Medication Summary
Medications used in the treatment of acute stroke include anticonvulsants such as diazepam, to prevent seizure recurrence; antihypertensive agents such as labetalol, to reduce blood pressure (BP) and other risk factors for heart disease; and osmotic diuretics such as mannitol, to decrease intracranial pressure in the subarachnoid space.
As previously mentioned, the treatment and management of patients with acute intracerebral hemorrhage depends on the cause and severity of the bleeding. However, there is currently no effective targeted therapy for hemorrhagic stroke.
Anticonvulsants, Other
Class Summary
Benzodiazepines are commonly used to control seizure activity and recurrence. Agents such as lorazepam and diazepam are often used acutely, in combination with either phenytoin or fosphenytoin loading.
Diazepam (Diastat, Diazemuls, Valium)
Diazepam controls active seizures by modulating the postsynaptic effects of gamma-aminobutyric acid type A (GABA-A) transmission, resulting in an increase in presynaptic inhibition. It appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. It also acts as an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders.
Diazepam should be augmented by longer-acting anticonvulsants, such as phenytoin or phenobarbital, because it rapidly distributes to other body fat stores.
Lorazepam (Ativan)
Lorazepam is a short-acting acting benzodiazepine with a moderately long half-life. It has become the drug of choice in many centers for treating active seizures.
Anticonvulsants, Hydantoins
Class Summary
Anticonvulsants prevent seizure recurrence and terminate clinical and electrical seizure activity. These agents are used routinely to avoid seizures that may be induced by cortical damage.
According to the American Heart Association/American Stroke Association (AHA/ASA) 2010 guidelines for management of spontaneous intracranial hemorrhage, treatment with antiepileptic drugs is indicated for those patients with clinical seizures or with electroencephalographic (EEG) seizure activity accompanied by a change in mental status. [1] Prophylactic use of anticonvulsants is controversial and should be used judiciously, if at all.
Phenytoin (Dilantin)
Phenytoin may act in the motor cortex, where it may inhibit spread of seizure activity, as well as in the brainstem centers responsible for the tonic phase of grand mal seizures. All doses should be individualized. The antiepileptic effect of phenytoin is not immediate. Concomitant administration of an intravenous benzodiazepine will usually be necessary to control status epilepticus. In addition, a larger dose before retiring should be administered if the dose cannot be divided equally.
Fosphenytoin (Cerebyx)
Fosphenytoin is a diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.
To avoid the need to perform molecular-weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express the dose as phenytoin sodium equivalents. Although fosphenytoin can be administered intravenously or intramuscularly, the intravenous route is the route of choice and should be used in emergency situations.
The antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, is not immediate. Concomitant administration of an intravenous benzodiazepine will usually be necessary to control status epilepticus.
Beta Blockers, Alpha Activity
Class Summary
Beta blockers are used to reduce BP and risk factors for heart disease. They are first-line agents for acute BP reduction in hemorrhagic stroke, but they are second-line agents for stroke prevention. Selective beta blockers obstruct access to beta-1 receptors more than they do to beta-2 receptors; nonselective beta blockers obstruct access to beta-1 and beta-2 receptors.
Labetalol (Trandate)
Labetalol blocks beta1-, alpha-, and beta2-adrenergic receptor sites to decrease BP. It is administered as a 5-20 mg intravenous bolus over 2 minutes, then as a continuous infusion at 2 mg/min (not to exceed 300 mg/dose).
Beta Blockers, Beta-1 Selective
Class Summary
Beta blockers are used to reduce BP and risk factors for heart disease. They are first-line agents for acute BP reduction in hemorrhagic stroke, but they are second-line agents for stroke prevention. Selective beta blockers obstruct access to beta-1 receptors more than they do to beta-2 receptors; nonselective beta blockers obstruct access to beta-1 and beta-2 receptors.
Esmolol (Brevibloc)
Esmolol is an ultra-short-acting agent that selectively blocks beta-1 receptors with little or no effect on beta-2 receptor types. This drug is particularly useful in patients with elevated arterial pressure, especially if surgery is planned, and its short half-life of 8 minutes allows for titration and quick discontinuation, if necessary.
Esmolol is also useful in patients at risk for experiencing complications from beta blockade, particularly those with reactive airway disease, mild to moderate left-ventricular dysfunction, and/or peripheral vascular disease.
