eMedicine Specialties > Emergency Medicine > Neurology

Subarachnoid Hemorrhage: Treatment & Medication

Author: Rami C Zebian, MD, Resident Physician, Department of Internal Medicine, University of Texas Medical School at Houston
Coauthor(s): A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
Contributor Information and Disclosures

Updated: Feb 25, 2009

Treatment

Prehospital Care

  • Address the ABCs.
  • Triage and transport patients with altered level of consciousness or an abnormal neurologic examination to the closest medical center with a CT scan and neurosurgical backup.
  • Ideally, avoid sedating these patients en route.

Emergency Department Care

  • In patients with a suspected grade I or II subarachnoid hemorrhage, ED care essentially is limited to diagnosis and supportive therapy.
    • Early identification of sentinel headaches is key to reduced mortality and morbidity rates.
    • Use sedation judiciously.
    • Secure intravenous (IV) access during ED stay and closely monitor the patient's neurologic status.
  • In patients with a grade III, IV, or V subarachnoid hemorrhage (ie, altered neurologic examination), ED care is more extensive.
    • Address the ABCs.
    • Endotracheal intubation of obtunded patients protects from aspiration caused by depressed airway protective reflexes.
    • Intubate to hyperventilate patients with signs of herniation.
      • Thiopental and etomidate are the optimal induction agents in subarachnoid hemorrhage during an intubation. Thiopental is short-acting and has a barbiturate cytoprotective effect. It should be used only in hypertensive patients because of its propensity to drop systolic blood pressure (SBP), which is the leading cause of secondary brain injury. In hypotensive and normotensive patients, use etomidate.
      • Use rapid sequence intubation if possible. In the process, to blunt ICP increase, ideally use sedation, defasciculation, short-acting neuromuscular blockade, and other agents with ICP-blunting properties (such as IV lidocaine).
      • Avoid excessive or inadequate hyperventilation. Target the pCO2 at 30-35 mm Hg to reduce elevated ICP. Excessive hyperventilation may be harmful to areas of vasospasm.
    • Avoid excessive sedation. It makes serial neurologic exams more difficult and has been reported to increase ICP directly.
  • Reliable neurologic examinations before and after initial treatment are critically important to optimizing management and to deciding on the appropriate neurosurgical intervention.
  • Use the following interventions early and judiciously to decrease elevated ICP when herniation is suspected:
    • Use osmotic agents, such as mannitol, which reduces ICP 50% in 30 minutes, peaks after 90 minutes, and lasts 4 hours.
    • Loop diuretics, such as furosemide, also decrease ICP without increasing serum osmolality.
    • IV steroid therapy to control brain edema is controversial and debated.
  • Monitoring
    • Monitor cardiac activity, oximetry, automated BP, and end-tidal carbon dioxide, when applicable.
    • End-tidal carbon dioxide monitoring of intubated patients enables the clinician to avoid excessive or inadequate hyperventilation. Target the pCO2 at about 30-35 mm Hg to reduce elevated ICP.
    • Invasive arterial line monitoring is indicated when dealing with labile BP (common in high-grade subarachnoid hemorrhage).
  • Antihypertensive agents
    • Antihypertensive agents previously were advocated for an SBP greater than 160 mm Hg or diastolic BP (DBP) greater than 90 mm Hg.
    • Keep systolic blood pressure 90-140 mm Hg before aneurysm treatment, then allow hypertension to keep systolic blood pressure less than 200 mm Hg.3
    • Consult critical care providers who will be involved in ongoing care of the patient, as individual practices vary.
    • Use medications that can be titrated rapidly.
    • Vasopressors may be indicated to keep SBP over 120 mm Hg; this avoids CNS damage in the ischemic penumbra from the reactive vasospasm seen in SAH.
  • Adjunctive therapies and measures
    • Provide supplemental oxygen for all patients with CNS impairment.
    • Elevate the head of the bed 30° to facilitate intracranial venous drainage.
    • Fluids and hydration
      • Maintain euvolemia (CVP, 5-8 mm Hg); if cerebral vasospasm is present, maintain hypervolemia (CVP 8-12 mm Hg, or PCWP, 12-16 mm Hg).3
      • Do not overhydrate patients because of risks of hydrocephalus.
      • Patients with SAH also may have hyponatremia from cerebral salt wasting.
    • Serum glucose: Maintain level at 80-120 mg/dL; use sliding or continuous infusion of insulin if necessary.3
    • Core body temperature: Keep at 37.2°C; administer acetaminophen (325-650 mg PO q4-6h) and use cooling devices if necessary.3
    • Consider antiemetics for nausea or vomiting.
    • Sedate cautiously to avoid masking the neurologic examination, which may jeopardize the reliability of the findings. However, avoid any increase in ICP due to excessive agitation from pain and discomfort.
  • Seizures
    • Prophylactic use of anticonvulsants does not acutely prevent seizures after subarachnoid hemorrhage, but use anticonvulsants in patients who have had a seizure or if local practice dictates routine use.
    • Begin with anticonvulsants that do not change the level of consciousness (ie, phenytoin first; barbiturates or benzodiazepines only to stop active seizures).
  • Calcium channel blockers decrease the incidence and severity of cerebral vasospasm.
    • Judicious use is essential because of the risk of detrimental primary or secondary hypotension.
    • Short-acting medication is recommended; discuss this intervention with the neurosurgeon.
  • Statins
    • Statins may improve cerebral vasomotor reactivity through cholesterol-dependent and cholesterol-independent mechanisms.
    • Their use is still controversial, but 2 small studies have shown promise. Acute treatment with statins ameliorated cerebral vasospasm and reduced vasospasm-related delayed ischemic deficits.7,8
  • Magnesium
    • New trials are now evaluating the role of magnesium sulfate to prevent delayed cerebral ischemia. It is a neuroprotective agent that acts as an NMDA-receptor antagonist and a calcium channel blocker. Phase 2 studies have shown a beneficial effect, and phase 3 trials are underway.9
  • Use of antifibrinolytics, such as epsilon aminocaproic acid, is controversial.
    • They competitively inhibit plasminogen activation and have been reported to reduce the incidence of rebleeding.
    • Other reports warn of their detrimental vasospastic effect and increased occurrence of hydrocephalus. Consult a neurosurgeon concerning their use.
  • Emergent ventricular drainage by the neurosurgeon may be necessary.

