Page 116 of 217

HOCM

With pregnancy HR and contractility with SVR worsen the

obstruction

-blockers is the treatment of choice

Synto no bolus, give slowly

hemodynamic Goals:

o preload , LUD

o R/R maintain sinus, treat arrhythmia aggressively

o Cont , avoid contractility (kitamine)

o Afterload , avoid sudden in SVR

Neo is the drug of choice if BP

Epidural very slow titration

With GA risk of CHF

Page 117 of 217

HTN

Essential or secondary.

With secondary look for the underlying cause: cushing, pheo, ….

Postponed if DBP > 110

Continue -blockers, and 2-agonist peri-op

D/C ACEI

A N/A

B N/A

C CHF, LVH, PVD, HTN, with labile BP

M intravascular volume

R renal impairment

CNS TIA, CVA, Rt shift of auto regulation curve

Hydrate pre-induction

Consider Art-line depend on Pt status and the procedure

Lab ECG, CBC, Lytes, BUN, creat

Page 118 of 217

Hydrocephalus:

Etiology:

o Trauma/hemorrhage IVH

o Congenital Arnold-chiari malformation

o Neoplastic tumor

o Post-inflammatory sbscess, meningitis

Pt may come for VP, VA, or LP shunt.

A impaired A/W reflex aspiration RSI

B impaired resp drive ABG

C Cushing reflex (brady, HTN)

D avoid ketamine and sux

N ICP, LOC

The rest of management as ICP card

Page 119 of 217

Hyperosmolar Nonketotic Coma

In type II (NIDDM)

elderly patient with minimal or mild diabetes may present with remarkably

high blood glucose levels and profound dehydration.

enough endogenous insulin activity to prevent ketosis; even with blood

sugar concentrations of 1000 mg·dl–1

, they are not in ketoacidosis.

it is the combination of an impaired thirst response and mild renal

insufficiency that allows the hyperglycemia to develop.

The marked hyperosmolarity may lead to coma and seizures,

with the increased plasma viscosity producing a tendency to intravascular

thrombosis.

responds quickly to rehydration and small doses of insulin.

One to 2 L of NS, or equivalent, infused over 1–2 hrs if there are no

cardiovascular contraindications.

Insulin, by bolus or infusion, should be administered.

Consider NaHCO3 if severe acidosis

With rapid correction of the hyperosmolarity, cerebral edema is a risk, and

recovery of mental acuity may be delayed after the blood glucose level and

circulating volume have been normalized.

Page 120 of 217

Hyperparathyroidism

Primary benign parathyroid adenoma (90% of cases) or hyperplasia (9%) and

very rarely to a parathyroid carcinoma, or as part of a (MEN) syndrome.

most Pt are hypercalcemic, most are asymptomatic at the time of diagnosis.

occurring during pregnancy is associated with a high maternal and fetal

morbidity rate (50%), The placenta allows the fetus to concentrate Ca,

promoting fetal hypercalcemia and leading to hypoparathyroidism in the

newborn.

Pregnant women with primary hyperparathyroidism should be treated with

surgery.

Secondary in parathyroid function as a result of conditions that produce

hypocalcemia or hyperphosphatemia.e.g. CRF, malabsorption

Tertiary development of hypercalcemia in a patient who has had prolonged

secondary hyperparathyroidism that has caused adenomatous changes in the

parathyroid gland and PTH production to become autonomous.

Surgery is the treatment of choice for the patient with symptomatic disease.

Page 121 of 217

Hyperthyroidism

most common etiology is the multinodular diffuse goiter of Graves' disease.

between the ages of 20 and 40 years and is predominant in women

A potential difficult if large goiter

B N/A

C hyperdynamic, HTN

D Avoid ketamin, and pancuronium

M Ca

Heme anemia, PLT

Consider giving -blockers peri-op, to HR, and the conversion of T4 to T3

Page 122 of 217

Hypertrophic Cardiomyopathy

AD, Peak 5th

decade of life, F>M, HTN is a common cause, Could associated with LVOFO

or without

Sport sudden death, Good EF due to hypercontractile state, MR is common

Could be dynamic obstruction by the anterior leaflet of the MV during systole systolic

anterior motion (SAM).

S/S

Angina, Syncope, Arrhythmia,CHF

A.fib systemic embolism

Atrial kick very important A.fib not well tolerated

CXR Cardiomegaly

ECG LVH

Treatment:

-blockers 1st choice by HR and contractility outflow obstruction.

CCB is other choice.

CHF is difficult to treat digoxin contractility obstruction, diuretics

hypovolemia obstruction.

Page 123 of 217

Hyponatremia < 130

or in serum Na & in ECV & PV, so it’s result from excess or deficit of water

total body Na regulated by aldosterone and ANP, where serum [Na] by ADH

S/S depend on the rate and severity of of Na: loss of apatite, N&V, cramps, weakness,

LOC, coma and seizure

Acute CNS S/S is due to cerebral edema

What is the serum osmolality see figure

Cerebral salt wasting syndrome, mediated by BNP, independent of SIADH, risk head

trauma, tumor, SAH, and infection

SIADH see other card

Rx < 120 with 3% NS @ 1-2 ml/kg/hr to serum Na 1-2 mEq/l/hr only for few hrs, not

more than 25 mEq/l/48 hrs

Rapid correction abrupt brain dehydration central pontine myelinolysis mild (transient behavioral disturbances or seizures) to severe (including pseudobulbar palsy and

quadriparesis).Within 3 to 4 weeks of the clinical onset of the syndrome, areas of

demyelination are apparent on MRI, risk factors (alcoholism, poor nutritional status, liver

disease, burns, and hypokalemia) , cerebral hemorrhage and CHF

Once serum Na > 120 fluid restriction is enough , Also treat the underlying causes

To calculate the net water loss necessary to [Na+] in hyponatremia, use the following

equation:

Current [Na+] × current TBW = desired [Na

+] × desired TBW TBW= 0.6x wt

Page 124 of 217

Hypoparathyroidism

underproduction of PTH or resistance of the end-organ tissues to PTH results in

hypocalcemia

normally: hypocalcemia PTH and 1,25(OH)2D synthesis Ca2+

mobilization from bone, GI absorption, and renal tubule reclamation.

most common cause of acquired PTH deficiency is inadvertent removal of the

parathyroid glands during thyroid or parathyroid surgery.

Other : 131

I therapy for thyroid disease, neck trauma, granulomatous disease, or

an infiltrating process (malignancy or amyloidosis).

Idiopathic is rare and may occur as an isolated disease or as part of an

autoimmune polyglandular process (hypothyroidism, adrenal insufficiency).

Pseudohypoparathyroidism is an inherited disorder in which parathyroid gland

function is normal but the end-organ response to the PTH is deficient.

Affected patients have hypocalcemia and hyperphosphatemia.

They are characterized by mental retardation, a short stature, obesity, and

shortened metacarpals.

Chvostek's sign is a contracture of the facial muscle produced by tapping the

facial nerve as it passes through the parotid gland.

Page 125 of 217

Hypotension

Preload:

Hypovolemia

Venodilation (spinal)

Tamponade

Tension Pneumothorax

R&R:

Too fast and too slow

Arrhythmias

Other (may affect any component):

Electrolytes imbalance

Acid-base

Hypoxia & hypercarbia

Contractility:

Ischemia

Valve dysfunction

CHF

Drugs

Afterload:

Drugs

Anaphylaxis

Sympathectomy

Hyperthermia

sepsis

Page 126 of 217

Hypothyroidism

Hashimoto’s thyroiditis may associated with other autoimmune disease e.g.

SLE, RA, DM, hypoparathyroidism, Addison’s disease.

May associated with amyloidosis.

A goiter altered A/W anatomy, with possible A/W obstruction

B OSA, hypoventilation, response to PCO2 and PO2, sensitivity to

narcotics, pul edema

C bradycardia, CHF, heart block, hypotension, edema

GI gastric emptying aspiration

M Na, possible SIADH, hypothermia, possible Addison’s disease

postponed if severe hypothyroid Pt until at least partially treated.

The management of hypothyroid patients with symptomatic CAD has been

a subject of particular controversy. In symptomatic patients or unstable

patients with cardiac ischemia, thyroid replacement should probably be

delayed until after coronary revascularization.

Maintain normal body temperature.

Consider adrenal insufficiency when intra-op hypotension not responding

to fluids and inotrops.

