Subarachnoid Hemorrhage

Case Conference 8/05/08

Epidemiology

n Most frequent cause – ruptured saccular aneurism.

n Other causes – trauma, av malformation, vasculitis, arterial dissection, coagulopathy, cocaine, amphetamines.

n Prevalence of saccular aneurisms – 5%n Aneurismal SAH: 2 – 22.5 per 100,000

population

Risk factors

n Family history – x 3- 5 in 1st degree relativesn ? Elastin gene on chromosome 7q11, ?othern Smoking (odds ratio 5.0 in 1 study)n Smokers with HTN – x 15 risk of SAHn Moderate to heavy drinkingn Phenylpropanolamine, estrogen deficiency

Diagnosis

n Noncontrast head CT sensitivity up to 92%n LP – for suspected SAH with normal CT (rbc,

xanthochromia ). Wait for at least 2h.n MRI / MRAn Cerebral angiographyn CTAn 14 – 22% - no angiographic cause of SAH

Clinical manifestations

n Release of blood into the CSF under arterial pressure. Rapid increase in ICP.

n “Worst HA in my life”n Sentinel HA may precede major SAH by 6 –

20 daysn LOC, Sz, N/V, meningismus, back pain

Fisher scale

n Group 1 – no blood detectedn Group 2 – diffuse or vertical layers < 1mmn Group 3 – localized clot and/or vertical layer >

= 1mmn Group 4 – intracerebral or intraventricular clot

with diffuse or no SAH

Carter an Ogilvy

Ø Age > 50Ø Hunt & Hess 4 – 5Ø Fisher score 3 – 4Ø Aneurism size > 10mmvScore 0 – 2 – 78% good outcomesvScore 3 – 67% good outcomesvScore 4 - 25% good outcomes

Complications

n Rebleeding from unsecured aneurism – 4% on day 1 and 1.5% /day up to day 28

More frequent in women, higher grade and with SBP> 170. Mortality > 75%

n Cerebral vasospasm – 70% (45% clinical)Day 4 – 6. risk of development minimal after day 14.

n Hydrocephalus; cardiac; volume / lytes; Sz

Vasospasm

n Symptomatic ischemia and infarction in 20 –30% of patients with aneurismal SAH

n Leading cause of disability and deathn Peak – day 7 – 8n Interference with NO production due to

endothelial damage; endothelin-1n Hyperglycemia; SSRI use; age<50; H-H 4-5;

GCS <14; long LOC = increased risk

Vasospasm

n 1st phase – vasoconstrictionn 2nd phase – proliferative arteriopathy with

necrosis of smooth muscle and fibrosis of the arterial wall.

n 40 – 60% of survivors have evidence of cerebral infarction on head CT.

Prevention of vasospasmn Nimodipine – improves outcomes, standard of care.

60 mg q 4h x 21dn Triple H therapy – hypervolemia, hypertension,

hemodilution. Few trials, benefit is uncertain. High euvolemic state and positive fluid balance is reasonable.

n Nicardipine – decreased angiographically diagnosed vasospasm; no difference in outcomes (J Neurosurg. 1993)

Treatment of vasospasm

n Triple H therapy: PAOP 15 – 18, pressors and/or inotropes. ? Hgb 10 – 11. Central line or Swan; A-line. No RCTs. Watch for pulmonary edema, htn encephalopathy.

n Angioplastyn Local papaverine infusionn Intrathecal nipride administration has been

reported.

Hydrocephalus

n 15% of patients in the 1989 Cooperative Aneurism Study.

n Intraventricular hemorrhage, posterior circulation aneurisms, antifibrinolytic agents, low GCS – all associated with increased risk.

n Causes of increased ICP (54% J Neurosurg Sep 2004) –hydrocephalus, increased CSF outflow resistance, reactive hyperemia, vasoparalysis.

Seizures

n Epileptogenic stimulus from cerebral infarction, hematoma or SDH

n Irritation from aneurism clippingn Reperfusion injuryn Late epilepsy 3 to 5%.n ?effects of iron on the cerebral cortex.n New onset Sz – 7% (Neurology 2003, 247 pts). Predictor of

poor outcome and late Sz.