Consultations

  • Obtain emergent neurosurgical consultation for definitive treatment.
  • Interventional radiology may be needed when surgical intervention is deemed necessary by the neurosurgical consultant (eg, a large clot causing a mass effect is present and needs to be evacuated emergently).
  • Many centers opt for early angiography in all patients.

Medication

The goals of therapy are to reduce pain, edema, and severity of cerebral vasospasm, relieve nausea and vomiting, and prevent convulsions.

Analgesics

Pain control is essential to quality patient care. It ensures patient comfort and promotes pulmonary toilet. Most analgesics have sedating properties that benefit patients who have sustained trauma.


Fentanyl citrate (Sublimaze)

A synthetic opioid that is 75-200 times more potent and much shorter half-life than morphine sulfate. Has less hypotensive effects and is safer in patients with hyperactive airway disease than morphine because of minimal-to-no associated histamine release. By itself, it causes little cardiovascular compromise, although addition of benzodiazepines or other sedatives may result in decreased cardiac output and blood pressure.
Highly lipophilic and protein-bound. Prolonged exposure leads to accumulation in fat and delays weaning process.
Consider continuous infusion because of the short half-life of fentanyl. Parenteral form is DOC for conscious sedation analgesia. Ideal for analgesic action of short duration during anesthesia and immediate postoperative period.
Excellent choice for pain management and sedation with short duration (30-60 min) and easy to titrate. Easily and quickly reversed by naloxone.
After initial parenteral dose, subsequent parenteral doses should not be titrated more frequently than q3h or q6h thereafter.
Transdermal form is used only for chronic pain conditions in opioid-tolerant patients. When using transdermal dosage form, most patients are controlled with 72-h dosing intervals; however, some patients require dosing intervals of 48 h.
Easily and quickly reversed by naloxone.

Adult

2-3 mcg/kg IV; not to exceed 50 mcg

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants may potentiate adverse effects of fentanyl when both drugs are used concurrently

Documented hypersensitivity; hypotension or potentially compromised airway where it would be difficult to establish rapid airway control

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypotension, respiratory depression, constipation, nausea, emesis, and urinary retention; idiosyncratic reaction, known as chest wall rigidity syndrome, may require neuromuscular blockade in order to increase ventilation

Antiemetics

These agents are used for the treatment of nausea or vomiting.