Page 127 of 217

ICP:

Normal ICP < 10 mmHg, to convert to cmH2O X by 1.32

A LOC, aspiration risk

B resp failure

C arrhythmias, hemodynamic instability, MI (ECG, Echo)

D avoid sux

N ICP, LOC, risk of herniation

M DI, SIADH, cerebral salt wasting

Monitors: routine, artline, ICP, CVP

Mx: 1- hyperventilate PaCO2 25-30 good only for 6 hrs

2- diuretics mannitol 0.25- 1.0 g/kg over 10 min, Lasix 0.5-1.0 mg/kg

3- Steroids need 6-24 hrs to work

4- head elevation

5- Barbiturate

6- CSF drain

Avoid neck twisting obstruction of IJ, avoid hyperglycemia

Maintain CPP, MAP > 60, avoid PEEP if possible

Page 128 of 217

IHD

Apart from atherosclerotic disease, other causes are: collagen vascular disease,

sickle cell disease, pheo, PIH, cocaine abuse

Avoid ergot, synto OK

Need continues sat and ECG monitor

Epidural is good prevent catecholamine and hyperventilation which

PCO2 coronary vasospasm

Neo is a better choice

Epidural best for C/S

Page 129 of 217

Immediate Hemolytic Transfusion Reactions

Catastrophic and life threatening with mortality 20-60%

Hemolysis of the donor RBC ARF, DIC, death

Intravascular and extravascular (RES)

Antibodies anti-A,B, Kell, Kidd, Lewis, and anti-Duffy

Ag-Ab complex activate Hageman factor(XII) kinin bradykinin

capillary permeability, also complement histamine , serotonin

S/S: fever, chills, N&V, diarrhea, rigor, flushing, hypotension, tachy, chest and

abdominal pain

Under GA most of S/S are masked only hypotension, tachycardia, bleeding,

Hemoglobinuria

Management: (keep index of suspicion)

o Stop Tx, re-check blood,

o 3 main objectives:

Maintain BP volume, inotrops

Preserve renal function diuretics, alk the urine (NaHCO3)

Prevent DIC no specific therapy, maintain BP, prevent stasis

o Blood sample should be collected in EDTA tubes for re-X match, direct

coombs test ( for definitive diagnosis)

Page 130 of 217

INDICATIONS FOR ONE-LUNG VENTILATION

ABSOLUTE 1. Isolation of each lung to prevent contamination of a healthy lung

a. Infection (abscess, infected cyst) b. Massive hemorrhage

2. Control of distribution of ventilation to only one lung

a. Bronchopleural fistula b. Bronchopleural cutaneous fistula

c. Unilateral cyst or bullae d. Major bronchial disruption or trauma

3. Unilateral lung lavage

4. Video-assisted thoracoscopic surgery

RELATIVE 1. Surgical exposure—high priority

a. Thoracic aortic aneurysm

b. Pneumonectomy

c. Upper lobectomy

2. Surgical exposure—low priority

a. Esophageal surgery

b. Middle and lower lobectomy

c. Thoracoscopy under general anesthesia

Page 131 of 217

Infratentorial Intracranial Tumors

Those tumors produce a mass effect on the brain stem, and ICP by obst hydro

A CN involvement + LOC unprotected A/W RSI

B Resp depression

C brady, HTN, arrhythmias ST-changes , prolonged QT

CNS ICP, LOC

Position sitting risk of VAE , CV instability in elderly, risk SC compression

Prone see other card

Monitors as Supratentorial tumors

Induction also the same

Post-op:

o need for continuous CV monitoring 24-48 hrs

o HTN is a common problem post-op, need to treated aggressively other

wise intracranial bleeding and edema

o Manipulation of CN IX, X, XII loss pharyngeal sensation may need

to keep intubated

Page 132 of 217

ITP

More common in young female, characterize by thrombocytopenia with

petechiae, where major cause of mortality is intracranial bleed

The main ttt is steroid, if not working splenectomy

Consider DDx: TTP, drug induced thrombocytopenia, Connective T disease,

HIV, other in preg PIH, DIC, essential thrombocytopenia

The main issues with Anesthesia Are

o A avoid traumatize the airway

o Avoid Regional

o Risk of bleeding PLT Tx

In Preg antibodies cress the placenta affect the fetus CNS bleed C/S

TTP

It’s: thrombocytopenia, fever, renal dysfunction, hemolysis, CNS involvement

Sz, and jaundice

ttt Tx plasma, plasmaphoresis, IVIG, steroids

also the same issues as ITP regarding anesthesia

Page 133 of 217

Kidney Tx

Of course for CRF

A RSI for possible gastroparesis

B pul edema if volume overloaded

C hyper/hypovolemia, pericardial effusion, pericarditis, arrhythmias

D altered drugs pharmacokinetics

G Gastroparesis

M K, secondary hyperparathyroidism with Ca and phos

Heme PLT dysfunction secondary to uremia

Lab CBC-D, CXR, ECG, Lytes, BUN, creat, X-match

monitorsCAS, Art-line, foley, CVP

Goals maximize the renal perfusion at the time of graft reperfusion by

maintaining a high BP, intravascular volume, and diuresis with lasix, and

mannitol

Possible problem Bleeding

Post-op pain epidural, PCA

Page 134 of 217

Lower Ext nerve inury:

Lumbosacral trunk:

Foot drop, with loss of ankle dorsiflexion

L5 dermatome loss of sensation lateral leg

In obstetric with prolonged labor and difficult vaginal delivery

Obturator:

Weakness of hip adduction and internal rotation

Peroneal N

With prolonged lithotomy position

At the knee level (injury) foot drop, with no sensory deficit

Femoral N:

Due to pelvic Sx, prolonged hip flexion, abduction, external rotation during

the 2nd

stage of labor, as well as lithotomy position

Walking OK, but unable to claim stairs, with loss of the patellar reflex

Meralgia paresthetica(Lateral femoral cutaneous nerve)

tingling, numbness, burning sensation over the lateral thigh

resolve spontaneous after giving birth

Page 135 of 217

Ludwig's Angina

An emergency and life threatening situation

generalized septic cellulitis of the submandibular region

occurs after dental extraction, especially of the second or third mandibular molars

it’s bilateral, involves 3 fascial spaces: submandibular, submental, and sublingual

Early S/S: chills, fever, drooling of saliva, inability to open the mouth, and

difficulty in speaking.

hemolytic streptococci, aerobic and anaerobic, including gas-forming bacteria

The infectious process may spread into the thorax, causing empyema, pericarditis,

pericardial effusion, and pulmonary infiltrates, Pneumothorax, necrotizing fasciitis

Review the CT/MRI, CXR for Pneumothorax

A difficult, difficult A/W

B hypoxia, pneumonia, effusion, empyema

C dehydration, pericardial effusion, pericarditis

Have the ENT surgeon in the room, scrubbed, and the neck is prepped, and the

difficult airway cart in the room, consider a reinforced and small size ETT

Awake FOI, give glycopyrolate, other option is inhalation induction

Post-op keep intubated to ICU until swelling subsided

Page 136 of 217

Lung volumes and

capacities

Page 137 of 217

TABLE 30–7. Underestimation of Left Ventricular End-Diastolic Pressure

CONDITION SITE OF

DISCREPANCY CAUSE OF DISCREPANCY

Decreased left ventricular compliance

Mean LAP<LVEDP Increased end-diastolic a wave

Aortic regurgitation LAP a wave<LVEDP Mitral valve closure prior to end-diastole

Pulmonic regurgitation PADP<LVEDP Bidirectional runoff for pulmonary artery flow

Right bundle branch block PADP<LVEDP Delayed pulmonic valve opening

Decreased pulmonary vascular bed

PAWP<LVEDP Obstruction of pulmonary blood flow

Page 138 of 217

Magnesium

mainly intracellular, 50% in bone, 25% muscle, and < 1% in the serum.

protein-bound (30%), chelated (15%), and ionized (55%)

Magnesium is necessary for enzymatic reactions involving DNA and protein

synthesis. As a primary regulator or cofactor in many enzyme systems, magnesium

is important for the regulation of the Na–K pump, Ca-ATPase enzymes, adenyl

cyclase, proton pumps, and slow Ca channels.

The distal tubule of the kidney is the major site of magnesium regulation.

Hypomagnesemia

clinical features of Mg, like Ca neuronal irritability and tetany.

can aggravate digoxin toxicity and CHF.

S/S: weakness, lethargy, muscle spasms, paresthesias, and depression. When

severe seizures, confusion, and coma.

CV coronary artery spasm, CHF, dysrhythmias, and hypotension.

is associated with K, Na, phos, and Ca.

Rarely resulting from inadequate dietary intake, most commonly caused by

inadequate GI absorption, excessive Mg losses, or failure of renal Mg

conservation. Excessive Mg loss is associated with prolonged nasogastric

suctioning, GI or biliary fistulas, and intestinal drains

Page 139 of 217

Magnesium

Mainly intracellular, distal tubule is the major site of magnesium regulation

Hypomagnesemia

Rarely from inadequate dietary intake, most commonly caused by

inadequate GI absorption, excessive Mg losses, or failure of renal Mg

conservation. Excessive Mg loss is associated with prolonged NGT,

gastrointestinal or biliary fistulas, and intestinal drains.

A N/A B N/A C arrhythmias, CHF, BP, coronary artery spasm.

M may associated with other electrolytes abnormality

Rx stop NGT, give Mg

Hypermagnesemia

Most common cause is iatrogenic, other Addison’s disease, lithium, hypothy

S/S depend on Mg level Hypotension Deep tendon hyporeflexia

Somnolence Respiratory insufficiency, deep tendon areflexia Heart

block, respiratory paralysis Cardiac arrest

Rx D/C Mg, IV CaCl, diuretics, dialysis

Page 140 of 217

Marfan syndrome:

AD, length of long bone

A TMJ laxity dislocation with intubation

B scoliosis, kyphoscoliosis, Pectus excavatum, restrictive lung defect

spontaneous Pneumothorax careful with PPV

C cystic media necrosis, aortic dissection, AR, MVP, MR, arrhythmia,

aneurysm Avoid sudden in contractility, -blockers and volatiles are

good, need endocarditis prophylaxis

Other lens dislocation, retinal detachment

Position careful

Neuraxial potential difficult, may need a bigger dose and volume of LA

Lab Echo, CT-chest and angio all for dissection, valve, tamponade,

CXR pneumo, ABG, CBC, lytes, BUN, creat, PFT

Page 141 of 217

Masseter Muscle Rigidity

most common in children and young adults. peak age incidence at 8–12 yrs of age.

Characteristically, anesthesia is induced by inhalation with halothane or sevo, after

sucx is given. Snapping of the jaw or rigidity on opening of the jaw is seen.

this rigidity can be overcome with effort and usually abates within 2–3 minutes.

A peripheral nerve stimulator usually reveals flaccid paralysis.

However, increased tone of other muscles also may be noted.

Repeat doses of succinylcholine do not relieve the problem.

Tachycardia and dysrhythmias are not infrequent.

(if the anesthetic is continued with a triggering agent), the initial signs of MH

appear in 20 minutes or more.

