Severe headache in a 54 year-old man

Coruña | Datukon | de Castro | de la LlanaApril 30, 2010 | Block G

NSS

CLINICAL HISTORY

General Data

• I.B.• 54/M• Right-handed• Farmer• Abra

Chief Complaint

• Severe headache

History of Present Illness

• 1 month PTA (3/14/2010)– (+) dizziness, (+) syncope– (+) severe headache – piercing, graded 10/10 – (+) left-sided weakness– Brought to Abra Provincial Hospital treated as a

case of CVD– CT scan done in Vigan ten days post-event

revealed subarachnoid hemorrhage

History of Present Illness

• 1 month PTA– (-) sensorial changes– (+) minimal nape pain– (-) facial asymmetry– Advised transfer to PGH for further evaluation and

surgery– Opted not to consult due to financial constraints

History of Present Illness

• 2 weeks PTA– Patient was discharged asymptomatic

• 1 week PTA– (+) headache - sudden onset, persistent, no noted

aggravating or relieving factors, piercing, (-) radiations, graded 10/10, constant

– (-) medications taken

History of Present Illness

• 1 week PTA– Consulted again in Abra Provincial Hospital

admitted for three days given unrecalled medications with some pain relief

– Opted to take physician’s advice to seek consult in our institution

Review of Systems• (-) fever• (-) cough• (-) colds• (-) dyspnea• (-) abdominal pain• (-) bowel changes• (-) dysuria

• (-) jaundice• (-) weight loss• (-) tinnitus• (-) blurring of vision• (-) rash• (-) orthopnea• (-) easy fatigability

Past Medical History• (-) HPN but with note of occasionally elevated

BP on casual checking, no consults done• (-) DM, BA, PTB• (-) previous surgeries• (-) known allergies to food and medications

Family Medical History• (+) HPN – siblings• (-) DM, BA, PTB, CA• (-) CVD

Personal/Social History• (-) smoking• (-) alcoholic beverage consumption• denies illicit drug use• Married, with 3 biological children and 6

stepchildren• Farmer

PHYSICAL EXAMINATION

Physical Examination• Conscious, coherent, not in distress• VS: BP 130/80 HR 100 RR 20 T 36.7oC• HEENT: pink conjunctivae, anicteric sclerae, (-)

neck vein engorgement, (-) cervical lymphadenopathy, (-) masses

• Chest/Lungs: equal chest expansion, clear breath sounds, (-) rales, (-) wheezes

Physical Examination• CVS: (-) heaves, (-) thrills, distinct heart

sounds, normal rate, regular rhythm, (-) murmurs

• Abdomen: flat, normoactive bowel sounds, soft, nontender, (-) masses, liver edge not palpable

• Extremities: pink nailbeds, (-) cyanosis, (-) edema, full & equal pulses

Neurologic Examination• Awake, coherent, oriented to three spheres• GCS 15 (E4V5M6) • Cranial Nerves

I – grossly normalII, III – pupils 3mm briskly reactive to lightIII, IV, VI – full, equal EOMsV – intact sensation at V1-3

V, VII - brisk corneal reflexesVII – shallow R nasolabial fold

Neurologic Examination• Cranial Nerves

VIII – intact gross hearingIX, X – intact gag, uvula midlineXI – good shoulder shrugXII – tongue midline

• Motor: good muscle tone, MMT 5/5 on all extremities

Neurologic Examination• Sensory: 100% on all extremities• DTR’s ++, (-) Babinski, (-) clonus• Meningeals: supple neck, (-) Kernig’s sign, (-)

Brudzinski’s sign

Summary

• 54 y/o non-hypertensive male• Apparently well until he presented with

sudden-onset headache and left-sided weakness

• Initially managed as a case of CVD, but with findings of subarachnoid hemorrhage on CT scan done 10 days post event

Summary

• Seen in our institution 39 days post-ictus• With essentially normal physical examination

findings except right central facial nerve palsy

ASSESSMENT

Subarachnoid hemorrhage probably secondary to ruptured aneurysm, Grade 1

DISCUSSION

Subarachnoid hemorrhageDifferential DiagnosesDiagnosticsManagementOutcome

Subarachnoid hemorrhage

• Extravasation of blood into the subarachnoid space between the pial and arachnoid membranes