Promethazine (Phenergan)

Antidopaminergic agent effective in treatment of emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.

Adult

12.5 mg PO/PR tid; 25 mg hs
25 mg IV/IM; repeat in 2 h prn

Pediatric

<2 years: Contraindicated
>2 years: 0.25-1 mg/kg PO/IV/IM/PR 4-6 times/d prn

Other CNS depressants or anticonvulsants may have additive effects; with epinephrine, may cause hypotension

Documented hypersensitivity; children younger than 2 y (incidences of death due to respiratory depression)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, impaired liver function, seizures, sleep apnea, and asthma

Anticonvulsants

These agents are used to prevent posttraumatic seizures. Use in patients with SAH who have not had seizures is controversial and dependent on individual neurosurgical preference; they usually are used only in patients who have had seizures. Conventional loading doses may be employed.


Phenytoin (Dilantin)

Appears to act in motor cortex, where it may inhibit spread of seizure activity; activity of brainstem centers responsible for tonic phase of grand mal seizures also may be inhibited.
Individualize dose; administer larger dose before retiring if dose cannot be divided equally.

Adult

Loading dose: 15-20 mg/kg PO/IV once or divided, followed by 100-150 mg/dose at 30-min intervals
Initial dose: 100 mg (125 mg susp) PO/IV tid
Maintenance dosage: 300-400 mg/d PO/IV divided tid (qd/bid if ER); increase to 600 mg/d (625 mg/d susp) prn; not to exceed 1500 mg/d; rate of infusion not to exceed 50 mg/min

Pediatric

Loading dose: 15-20 mg/kg PO/IV once or in divided doses
Initial dose: 5 mg/kg/d PO/IV divided bid/tid
Maintenance dose: 4-8 mg/kg PO/IV divided bid/tid
>6 years: May require minimum adult dose (300 mg/d); not to exceed 300 mg/d

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity
Barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate may decrease effects
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid

Documented hypersensitivity; due to effect on ventricular automaticity, do not use in sinoatrial block, sinus bradycardia, second- and third-degree AV block, or Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalysis when therapy begins and at monthly intervals for several months to monitor for blood dyscrasias; discontinue use if skin rash appears—if rash is exfoliative, bullous, or purpuric do not resume use; death from cardiac arrest after too-rapid IV administration may occur (sometimes preceded by marked QRS widening); hypotension and arrhythmias can occur if rate of infusion (adults) exceeds 50 mg/min; administer cautiously to patients with acute intermittent porphyria; exercise caution when administering to patients with diabetes as it may raise blood glucose levels; discontinue if hepatic dysfunction occurs


Fosphenytoin (Cerebyx)

Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin; plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin; phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.
Dose expressed as phenytoin equivalents (PE) to avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses.
IV is route of choice and should be used in emergency situations.

Adult

Loading dose: 15-20 mg PE/kg IV/IM at 100-150 mg PE/min
Maintenance dose: 4-6 mg PE/kg/d IV/IM at 150 mg PE/min to minimize risk of hypotension

Pediatric

Loading dose: 15-20 mg PE/kg IV/IM
Initial dose: 5 mg PE/kg/d IV/IM
Maintenance dose: 4-8 mg PE/kg IV/IM
>6 years: May require minimum adult dose (300 mg PE/d); not to exceed 300 mg PE/d

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, disulfiram, ethanol (acute ingestion), fluconazole, isoniazid, metronidazole, miconazole, omeprazole, phenacemide, phenylbutazone, succinimides, sulfonamides, trimethoprim, and valproic acid may increase toxicity
Barbiturates, carbamazepine, diazoxide, ethanol (chronic ingestion), rifampin, theophylline, antacids, charcoal, and sucralfate may decrease effects
May decrease effects of acetaminophen, amiodarone, carbamazepine, cardiac glycosides, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, methadone, metyrapone, mexiletine, oral contraceptives, quinidine, theophylline, and valproic acid