If the anesthetic is discontinued, the patient usually recovers uneventfully.

However, within 4–12 hours, myoglobinuria occurs and CK elevation is detected.

Muscle biopsy with caffeine–halothane contracture testing has shown that approx

50% of Pt who experience MMR are also susceptible to MH.

DDx of MMR are: (1) myotonic syndrome, (2) TMJ dysfunction, (3) underdosing

with Sux, (4) not allowing sufficient time for Sux to act before intubation, (5)

increased resting tension after succinylcholine in the presence of fever or elevated

plasma epinephrine.

Page 142 of 217

Maxillofacial trauma

Lower 1/3 mandible (30% in the body of the mandible)

Middle 1/3 maxilla, zygomatic, orbital, nasal LeForte I, II, III

Upper 1/3 frontal and cranium ( CNS)

Airway

100% O2, and clear the A/W from foreign bodies, blood, # teeth (count), if

there is bleeding apply pressure, nasal packing, and consider a close

reduction for a #

In case of tongue injury laceration edema/swelling difficult

intubation

In case of mid and upper facial injury avoid nasal intubation Bleeding,

and possible basal skull #

Laryngeal injury

S/S hoarseness, stridor, sub-Q emphysema with crepitus void blind

technique

After intubation with direct vision bypass the injury and make sure that the

cuff is beyond the injury

Trismus after facial injury due to muscle spasm relived by GA

Page 143 of 217

Meconium Aspiration:

Risk of PPHTN.

risk with post-term pregnancy

The new recommendation it does not matter thin or thick meconium

If there is meconium suction the hypopharynx

Apply NALS

If not vigorous (HR < 100, resp depression) ETT suction, 100% O2

If vigorous no need for ETT or tracheal suctioning

Page 144 of 217

MH acute crisis

Manifestations :

Hypercarbia, Tachycardia, Tachypnea, Temp (1°C–2°C increase every 5

minutes), HTN, Cardiac dysrhythmias, Acidosis, Arterial hypoxemia,

Hyperkalemia, Skeletal muscle activity, Myoglobinuria

DDx: pheo, thyroid storm, carcinoid

Management:

Call for help

Discontinue inhaled anesthetics and succinylcholine

Hyperventilate the lungs with 100% O2

Administer dantrolene (2.5 mg/kg iv) with repeated doses (up to a maximum of 10

mg/kg iv) based on Paco2, heart rate, and body temperature (each ampule of 20 mg

is mixed with 50 ml of distilled water)

If Dantrolene is not available, give procainamide IV 1mg/kg up to 15mg/kg

Treat persistent acidosis with sodium bicarbonate (1–2 mEq/kg iv)

Control body temperature (gastric lavage, external ice packs until 38°C)

Replace anesthetic circuit and canister

Monitor with capnography and arterial blood gases

Be prepared to treat hyperkalemia and cardiac dysrhythmias

Page 145 of 217

Mineralocorticoid Physiology

Aldosterone is a major regulator of extracellular volume and K homeostasis

through the resorption of Na and the secretion of K.

Renal perfusion pressure+ sympathetic stimulation+ Na, and

hypovolemia renin from juxtaglomerular Renin splits

angiotensinogen to angiotensin I ACE in the lung Angiotensin II

aldosterone.

Other stimuli that aldosterone includeK and, to a limited degree, Na,

PGE, and ACTH.

So aldosterone K and Na and HTN, while is the opposite

Mineralocorticoid Insufficiency:

Common in CRF, and DM, Pt usually on fludrocortisone 0.05-0.1 mg/d

C hypovolemia, heart block due to K,

M K, Na, and metabolic acidosis (hyperchloremic)

D Avoid Sux, and NSAID PGE Renin exacerbation

Page 146 of 217

Mitral Regurgitation

Chronic regurgitation caused by abnormal leaflet anatomy can be due to congenital or

rheumatic disease, myxomatous degeneration(MVP), CTD, infective endocarditis and LV

hypertrophy.

CTD associated with MR include SLE, rh arthritis, ank spondylitis, and scleroderma.

Valvular involvement in CTD is variable; about 50% of patients with SLE have detectable

MR, and approximately 25% have significant regurgitation.

Acute severe MR is caused by infective endocarditis which result in chordae tendineae,

acute MI with papillary muscle rupture or retraction usually from RCA, or prosthetic valve

dysfunction. Almost always associated with MS.

Pathogenesis

Long latent period 30-40 yrs. LA volume overload LV volume overload with foreword

LV SV, Eccentric hypertrophy of the LV, Regurgitation fraction > 0.6 associated with

severe MR, PAWP giant V wave, In acute MR there is sudden in LAP pul edema.

History

Patients with chronic MR remain asymptomatic for an extended period.

Later, patients develop symptoms of fatigue and exertional dyspnea, followed by more overt

symptoms of CHF, including orthopnea and paroxysmal dyspnea.

When CHF develops rapid deterioration with 5 yrs mortality rate 50%

Physical Findings

Page 147 of 217

Mitral Stenosis

normal MVA 4.0 to 6.0 cm2, Symp(exercise or tachycardia) 2.0 to 2.5 cm

2; rest < 1.5 cm

2.

mild gradient < 5 mm Hg and VA >1.5 cm2. Severe gradient > 10 mmHg, and valve area

< 1 cm2. MS in adults is predominantly of rheumatic origin. F>M.

The MV is the most common site of rheumatic valve disease. Long latent period > 20 yrs.

Pathogenesis

Obstruction to LV inflow LA dilation and HTN and resultant pul venous HTN

interstitial edema work of breathing dysponea, and predispose to supraventricular

tachyarrythemia.

Pul arteriolar and capillary vasoconstriction protect against pul edema, although PVR

exacerbates pul arterial and RV HTN and causes RVH.

Pul HTN can be severe late in the course of MS, with eventual RV systolic dysfunction.

Acute decompensation occur due to stress e.g. sepsis, pregnancy, A fib, PE which can

lead to pul edema

Stasis of the blood in the LA thrombi A fib systemic emboli.

History

Early fatigue or dyspnea precipitated by events with associated tachycardia, including

strenuous physical exercise, emotional stress, fever, pregnancy, or surgery.

Page 148 of 217

MR

Well tolerated in pregnancy

risk of A.fib with systemic embolization due to hypercoaglable state in

pregnancy

hemodynamic Goals:

o preload maintain, LUD, avoid overload

o R/R slightly maintain sinus, aggressively treat arrhythmia

o Cont maintain, avoid cardiodepressant

o Afterlaod

o PVR avoid pain, hypoxia, PCO2

If mild no need for aggressive monitoring, but if severe then art-line, CVP/PAC

MVP manage as MR

Page 149 of 217

MS

Not well tolerated, with risk of pul edema.

Arrhythmias are not tolerated at all, and needs to treated very aggressively with

-blockers, Digoxin, over even cardioversion, then lasix

mortality during labor/post-partum

Mild is usually tolerated ok

But mod/severe pregnancy worsen NYHA by 1-2 classes

Need invasive hemodynamic monitoring art-line, PAC, O2 all the time

In the 2nd

stage avoid explosive effort valsalva VR pul edema

Avoid overzealous hydration pul edema

Tachycardia -blockers

hemodynamic Goals:

o preload maintain, LUD, avoid overhydration

o R/R slow and sinus

o Cont maintain, avoid cardiodepressant

o Afterlaod maintain, avoid sudden in SVR

o PVR avoid by pain, hypoxia, PCO2

Neo is the best choice in case of hypotension

Page 150 of 217

Mucopolysaccharoidosis:

I H Hurler

I H/S Hurler/Scheie

I S Scheie

II Hunter

III Sanfilippo

IV Morquio

A Coarse facial features, macrogolssia, short neck difficult A/W

B Restrictive defect

C CAD, VHD, AR, Cardiomyopathy

GI hepatosplenomegaly

MSK joint stiffness, AO instability, odontoid hypoplasia, kyphoscoliosis,

Dwarfism

Routine lab + Echo, CXR

Page 151 of 217

Multiple Sclerosis

demyelination in the brain and spinal cord, F>M

symptoms depend on the sites: visual disturbances, nystagmus, limb weakness and

paresthesias, The legs are affected more than the arms.

Bowel retention and urinary incontinence are frequent complaints.

Involvement of the brain stem can produce diplopia, trigeminal neuralgia, cardiac

dysrhythmias, and autonomic dysfunction, while alterations in ventilation can lead

to hypoxemia, apnea, and respiratory failure.

As is typical in many immune disorders, pregnancy is associated with an

improvement in symptoms, but relapse frequently occurs in the first three

postpartum months.

treatment Corticosteroids, immunosuppressants (azathioprine, methotrexate,

cyclophosphamide, and cyclosporine)

Symptoms exacerbation with stress (emotional, surgical) temp, infections

Management of Anesthesia

Possible exacerbation post-op

Document neurological symptoms pre-op, re-exam post-op

the patient should be advised that surgery and anesthesia could produce a relapse

despite a well managed anesthetic

Page 152 of 217

Murmurs

Innocent murmurs: soft, systolic and not radiated, may vary with position, not

characteristic of any lesions

Noninnocent murmurs: all diastolic murmurs, all pansystolic, continues, late

systolic and transmitted murmurs

For innocent murmurs no need for surgical delay, and no need for prophylaxis

Not noninnocent one’s if heard in the pre-op delay, and further investigation

Page 153 of 217

Midsystolic

flow across aortic or pulmonic valve (e.g., secondary to AR or ASD)

Aortic valve leaflet sclerosis (e.g., in elderly patients)

Aortic or pulmonic outflow obstruction (valvular, subvalvular, supravalvular)

Dilatation of aortic root or proximal pulmonary artery

Papillary muscle dysfunction

Holosystolic MR, TR, VSD

Late Systolic MVP, Papillary muscle dysfunction

Early Diastolic Aortic or pulmonic valve insufficiency

Mid-Diastolic MS, TS

flow across nonstenotic AV valve (e.g., secondary to MR or ASD)

Presystolic MS (with sinus rhythm)

Continuous Murmurs PDA

Page 154 of 217

Muscular dystrophy

7 main types with progressive and variable rate in losing of muscle function.

