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| == Background ==
| | ''Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space. Clinical approach differs by etiology — see the appropriate page below:'' |
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| === Pearls ===
| | *[[Aneurysmal subarachnoid hemorrhage]] — spontaneous/non-traumatic SAH (most commonly ruptured cerebral aneurysm) |
| | *[[Traumatic subarachnoid hemorrhage]] — SAH due to blunt or penetrating head trauma |
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| #Obtain GCS before intubation
| | [[Category:Neurology]] |
| #If intubate prevent HTN (rebleeding)
| | [[Category:Critical Care]] |
| ##Pretreatment
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| ###Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)
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| ###Fentanyl 200mcg (sympatholytic)
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| ##Sedation
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| ###If pt has high BP - use propofol
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| ###If pt has adequate BP - use etomidate
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| ##Treat pain
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| ###Prevents incr catacholamines / incr BP
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| === Epidemiology ===
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| *Of All pts in ED who p/w HA:
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| **1% will have SAH
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| **10% will have SAH if c/o worst HA of life
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| **25% will have SAH if c/o worst HA of life + any neuro deficit
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| === Risk Factors ===
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| #Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
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| #Hypertension
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| #Atherosclerosis
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| #Cigarette smoking
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| #Alcohol
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| #Age >50
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| #Cocaine use
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| #Estrogen deficiency
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| === Etiology of Spontaneous SAH ===
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| #Ruptured aneurysm (85%)
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| #Nonaneurysmal (15%)
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| ##Perimesencephalic hemorrhage (10%) - lower risk of complications
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| ##Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis
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| == Clinical Features ==
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| #Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
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| ##Sudden onset is more important finding than worst HA
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| #May be a/w syncope, seizure, nausea/vomiting, meningismus
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| ##Meningismus may not develop until hrs after bleed (blood breakdown -> aseptic meningitis)
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| #Retinal hemorrhage
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| ##May be the only clue in comatose patients
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| #Sentinel bleed/HA 6-20d before SAH (30-50% of pts)
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| == DDX ==
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| #Other intracranial hemorrhage
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| #Drug toxicity
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| #Ischemic stroke
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| #Meningitis
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| #Encephalitis
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| #Intracranial tumor
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| #Intracranial hypotension
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| #Metabolic derangements
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| #Venous thrombosis
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| #Primary headache syndromes (benign thunderclap headache, migraine, cluster headache)
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| == Diagnosis ==
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| '''If concerned for SAH and CT normal strongly consider LP'''
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| #Non-Contrast Head CT
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| ##Sensitivity
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| ###Within 12hr of onset of symptoms: 98% Sn
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| ###Within 24hr of onset of symptoms: 93% Sn
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| ###Within 5d of onset of symptoms: 50% Sn
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| ###Not as sensitive/specific for minor bleeds
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| ##Findings
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| ###SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
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| ###SAH due to trauma - look at convexities of frontal and temporal cortices
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| #Lumbar Puncture
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| ##Findings:
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| ###Elevated RBC count that doesn't decrease from tube one to four
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| ####Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
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| ###Opening pressure >20 (60% of pts)
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| ####Can help differentiate from a traumatic tap (opening pressure expected to be normal)
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| ####Elevated opening pressure also seen in cerebral venous thrombosis, IIH
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| ###Xanthrochromia
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| ####May help differentiate between SAH and a traumatic tap
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| ####Takes at least 2hr after bleed to develop (beware of false negative if measure early)
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| ####Sn (93%) / Sp (95%) highest after 12hr
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| ##If unable to obtain CSF consider CTA
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| ###CTA also highly sensitive for predicting delayed cerebral ischemia
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| == Treatment ==
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| 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.