Documented hypersensitivity; due to effect on ventricular automaticity, do not use in sinoatrial block, sinus bradycardia, second- and third-degree AV block, or Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalysis when therapy is begun and at monthly intervals for several months thereafter, as blood dyscrasias have occurred; discontinue use if skin rash appears—if rash is exfoliative, bullous, or purpuric, do not resume use; death from cardiac arrest has occurred after too-rapid IV administration, sometimes preceded by marked QRS widening; administer cautiously to patients with acute intermittent porphyria; caution when administering to patients with diabetes, as it may raise blood glucose levels; discontinue if hepatic dysfunction occurs; coadministration of IV benzodiazepine usually necessary to control status epilepticus; full antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, not immediate

Osmotic agents

These agents are used in an attempt to lower ICP and cerebral edema by creating an osmotic gradient across an intact blood-brain barrier; as water diffuses from the brain into the intravascular compartment, ICP decreases.


Mannitol (Osmitrol, Resectisol)

May reduce subarachnoid space pressure by creating osmotic gradient between CSF in arachnoid space and plasma; not for long-term use.

Adult

Initially assess for adequate renal function by administering test dose of 200 mg/kg IV over 3-5 min (should produce urine flow of at least 30-50 mL/h of urine over 2-3 h)
1.5-2 g/kg as 20% solution (7.5-10 mL/kg) or 15% solution (10-13 mL/kg) IV for as little as 30 min

Pediatric

Initially assess for adequate renal function by administering test dose of 200 mg/kg IV over 3-5 min; should produce a urine flow of at least 1 mL/kg/h over 1-3 h; if adequate renal function observed, administer as follows:
0.5-1 g/kg IV, followed by maintenance dose of 0.25-0.5 g/kg IV q4-6h

Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Carefully evaluate cardiovascular status before rapid administration, since sudden increase in extracellular fluid may lead to fulminating CHF; to avoid pseudoagglutination when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

Diuretics

These agents are used to decrease plasma volume and edema by causing diuresis.


Furosemide (Lasix)

Used in acute setting for reduction of increased ICP. Proposed mechanisms in lowering ICP include following: (1) suppression of cerebral sodium uptake, (2) carbonic anhydrase inhibition resulting in decreased CSF production, and (3) inhibition of cellular membrane cation-chloride pump, thereby affecting transport of water into astroglial cells. Dose must be individualized.

Adult

20-40 mg/d IV/IM given slowly; depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs

Pediatric

Neonates: 1 mg/kg IV/IM slowly under close supervision; titrate with 1 mg/kg/dose increments, no sooner than 2 h following initial dose, until satisfactory effect achieved
Children: 1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents; antagonizes muscle-relaxing effect of tubocurarine; aminoglycosides appear to increase auditory toxicity—hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin; may increase lithium plasma levels and toxicity

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Observe for blood dyscrasias and liver or kidney damage; may increase urinary excretion of magnesium and calcium

Calcium channel blockers

These agents may attenuate deleterious effects of calcium influx in patients with acute neurotrauma. Unfortunately, experimental studies using conventional calcium channel blockers in head injury models have been disappointing overall; however, some studies have suggested that calcium channel blockers may be effective in attenuating cerebral edema and postinjury cognitive dysfunction compared to placebo.


Nimodipine (Nimotop)

Used for improvement of neurologic impairments resulting from spasms following SAH caused by ruptured congenital intracranial aneurysm in patients in good neurologic condition postictus. While studies show such benefit, no evidence indicates drug either prevents or relieves spasms of cerebral arteries; thus, actual mechanism of action unknown.
Begin therapy within 96 h of SAH. If patient cannot swallow capsule because undergoing surgery or unconscious, make holes at both ends of capsule with 18-gauge needle and extract contents into syringe, empty contents into patient's in situ nasogastric tube, and wash it down tube with 30 mL isotonic saline.

Adult

60 mg PO/NG q4h for 21 d

Pediatric

Not established

Beta-blockers, although advantageous in some patients, may result in increased adverse effects due to depressant effects on myocardial contractility or AV conduction; fentanyl may cause severe hypotension or increased fluid volume requirements; cimetidine may increase blood levels

Documented hypersensitivity; hypotension (SBP <90 mm Hg); sick sinus syndrome; second- or third-degree AV block except in patients with pacemaker

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In rare cases, LDH, alkaline phosphatase, and ALT may be elevated

Hemostatic agents

These agents are potent inhibitors of fibrinolysis and can reverse states that are associated with excessive fibrinolysis. Use is controversial; consultation with admitting physicians is urged prior to use.