Etiologies

• Trauma– MOST COMMON cause of SAH

• Spontaneous– Ruptured aneurysms

(75-80%)– Cerebral AVMs– CNS vasculitides– Cerebral artery

dissection– Coagulation disorders– Dural sinus thrombosis– No cause determined

Risk Factors

• Hypertension• OCPs• Substance abuse—cigarette smoking, cocaine

abuse, alcohol consumption• Diurnal variation in BP• Pregnancy and parturition• During LT or cerebral angiography in those with

aneurysms• Advancing age

Cerebral AneurysmsCerebral vs Extracranial blood vessels• Less elasticity of tunica media and adventitia• Tunica media has less muscle• Adventitia is thinner• More prominent internal elastic lamina• Subarachnoid space has very little supportive

tissue

Cerebral Aneurysms• Early precursors of aneurysms are small

outpouchings through defects in the media of the arteries

• These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations

Cerebral AneurysmsEtiologies• Congenital (Medial gap: defect in muscular

layer of arterial wall)• Atherosclerotic or hypertensive• Embolic (atrial myxoma)• Infectious (mycotic aneurysms)• Traumatic• Associated with other conditions

Cerebral AneurysmsLOCATION• Saccular aneurysms (berry aneurysms)– Located on major arteries at the apex of branch

points (site of maximum hemodynamic stress on a vessel)

• Fusiform aneurysms– More common in the vertebrobasilar system

Cerebral Aneurysms• Saccular aneurysms location– 85-95% in carotid system, with the ff most

common locations• ACoA: 30%• P-comm: 25%• MCA: 20%

– 5-15% in the posterior circulation (vertebro-basilar)

– 20-30% would have multiple aneurysms

Clinical Features: Symptoms

MAJOR RUPTURE IS THE MOST FREQUENT PRESENTATION• Headache– Most common, present in 97% of cases– “Worst headache of my life”– Severe and sudden

• Vomiting• Syncope• Photophobia• Neck pain• Focal cranial nerve deficits (diplopia, ptosis)

Clinical Features: Signs• (+) Kernig’s or Brudzinksi’s• Coma

– Increased ICP– Damage to brain tissue– Hydrocephalus– Diffuse ischemia– Seizure– Low blood flow

• Ocular hemorrhage– Due to compression of the central retinal vein and the

retinochoroidal anastomoses by elevated CSF pressure causing venoud HPN and disruption of retinal veins

Aneurysmal Rupture• The probability of rupture is related to the

tension on the aneurysm wall• Law of La Place: tension is determined by the

radius of the aneurysm and the pressure gradient across the wall of the aneurysm

• The rate of rupture is directly related to the size of the aneurysm– < 5 mm: 2% risk of rupture– 6-10 mm: 40% have already ruptured upon diagnosis

Aneurysmal Rupture• Blood extravasates under arterial pressure

into the subarachnoid space and quickly spreads through the CSF around the brain and spinal cord– Direct damage to local tissues– Increased ICP– Meningeal irritation

Grading SAH

Hunt and Hess Classification of SAHGrade Description

1 Asymptomatic or mild H/A and slight nuchal rigidity

2 CN palsy (III, VI), moderate to severe H/A, nuchal rigidity

3 Mild focal deficit, lethargy, confusion

4 Stupor, moderate to severe hemiparesis, early decerebrate rigidity

5 Deep coma, decerebrate rigidity, moribund appearance

Add one grade for serious systemic disease (HPN, DM, severe atherosclerosis, COPD), or severe vasospasm on arteriography.

Grading SAH

• Grades 1 & 2: operated ASAP as soon as an aneurysm is diagnosed

• Grade > 3 managed until condition improved to grade 2 or 1

• Exception: life threatening hematoma or multiple bleeds (operated on regardless of grade)

Grading SAH

MORTALITY• Admission Grade 1 or 2: 20%• OR Grade 1 or 2: 14%• Rebleed: major cause of death for Grade 1 or

2• Signs of meningeal irritation increases surgical

risk

Grading SAH

WFNS SAH GradeWFNSGrade

GCS Score Major Focal Deficit

0**1 15 -2 13-14 -3 13-14 +4 7-12 + or -5 3-6 + or -

*aphasia, hemiparesis or hemiplegia** intact anseurysm

Grading SAH

Fischer Scale (CT scan appearance)

Grade Description1 No blood detected2 Diffuse deposition of subarachnoid blood, no clots, and

no layers of blood greater than 1 mm3 Localized clots and/or vertical layers of blood 1 mm or

greater in thickness4 Diffuse or no subarachnoid blood, but intracerebral or

intraventricular clots are present

SAH Grading

• The Hunt and Hess and the WFNS grading systems correlate well with patient outcome

• The Fischer classification predicts the likelihood of symptomatic cerebral vasospasm, one of the most feared complications of SAH

• All 3 grading systems are useful in determining the indications for and timing of surgical management

DIFFERENTIAL DIAGNOSES

Differential Diagnoses• Stroke• Aphasia• First Seizure in Adulthood• AVMs• Frontal Lobe Syndromes• Aseptic Meningitis• Hydrocephalus• Basilar Artery Thrombosis

Differential Diagnoses• Intracranial Hemorrhage• Cerebellar Hemorrhage• Cerebral Aneurysms• Cerebral Venous Thrombosis• Meningococcal Meningitis• Epidural Hematoma• Migraine Headache

DIAGNOSTICS

Workup

• Serum Chemistry Panel• CBC• PT PTT• Blood Typing/Screening tests• Imaging – CT without contrast is the most sensitive imaging

study in subarachnoid hemorrhage.

