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Intracranial Hemorrhage Medication

  • Author: David S Liebeskind, MD; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: May 10, 2016
 

Medication Summary

Antihypertensive agents reduce blood pressure to prevent exacerbation of intracerebral hemorrhage. Osmotic diuretics, such as mannitol, may be used to decrease intracranial pressure.

As hyperthermia may exacerbate neurological injury, acetaminophen may be given to reduce fever and to relieve headache.

Anticonvulsants are used routinely to avoid seizures that may be induced by cortical damage. Levetiracetam has shown efficacy in children for prophylaxis of early posthemorrhagic seizures.[13] Additional data suggest that levetiracetam is more effective than phenytoin for seizure prophylaxis without suppression of cognitive abilities in patients with ICH.[14] Vitamin K and protamine may be used to restore normal coagulation parameters. Antacids are used to prevent gastric ulcers associated with intracerebral hemorrhage.

Accumulating data suggest that statins have neuroprotective effects; however, their association with intracerebral hemorrhage outcome has been inconsistent.[16] Antecedent use of statins prior to intracerebral hemorrhage is associated with favorable outcome and reduced mortality after intracerebral hemorrhage. This phenomenon appears to be a class effect of statins.

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Antihypertensive agents

Class Summary

These agents reduce blood pressure to prevent exacerbation of intracerebral hemorrhage.

Labetalol (Normodyne, Trandate)

 

Antagonizes adrenergic receptors, thereby reducing blood pressure.

Nicardipine (Cardene, Cardene SR)

 

Calcium channel blocker. Potent rapid onset of action, ease of titration, and lack of toxic metabolites. Effective but limited reported experience in hypertensive encephalopathy.

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Osmotic diuretics

Class Summary

Osmotic diuretics reverse pressure gradient across the blood-brain barrier, reducing intracranial pressure.

Mannitol (Osmitrol, Resectisol)

 

Reduces cerebral edema with help of osmotic forces and decreases blood viscosity, resulting in reflex vasoconstriction and lowering of intracranial pressure.

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Antipyretics, analgesics

Class Summary

These agents reduce fever and relieve pain.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

 

Reduces fever, maintains normothermia, and reduces headache.

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Anticonvulsants

Class Summary

These agents reduce the frequency of seizures and provide seizure prophylaxis.

Fosphenytoin (Cerebyx)

 

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 IV benzodiazepine usually necessary to control status epilepticus. Full antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, not immediate.

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Antidotes

Class Summary

This agent reverses some coagulopathies or bleeding diatheses.

Phytonadione; vitamin K (Konakion, Mephyton, AquaMEPHYTON)

 

Promotes hepatic synthesis of clotting factors that inhibit warfarin effects.

Protamine

 

Forms a salt with heparin and neutralizes its effects.

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Antacids

Class Summary

These agents provide prophylaxis of gastric ulcers.

Famotidine (Pepcid)

 

Minimizes development of gastric ulcers.

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentration.

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Contributor Information and Disclosures
Author

David S Liebeskind, MD Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California, Los Angeles, David Geffen School of Medicine; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center

David S Liebeskind, MD is a member of the following medical societies: American Academy of Neurology, Stroke Council of the American Heart Association, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Jeffrey L Saver, MD, FAHA, FAAN Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine

Jeffrey L Saver, MD, FAHA, FAAN is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, National Stroke Association

Disclosure: Received the university of california regents receive funds for consulting services on clinical trial design provided to covidien, stryker, and lundbeck. from University of California for consulting.

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Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease.
This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.
This CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.
This MRI reveals hemorrhagic transformation of an ischemic infarct.
Table 1. MRI Appearance of Intracerebral Hemorrhage
Phase Time Hemoglobin T1 T2
Hyperacute < 24 hours Oxyhemoglobin (intracellular) Iso or hypo Hyper
Acute 1-3 days Deoxyhemoglobin (intracellular) Iso or hypo Hypo
Early subacute >3 days Methemoglobin Hyper Hypo
Late subacute >7 days Methemoglobin (extracellular) Hyper Hyper
Chronic >14 days Hemosiderin (extracellular) Iso or hypo Hypo
Table 2. Grading of Subependymal Hemorrhage
Grade Hemorrhage Location
I Subependymal hemorrhage
II Intraventricular hemorrhage without ventriculomegaly
III Intraventricular hemorrhage with ventriculomegaly
IV Intraventricular hemorrhage with parenchymal hemorrhage
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