Subarachnoid Hemorrhage (SAH) William J. Jones, M.D. Assistant Professor of Neurology Co-Director, UCH Stroke Program Click to edit Master title style Disclosures/Relationships No conflicts of interest Click to edit Master title style SAH Objectives Recognize and appropriately evaluate suspected SAH Apply appropriate strategies to prevent re-bleeding Apply appropriate strategies to reduce intracranial pressure Use appropriate treatment for seizures or to prevent seizures
SS1280 Case 1 28 year old woman, presented to an outside ED Sudden HA while doing kettlebell exercises Sharp right parietal pain, radiating down neck, with limited movement of head and neck due to pain Associated photophobia Described as the worst headache of her life PMH: Migraine Questions What evaluation should she have? Other than the history of migraine she had no significant PMH Neurological examination was reportedly normal Non-contrast head CT was reportedly normal A Spinal tap was not done SS1280 Case 1 Four days later she returned to the kettlebell class and again had sudden similar headache but even worse She returned to the ED with headache, lightheadedness, numbness and tingling, and nausea and vomiting She was treated with IV fluids and anti-emetics in the ED and discharged with a prescription for oxycodone
SS1280 Case 1 Since then she continued to have severe headache, worse with valsalva (sneezing, coughing, etc.) and associated with Nausea and vomiting Severe lower back pain Difficulty walking Twelve days after the initial headache she drove from New Mexico to her parents home in Aurora and was seen in the Neurology Outpatient clinic SS1280 Case 1 She reports a severe headache which is much different than she has ever experienced with migraine Examination: Pain with eye movement and transient bilateral horizontal nystagmus with lateral gaze Intense pain with neck flexion Normal sensory examination SS1280
SS1280 Case 1 Spinal tap Non-traumatic Cloudy, light pink fluid Tube #1: Bloody, slight xanthochromia 16 WBCs 5184 RBCs Tube #4: Bloody, slight xanthochromia 26 WBCs 3610 RBCs SS1280 Symptoms suspicious for acute SAH The worst headache of my life is described by ~80% of patients who can give a history A warning or sentinel headache is also described by 20% Most intracranial aneurysms remain asymptomatic until they rupture Aneurismal SAH occurs frequently during physical exertion or stress but can occur at any time Other signs and symptoms are often associated with headache: Nausea and/or vomiting (~77%) Stiff neck (~35%) Brief loss of consciousness (~53%) Focal neurological deficits (including cranial nerve palsies) Up to 12% die before receiving medical attention
Risk Factors for SAH Hypertension Smoking Heavy alcohol use Sympathomimetic drugs (especially in younger patients) Cocaine Methylphenidate Diabetes does not appear to be a risk factor for SAH Evaluation of suspected acute SAH SAH is a medical emergency and is frequently misdiagnosed A high level of suspicion for SAH should exist in patients with acute onset of severe headache CT scanning for suspected SAH should be performed If the CT is negative lumbar puncture is strongly recommended Selective cerebral angiography should be performed in patients with SAH to document the presence and anatomic features of aneurysms MRA and/or CTA may be considered when conventional angiography cannot be performed in a timely fashion PZ1131 Case 2 78 year old woman presented to outside ED Awoke with 10/10 bitemporal headache, nausea, and vomiting BP 156/79 (123-171/59-87), HR 122 (73-122) Regular, unlabored, and protecting airway Lethargic but follows directions, pupils pinpoint, grip is weak on the right
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Questions What are three common and serious cerebral complications of SAH? Re-bleeding Cerebral Vasospasm Typically occurs 3-5 days (up to 14 days) after SAH Nimodipine, 60 mg PO/NG q 4 hours X 21 days After aneurysm is secured Volume expansion Mild-moderate HTN Elevated intracranial pressure (ICP) Question Should empiric anticonvulsant treatment be started? Yes No Hunt and Hess scale for non-traumatic SAH Description Grade Survival Unruptured aneurysm 0 Asymptomatic, mild headache, slight nuchal rigidity 1 70% Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy 2 60% Drowsiness / confusion, mild focal neurologic deficit 3 50% Stupor, moderate-severe hemiparesis 4 20% Coma, decerebrate posturing 5 10%
Modified Fisher grade classification of SAH on CT scan Grade 1 None evident 2 Less than 1 mm thick 3 More than 1 mm thick Appearance of hemorrhage 4 Any thickness with intraventricular hemorrhage or parenchymal extension World Federation of Neurosurgeons (WFNS) classification of SAH Grade GCS* Focal neurological deficit 1 15 Absent 2 13-14 Absent 3 13-14 Present 4 7-12 Absent of present 5 <7 Absent or present *Glasgow Coma Scale Re-bleeding after initial SAH Re-bleeding is associated with ~ 70% fatality rate Re-bleeding is currently the most treatable cause of poor outcomes ~ 4% of re-bleeding occurs within the first 24 hours ~1-2% per day for the first month With conservative therapy (not clipped or coiled) the risk of re-bleeding is ~ 20-30% within the first month and ~ 3% per year thereafter Risk factors for re-bleeding: Longer interval from hemorrhage to admission and treatment Higher initial blood pressure Worse neurological status on admission (Hunt & Hess, Fisher, WFNS) Recent evidence suggests that ultra-early re-bleeding (within 24 hours of initial SAH) may be as high as 15% ~70% of ultra-early re-bleeds may occur within 2 hours of the initial SAH