Workup: CT Scan

• Findings may be negative in 10-15% of patients with SAH

• Maximum sensitivity is within 24 hours post-injury

• Sensitivity is 80% at 3 days, 50% at 1 week

Workup: CT Scan

• Look for evidence of hydrocephalus– trapped temporal horns and "Mickey Mouse"

appearance of ventricular system• Intraparenchymal clot, intraventricular

hematoma, and interhemispheric hematoma• Degree and location of SAH are significant

prognostic factors.

Workup: Cerebral Angiography

• To assess the vascular anatomy• To determine site of bleed• To document presence or absence of other

aneurysms (about 20% have multiple aneurysms)

• For operative planning

Workup: Cerebral Angiography

• Negative angiographic findings do not rule out aneurysm.

• ~ 10-20% of patients with clinically diagnosed SAH (CT and/or lumbar puncture) have negative angiographic findings.

• Repeat angiogram usually required in 10-21 days

Four-Vessel Angiogram

• The gold standard for evaluation of cerebral aneurysms

• Four vessels: – R and L verterbral arteries– R and L carotid arteries

Four-Vessel Angiogram

Workup

• MRI is inferior to CT in an acute setting to detect SAH.

• MR angiography (MRA) is less sensitive than cerebral angiography to detect small aneurysms.

• CT angiography is beneficial in very unstable patients who cannot undergo angiography or in emergent settings prior to operative intervention for clot evacuation.

Workup

• ECG– Nonspecific ST and T changes, prolongation of QRS

segments or QT intervals, deeply inverted T waves, and U waves sometimes are seen in SAH

– Patients with SAH can have myocardial ischemia due to the increased level of circulating catecholamines or to autonomic stimulation from the brain.

Workup

• Lumbar puncture– Performed if CT scan shows no subarachnoid

hemorrhage presence of RBCs and xanthochromia

– Most sensitive 12 hours after onset of symptoms– Findings can be negative in ~10-15% of patients

with SAH.– Patients with negative CT and LP findings have a

favorable prognosis.

MANAGEMENT

General Symptomatic Treatment

• Absolute bed rest in quiet, comfortable environment

• Cardiac monitoring and frequent assessment of neuro-vital signs

• Soft diet for alert patients, nasogastric-tube (NGT) feedings if with impaired consciousness

• Analgesics for headache. Avoid aspirin.

General Symptomatic Treatment

• Paracetamol and cooling blankets• Maintenance of euglycemia• Sedatives• Antiemetics• Stool softeners

Early Specific Treatment

• Nimodipine– Significant reduction in poor outcomes with

calcium antagonists.• Evidence rests mainly on one large trial with oral

nimodipine.

– Uncertain whether acts through neuroprotection or through reduction of the frequency of vasospasm, or both.

– 60 mg every 4 hours x 3 weeks

Early Specific Treatment

• Anticonvulsants– Short-term anticonvulsants recommended for

patients with documented seizures in the acute phase.

– In patients with significant cortical damage, thick cisternal clot, parenchymal hemorrhage, or those in coma

– Phenytoin 15 mg/kg LD then 3-5 mg/kg/day (100mg TID) in divided doses

Early Specific Treatment

• Steroids– Dexamethasone may help with headache and

nape pain.– Effect on edema controversial– Corticosteroids have no proven role and are not

recommended for use in SAH.