Aminocaproic acid (Amicar)

Inhibits fibrinolysis via inhibition of plasminogen activator substances and, to lesser degree, through antiplasmin activity. Main problem with use is that thrombi that form during treatment are not lysed and effectiveness is uncertain. Has been used to prevent recurrence of SAH.

Adult

36 g/d PO/IV in 6 divided doses; not to exceed 30 g/d

Pediatric

5-30 g/d PO/IV q3-6h divided; not to exceed 18 g/m2/d

Estrogens or oral contraceptives increase clotting factors, which may lead to hypercoagulable state

Documented hypersensitivity; active intravascular clotting process; DIC

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

If administered to patient with DIC, may produce thrombus that can be fatal, thus important to differentiate between hyperfibrinolysis and DIC
Do not administer in absence of definite diagnosis or if laboratory findings do not show hyperfibrinolysis (hyperplasminemia); caution in cardiac, hepatic, or renal disease

Antihypertensive agents

These agents are used to attempt to reduce ICP by reducing peripheral PB.


Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of heart. Short-acting and potent. Close monitoring essential.

Adult

Starting dose: 0.3-0.5 mcg/kg/min IV; increase in increments of 0.5 mcg/kg/min, titrating to desired hemodynamic effect
Average dose 3 mcg/kg/min

Pediatric

Administer as in adults

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with ICP, hepatic failure, severe renal impairment, or hypothyroidism; in renal or hepatic insufficiency, levels may increase and can cause cyanide toxicity; sodium nitroprusside can lower BP and thus should be used only in patients with MBP >70 mm Hg


Labetalol (Trandate, Normodyne)

Blocks alpha-, beta1-, and beta2-adrenergic receptor sites, decreasing BP.

Adult

20-30 mg IV over 2 min followed by 40-80 mg at 10-min intervals; not to exceed 300 mg/dose

Pediatric

Suggested dose: 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Decreases effects of diuretics; increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; AV block, uncompensated CHF; reactive airway disease; severe bradycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with impaired hepatic function; discontinue if signs of liver dysfunction; older patients may have lower response rate and higher incidence of toxicity

General anesthetics

These agents provide sedation when neuromuscular blocking agents are used for intubation.


Thiopental (Pentothal)

Short-acting barbiturate sedative-hypnotic with rapid onset and duration of action of 5-20 min. Like methohexital, most commonly used as induction agent for intubation. Depresses consciousness and diminishes or terminates seizure effects; facilitates transmission or impulses from thalamus to cortex of brain, resulting in imbalance in central inhibitory and facilitatory mechanisms. To use as sedative, titrate in dosage increments of 25 mg (adjust to lower dose in children).

Adult

2-4 mg/kg IV; may use lower doses in critically ill or elderly patients

Pediatric

2-3 mg/kg/dose IV; repeat prn

CNS depressants, salicylates, and sulfisoxazole increase toxicity

Documented hypersensitivity (rare); porphyria; severe hypovolemia or unstable hemodynamics; lack of familiarity with drug; inability to manage airway

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic or renal insufficiency, asthma, severe cardiovascular disease, unstable aneurysm, hypotension, laryngospasm, or bronchospasm


Amidate (Etomidate)

Nonbarbiturate imidazole compound with sedative properties. Short-acting and rapid onset of action; duration of action is dose dependent (15-30 min). Most useful feature as induction agent is that it produces deep sedation while causing minimal cardiovascular effects. Major application is induction for endotracheal intubation, particularly in patients with, or at risk for, hemodynamic compromise. Has been shown to depress adrenal cortical function; however, effect is not significant clinically during short-term administration. Since drug mixed in propylene glycol, continuous infusion not recommended.

Adult

0.3 mg/kg/dose IV; repeat prn

Pediatric

Administer as in adults

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients undergoing severe stress may require exogenous corticosteroid replacement

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Multimedia: Subarachnoid Hemorrhage
References
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Further Reading

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Contributor Information and Disclosures

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Rami C Zebian, MD, Resident Physician, Department of Internal Medicine, University of Texas Medical School at Houston
Rami C Zebian, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Richard S Krause, MD, Senior Faculty, Department of Emergency Medicine, State University of New York at Buffalo School of Medicine
Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
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CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
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