Duchenne’s muscular dystrophy The most common, and the most severe form.

Due to lack of protein Dystrophin.

Painless degeneration of the skeletal muscle.

X-linked trait (boys)

S/S 2-5 yrs old.

In the wheelchair by age of 12.

The affected muscle may become enlarged, due to fatty infiltration.

Death by 15-25.

Secondary to CHF and pneumonia.

Serum CK reflect the progression of the disease, with 30-300 folds above

normal, later with complete degeneration the level well .

Smooth muscle involvement GI hypomotility and gastroparesis.

CVS

o myocardial degeneration loss of R-wave in the lateral leads

o contractility dilated cardiomyopathy, and arrhythmias

Page 155 of 217

MVP:

More common in young female than in male

May associated with other disease e.g. marfan syndrome, connective tissue

disease.

Risk of endocarditis, stroke, arrhythmias, sudden death

If associated with MR or CHF, Pt could be on ACEI, -blockers, Diuretics,

antiarrhythmics, anticoagulants

P/E late systolic click, if MR late systolic murmur

A N/A unless associated with other disease

B if CHF plu edema, ? scoliosis restrictive lung defect

C CHF, Arrhythmias, Endocarditis prophylaxis

D avoid histamine releasing drugs, and ketamine

CNS Stroke, anxious Pt may benefit from pre-op meds

Hemodynamic goals

Preload maintain

Contractility avoid

R & R sinus, little fast

Afterload avoid , better

Page 156 of 217

Myasthenia Gravis

Osserman and Genkins classification:

• Class I—ocular symptoms only

• Class IA—ocular S’s with EMG evidence of peripheral muscle involvement

• Class IIA—mild generalized symptoms

• Class IIB—more severe and rapidly progressive symptoms

• Class III—acute, presenting in weeks to months with severe bulbar symptoms

• Class IV—late in the course of the disease with severe bulbar symptoms and marked

generalized weakness

autoimmune disease with anti-acetylcholine receptor antibodies, F>M

Abnormal thymus glands 75% of pts(85% show hyperplasia; 15% thymoma).

75% of pts either go into remission or are improved post-op

Medical ttt: anticholinesterase, steroids, other immunosuppressant (azathioprine,

cyclophosphamide, cyclosporine)and plasmapheresis.

underdosage ―myasthenic crisis‖ whereas overdosage will produce a

―cholinergic crisis.‖ Excessive doses of cholinesterase inhibitors produce

abdominal cramping, vomiting, diarrhea, salivation, bradycardia, and skeletal

muscle weakness that mimics the weakness of myasthenia , to differentiate

Page 157 of 217

Myasthenic Syndrome (Lambert-Eaton Syndrome)

Associated with small cell ca of the lung

IgG antibodies against Ca channel in the presynaptic membrane Ach

release in response to nerve stimulator

M>F, age 50-70

Mainly proximal muscle weakness

A

B rarely respiratory failure

C autonomic dysfunction orthostatic hypotension

D sensitive to both Sux and NDMR, Pt could be on diaminopyridine Sz

Keep high index of suspicion in a Pt with Lung Ca

Consider Art-line

Page 158 of 217

Page 159 of 217

NALS

Exam table goes trend for drainage and reverse trend to PO2

Avoid hypothermia VO2 metabolic acidosis

Assess for choanal atersia usually cyanotic and resp depression at rest, pink

when crying

If Apgar score < 8 with not resp depression give O2 by ―blow by‖

So If not breathing or cyanotic suction the A/W, warmth, dry, tactile

stimulation by rubbing the back, flicking the soles of the foot, give O2 not

breathing or HR < 100 PPV with initial P 30-40 cmH2O for 4-5 sec to open

the alveoli, the vent @ rate 40-60 min if HR > 100, and Pink ongoing care, if

HR < 60 PPV and start Chest compression for 30 sec if still HR < 60 five

Epi ….. Bicarb………..

For vent I:E = 1:1, @ 40-60 min, after the 1st breath the P 20-30 cm H2O

For chest compression to vent 3:1 1,5:0.5 sec 90:30 pre minute

Chest compression using two thumbs just below a line drown between two

nipples to compress the AP diameter by 1/3 to ½

Intubation can be considered at any time

If Vent without ETT for > 2-3 min decompress the stomach

Page 160 of 217

Necrotizing fasciitis

Emergency and life threatening with high mortality rate

Possible underlying disease: DM, alcoholism, malnutrition, renal and CV

diseases

Septic shock, possible under resuscitated

A full stomach RSI

B ARDS, respiratory failure, pul edema

C septic shock with SVR, CO

M lactic acidosis, lytes abnormalities

R ARF

CNS LOC

Lab and Mx as septic shock

Post-op ICU

Page 161 of 217

Neonatal Considerations:

In addition to the pediatrics considerations

Metabolic risk of hypoglycemia S/S: apnea, convulsion

Glucose infusion @ 4-8 mg/kg/min

hyperglycemia cerebral hemorrhage, glucosuria H2O and

lytes depletion

Physiological jaundice alter drugs pharmacokinetics, and free

bili kernicterus, which by hypoxia, acidosis, hypothermia

Renal Na loss, immature renal function

CNS fragile cerebral vessels risk of IVH by hypoxia, hypercarbia,

Na, fluctuation in BP, low Hb, rapid administration od NHCO3

Eye ROP maintain O2 sat 90-95% or PO2 50-70

Page 162 of 217

Peri-op nerve injury:

History:

Symptoms: pain, paresthesia, motor weakness, where, when did it start

Presence of risk factors or conditions that may have neuropathy as a

symptoms: DM, Obesity, R Arthritis, PVD, smoking, alcohol,

Drugs that may cause neuropathies chemo, anti-virals

Review anesthetic records, OR note for documentation of padding, position

A block done or not if yes any symptom at the time of the block pain or

paresthesias with injection

If the surgical procedure done in the same side ? surgical complication

or prolonged use of a tourniquet, also BP cuff may cause injury

Exam:

V/S, complete neurological exam, and mainly examining the affected side

sensory, motor, reflex, and looking for any pressure demarcation

Also assess for nerve or dermatomal distribution

Obtain a Neurology consult for further evaluation and need for nerve

conduction study, and possible MRI

Sensory only F/U in 2wks, motor further evaluation

Page 163 of 217

Neuraxial Anesthesia and anticoagulation

IV heparin e.g. vascular Sx delay IV heparin 1hr post catheter

placement, and catheter removal 2-4 hr after the last dose or one hr before

the next dose

S.C heparin also delay catheter placement 2-4 hrs, or delay the heparin 1 hr

post catheter placement

LMWH: needle placement 10-12hrs after the last dose of LMWH, if Pt

receiving a higher dose 1mg/kg delay 24hr

Post-op 1st dose of LMWH delay 24 hr, and may keep the catheter until

next AM, give LMWH 2hrs later

Anti-PLT: plavix ?? no data, but better at least 10 days before needle

placement, NSAID are OK

Pt on oral med (Warfarin) stop 5 days per-op INR= 1.4 is OK

Page 164 of 217

Neurofibromatosis

AD, café-au-lait spots >6, with > 1.5 in diameter, with CNS vascular and

skin involvement, and short stature

Could be a part of MEN IIB

A difficult intubation, due to laryngeal or tracheal compression

B restrictive lung defect, interstitial lung disease, possible mediastinal mass

C HTN due to renovascular, Pheo, coarctation, Wilm’s tumor

CNS Astrocytoma, meningioma (ICP), spinal cord tumor, Sz disorder

M diffuse endocrine disorder as well as carcinoid tumor

MSK Kyphoscoliosis

Regional Anesthesia could be difficult, Avoid if there is spinal cord

tumor

Lab CBC, Lytes, BUN, creat, ECG, Echo, CXR, PFT with F/V loop

Page 165 of 217

Neuroleptic Malignant Syndrome (NMS)

S/S include fever, rhabdomyolysis, tachycardia, hypertension, agitation, muscle

rigidity, and acidosis, mental changes, and stupor, hypoxia, acidosis, CK, and

myoglobinuria

The mortality rate is unknown, but may be as high as 20%. Dantrolene is an

effective therapeutic modality in many cases of NMS.

there are significant differences between the two. MH is acute, whereas NMS

often occurs after longer term drug exposure.