Early Specific Treatment

• Antifibrinolytic agents are NOT recommended.– Reduce risk of rebleeding, BUT…– Associated with higher rate of cerebral ischemia

Early Specific Treatment

• Manage increased ICP• BP control– Best antihypertensive agent unsettled– IV nicardipine– Target SBP<150 mmHg in the pre-operative phase

Management of Vasospasm

• Monitoring– Serial transcranial Doppler (TCD) recommended

for diagnosis and monitoring of vasospasm

Management of Vasospasm

• Maintenance of euvolemia– Evidence on use of blood volume expansion alone

or in combination with induced hypertension and hemodilution (triple H therapy) in the prophylaxis and management of secondary ischemia (vasospasm) following aneurysmal SAH lacking

Management of Vasospasm

• Endovascular angioplasty (chemical +/- mechanical) – Transluminal balloon angioplasty– Early intervention (before irreversible infarction

signs are noted)• CCB may provide neuroprotection• Magnesium sulfate and statins under

investigation

Management

• Main goal: excluding the aneurysm from the circulation– “Nonsurgical” / endovascular: trapping (distal &

proximal arterial interruption, proximal ligation for giant aneurysms, endovascular coiling, balloon embolization

– Surgical: clipping (“gold standard”), wrapping or coating the aneurysm

Timing of Surgery

• Early surgery - performed within 72 hours from ictus– Eliminates rebleeding risk if successful– Facilitates treatment of vasospasm– Lower mortality (but higher operative mortality)

• Late surgery - performed more than 3 days from ictus

Timing of Surgery

• Early, immediate surgery recommended for good to moderate grade (Hunt and Hess I-III) aneurysmal SAH patients to minimize chance of devastating rebleed

• For poor grade patients (Grade IV-V), early surgery is recommended in the presence of:– Hematoma– Hydrocephalus

Timing of Surgery

• Surgery may be delayed in the presence of:– Ischemia or infarction– Severe angiographic vasospasm– Casted ventricles– Diffuse SAH (Fisher Grade III) Complex aneurysm

on angiography• Maximum cut-off age for early surgical

management (for the elderly) not recommended in the absence of organ failure

Coiling

• Can be performed early in both good- and poor-grade patients.

• Reduces rebleed rate for poor-grade patients who would otherwise be treated conservatively.

• Vasospasm is not a contraindication and can be dealt with endovascularly during coiling.

• Can be performed under local anesthesia

Where to Admit

• Stroke Unit or Intensive Care Unit• In the absence of an ASU/ICU, may place

patient is a quiet, regular room with very close monitoring.

Rehabilitation

• Supportive rehabilitation done initially in the pre-operative phase

• Early rehabilitation recommended for all SAH patients in postoperative period

Outcome of Aneurysmal SAH

• 10-15% die before reaching medical care• 45% overall mortality rate• NO SURGERY: Rebleeding is the major cause of

M&M in 15%• SURGERY: Vasospasm kills 7%• 66% who underwent clipping never return to

the same quality of life

COURSE IN THE WARDS

Course in the Wards

HD 1

•D39 post ictus•Admitted to the NSSCU•Labs: CBC, BT, PT/PTT, Na, K, Ca, Cl, BUN, Crea, FBS, CXR PA, 12L ECG, U/A, CT scan•Meds:•Amlodipine 5mg, 1 tab HS•Phenytoin 100mg/tab 1 tab q8•Simvastatin 20mg HS•Tramadol 50mg q8•Lactulose 30cc HS

HD 2

•D40 post ictus•Referred to Interventional Radiology for 4V angiography•Referred to SAPOD for clearance

Laboratory Results• Blood Type: A+• CBC– 04/23/10: Hgb 163, Hct 0.458, WBC 5.8, Plt 266, L

0.615, N 0.263– 04/27/10: Hgb 115, Hct 0.321, WBC 9.41, Plt 248,

L 0.878, N 0.079

Laboratory Results• PT/ PTT (04/23/10)– PT: 11.5/10.5/>1.0/1.01– aPTT: 34.7/34.4

• Blood Chemistry– 04/23/10: Glu 6.01, BUN 11.58, Crea 69, Na 132, K

3.7, Cl 90– 04/26/10: BUN 3.99, Crea 52, Na 196, K 3.4, Cl 112

Laboratory Results• U/A– 04/24/10: yellow, turbid, pH 8.0, Sp Gr 1.010, CHO

(-), CHON (-), RBC 9, WBC 2, EC 2, Cast 0, Crystals 0, Bac 17

Course in the Wards

HD 3

• D41 post ictus• E4V5M6

• Scheduled for four-vessel angiogram

HD 4

• D42 post ictus• s/p 4V angiogram• Phenytoin discontinued

Patient’s 4VA Result• R transfemoral, B ICA, and L vertebral

angiograms were done using non-ionic contrast media (Ultravist – Lopromide)

• Saccular aneurym, L ACA – Acomm junction site, with slight vasospasm

• Aplastic A1 segment, R ACA, Patent Acomm

Course in the Wards

HD 5

• D43 post-ictus• s/p clipping of aneurysm tolerated procedure well

Course in the Wards• Presently on 8th hospital day• No subjective complaints• No neurologic deficits noted