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Subarachnoid Hemorrhage (SAH)

William J. Jones, M.D. Assistant Professor of Neurology Co-Director, UCH Stroke Program

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Disclosures/Relationships

No conflicts of interest

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

PZ1131

PZ1131

PZ1131

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 Appearance of hemorrhage 1 None evident 2 Less than 1 mm thick 3 More than 1 mm thick 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 re-bleeding 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

Questions