Phenothiazines and haloperidol or any of the newer potent antipsychotic agents

alone or in combination are usually triggering agents for NMS

Sudden withdrawal of drugs used for Parkinson's disease may also trigger NMS

(ECT) with Sux does not appear to trigger the syndrome.

does not seem to be inherited, .

possible due to dopamine depletion in the CNS by psychoactive agents.

bromocriptine, a dopamine agonist, is often useful in treatment of NMS

with dehydration, rapid titration of triggering drugs, and psychomotor agitation

Other DDx: CNS diseases meningitis, tumor,

Page 166 of 217

Non-obstetrical surgery during pregnancy

Obstetric consideration

Risk of abortion and premature labor

Minimize the amount of drugs as much as possible

Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids,

Ketamine, Etomidate)

If urgent Sx consider delay to the 2nd

trimester

Have an obstetric consultation

For GA < 16 wks have FHM pre, and post op, for >16 wks have it intra-op

for abdominal procedure consider a transvagainal monitor

FHR variability present @25-27 wks

Maintain normal maternal BP, Oxygenation, acid-base status, avoid

aortocaval compression

For pelvic and lower limb and upper limb consider regional technique

For laparoscopic procedures max peritoneal inflation pressure 8-12 mm Hg

For spinal or epidural give a fluid bolus before

Always give reflux prophylaxis, and do RSI, with maintaining LUD

Page 167 of 217

Obesity

A difficult intubation

B OSA, pickwickian syndrome, restrictive defect, with FRC and Pul HTN

C HTN, CAD, pul HTN with cor-pulmonale, RV and LV dysfunction

GI GERD, gastric acidity, fatty liver with liver dysfunction

M DM

D calculate the drug dosage according to the lean body mass

H/P evidence of OSA, and RV/LV dysfunction snoring, orhtopnea,

PND, EXAM RV/LV failure

LAB CBC-D, Lytes, BUN, Creat, ABG, PFT, ECG,LFT, and consider

Echo

Difficult IV access, and regional anesthesia

Page 168 of 217

Obstetric considerations:

Physiological and anatomical changes

A difficult A/W, Full stomach, ,RSI

B easy desat FRC, VO2

C hyperdynamic state, Aortocaval compression BP, UP blood flow

D MAC, cholinesterase, albumin Free F of drugs, placental drug

transfer

GI/Hepatic full stomach, gastric empting, liver enzyme

Page 169 of 217

Omphalocele and Gastroschisis

o Impaired blood supply to the herniated organs, and intestinal obstruction

o Major intravascular fluid shift and dehydration full-strength balanced salt

solution

o Hypothermia and hypoglycemia

A possible difficult airway Beckwith-Wiedemann syndrome consists of

mental retardation, hypoglycemia, congenital heart disease, a large tongue, and

an omphalocele.

B respiratory failure

C CHD in 20% of infants with omphalocele.

Induction: NG aspirate gastric content then RSI , need large IV , possible

central, and arterial line

Post-op keep intubated

M intravascular volume, with lytes abnormality

Page 170 of 217

Organophosphate poisoning

Bind to acetylcholinestrase enzyme

S/S: Nicotinic: muscle weakness, fasciculation

Muscarinic: DUMBELS syndrome

D diaphoresis, diarrhea

U urination

M miosis

B bradycardia, bronchorrhea, bronchospasm

E Emisis

L lacremation

S salivation

A salivation, aspiration

B Respiratory failure, , bronchorrhea, bronchospasm

C hypotension, bradycardia, shock, arrhythmias, QT(poor prognosis)

D Avoid aminoglycosids ABx

M lytes abnormalities, acidosis, dehydration

GI N&V, diarrhea

Page 171 of 217

Osteogenesis Imperfecta:

A connective tissue disorder with 4 subtypes

Multiple #, short stature, blue sclera

A deformity of the base of the skull, vertebral # Awake FOI

B kyphoscoliosis restrictive lung defect

C Cor-pulmonale

Heme impaired PLT function

Page 172 of 217

Other hemolytic anemia’s:

Spherocytosis:

Membrane defect abnormal shape RBC hemolysis

May have a hemolytic crisis which can triggered by infection and folate

deficiency

May come for splenectomy

G6PD Deficiency:

RBC enzyme defect

Can have a hemolytic crisis if exposed to some food and drugs: Fava beans,

PNC, Tyhlenol, antimalarial drugs, methylene blue, ASA in large dose

Usually happened 2-5 day after ingestion

May have DIC

Page 173 of 217

Oxygen Delivery and Oxygen Consumption

Oxygen Delivery.

Oxygen delivery is a function of arterial oxygen content (Cao2) and cardiac output.

Cao2 is expressed as the number of milliliters of oxygen contained in 100 ml of

blood and is calculated as follows:

Cao2 = (Hgb × 1.34 × Sao2) + (0.003 × Pao2)

DO2 = CO × Cao2

Oxygen Consumption.

O2 consumption = CO x (CaO2-CvO2)

Oxygen extraction Ratio

ER= O2 consumption / O2 delivery

ER= [ CO x (CaO2-CvO2)] / CO x CaO2 = CaO2 – CvO2/CaO2

Page 174 of 217

Pancreatitis:( acute, chronic)

Associated with: chronic alcohol abuse, blunt abdominal trauma, gallstone,

perforated PUD

Lab amylase

DDx cholecystitis , MI, Pneumonia

Chronic mainly with alcoholism, CF, old blunt trauma

A RSI, for GI ileus

B ARDS

C hypovolemia, hypotension

D narcotic tolerant, malnourished albumin free fraction of drugs

careful titration

M Ca, acidosis, DM, acute alcohol withdrawal

Renal ARF due to dehydration

CNS encephalopathy

Heme anemia, DIC

Consider art-line , CVP

Post-op ICU, pain management

Page 175 of 217

Parkinson's Disease

degenerative disease of the CNS caused by loss of dopaminergic fibers in the

basal ganglia of the brain.(substantia nigra)

clinical features are resting tremor, cogwheel rigidity of the extremities,

bradykinesia, shuffling gait, stooped posture, and facial immobility.

A laryngospasm, muscle rigidity before giving MR difficult vent consider RSI

B frequent aspiration, VC, COPD

C arrhythmias due to L-dopa, autonomic dysfunction, intravascular volume

D L-dopa(sinemet) Levodopa+ a peripheral dopamine decarboxylase inhibitor

carbidopa to systemic side effect give in AM t1/2 6-12, avoid Maxran,

Demerol, alfenta, droperidol, sux may use for RSI, K one case report

Post-op: In the postoperative period, patients with Parkinson's disease are more

susceptible to the development of mental confusion and even hallucinations.

Page 176 of 217

PDPH

In a supine position very mild, sitting severe fronto-occipital headache

May associated with cranial N symptoms: diplopia, tinnitus, N&V

DDx: meningitis, migraine

Action:

Review anesthetic Record for Neuraxial procedure, type and size of needle

for spinal, and wet tab documentation, and any other complications

Review past-medical Hx neurological Hx (headache)

Headache: character, severity, aggravating and relieving factors (position),

associated symptoms, and the location of the headache

Exam: V/S include Temp, meningeal signs (meningismus, photophobia,

fever), Neuro Exam looking for any sensory or motor deficit

Rx: bed rest, hydration, caffeine 300mg PO q8-12hrs, Tylenol, and

NSAID’s if not working or severe headache Epidural blood patch

Peri-tonsilar abscess

Emergency and potential life threatening

A airway obstruction, with trismus , possible full stomach, do a gas induction

with no muscle relaxant , gentle intubation avoid rupture the abscess

Page 177 of 217

Pheochromocytoma

In normal medulla, norepinephrine account for only 20% of the secretion,

where it is greater in a Pt with pheochromocytoma.

halothane and histamine-releasing drugs, can exacerbate the life-threatening

cardiovascular effects of the catecholamines secreted by these tumors.

Most (85–90%) are solitary tumors localized to a single adrenal gland,

usually the right, 10% of adults and 25% of children have bilateral tumors.

extra-adrenal sites (10%) along the paravertebral sympathetic chain.

95% in the abdomen, a small % located in thorax, urinary bladder, or neck.

Malignant spread of highly vascular tumors in approximately 10% of cases.

In about 5% of cases, this tumor is inherited as a familial AD trait.

It may be part of the polyglandular syndrome as MEN Type IIA or IIB.

Type IIA includes: medullary carcinoma of the thyroid, parathyroid

hyperplasia, pheochromocytoma;

Type IIB consists of: medullary carcinoma of the thyroid,

pheochromocytoma, neuromas of the oral mucosa.

may also arise in association with von Recklinghausen's neurofibromatosis

or von Hippel-Lindau disease (retinal and cerebellar angiomatosis).

Page 178 of 217

Phosphate

distributed in similar concentrations throughout intracellular and

extracellular fluid.90% in bone, 10% is intracellular, and <1%, in the ECF.

free ion (55%), complexed ion (33%), and in a protein-bound form (12%).

Control of phos concentration by altered renal excretion and redistribution

within the body compartments.

Absorption occurs in the duodenum and jejunum and is largely unregulated.

Phos reabsorption in the kidney is primarily regulated by PTH, dietary

intake, and insulin-like growth factor.

Phos provide the primary energy bond in ATP and creatine phosphate.

Therefore, severe phosphate depletion results in cellular energy depletion.

Phos is an essential element of second-messenger systems, including cAMP

and phosphoinositides, and a major component of nucleic acids,

phospholipids, and cell membranes.

As part of 2,3-DPG, phos is important for off-loading oxygen from the

hemoglobin molecule.