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| {{AHA SAH BP Guidelines}}
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| #Avoid hypotension
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| ##Maintain MAP >80
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| ##Give IVF
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| ##Give pressors if IVF ineffective
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| #Discontinue/reverse all anticoagulation
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| ##Coumadin - (Prothrombin complex conc or FFP) + vit K
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| ##Aspirin - DDAVP
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| ##Plavix - Platelets
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| #Nimodipine
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| ##Prevents vasospasm (a/w improved neuro outcomes and decreased cerebral infarction)
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| ##Give 60mg q4hr PO or NGT only (never IV) within 96hr of symptom onset. NNT 13 to prevent one poor outcome
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| ##Keep an eye on BP for fluctuations
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| #Magneisum
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| ##Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain b/w 2-2.5 mmol/L
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| #Seizure prophylaxis
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| ##Controversial; 3 day course may be preferable
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| ##Phenytoin, levetiracetam, carbamazepine and phenobarb. Phenytoin can be a/w worse neurologic & cognitive outcome
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| #Glucocorticoid therapy
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| ##Controversial; evidence suggests is neither beneficial nor harmful
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| #Glycemic control
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| ##Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
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| #Keep head of bed elevated
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| #Aneurysm Tx
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| ##Surgical clipping and endovascular coiling are definitive tx
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| ##Antifibrinolytic - Controversial; if delayed aneurysmal tx, consider short term therapy (<72 hrs) with TXA or aminocaproic acid
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| == Complications ==
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| #Rebleeding
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| ##Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours
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| ##Usually diagnosed by CT after acute deterioration in neuro status
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| ##Only aneurysm treatment is effective in preventing rebleeding
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| #Vasospasm
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| ##Leading cause of death and disability after rupture
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| ##Typically begins no earlier than day three after hemorrhage
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| ##Characterized by decline in neuro status
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| ##Aggressive treatment can only be started after aneurysm has been treated
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| ###Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), ballon angioplasty, or intra-arterial vasodilators.
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| ####Studies have not provided strong evidence of benefit Triple-H therapy
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| #Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
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| ##Ischemia
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| ###Elevated troponin (20-40% of cases)
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| ###ST segment depression
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| ##Rhythm disturbances
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| ###Torsades, A-fib/flutter
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| ##QT prolongation
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| ##Deep, symmetric TWI
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| ##Prominent U waves
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| #Hydrocephalus
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| ##Consider ventricular drain placement for deteriorating LOC + no improvement w/in 24hr
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| #Hyponatremia
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| ##Usually due to SIADH
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| ###Treat via isotonic, or if necessary, hypertonic saline (do not treat via H2O restriction)
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| ##Rarely due to cerebral salt-wasting
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| ###Volume depleted, so treat with isotonic saline
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| == Prognosis ==
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| === Hunt and Hess ===
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| Subjective terminology, but good interobserver variability
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| *Grade 0: Unruptured aneurysm
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| *Grade 1: Asymptomatic or mild HA and slight nuchal rigidity
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| :Grade 1a: No acute meningeal/brain reaction, with fixed neurological def
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| *Grade 2: Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy
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| *Grade 3: Mild mental status change (drowsy or confused), mild focal neurologic deficit
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| *Grade 4: Stupor or moderate to severe hemiparesis
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| *Grade 5: Coma or decerebrate rigidity
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| <br>
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| :Grade 1 or 2 have curable disease
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| :Add one grade for serious systemic disease (HTN, DM, severe atherosclerosis, COPD)
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| === World Federation of Neurosurgical Societies (WFNS) ===
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| Objective terminology, and fair interobserver variability
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| *Grade 1: GCS of 15, no motor deficits
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| *Grade 2: GCS of 13 or 14, no motor deficits
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| *Grade 3: GCS of 13 or 14, with motor deficits
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| *Grade 4: GCS of 7–12, with or without motor deficits
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| *Grade 5: GCS of 3–6, with or without motor deficits
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| 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).
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| Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.
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| == See Also ==
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| *[[Intracranial Hemorrhage (Main)]]
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| *[[Head Trauma]]
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| == Source ==
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| *EB Emergency Medicine, July 2009
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| *EMCrit Podcast 8
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| <references/>
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| *www.epmonthly.com/features/current-features/lp-for-subarachnoid-hemorrhage-the-700-club
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| [[Category:Neuro]] | |