Antiepileptic therapy

n 6 months for acute seizure following SAHn Late epilepsy (>2 weeks after surgery)– only

in 4.9% patients.n Therapy may not be necessary in most

patients, esp. with good grade and no early seizures.

n Dilantin, tegretol

Hyponatremia

n Cerebral salt wasting due to enhanced release of natriuretic peptides from the brain.

n Isotonic volume loss with hypovolemia.n Appropriate ADH responsen SIADHn Avoid hypovolemia

Hyponatremia

n Salt wasting with excess ADH is likely.n Volume status evaluation; urine Na,

osmolality; serum osm and uric acid n Risk of cerebral ischemia with water

restrictionn Rapidly developing hypo-osmolality –

neuronal edema, Sz, increased ICPn 3% saline, replacement of UO and insensible

losses, salt tabs.

Cerebral salt wasting

n Release of BNP – decreased Na absorption and inhibition of renin release.

n BNP is released from hormone-producing neurons in response to elevated ICP.

n Renal salt wasting – volume depletion- ADH release – inability of the kidney to dilute urine

Is cerebral salt wasting real?

n Physiologic Na excretion due to vasoconsrtriction or due to volume expansion.

n Volume depletion may worsen cerebral perfusion

n Hypotension may precipitate vasospasmn HypoNa-emia may worsen cerebral edema

Diagnosis

n Na < 135 and low plasma osmolalityn Inappropriately elevated urine osmolalityn Urine Na > 40 meq/ln Low serum uric acid due to urate wasting in

urinen Clinical evidence of hypovolemia (low BP,

decreased skin turgor, elevated Hct)n Net negative sodium balancen Volume depletion will distingwish CSW from

SIADH

Treatment

n CSW: restoration of euvolemia will remove stimulus to ADH release. Urine osmolality should decrease to 100 mosmol/kg

n Salt tabletsn Isotonic saline may make SIADH worsen CSW + SIADH: osmolality of IVF should be

greater than urine osmolality

CV complications

n Neurocardiogenic hypothesis - centrally mediated release of catecholamines within the myocardium. Myocardial O2 demand; low Mg.

n Relationship between the degree of neurologic injury and troponin levels (Stroke 2004)

n Cardiac arrhythmias including torsades.n Myocardial ischemia n Cardiogenic and noncardiogenic pulmonary

edema.

BP managementn SBP< 140 and MAP< 100 before aneurism obliterationn Nimodipine, labetalol, enalaprilat – 1st linen Nicardipinen Esmololn Hydralazinen Nipriden Lowering BP: decrease risk of rebleeding, increase risk of

infarction

BP management

n BP is allowed to rise after aneurism obliteration

n Guides: CPP, LOC, neuro exam, degree of vasospasm

n Rising the SBP to 150 – 180 is not uncommon

n Norepinephrine, neosynephrine, dopamine

ICU care

n Nutritionn DVT prophylaxisn Stress ulcers prophylaxis in intubated

patientsn Replacement of electrolytes, esp. Mgn Prevention of aspiration, infections.

Subdural Hemorrhage

Epidural Hemorrhagen Associated with low-energy trauman Source of bleeding – (arterial)

n meningeal arteries (often the middle meningeal artery)n occasionally dural venous sinuses

n Often occurs from a high-pressure arterial sourcen May result in rapid expansion of hematoma and herniation of brain contents

n Presentation: n Classic ‘three stage’ presentation

n patient bcomes unconscious initially from the concussive aspect of the head trauma.

n It is followed by a lucid interval while the hematoma subclinically expands

n As the volume of the hematoma grows, the decompensated region of the pressure-volume curve is reached, the ICP increases, and the patient becomes lethargic and herniates.

n Uncal herniation from an EDH classically causes ipsilateral third nerve palsy and contralateral hemiparesis

CT Scan Findings: EDH does not cross sutural marginscrosses dural attachments because it is located in the potential space between dura and skull. has a lens-shaped appearanceTypical location of blood: cerebral convexities

Epidural Hemorrhage

Factor VII

n Randomized placebo controlled study (NEJM 5/08)

n Treatment with 80 mug/kg resulted in significant reduction of hemorrhage growth (26 vs 11% or by 3.8 ccin 80 vs placebo arm)

n No difference in primary outcome (severe disability or death)

n Rate of MI and CVA 8 vs 4%n Investigational use