Background

Anatomy of the meninges

Defined as hemorrhage into the subarachnoid space (between the arachnoid membrane and the pia mater). This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury.

Epidemiology

The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. [1]

Risk Factors

Genetics (polycystic kidney disease, Ehler-Danlos, family history)

Hypertension

Atherosclerosis

Cigarette smoking

Alcohol

Age >50

Cocaine use

Estrogen deficiency

Etiology of Spontaneous SAH

Ruptured aneurysm (85%)

Nonaneurysmal (15%) Perimesencephalic hemorrhage (10%) - lower risk of complications Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis



Traumatic Subarachnoid Hemorrhage

Differentiate from aneurysmal rupture

Supportive care with prevention of hypertension, elevated ICP, and vasospasm with PO nimodipine

Patients with normal neurologic exam NOT on anticoagulation may not need a repeat head CT [2] [3] Recommend 6 hour observation



Clinical Features

Sudden, severe headache that reaches maximal intensity within minutes (97% of cases) Sudden onset is more important finding than worst headache

May be associated with syncope, seizure, nausea/vomiting, meningismus Meningismus may not develop until hrs after bleed (blood breakdown → aseptic meningitis)

Retinal hemorrhage May be the only clue in comatose patients

Sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients

Differential Diagnosis

Other

Evaluation

Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).

More subtle CT showing subarachnoid hemorrhage (white area in the frontal area stretching into the sulci).

[4] Ottawa SAH Rules

Never has been externally and prospectively validated, authors caution implementation into routine use

100% sensitive to rule out SAH (97.1%-100%)

Can exclude SAH if all of the following are true Age < 40 No neck pain or stiffness No witnessed LOC No onset during exertion No thunderclap symptomatology (max intensity at onset) No limited neck flexion on physical exam



If concerned for SAH and CT normal strongly consider LP, especially if CT obtained >6 hrs after symptom onset

Time from onset of symptoms Sensitivity of CT <6 hours ~100%[5] 6-12 hours 98% 12-24 hours 93%[6] 24 hours - 5 days <60%

SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)

SAH due to trauma - look at convexities of frontal and temporal cortices

Elevated RBC count that does not decrease from tube one to four Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl

Opening pressure >20 (60% of patients) Can help differentiate from a traumatic tap (opening pressure expected to be normal) Elevated opening pressure also seen in cerebral venous thrombosis, IIH

Xanthochromia May help differentiate between SAH and a traumatic tap Takes at least 2hr after bleed to develop (beware of false negative if measure early) Sn (93%) / Sp (95%) highest after 12hr

If unable to obtain CSF consider CTA CTA also highly sensitive for predicting delayed cerebral ischemia

If traumatic tap is suspected Tube 4 RBC count <500 has negative predictive value of 100% for SAH. Tube 4 RBC decrease of 70% compared to tube 1 excludes a radiographically detectable SAH. [7] One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added. [8]



CT Angiogram

A CT followed by CTA is an acceptable alternative to CT and LP [9]

CTA has a 98% sensitivity for aneurysms >3mm

Management

Physiologic derangements, such as hypoxemia, metabolic acidosis, hyperglycemia, BP instability, and fever, can worsen brain injury and has been independently associated with increased M&M, but no studies showing benefit of corrections.

Avoid hypotension Maintain MAP>80 (CPP of 60 as long as ICP<20)

Give IVF

Give pressors if IVF ineffective Hypertension AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable [10]

Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome [11] , but more recent work has found no difference between SBP <140 and <180 [12]

, but more recent work has found no difference between SBP <140 and <180 Ensure appropriate pain control and sedation before adding antihypertensives Discontinue/reverse all anticoagulation Coumadin → (Prothrombin complex concentrate (Kcentra) or FFP) + vitamin K