Vasodilators
Class Summary
Vasodilators lower BP through direct vasodilation and relaxation of the vascular smooth muscle. They are used more for BP lowering in refractory situations.
Hydralazine (Apresoline)
Hydralazine decreases systemic resistance through direct vasodilation of arterioles and is used to treat hypertensive emergencies. The use of a vasodilator will reduce the stroke volume ratio (SVR), which, in turn, may allow forward flow, improving cardiac output. Hydralazine is typically not a first-line agent, because of its side-effect profile.
Calcium Channel Blockers
Class Summary
Calcium channel blockers are used to lower BP by relaxing the blood vessels and increasing the amount of blood and oxygen that is delivered to the heart, while reducing the heart’s workload. In acute situations, intravenous calcium channel blockers are frequently used to control BP. These are first-line agents for long-term BP control in stroke patients (along with thiazides, ACEIs, and angiotensin receptor blockers [ARBs]).
Nicardipine (Cardene, Cardene IV, Cardene SR)
Nicardipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.
Angiotensin-converting Enzyme Inhibitors
Class Summary
ACEIs prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. These are first-line agents for emergent and long-term BP control in hemorrhagic stroke patients.
Enalapril (Vasotec)
Enalapril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It helps to control BP and proteinuria.
Ramipril (Altace)
Ramipril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Lisinopril (Zestril)
Lisinopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Angiotensin Receptor Blockers
Class Summary
ARBs may be used as an alternative to ACEIs in patients who develop adverse effects, such as a persistent cough.
Losartan (Cozaar)
Losartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACEIs do. In addition, it does not affect the response to bradykinin and is less likely to be associated with cough and angioedema.
Candesartan (Atacand)
Candesartan blocks vasoconstriction and the aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACEIs do. In addition, it does not affect response to bradykinin and is less likely to be associated with cough and angioedema.
Valsartan (Diovan)
Valsartan produces direct antagonism of angiotensin II receptors. It displaces angiotensin II from the AT1 receptor and may lower BP by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.
Diuretics, Thiazide
Class Summary
Thiazide diuretics inhibit sodium and chloride reabsorption in the distal tubules of the kidney, resulting in increased urinary excretion of sodium and water.
Hydrochlorothiazide (Microzide)
Hydrochlorothiazide inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as potassium and hydrogen ions.
Chlorthalidone (Diuril)
Chlorthalidone inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as potassium and hydrogen ions.
Diuretics, Osmotic Agents
Class Summary
Osmotic diuretics, such as mannitol, may be used to decrease intracranial 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)
Mannitol reduces cerebral edema with the help of osmotic forces. It also decreases blood viscosity, resulting in reflex vasoconstriction and lowering of intracranial pressure.
Analgesics, Other
Class Summary
Because hyperthermia may exacerbate neurologic injury, these agents may be given to reduce fever and relieve pain.
Acetaminophen (Tylenol, FeverAll, Aspirin Free Anacin)
Acetaminophen reduces fever, maintains normothermia, and reduces headache.
Hemostatics
Class Summary
Vitamin K is used to promote the formation of clotting factors. Phytonadione can overcome the competitive block produced by warfarin and other related anticoagulants. A fresh frozen plasma (FFP) infusion followed by oral vitamin K should be given without delay in the emergency department to manage warfarin-related intracranial hemorrhage.
Vitamin K1 (phytonadione; vitamin K, Mephyton, AquaMephyton)
Phytonadione can overcome the competitive block produced by warfarin and other related anticoagulants. Vitamin K3 (menadione) is not effective for this purpose. There is a delay of the clinical effect for several hours while liver synthesis of the clotting factors is initiated and plasma levels of clotting factors II, VII, IX, and X are gradually restored.
Phytonadione should not be administered prophylactically and is used only if evidence of anticoagulation exists. The required dose varies with the clinical situation, including the dose and duration of action of the anticoagulant ingested. Intravenous phytonadione is recommended for life-threatening bleeding, including intracerebral hemorrhage complicating warfarin therapy, although it carries a small risk of anaphylaxis.
Blood Components
Class Summary
These agents are indicated for the correction of abnormal hemostatic parameters.
Fresh frozen plasma
Plasma, the fluid component of blood, contains the blood's soluble clotting factors. FFP is created by separating plasma from a unit of blood and freezing it for use in patients with blood-product deficiencies.
