Subarachnoid hemorrhage: Difference between revisions
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***If has high BP - use [[propofol]] | ***If has high BP - use [[propofol]] | ||
***If has adequate BP - [[ | ***If has adequate BP - use [[etomidate]] | ||
**Treat pain | **Treat pain | ||
***Prevents increased catacholamines / increased BP | ***Prevents increased catacholamines / increased BP |
Revision as of 04:42, 14 December 2015
Background
Pearls
- Obtain neuro exam before intubation
- If intubate prevent hypertention (rebleeding)
- Pretreatment
- Induction
- Treat pain
- Prevents increased catacholamines / increased BP
Epidemiology
- Of All pts in ED who present with headache:
- 1% will have SAH
- 10% will have SAH if c/o worst headache of life
- 25% will have SAH if c/o worst headache 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%) - lower risk of complications
- 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 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
Intracranial Hemorrhage Types
- Intra-axial
- Hemorrhagic stroke (Spontaneous intracerebral hemorrhage)
- Traumatic intracerebral hemorrhage
- Extra-axial
- Epidural hemorrhage
- Subdural hemorrhage
- Subarachnoid hemorrhage (aneurysmal intracranial hemorrhage)
Other
- Drug toxicity
- Ischemic Stroke
- Meningitis
- Encephalitis
- Intracranial tumor
- Intracranial hypotension
- Metabolic derangements
- Cerebral venous thrombosis
- Primary headache syndromes (benign thunderclap headache, Migraine, Cluster Headache)
Diagnosis
Ottawa SAH Rules[2]
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
Non-Contrast Head CT
Time from onset of symptoms | Sensitivity of CT |
<6 hours | ~100%[3] |
6-12 hours | 98% |
12-24 hours | 93%[4] |
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
Lumbar Puncture
- 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
- 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.[5]
- One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.[6]
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
- Discontinue/reverse all anticoagulation
- Nimodipine
- Only CCB studied that has been shown to prevent vasospasm (associated with improved neuro outcomes and decreased cerebral infarction)
- 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
- Magneisum sulfate
- Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain b/w 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 pt stay in ED while awaiting ICU bed
- Keep head of bed elevated
- Aneurysm treatment
- Surgical clipping and endovascular coiling are definitive tx
- Antifibrinolytic - Controversial; if delayed aneurysmal tx, consider short term therapy (<72 hrs) with TXA or aminocaproic acid
AHA Aneurysmal SAH BP Guidelines[7]
- 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)
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
- Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), ballon angioplasty, or intra-arterial vasodilators.
- Studies have not provided strong evidence of benefit Triple-H therapy
- Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), ballon angioplasty, or intra-arterial vasodilators.
- Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
- Ischemia
- Elevated troponin (20-40% of cases)
- ST segment depression
- Rhythm disturbances
- QT prolongation
- Deep, symmetric TWI
- Prominent U waves
- Ischemia
- Hydrocephalus
- Consider ventricular drain placement for deteriorating LOC + no improvement w/in 24hr
- Hyponatremia
- Usually due to SIADH
- Treat via isotonic, or if necessary, hypertonic saline (do not treat via H2O restriction)
- Rarely due to cerebral salt-wasting
- Volume depleted, so treat with isotonic saline
- Usually due to SIADH
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 (HTN, 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
- ↑ Fact or Fantasy? Lidocaine for RSI in Patients with Major Head Injury. JWatch Emergency Med. 2002;2002:227 10
- ↑ Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018
- ↑ Perry JJ, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011; 343:d4277.
- ↑ van Gijn J and van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology. 1982; 23:153–156.
- ↑ Gorchynski J, Oman J, and Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007; 8(1): 3–7.
- ↑ Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ : British Medical Journal. 2015;350:h568.
- ↑ Bederson J. et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association. Stroke. 2009;40:994-1025 PDF