Aspirin → DDAVP

Plavix → Platelets

Dabigatran (Pradaxa) → Idarucizumab (Praxbind): 5 grams IV Nimodipine Only CCB studied that has been shown improve outcomes (contrary to popular belief, it does not affect large-vessel vasospasm but does decrease incidence of delayed cerebral ischemia) [13]

Give 60mg q4hr PO or NGT only (never IV) within 96hr of symptom onset. NNT 13 to prevent one poor outcome

Keep an eye on BP for fluctuations Magnesium sulfate Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain between 2-2.5 mmol/L Seizure prophylaxis Controversial; 3 day course may be preferable

Phenytoin, levetiracetam, carbamazepine and phenobarb. Phenytoin can be associated with worse neurologic & cognitive outcome Glucocorticoid therapy Controversial; evidence suggests is neither beneficial nor harmful Glycemic control Controversial; consider sliding scale if long patient stay in ED while awaiting ICU bed Keep head of bed elevated Aneurysm treatment Surgical clipping and endovascular coiling are definitive treatment

Antifibrinolytic - Controversial; if delayed aneurysmal treatment, consider short term therapy (<72 hrs) with TXA or aminocaproic acid

Intubation

Consider neuroprotective intubation 3 minutes before intubation Lidocaine 1-2mg/kg to blunt sharp MAP increase Fentanyl 2-5mcg/kg as sympatholytic [14] Sedation Etomidate if blood pressure normal Propofol if blood pressure high Succinylcholine without defasciculating dose

Ensure patient is pain-free for post-intubation sedation Propofol with fentanyl Try to prioritize pain control with fentanyl



[15] AHA Aneurysmal SAH BP Guidelines

No well-controlled studies exist that answer whether BP control influences rebleeding BP should be controlled to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I, Level of Evidence B). Nicardipine, labetalol, and esmolol are appropriate choices for BP control (Sodium nitroprusside may raise intracranial pressure and cause toxicity with prolonged infusion and should be avoided)

Disposition

Admit

Complications

Rebleeding

Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours

Usually diagnosed by CT after acute deterioration in neuro status

Only aneurysm treatment is effective in preventing rebleeding

Vasospasm

Leading cause of death and disability after rupture

Typically begins no earlier than day three after hemorrhage

Characterized by decline in neuro status

Aggressive treatment can only be started after aneurysm has been treated treatment for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), balloon angioplasty, or intra-arterial vasodilators [ citation needed ] Studies have not provided strong evidence of benefit Triple-H therapy [ citation needed ]



Cardiac abnormalities

Most likely related to the release of catecholamines due to hypoperfusion of hypothalamus

Ischemia Elevated troponin (20-40% of cases) ST segment depression

Rhythm disturbances Torsades, A-fib/flutter

QT prolongation

Deep, symmetric TWI

Prominent U waves

Consider ventricular drain placement for deteriorating LOC + no improvement within 24hr

Hyponatremia is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU. [16]

Cerebral Salt Wasting and SIADH are the two most common causes[17]

Prognosis

Hunt and Hess

Subjective terminology, but good interobserver variability

Grade Description Survival Rate 0 Unruptured aneurysm - 1 Asymptomatic or mild HA and slight nuchal rigidity 70% 1a No acute meningeal/brain reaction, with fixed neurological def - 2 Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy 60% 3 Mild mental status change (drowsy or confused), mild focal neurologic deficit 50% 4 Stupor or moderate to severe hemiparesis 20% 5 Coma or decerebrate rigidity 10%

Grade 1 or 2 have curable disease

Add one grade for serious systemic disease (hypertension, DM, severe atherosclerosis, COPD)

World Federation of Neurosurgical Societies (WFNS)

Objective terminology, and fair interobserver variability

Grade GCS Focal neurological deficit 1 15 Absent 2 13–14 Absent 3 13–14 Present 4 7–12 Present or absent 5 <7 Present or absent

Other scales are also available, including the Ogilvy and Carter scale (comprehensive, yet complex), and the Fisher scale or Claassen grading system (vasospasm index risk).

Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.

See Also

References