Page 179 of 217

Physiological changes in pregnancy:

A venous engorgement, edema, by PIH, URTI and fluid overload, easy nasal

bleed

B FRC, TLC, ERV, IRV, TV, minute vent, and O2 consumption, shunt

from 5% to 14 %, shift of O2-Hgb curve to the Rt with P50 30mmHg

C CO, Normal BP due SVR, plasma volume

Pierre Robin Syndrome:

A difficult A/W due to micrognathia, glossoptosis, cleft palate

B obstruction pul edema, Aspiration

C CHF, pul HTN, cor pulmonale, associated CHD

CNS Sz due to hypoxic brain injury

Do awake FOI, have ENT surgeon in the room for possible trach

A/W obstruction improve with age

Extubate awake only

Page 180 of 217

PIH and HELLP

In addition to the changes in pregnancy

A airway edema, difficult intubation difficult A/W cart in the room

B pul edema, more after delivery

C CHF, BP, volume, oncotic pressure

D Mg, other meds, could be on ASA

M Mg, albumin

Heme anemia, hemolysis, thrombocytopenia , fibrinogen

CNS LOC, headache, blurred vision, seizure, bleeding , edema

Renal GFR, oliguria, ARF

GI/Hepatic RUQ pain, liver rupture

Rx start Mg bolus 4g then infusion @ 1-3 g/h, consider other anti-HTN meds

e.g. labetolol, SNP, NTG, hydralazine, (ACEI are C/I due to fetal effect)

Monitor Mg level avoid Mg toxicity, consider early epidural help BP,

improve UP blood flow (if PLT are OK)

Monitors: art line, fetal monitoring, CVP/PAC

Before giving any fluid bolus look for evidence of CHF

Lab: CBC-D, Lytes, BUN, Creat, Mg, PT, PTT, fibrinogen, LFT, BT

Page 181 of 217

Pituitary Tumors, and transsphenoidal approach

Ant regulated by the hypothalamus secret 7 hormones

Post ADH, Oxytocin

Tumors could be non-functioning, or hyper secreting

The non-functional mass effect headache impaired vision, N&V, CN palsy,

and ICP, or pan-hypopitutarism

hyper secreting could be a MEN I, usually small, the most common is adenoma

secreting prolactin , then GH, then ACTH, other effect hyperthyroid, DM

pituitary apoplexy due to sudden hemorrhage neuro deficit and pituitary

function Mx steroids and surgical decompression

May not develop DI until after starting steroids therapy

Monitors routine with art-line for acromegaly, CVP if head-op position

Lab CBC, lytes, ABG, CXR, ECG, lateral neck XR

Critical structures internal carotid artery, cavernous sinuses, CN III, IV, V, VI

A possible difficult intubation

B OSA

C HTN, Cardiomegaly, cardiomyopathy

D hormone replacement, stress dose steroid,

Page 182 of 217

Placenta previa

Risks: previous C/S, previa

Painless vaginal bleeding in the 2nd

-3rd

trimester

Risk of abruption and IUGR

Avoid vaginal exam and tocolytic therapy

A and B obst

C hypovolemia, shock

D avoid tocolytic

Heme DIC rare, most are dilutional thrombocytopenia

Mx:

lab as in abruption

shock as in abruption

GA Vs spinal/epidural depend wither if the placenta is anterior or >1 C/S with

risk of accreta GA, if posterior may consider spinal/epidural if the Pt is stable

Page 183 of 217

Porphyrias

A group of inborn error of metabolism, with defect in heme synthesis

Complete deficiency of enzymes is incompatible with life

Deficiency of one enzyme will lead to accumulation of one or more

intermediates molecules which will give the clinical manifestation of Porphyria.

The rate-limiting step in heme synthesis is the conjugation of succinyl-CoA

with glycine to form D-aminolevulinic acid ALA (the enzyme is aminolevulinic

acid synthetase).

generally manifest after puberty. Inheritance is an AD pattern,

but congenital erythropoietic porphyria is inherited as an AR pattern.

A functional classification for the anesthesiologist is based on a division of the

porphyrias into:

o Inducible: acute symptoms are precipitated on drug exposure, which are:

Acute intermittent Porphyria

variegate Porphyria ( 80% photosensitive)

hereditary coproporphyria

o noninducible forms.

Page 184 of 217

Post-op Stridor:

Emergency, and life threatening

Proceed immediately to the PARR

Review the V/S, and quick AMPLE history , 100% O2, and Call for help,

do jaw thrust, apply oral A/W, apply CPAP, suction the A/W

DDx: 1-Laryngeospasm, 2-laryngeal edema due to volume overload or

Trendelenburg position intra-op,3- VC paralysis due to neck or thoracic Sx,

or residual NM blockade, 4- A/W foreign body (secretion, blood, vomit

Page 185 of 217

Post-op Altered LOC/Agitation:

With LOC could be life threatening, agitation potential harm to him self

and nurses

Proceed immediately to the PARR

ABC, restrain the Pt if needed, 100% O2. obtain new V/S

Review anesthetic chart/ talk to the anesthetist who did the case, review the

old chart

DDx:

o Psychological response to emergence

o Co-existing mental/psychological problem (post-traumatic stress)

o Intra-op re-call

o Residual anesthetics, NMB Agents, Ketamine.

o Drugs/alcohol withdrawal

o Withdrawal of anti-psychotic, seizure, Parkinson meds

o Surgical pain, bladder distention

o A/W obstruction with hypoxia and hypercarbia

o Other metabolic abnormalities Na, Ca, hypoglycemia

o CNS: hypoperfusion, CVA, Sz, postictal

Page 186 of 217

Post-op hepatic dysfunction

Classify as pre, intra and post hepatic

The main S/S is jaundice

Need repeat measurement of bili, AST/ALT, and ALP

Most likely multifactorial

One of the main factors could be intra-op hepatic hypoxemia

Steps:

1) Review all meds given to the Pt without any exclusion peri-op, includes

intra-op use of vasopressors splanchnic vasoconstriction B flow

2) Look for source of infection

3) Blood Tx bili load in Pt with co-existing liver dysfunction

4) Look for hematoma hyperbilirubinemia

5) Role out hemolysis Hb, retics

6) Review anesthetic and PARR records for any evidence of hypoxemia,

hypotension, hypovent, hypovolemia

7) Look for extra-hepatic source of liver dysfunction CHF, resp failure, PE,

RF

8) Could be benign post-op intrahepatic cholestasis

Page 187 of 217

Post-tonsillectomy bleeding

Emergency and potential life threatening

Go immediately to see the Pt

OR emerg meds , airway equipment double setup X2 suction , X2 scops

A full stomach, possible difficult airway use ketamine for induction, RSI

B hypoxia

C hemorrhagic shock, resuscitate the Pt

H possible bleeding disorder.

Lab CBC, lytes, PT, PTT, X-match

Page 188 of 217

Pre-op Cardiac evaluation:

See other card for clinical predictors

See other card for stratification for noncardiac surgical procedure

See the algorithm

Recent MI wait 4-6 wks for elective surgery

Lab evaluation

o Resting LV function is not a predictor for ischemic event

o 12 leads ECG

o Exercise or pharma stress test for Pt with intermediate risk, or when Pt

is unreliable

o Angio for Pt suspected or known CAD

Pre-op therapy

o CABG for high risk Pt, with possibility to improve outcome

o PCA: no controlled trial for PCA vs medical therapy, If Pt had PCA,

with balloon dilation only, wait only for one week for elective

procedure, if stent 4-6 wks with minimum 2 wks, for anti-PLT therapy

o Medical: -blokers

Anesthetic consideration

o No technique is superior

Page 189 of 217

Preterm labor

Between 20-37 wks

fetal M&M

Pt may given tocolytic therapy if there is no C/I

-agonist: Ritodrine and terbutaline

o For short term only to allow time for lung maturity after steroids

o The effect persist to 60-90 min after D/C, need at least 10 min D/C

before giving anesthetic

o S/E: hyperglycemia, tachycardia, with possible arrhythmia, pul edema,

myocardial ischemia, hypotension, cerebral vasospasm, fetal

tachycardia, rebound hypoglycemia

o Avoid overzealous hydration which may risk of pul edema, and

hyperventilation K

o Lidocaine IV may prevent arrhythmia

MgSO4

o See PIH for S/E, less severe than -agonist

o Risk of hypotension with spinal/epidural

o sensitivity to NDMR

Page 190 of 217

Prone position

Difficult access to the A/W

Difficult resuscitation

Difficult to add invasive monitoring art-line, CVP, TEE

Pressure injury to eyes, nose, iliac crest, knees, toes, breast, genitalia

Brachial plexus injury

CI, SV, Venus return due to pressure on the abdomen vena caval

pressure epidural vein engorgement

Page 191 of 217

Protein C and Protein S Deficiency

Congenital AD, or Acquired due to hepatic dysfunction, vit K deficiency,

and DIC, post-op, hemodialysis, postpartum

risk of thrombo-embolic phenomena post-op

A N/A

B PE, with possible Pul HTN,

C IHD (MI, angina), Peripheral vascular disease

D on coumadin stop pre-op and start heparin

G bowel ischemia

R renal vein and artery thrombosis.

CNS sagital sinus thrombosis stroke, TIA’s

for neuraxial anesthesia look in the ASRA guidelines

may give FFP to protein C level.

Antithrombin III deficiency

risk of thrombo-embolic phenomena

Resistance to heparin, may give Antithrombin III concentrate, or FFP

Page 192 of 217

Pul HTN

The pulmonary vessels are more reactive compared to Eisenmenger

High mortality rate

Hemodynamic Goals:

o preload maintain, LUD

o R/R maintain normal and sinus

o Cont maintain, avoid cardiodepressant

o Afterlaod maintain, avoid sudden in SVR

o PVR Avoid any thing that PVR pain, hypoxia, acidosis, PCO2

O2 all the time, Art-line,

Consider: NO, prostacycline, CCB, NTG to PVR

PAC risk/benefit

No spinal, epidural slowly titrate

GA same problem as in Eisenmenger

Post-op ICU

Page 193 of 217

Pulmonary embolism

Associated with hyper-coagulation state (protein C and S deficiency ),

trauma, prolonged bed rest

High M&M

Pathophysiology:

o Pulmonary arteries obstruction dead space ventilation

hypoxemia , hypercarbia

o PVR, Bronchospasm

o RV dysfunction and arrhythmias

Pt may present to the OR for emergency surgery, insertion of IVC filter or

surgical embolectomy

Also Pt may present with previous history of PE, and now anticoagulated

have a hematology consult (Q: risk/benefit of holding meds pre-op) also

discuss with the surgeon regarding continuing the anticoagulation med peri-

op

Have PT, PTT, and PLT count (HIT)

