Stroke, Hemorrhagic



Denise Nassisi, MD, Assistant Professor, Department of Emergency Medicine, Mount Sinai Medical Center

Nothing to disclose.

Specialty Editor(s)

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

eMedicine Salary Employment

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center

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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

Nothing to disclose.

Richard S Krause, MD, Senior Faculty, Department of Emergency Medicine, State University of New York at Buffalo School of Medicine

Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital

WebMD Salary Employment


The terms intracerebral hemorrhage (ICH) and hemorrhagic stroke are used interchangeably in this discussion and are regarded as separate entities from hemorrhagic transformation of ischemic stroke. Intracerebral hemorrhage accounts for 10-15% of all strokes and is associated with higher mortality rates than cerebral infarctions.[1]

Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke. Prior literature indicates that only 8-18% of strokes were hemorrhagic. However, a recent retrospective review from a stroke center found that 40.9% of 757 strokes were hemorrhagic. However, the authors state that the increased percentage of hemorrhagic stroke may be due to improvement of CT scan availability and implementation unmasking a previous underestimation of the actual percentage, or it may be due to an increase in therapeutic use of antiplatelet agents and warfarin causing an increase in the incidence of hemorrhage.[2]

Patients with hemorrhagic stroke present with similar focal neurologic deficits but tend to be more ill than patients with ischemic stroke. Patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension; however, none of these findings reliably distinguishes between hemorrhagic stroke and ischemic stroke.[3]

An intracerebral hemorrhage is shown in the CT below.

View Image

Large intracerebral hemorrhage with midline shift.


In intracerebral hemorrhage (ICH), bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse. Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. A general increase in intracranial pressure may occur.



United States

Intracerebral hemorrhage accounts for 10-15% of all strokes.[1] Recent reports indicate an incidence exceeding 500,000 new strokes of all types per year.



African Americans have a higher incidence of hemorrhagic and ischemic strokes than other races in the United States. The incidence of hemorrhagic stroke in the Japanese population is increased.


The risk of stroke increases with age.




Laboratory Studies

Imaging Studies

Other Tests

Prehospital Care

Emergency Department Care


Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Class Summary

Anticonvulsants prevent seizure recurrence and terminate clinical and electrical seizure activity.

Fosphenytoin (Cerebyx)

Clinical Context:  Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.

To avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents (PE). Although can be administered IV and IM, IV route is route of choice and should be used in emergency situations.

Concomitant administration of an IV benzodiazepine will usually be necessary to control status epilepticus. The antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, is not immediate.

Phenytoin (Dilantin)

Clinical Context:  May act in motor cortex where may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited.

Dose to be administered should be individualized. Administer larger dose before retiring if dose cannot be divided equally.

Diazepam (Diastat, Diazemuls, Valium)

Clinical Context:  Useful in controlling active seizures and should be augmented by longer-acting anticonvulsants, such as phenytoin or phenobarbital.

Modulates postsynaptic effects of GABA-A transmission, resulting in an increase in presynaptic inhibition. Appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. Also has been found to be an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders.

Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of Cmax.

Individualize dosage and increase cautiously to avoid adverse effects.

Lorazepam (Ativan)

Clinical Context:  Short-acting benzodiazepine with moderately long half-life. Has become drug of choice in many centers for treating active seizures.

Class Summary

The treatment of hypertension should be designed to reduce the blood pressure and other risk factors of heart disease. Pharmacologic therapy should be individualized based on a patient's age.

Labetalol (Trandate)

Clinical Context:  Blocks beta1-, alpha-, and beta2-adrenergic receptor sites decreasing blood pressure.

Esmolol (Brevibloc)

Clinical Context:  Ultra–short-acting agent that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. Particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac events compared to placebo. Can be discontinued abruptly if necessary. Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Hydralazine (Apresoline)

Clinical Context:  Decreases systemic resistance through direct vasodilation of arterioles. Used to treat hypertensive emergencies. The use of a vasodilator will reduce SVR, which, in turn, may allow forward flow, improving cardiac output.

Nicardipine (Cardene, Cardene IV, Cardene SR)

Clinical Context:  Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

Class Summary

These agents are used in an attempt to lower pressure in the subarachnoid space. As water diffuses from the subarachnoid space into the intravascular compartment, pressure in the subarachnoid compartment may decrease.

Mannitol (Osmitrol)

Clinical Context:  Reduces cerebral edema with help of osmotic forces and decreases blood viscosity, resulting in reflex vasoconstriction and lowering of ICP.

Class Summary

Vitamin K is used to promote the formation of clotting factors.

Phytonadione (Mephyton)

Clinical Context:  Can overcome competitive block produced by warfarin and other related anticoagulants. Vitamin K-3 (menadione) is not effective for this purpose. Clinical effect is delayed several hours while liver synthesis of clotting factors is initiated and plasma levels of clotting factors II, VII, IX, and X are gradually restored.

Not to be administered prophylactically. Use only if evidence of anticoagulation exists. Required dose varies with clinical situation, including amount of anticoagulant ingested and whether it is a short-acting or long-acting anticoagulant.

Class Summary

These agents are indicated for the correction of abnormal hemostatic parameters.

Fresh Frozen Plasma

Clinical Context:  Plasma is the fluid compartment of blood containing the soluble clotting factors. For use in patients with blood product deficiencies.


Clinical Context:  Platelet activity may be abnormal.

Prothrombin complex concentrate (Bebulin VH, Profilnine SD)

Clinical Context:  A mixture of vitamin K–dependent clotting factors found in normal plasma. Replaces deficient clotting factors. Provides increase in plasma levels of factor IX and can temporarily correct coagulation defect of patients with factor IX deficiency.

Class Summary

This agent is used to neutralize the effects of anticoagulants.

Protamine sulfate

Clinical Context:  Forms a salt with heparin and neutralizes its effects.

Class Summary

These agents improve bleeding time and hemostasis.

Desmopressin acetate (DDAVP, Stimate)

Clinical Context:  Releases von Willebrand protein from endothelial cells. Improves bleeding time and hemostasis in patients with some vWf (mild and moderate von Willebrand disease without abnormal molecular forms of von Willebrand protein). Effective in uremic bleeding. Tachyphylaxis usually develops after 48 h, but the drug can be effective again after several days.

Further Inpatient Care





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Large intracerebral hemorrhage with midline shift.

CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.

A 59-year-old female with hypertension who presented with left-sided weakness demonstrated a right putaminal hemorrhage on noncontrast CT examination of the head. Tiny hyperdense foci in the basal ganglia and pineal gland represent calcifications.

A 62-year-old female with hypertension who presented with acute-onset ataxia and confusion. Noncontrast CT examination of the head showed a large right cerebellar hemorrhage, which was evacuated to relieve the mass effect on the brainstem and fourth ventricle.

Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.