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| ==Background==
| | ''Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space. Clinical approach differs by etiology — see the appropriate page below:'' |
| [[File:Meninges-en.svg|thumb|Anatomy of the meninges]]
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| 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.
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| ===Epidemiology===
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| The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. <ref>Dubosh NM et al. Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis. Stroke 2016. PMID: 26797666</ref>
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| ===Risk Factors===
| | *[[Aneurysmal subarachnoid hemorrhage]] — spontaneous/non-traumatic SAH (most commonly ruptured cerebral aneurysm) |
| *Genetics (polycystic kidney disease, Ehler-Danlos, family history)
| | *[[Traumatic subarachnoid hemorrhage]] — SAH due to blunt or penetrating head trauma |
| *[[Hypertension]] | |
| *Atherosclerosis
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| *Cigarette smoking
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| *[[Alcohol]] | |
| *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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| ===Traumatic Subarachnoid Hemorrhage===
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| *Differentiate from aneurysmal rupture
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| *Supportive care with prevention of hypertension, elevated ICP, and vasospasm with PO nimodipine
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| *Patients with normal neurologic exam NOT on anticoagulation may not need a repeat head CT<ref>Borczuk, et al. Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention. J Am Coll Surg. 2014; 219.</ref><ref>Nahmias JT, et al. Mild Traumatic Brain Injuries Can Be Safely Managed Without Neurosurgical Consultation: The End of a Neurosurgical "Nonsult"? American Association for the Surgery of Trauma. Annual Meeting. 2016</ref>
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| **Recommend 6 hour observation
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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 [[headache]]
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| *May be associated with [[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 headache 6-20 days before serious SAH in 30-50% of patients
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| ==Differential Diagnosis==
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| {{Intracranial hemorrhage DDX}}
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|
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| ===Other===
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| *Drug toxicity
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| *Ischemic [[Stroke (Main)|Stroke]]
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| *[[Meningitis]]
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| *[[Encephalitis]]
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| *[[brain tumor|Intracranial tumor]]
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| *Intracranial hypotension
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| *[[Metabolic derangements]]
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| *[[Cerebral venous thrombosis]]
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| *Primary headache syndromes (benign thunderclap headache, [[Migraine]], [[Cluster Headache]])
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| ==Evaluation==
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| [[File:SubarachnoidP.png|thumb|Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).]]
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| [[File:PMC2823144 JETS-03-52-g004.png|thumb|More subtle CT showing subarachnoid hemorrhage (white area in the frontal area stretching into the sulci).]]
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| ===Ottawa SAH Rules<ref>Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018</ref>===
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| ''Never has been externally and prospectively validated, authors caution implementation into routine use''
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| *100% sensitive to rule out SAH (97.1%-100%)
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| *Can exclude SAH if all of the following are true
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| **Age < 40
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| **No neck pain or stiffness
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| **No witnessed LOC
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| **No onset during exertion
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| **No thunderclap symptomatology (max intensity at onset)
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| **No limited neck flexion on physical exam
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| '''If concerned for SAH and CT normal strongly consider LP, especially if CT obtained >6 hrs after symptom onset'''
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| ===Non-Contrast [[Head CT]]===
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| {| class="wikitable"
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| | align="center" style="background:#f0f0f0;"|'''Time from onset of symptoms'''
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| | align="center" style="background:#f0f0f0;"|'''Sensitivity of CT'''
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| |-
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| | <6 hours||~100%<ref>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.