Better to avoid Neuraxial technique in those Pt

If diagnosis is in doubt Spiral CT, V/Q scan, Echo

Page 194 of 217

Pulmonary HTN

@ rest mean of 25, with exercise > 30

Primary (idiopathic) F:M 3:1, age 20-40

Secondary:

o pul disease: asthma, COPD, restrictive lung disease, cystic fibrosis,

o heart disease: MS, AS, ASD, VSD

o collagen vascular disease

o thromboembolic disease: PE, sickle cell

S/S SOBOE, easy fatigue wheezing, graham steel murmur

Lab: CXR, ECG(RVH, RAD, Rt atrial enlargement), Echo, ABG, PFT, NO

test to if responsive or not (Viagra)

Cardiology consult and ICU

Monitors: CAS, 5 leads EGC, art-line, CVP, PAC???, TEE, ECG look for

acute strain pattern in leads II, III and aVF

Options RA Vs GA, better RA

Have NO ready, and inotropic support (milrinon, dobutamine) SNP, NTG

Keep 100 O2 all time

Avoid things PVR ( hypoxia, acidosis, hypothermia, PCO2)

Page 195 of 217

Pyloric stenosis

M>F

Not a surgical emergency, S/S appear 2-6wks

With the consideration of neonate

A full stomach RSI

B compensated resp acidosis hypoventilation

C hypovolemia shock

M hypochloremic metabolic alkalosis, dehydration

Pre op assess the level hydration skin turgor, anterior fontanel, moist tongue,

urine OP, V/S

Check lytes Na >132, Cl>88, K > 3.2,

Give K, if + urine OP

Induction give atropine, insert NGT, or OGT to empty the stomach (no

guaranteed) and pre-oxygenate

RSI with cricoid pressure

Maintenance need to be paralyzed if not risk of mucosal perforation

Infiltrate Marcaine with epi, give Tylenol 15mg/kg PR for pain control

Page 196 of 217

Restrictive Cardiomyopathy

Causes:

o Toxic :Methysergide, Anorectic agents, Radiation

o Infectious: viral myocarditis

o Infiltration: endomyocardial fibrosis

o Genetic

o Idiopathic

o Infiltration

Sarcoid, Hemochromatosis, Amyloidosis ,Glycogen storage

disease

Impaired diastolic filling

Have the same clinical picture of constrictive pericarditis

Except that the LV is more affected than RV

Management of anesthesia:

o As Tamponade

Page 197 of 217

Restrictive lung disease

The main feature is lung compliance with TLC, normal FEV1/FVC,

and VC N 70ml/kg, as low as 15ml/kg, and possible

hyperventilation with PCO2

Could be acute Vs chronic, where the acute component could be reversible

Causes:

o intrinsic lung disease ( edema, pneumonia, aspiration, ARDS,

fibrosis due to drugs, or idiopathic, and plural diseases)

o Neuromuscular diseases: spinal cord transection, Guillian barre,

muscular dystrophy, myasthenia, and myasthenic syndrome

o MSK scoliosis, sternal deformity

o Extrinsic: obesity, pregnancy, ascites

S/S SOBOE, exercise tolerance, cough, breathing pattern Vt, RR

With severe disease Pt may have pul HTN, with S/S of Rt heart failure

Pre-op: determine the severity by H/P and Lab, and treat the possible acute

reversible component

A VC < 15ml/kg with PCO2 high risk

Lab: CBC-D, lytes, BUN, creat, CXR, ABG, PFT, ECG, Echo

Page 198 of 217

Rheumatoid arthritis

F> M, Age 30-50

The hands and wrists are involved first, particularly the metacarpophalangeal and proximal

interphalangeal joints.

A:C-spine: atlantoaxial subluxation, The degree of cord compression does not correlate

well with the patient's symptoms, and asymptomatic patients may have a high degree of

spinal canal stenosis., TMJ involvement, Cricoarytenoid arthritis which may cause pain,

horseness, dyspnea, stridor and airway edema.

So be caution with intubation and consider Fiberoptic intubation, and risk of post-

extubation stridor.

B: pleural effusions, pulmonary nodules, interstitial lung disease, obstructive lung disease,

restrictive lung disease. more common due to costochondral involvement

Several of the antirheumatic drugs cause pulmonary dysfunction as well

V/Q mismatch and hypoxia

Consider PFT and possible post-op ICU bed

C: Pericarditis in 30%, chronic constrictive pericarditis or pericardial tamponade

myocarditis, coronary arteritis

dysrhythmias secondary to development of rheumatoid nodules in the cardiac

conduction system

aortitis, producing aortic root dilation and aortic insufficiency, Valve fibrosis

Page 199 of 217

Risk of RBC Tx

Citrate Intoxication

o CPDA citrateionized calcium.

o Signs hypotension, narrow pulse pressure, VEDP, and CVP

o ECG changes: prolonged Q-T interval, widened QRS, and flattened T waves.

o The hypocalcemia is directly related to the rate and volume of blood Tx.

o Citrate is metabolized efficiently by the liver, Impaired liver function or

perfusion will lower the rate threshold for developing citrate intoxication.

o Treatment: CaCl

Acid–Base Changes ? metabolic acidosis

2,3-DPG left shift of the O2–Hgb dissociation curve

Hyperkalemia with rapid Tx by acidosis, hypovolemia, and hypothermia

o ECG peaked T waves, a prolonged PR interval, and a widened QRS.

o If ECG changes are observed the transfusion should be stopped and

intravenous calcium should be administered. Bicarbonate, dextrose, and

insulin may also be appropriate according to the severity of the episode

Volume Overload

Hypothermia CO, left shift of O2-Hgb, acidosis, coags

Microaggregate Delivery

Page 200 of 217

Sarcoidosis:

More common in African-American, F:M 2:1

A distorted anatomy with possible A/W obstruction difficult A/W FOI

B restrictive lung disease with pulmonary fibrosis

C Arrhythmias, heart block, CHF

D on Steroid and immunosuppressant (stress dose)

GI liver involvement

CNS SOL, neuropathy, Sz

Lab/DI CBC-D, Lytes, BUN, creat, ABG, CXR, PFT, ECG, LFT

Consider ICU backup if bad PFT

Page 201 of 217

SARS:

Not contagious until Pt become symptomatic with in 4-6 days(2-10)

Transmission by close contact, and in a contact with resp secretion

S/S and Lab:

Fever, chills, headache, myalgia (nonspecific)

Nonproductive cough, with SOB, other N&V, diarrhea

Radiological evidence of pneumonia within 7-10 days of symptoms onset

Lab: lymphopenia, PLT, PTT and Liver enzymes and CK

SARS serum Antibodies positive

SARS CoV isolation in cell culture

PCR positive for SARS CoV RNA

Action:

Suspected Pt should be in resp isolation room ASAP if history contact with

Pt with SARS or been in an epidemic area

During Pt transfer have a surgical mask over the Pt

Do CXR, pulse oxi, blood C/S, CBC-D, sputum for gram stain and C/S

Test for other respiratory pathogens inf A, B, RSV, pneumococcal

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Scleroderma

Progressive systemic sclerosis:Inflammation, Vascular sclerosis, Fibrosis of skin and

viscera

Tissue edema

Some Pts have CREST syndrome, C: calcinosis, R: Raynaud’s phenomenon, E:

esophageal hypomotality, S: scleroderma, T: Telengectesia

F>M, Age 20-40

Pregnancy the progression of the disease in 50% of the Pt.

A: flexion contracture difficult airway due to limited mouth opening, motility, LOS

tone GERD need RSI

B: A major cause of M&M, Chronic aspiration, Diffuse lung fibrosis restrictive lung

disease, diffusion capacity

C: risk of IHD, fibrosis of the conductive system arrhythmia, cardiomyopathy CHF,

systemic and pulmonary HTN, pericarditis effusion tamponade, with systemic HTN

intravascular volume hypotension , Raynaud’s phenomenon in 70% risk of ischemia

with art-line

CNS: peripheral and cranial nerve neuropathy

o Eye: conjunctivitis and corneal abrasion

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Scoliosis Sx

Need two stage Sx, 1st anterior approach to release the anterior spinal artery, and

diskectomy, the 2nd

stage to posterior instrumentation

The scoliosis could be secondary to muscular disease ( muscular dystrophy)

A Reflux RSI

B Restrictive lung disease, risk of PPC (pneumonia, atelectasis)

C myopathy, arrhythmias

D avoid Sux

Heme consider autologus blood donation pre-op

Consult (ICU, Heme), talk to the Pt regarding awake test

Lab:CBC-D, Lytes, BUN, creat, X-match, CXR, PFT, ABG, ECG, Echo if needed

OR: blood in the OR, bear hugger, Art-line, IV wormer

Position: prone check all pressure points, and frequent checking

May consider deliberate hypotension if there is no C/I, with that HR will , so

consider -blockers

SSEP: if latency by 10% or amp by 60% BP, ask the surgeon to stop

Volatiles have the least effect on SSEP See SSEP card

Post-op: pain, PPC, ICU

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SEP

Any injury will cause in latency & amplitude

SSEP 50% in amp to surgical maneuver significant

Cortical ( SSEP, VEP) are more vulnerable to anesthetic drug effect

brain stem/subcortical (SSEP, BAEP) are more resistance

key points:

maintain a constant anesthetic level, and avoid any sudden changes

or a bolus doses of any drugs

maintain and control other factors that may affect the SEP like

temp, BP, PaO2 and PaCO2

Effect of inhalational agents:

SSEP all lat/amp, except enf /, N2O 0/

VEP all lat/ amp

BAEP alt/0 amp

Effect of IV drugs:

All drugs lat/ amp except ketamine and etomidate /, with 0/

effect on the VEP and no effect on BAEP at regular doses

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Septic shock:

A LOC, full stomach

B resp failure, ARDS, pul edema

C low or high output failure, SVR,

D Abx, APC, steroids, inotrops, vasopressors

Met lactic acidosis, base deficit, K, lytes disturbance, adrenal insufficiency

Renal ATN, ARF

Heme thrombocytopenia, DIC

Management:

ABC

ECG, Sat, Art-line, CVP/PAC, frequent ABG,

Lab: CXR, ABG, ECG, CBC-D, Blood C/S, sputum, and urine, lytes, BUN,

creat, LFT, PT, PTT, Fibrinogen, D-dimer, ACTH stim test, if suspecting a

source of infection do further investigation e.g. TEE or TTE for ? edocarditis,

abdominal CT…..