Prevention of re-bleeding Surgical clipping or endovascular coiling should be performed to reduce the rate of rebleeding after aneurismal SAH Early referral to high-volume centers that have both experienced cerebrovascular surgeons and endovascular specialists is recommended Treat hypertension Antithrombolytics (±) Prevention of re-bleeding (elevated blood pressure) No well-controlled studies of blood pressure control on the rate of re-bleeding Retrospective studies have shown: Re-bleeding is less frequent in patients treated with antihypertensive medication Even though blood pressures were still higher in the treated than non-treated patients An increase in blood pressure immediately before re-bleeding Re-bleeding associated with systolic blood pressure > 150 mm Hg Re-bleeding associated with systolic blood pressure > 160 mm Hg ~ 13.6% of re-bleeds in the ambulance or while still at the referring hospital with a peak incidence within 2 hours of the initial hemorrhage Re-bleeding rate of only 6.9% with no relationship to blood pressure When blood pressure is elevated, short-acting continuous-infusion intravenous agents with a reliable dose-response relationship and favorable safety profile are desirable to reduce SBP <150 mm Hg: Nicardipine, labetalol, and esmolol reportedly best meet these criteria However, sodium nitroprusside is more reliable at quickly and effectively lowering blood pressure but may raise intracranial pressure and causes toxicity with prolonged infusion Prevention of re-bleeding (antifibrinolytics) Antifibrinolytic agents (epsilon-aminocaproic acid, 36 gm/ day; or tranexamic acid, 6 to 12 gm/day): 40-60% reduction in re-bleeding in treated versus control subjects Nearly one third of treated patients in these trials were clinically worse at 14 days Up to 43% increase in the rate of cerebral infarction No difference in re-bleeding between subjects receiving tranexamic acid versus control subjects Similar results have been found with either epsilon-aminocaproic acid (36 gm/d) or tranexamic acid (6 to 12 gm/d) More recently, a prospective, randomized trial of tranexamic acid administered immediately after the diagnosis of SAH followed by early clipping or coiling demonstrated reduced re-bleeding rates and adverse outcomes
Prevention of re-bleeding Quiet bed-rest may be helpful but is not sufficient to prevent re-bleeding without being combined with broader treatment strategies Blood pressure should be monitored and controlled to balance the risk of stroke, hypertension-related re-bleeding, and maintenance of cerebral perfusion pressure Within the first 24 hours when risk of vasospasm is low (typically occurs between 3-14 days) and the risk of re-bleeding is highest, SBP should be maintained < 150 mm Hg Recent evidence suggests that early treatment with a short course of antifibrinolytic agents combined with early aneurysm treatment followed by discontinuation of the antifibrinolytic may be reasonable avoid hypovolemia and vasospasm (±) Aminocaproic acid 4-5 gm IV over one hour, then 1 gm IV per hour for 24 hours or until clipped or coiled Increased intracranial pressure Increased ICP is common following SAH may be caused by one or more of: Hydrocephalus May occur with or without intra-ventricular blood Is associated with the amount of cisternal blood when intra-ventricular blood is absent Intra-parenchymal hemorrhage Cerebral edema Increased intracranial pressure Most patient require ICP monitoring Intracranial pressure monitor (bolt) Intra-ventricular drain (s) can also be used to treat hydrocephalus and elevated ICP Mannitol 0.8-0.9 gm/kg will reduce ICP May cause hyponatremia May cause volume depletion and thus decreased cerebral perfusion Hyperventilation temporarily reduces ICP
Anticonvulsant treatment The risk and implications of seizures associated with SAH are not well defined, and the need for and efficacy of routinely administered anticonvulsants after SAH are not well established Seizure-like episodes have been associated with aneurismal rupture In retrospective reviews seizures frequency ranges from 6% to 18% Most seizures occurred before medical presentation and in-hospital seizures are rare in patients given prophylactic anticonvulsants The relationship between seizures and outcome is not clear In one series of patients who underwent continuous EEG monitoring found 19% of stuporous or comatose patients had non-convulsive seizures All were receiving prophylactic anticonvulsants, and all died Risk factors for seizures after SAH include: middle cerebral artery aneurysms intraparenchymal hematoma cerebral infarctions history of hypertension Anticonvulsant treatment Anticonvulsants should be administered in patients with seizures Prophylactic anticonvulsants may be considered in the immediate post-hemorrhagic period Dilantin (phenytoin) Typically avoid phenytoin because cardiac rhythm disturbances are common with SAH and phenytoin may also cause arrhythmias Keppra (levetiracetam) 500-1000 mg IV BID Valproic acid 10-15 mg/kg per day divided TID, may increase up to 30-60 mg/kg per day SAH recommendations Prevention of re-bleeding Secure aneurysm ASAP Maintain SBP < 150 mm Hg until aneurysm is secured Nicardipine, 3-15 mg per hour IV drip Nipride (nitroprusside), 3-10 mcg/kg per minute IV drip ±Amicar (aminocaproic acid) immediately and for 24 hours or until aneurysm is secured Treatment of ICP ICP monitor or intra-ventricular drain (s) Mannitol 0.8-0.9 gm/kg Anticonvulsants Keppra (levetiracetam), 500-1000 mg BID Depacon (valproate), 10-60 mg/kg per day, divided TIA
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