</ref>
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| |-
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| | 6-12 hours||98%
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| |-
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| | 12-24 hours||93%<ref>van Gijn J and van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology. 1982; 23:153–156.</ref>
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| |-
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| | 24 hours - 5 days||<60%
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| |}
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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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| *Elevated RBC count that does not 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 patients)
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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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| *Xanthochromia
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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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| *If traumatic tap is suspected
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| **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.<ref>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.</ref>
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| **One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.<ref>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.</ref>
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| ===CT Angiogram===
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| *A CT followed by CTA is an acceptable alternative to CT and LP<ref>Walsh B, Vilke GM, Coyne CJ. Clinical Guidelines for the Emergency Department Evaluation of Subarachnoid Hemorrhage. Meurer WJ, JEM. 2016; 50(4) 696-701.</ref>
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| *CTA has a 98% sensitivity for aneurysms >3mm
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| ==Management==
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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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| #Avoid [[hypotension]]
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| #*Maintain MAP>80 (CPP of 60 as long as ICP<20)
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| #*Give [[IVF]]
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| #*Give [[pressors]] if IVF ineffective
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| #Hypertension
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| #*AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable<ref>Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012; 43(6):1711-1737.</ref>
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| #*Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome<ref>Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.</ref>, but more recent work has found no difference between SBP <140 and <180<ref>Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].</ref>
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| #*Ensure appropriate pain control and sedation before adding antihypertensives
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| #Discontinue/reverse all anticoagulation
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| #*[[Coumadin]] → (Prothrombin complex concentrate (Kcentra) or [[FFP]]) + vitamin K
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| #*[[Aspirin]] → [[DDAVP]]
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| #*[[Plavix]] → [[Platelets]]
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| #*[[Dabigatran]] (Pradaxa) → [[Idarucizumab]] (Praxbind): 5 grams IV
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| #[[Nimodipine]]
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| #*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)<ref>Francoeur CL, Mayer SA. Management of delayed cerebral ischemia after subarachnoid hemorrhage. Crit Care. 2016;20(1):277.</ref>
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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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| #[[Magnesium sulfate]]
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| #*Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain between 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 associated with 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 patient stay in ED while awaiting ICU bed
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| #Keep head of bed elevated
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| #Aneurysm treatment
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| #*Surgical clipping and endovascular coiling are definitive treatment
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| #*Antifibrinolytic - Controversial; if delayed aneurysmal treatment, consider short term therapy (<72 hrs) with TXA or aminocaproic acid
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| {{Intubation with ICH}}
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| {{AHA SAH BP Guidelines}}
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| ==Disposition==
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| *Admit
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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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| **treatment for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), balloon angioplasty, or intra-arterial vasodilators{{Citation needed|reason=Reliable source needed|date=February 2016}}
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| **Studies have not provided strong evidence of benefit Triple-H therapy{{Citation needed|reason=Reliable source needed|date=February 2016}}
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| ===Cardiac abnormalities===
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| Most likely related to the release of catecholamines due to hypoperfusion of hypothalamus
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| *[[myocardial ischemia|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 within 24hr
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| ===[[Hyponatremia]]===
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| *[[Hyponatremia]] is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU.<ref>Woo, M.H, Kale-Pradhan, P.B. Fludrocortisone in the treatment
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| of subarachnoid hemorrhage-induced hyponatremia. Annals of Pharmacotherapy. 1997. 31, 637–639.</ref>
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| *Cerebral Salt Wasting and [[SIADH]] are the two most common causes<ref>Albanese, A. et al. . Management of hyponatremia in patients with acute cerebral insults. Archives of Disease in Childhood, 85. (2001). 246–251.</ref>
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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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| {| class="wikitable"
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| | align="center" style="background:#f0f0f0;"|'''Grade'''
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| | align="center" style="background:#f0f0f0;"|'''Description'''
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| | align="center" style="background:#f0f0f0;"|'''Survival Rate'''
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| |-
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| |0 ||Unruptured aneurysm||-
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| |-
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| |1 ||Asymptomatic or mild HA and slight nuchal rigidity||70%
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| |-
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| |1a ||No acute meningeal/brain reaction, with fixed neurological def||-
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| |-
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| |2 ||Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy||60%
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| |-
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| |3 ||Mild mental status change (drowsy or confused), mild focal neurologic deficit||50%
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| |-
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| |4 ||Stupor or moderate to severe hemiparesis||20%
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| |-
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| |5 ||Coma or decerebrate rigidity||10%
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| |}
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| :Grade 1 or 2 have curable disease
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| :Add one grade for serious systemic disease (hypertension, 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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| {| class="wikitable"
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| |-
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| !width="50"| Grade
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| ! GCS
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| ! Focal neurological deficit
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| |-
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| ! 1
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| | 15 || Absent
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| |-
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| ! 2
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| | 13–14 || Absent
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| |-
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| ! 3
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| | 13–14 || Present
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| |-
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| ! 4
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| | 7–12 || Present or absent
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| |-
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| ! 5
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| | <7 || Present or absent
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| |}
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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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| *[[Lumbar Puncture]]
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| *[[EBQ:Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage]]
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| ==External Links==
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| *[http://emcrit.org/podcasts/sah/ EMCrit Podcast - Subarachnoid Hemorrhage]
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| ==References==
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| <references/>
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| [[Category:Neurology]] | | [[Category:Neurology]] |
| | [[Category:Critical Care]] |