Early goal directed therapy( CVP 8-12, MAP >65, Urine>0.5ml/kg/hr,

SvO2>70%)

Broad spectrum ABx

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Class I Class II Class III Class IV

Blood loss (ml) 750 750–1500 1500–2000 2000

Blood loss (%) 15 15–30 30–40 40

HR (per min) <100 >100 >120 140

Blood pressure Normal Normal

Pulse pressure Normal or

RR 14–20 20–30 30–40 <35

Urine ml/hr 30 20–30 5–15 Negligible

Mental status Slightly

anxious

Mildly

anxious

Anxious and

confused

Confused,

lethargic

Fluid (3:1 rule)‡ Crystalloid Crystalloid Crystalloid +

blood

Crystalloid +

blood

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Shoulder Sx:

Arthroplasy, and arthroscopy, and rotator cuff repair

Use of a beach chair position VAE risk

Limited access to the airway tighten the connection, reinforce with tap

Possible eye and ears injury

Avoid excessive head rotation brachial plexus injury

Options GA, interscalene or combined

Assess the arm before doing the block for any neurological deficit

Risk of post-op neurological deficit the level of the injury is at the level

of the trunk (same as interscalene) difficult to determine the cause (surgical

Vs block) Neurapraxia 90% resolve within 3-4 months

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Inappropriate Secretion of Antidiuretic Hormone (SIADH)

Causes: head injuries,intracranial tumors, pulmonary infections, small cell

carcinoma of the lung and hypothyroidism.

Clinical manifestations

occur as a result of a dilutional hyponatremia, serum osmolality, and a reduced

urine output with a high osmolality. Weight gain, skeletal muscle weakness, and

mental confusion or convulsions are presenting symptoms. Peripheral edema

and hypertension are rare. The diagnosis of the (SIADH) is one of exclusion,

and other causes of hyponatremia must first be ruled out. The prognosis is

related to the underlying cause of the syndrome.

Treatment:

Pt with mild/mod H2O intoxication is restriction of fluid intake to 800 ml·day–

1.

Pt with severe water intoxication associated with hyponatremia and mental

confusion may require more aggressive therapy, with the iv administration of a

hypertonic saline solution. This may be administered in conjunction with lasix

Caution must be observed in patients with poor LV function. Isotonic saline is

substituted for hypertonic solutions once the serum Na is in a safe range.

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Sickle cell anemia

The defect in -chain, position 6 glutamic acid substituted by valine

3 types of crisis

o hemolytic further anemia

o sickling pain & vaso-occlusive

o Aplastic may cause death.

Ethnic background: Mediterranean and African-American.

In infancy Hb F is protective.

% of Hb S

o trait (mild)

o < 50% is Hb S

o sickling do not occur under normal physiological conditions

o may happen under extreme conditions e.g severe hypoxemia.

o Disease (severe)

o Hb S > 75% may up to 95%

o Could be associated with other abnormal Hb e.g Hb C

o Pt with Hb SC have a normal Hb level, but at a greater risk of sickling.

Pre-op you need to knew what is the result of the Hb electrophoresis.

mortality with in the number of the painful crisis in adult per-year.

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Status asthmaticus

Emergency and life threatening

Result in respiratory failure with hypoxia, hypercarbia, and

respiratory/metabolic acidosis

Management:

o ABC, 100% O2

o Intubate deep/ also may consider BiPAP

o Ventoline, ipratrupium bromide, steroids, thiophylline, leukotrine

inhibitor, ABx if suspect infection

o Other consider Ventoline IV, Isoprel/pei gtt, Ketamine, BNZ

o Last volatile agent, and paralyze

o Ventilation: volume control Vt 6-10ml/kg, PEEP 5-10, target

normal PO2, pH, and PCO2, keep the platue pressure < 30cmH2O

o If need switch to pressure control

o Also may consider Heliox

o Be aware of AutoPEEP disconnect the bag, if on vent reverse

ratio ventilation

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Stroke & TIA:

Hemorrhagic or ischemic

Etiology: Atherosclerosis, embolic MI, A.fib, VHD, post-op CEA,

trauma, severe HTN

A LOC, loss of A/W reflux (RSI)

B hypoventilation

C HTN, CAD, VHD, A.fib, arrhythmias ECG, Echo

D anti-PLT, ASA, coumadin, Avoid Sux, N. stimulator resistance

N LOC, neuro deficit

Peri-op

Avoid swinging in BP, and hyperglycemia

With chronic HTN the cerebral autoregulation curve shifted to the Rt

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Supratentorial Intracranial Tumors

Review Pt overall medical condition

Focus on Neuro-evaluation: LOC, S/S of ICP: headache, N&V, papilledema,

unilateral pupil dilation, and the presence and extent of focal neurological deficit

May have fluid and lytes abnormality

Review CT/MRI head

Lab: CBC, lytes, BUN, creat, ECG

The main effect of Supratentorial masses is intracranial HTN

The main anesthetic goal is to maximize the therapeutic modality to ICP, and to

avoid any factor that may ICP

ICP control SEE ICP card

Monitoring: Standard + Art line, CVP, Foley cath, for the art-line have the

transducer at the level of external auditory meatus ( level of circle of Willis)

Induction: may need RSI, if CN involvement or LOC, give Lidocaine IV, with

other standard induction drugs, Avoid Sux

Maintenance: Isoflurane, No N2O

Emergence: give Lidocaine IV 90 sec before extubation, and consider using

antihypertensive Meds(labetolol), assess for any neurological deficit

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Systemic Lupus Erythematosus

A cricoarytenoid arthritis hoarseness, stridor, or airway obstruction (awake

intubation), post-extubation edema

B effusion, pneumonitis, pul HTN, and alveolar hemorrhage. high correlation

of pul HTN with Raynaud's phenomenon in patients with SLE.(CXR, PFT)

C pericardial effusion, tamponade, Cardiomyopathy, cardiac conduction

abnormalities, ventricular function, and coronary arteritis, noninfectious

endocarditis (Libman-Sacks endocarditis) mitral insufficiency (ECG, ECHO)

D immunosuppressants (corticosteroids) or cytotoxic drugs

(cyclophosphamide, azathioprine, cyclosporine),avoid Drug-induced lupus

quinidine, hydralazine, methyldopa, captopril, enalapril, clonidine, isoniazid,

Hanti-phospholipid antibodies thromboembolic complications, anemia

R common cause of M&M in patients with SLE, CRF

CNS seizures, stroke, dementia, psychosis, and peripheral neuropathy

GI peritonitis, pancreatitis, bowel ischemia, protein-losing enteropathy, and

lupoid hepatitis

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Tamponade:

Emergency and life threatening

In acute as little as 200 ml cause S/S

In chronic up to 1000 ml cause S/S

Causes:

o Infection: bacterial, viral, fungal, TB

o Inflammatory disease with vasculitis: R.Arthritis, SLE, scleroderma

o Metabolic: RF, myxedema

o Radiation, malignancy, trauma, post-heart

Pathophysiology: VEDV, SV, CO, SBP, CVP, Rt=Lt pressure

Dx by keeping in mind a high index of suspicion with clinical S/S and lab

Beck’s triad: hypotension, distended neck veins, muffled heart sound

S/S: tachypnea, BP, narrow pulse pressure, HR, pulses paradoxus

Signs of systemic hypoprefusion: oliguria, lactic acidosis, cool extr

DDx: tension Pneumo, RV infarction, Pul HTN, cardiac herniation

ECG: diffuse ST-changes, low voltage

Lab: ECG, Echo, CXR, CT

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TCA overdose:

Gives anticholinergic syndrome, So no Atropine

Cardiac toxicity is the major cause of death

No correlation between serum level and symptom

A LOC RSI

B depression, ARDS

C toxicity, QT, wide QRS, sinus tach, heart block, hypotension due

contractility, and vasodilation by -blockade, arrest

CNS hallucination, coma, seizure

M metabolic acidosis

Management:

o ABC

o Gastric lavage

o Activated charcoal 1g/kg with 60 ml sorbitol

o Bicarb is the Key in the management 2 mEq/kg bolus then infusion

150mEq in 850 D5W to maintain pH 7.45-7.50

o For Vent arrhythmia give Lidocaine, Class 1A,1C are C/I

o Hypotension Norepi gtt

o Bradycardia Isoprel or pacing No Atropine

Page 216 of 217

TEF

30% premature, associated CHD, and VATER, VACTREL syndromes

Depend on the infant stability if stable complete repair, if not stage repair, with

insertion of G-tube under LA, the ligation of the fistula, and reanastomosis of the

esophagus

A subglottic stenosis

B resp distress, RDS, pneumonia

C CHD, decompensation and CHF

M dehydration, metabolic acidosis

Worm up the room, big IV, standard CAS monitors, Art-line

Lab CBC-D, lytes, ABG, Cap gas or VBG, CXR, Echo, X-match with 2U peds

in the room

Give atropine, not muscle relaxant until chest open,

Inhalation induction bronch, then intubate after further mask ventilation to

deepen the Pt, have different size ETT, after intubation with the bevel directed

posteriorly, listen to the chest and initially intubate the Rt main bronchus, with

listening to the chest withdraw the tube slowly till you here bilateral breath sound.

Consider caudal epidural for post-op pain

Run maintenance fluids with glucose maintenance as well

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