Subarachnoid hemorrhage
Background
Pearls
- Obtain GCS before intubation
- If intubate prevent HTN (rebleeding)
- Pretreatment
- Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)
- Fentanyl 200mcg (sympatholytic)
- Sedation
- If pt has high BP - use propofol
- If pt has adequate BP - use etomidate
- Treat pain
- Prevents incr catacholamines / incr BP
- Pretreatment
Epidemiology
- Of All pts in ED who p/w HA:
- 1% will have SAH
- 10% will have SAH if c/o worst HA of life
- 25% will have SAH if c/o worst HA of life + any neuro deficit
Risk Factors
- Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
- Hypertension
- Atherosclerosis
- Cigarette smoking
- Alcohol
- Age >50
- Cocaine use
- Estrogen deficiency
Etiology of Spontaneous SAH
- Ruptured aneurysm (85%)
- Nonaneurysmal (15%)
- Perimesencephalic hemorrhage (10%)
- Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis
Clinical Features
- Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
- Sudden onset is more important finding than worst HA
- May be a/w 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/HA 6-20d before SAH (30-50% of pts)
DDX
- Other intracranial hemorrhage
- Drug toxicity
- Ischemic stroke
- Meningitis
- Encephalitis
- Intracranial tumor
- Intracranial hypotension
- Metabolic derangements
- Venous thrombosis
- Primary headache syndromes (benign thunderclap headache, migraine, cluster headache)
Diagnosis
If concerned for SAH and CT normal must perform LP
- Non-Contrast Head CT
- Sensitivity
- Within 12hr of onset of symptoms: 98% Sn
- Within 24hr of onset of symptoms: 93% Sn
- Within 5d of onset of symptoms: 50% Sn
- Not as sensitive/specific for minor bleeds
- Findings
- SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
- SAH due to trauma - look at convexities of frontal and temporal cortices
- Sensitivity
- Lumbar Puncture
- Findings:
- Elevated RBC count that doesn't 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 pts)
- Can help differentiate from a traumatic tap (opening pressure expected to be normal)
- Elevated opening pressure also seen in cerebral venous thrombosis, IIH
- Xanthrochromia
- 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
- Elevated RBC count that doesn't decrease from tube one to four
- If unable to obtain CSF consider CTA
- Findings:
Treatment
- Nimodipine
- Associated with improved neuro outcomes and decreased cerebral infarction
- Give 60mg q4hr PO or NGT only! (never IV)
- BP control
- No consensus on HTN (incr BP may maintain CPP but may also increase rate of bleeding)
- If pt is alert this means CPP is adequate so consider lowering sbp to 120-140
- If pt has history of HTN consider lowering sbp to ~160
- If pt is ALOC consider leaving BP alone as the ALOC may be 2/2 reduced CPP
- If pt is alert this means CPP is adequate so consider lowering sbp to 120-140
- If BP control is necessary use NICARDIPINE, LABETALOL, or ESMOLOL
- Avoid vasodilators such as nitroprusside or NTG (increase cerebral blood volume > increased ICP)
- Avoid hypotension
- Maintain MAP > 80
- Give IVF
- Give pressors if IVF ineffective
- Maintain MAP > 80
- No consensus on HTN (incr BP may maintain CPP but may also increase rate of bleeding)
- Discontinue/reverse all anticoagulation
- Coumadin - give (prothrombin complex conc or FFP) and vit K)
- Aspirin - give DDAVP
- Plavix - give platelets
- Seizure prophylaxis
- Controversial; 3 day course may be preferable
- Phenytoin load
- Glucocorticoid therapy
- Controversial; evidence suggests is neither beneficial nor harmful
- Glycemic control
- Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
- Keep head of bed elevated
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 initiated after the aneurysm has been treated (sx or intraluminal tx)
- Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia)
- Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
- Ischemia
- Elevated troponin (20-40% of cases)
- ST segment depression
- Rhythm disturbances
- Torsades, a fib, a flutter
- QT prolongation
- Deep, symmetric TWI
- Prominent U waves
- Ischemia
- Hydrocephalus
- Consider ventricular drain placement for deteriorating LOC + no improvement within 24 hours
- Hyponatremia
- Usually due to SIADH
- Treat via isotonic, or if necessary, hypertonic saline (do not treat via H2O restriction)
- Usually due to SIADH
Prognosis
Hunt and Hess
- Grade 0: Unruptured aneurysm
- Grade 1: Asymptomatic or mild HA and slight nuchal rigidity
- Grade 1a: No acute meningeal/brain reaction, with fixed neurological def
- Grade 2: Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy
- Grade 3: Mild mental status change (drowsy or confused), mild focal neurologic deficit
- Grade 4: Stupor or moderate to severe hemiparesis
- Grade 5: Coma or decerebrate rigidity
- Grade 1 or 2 have curable disease
- Add one grade for serious systemic disease (HTN, DM, severe atherosclerosis, COPD)
World Federation of Neurosurgical Societies (WFNS)
- Grade 1: GCS of 15, no motor deficits
- Grade 2: GCS of 13 or 14, no motor deficits
- Grade 3: GCS of 13 or 14, with motor deficits
- Grade 4: GCS of 7–12, with or without motor deficits
- Grade 5: GCS of 3–6, with or without motor deficits
See Also
Source
- UpToDate
- EB Emergency Medicine, July 2009
- EMCrit Podcast 8
- Tintinalli