Platelets
Platelets are fragments of large bone marrow cells found in the blood that play a role in blood coagulation. A single random donor unit of platelets per 10 kg is administered in adults when the platelet count drops below 50,000/µL.
Prothrombin complex concentrate (Bebulin VH, Profilnine SD)
Prothrombin complex concentrate (PCC) is a mixture of vitamin K-dependent clotting factors found in normal plasma that replaces deficient clotting factors, provides an increase in plasma levels of factor IX, and can temporarily correct a coagulation defect in patients with factor IX deficiency. PCC is usually reserved for situations in which volume overload is a concern.
Antidotes, Other
Class Summary
Protamine is used to neutralize the effects of anticoagulants.
Protamine
Protamine sulfate forms a salt with heparin and neutralizes its effects. The dosage administered is dependent on the amount of time that has passed since heparin was given.
Vasopressin-Related
Class Summary
These agents improve bleeding time and hemostasis.
Desmopressin acetate (DDAVP, Stimate)
Desmopressin releases von Willebrand protein from endothelial cells. It improves bleeding time and hemostasis in patients with mild and moderate von Willebrand disease without abnormal molecular forms of von Willebrand protein. It is effective in uremic bleeding. Tachyphylaxis usually develops after 48 hours, but the drug can be effective again after several days.
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Axial noncontrast computed tomography scan of the brain of a 60-year-old man with a history of acute onset of left-sided weakness. Two areas of intracerebral hemorrhage are seen in the right lentiform nucleus, with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle, with intraventricular extension of the hemorrhage.
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Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region, with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance imaging scan (middle image) again demonstrates the hemorrhage, with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma, with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.
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Noncontrast computed tomography scan (left) obtained in a 75-year-old man who was admitted for stroke demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right), with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted, with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.
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Noncontrast computed tomography (CT) scanning was performed emergently in a 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT scan (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. There is diffuse loss of gray-white differentiation. The fluid-attenuated inversion-recovery (FLAIR) image (right) demonstrates high signal throughout the cortical sulci and in the basilar cisterns, as well as in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage; the suppression of high cerebrospinal fluid signal aids in making subarachnoid hemorrhage more conspicuous than do conventional magnetic resonance imaging sequences.
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Computed tomographic angiography examination and subsequent cerebral angiography were performed in 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery injection. Balloon-assisted coil embolization was performed.
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Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.
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Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and sylvian triangle. The pericallosal artery has been described as arising distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: (1) the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery, (2) A2 extends to the junction of the rostrum and genu of the corpus callosum, (3) A3 extends into the bend of the genu of the corpus callosum, and (4) A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the sylvian point.
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Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries.
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Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).
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Frontal view from a cerebral angiogram in a 41-year-man who presented 7 days earlier with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm (which was treated with surgical clipping). There is significant narrowing of the proximal left ACA, left M1 segment, and left supraclinoid internal carotid artery, indicating vasospasm.
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Angiographic view in a 41-year-man who presented 7 days earlier with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm (which was treated with surgical clipping). Superimposed road map image demonstrates placement of a wire across the left M1 segment and balloon angioplasty. The left proximal ACA and supraclinoid internal carotid artery (ICA) were also angioplastied, and intra-arterial verapamil was administered. Follow-up image on the right after treatment demonstrates resolution of the left M1 segment and distal ICA, which are now widely patent. Residual narrowing is seen in the left proximal ACA.
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A cerebral angiogram was performed in a 57-year-old man with a family history of subarachnoid hemorrhage and who was found on previous imaging to have a left distal internal carotid artery (ICA) aneurysm. The lateral projection from this angiogram demonstrates a narrow-necked aneurysm arising off the posterior aspect of the distal supraclinoid left ICA, with an additional nipplelike projection off the inferior aspect of the dome of the aneurysm. There is also a mild, lobulated dilatation of the cavernous left ICA.
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Follow-up cerebral angiogram after coil embolization in a 57-year-old man with a left distal internal carotid artery aneurysm. Multiple coils were placed with sequential occlusion of the aneurysm, including the nipple at its inferior aspect. A small amount of residual filling is noted at the proximal neck of the aneurysm, which may thrombose over time.
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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Medication
- Medication Summary
- Anticonvulsants, Other
- Anticonvulsants, Hydantoins
- Beta Blockers, Alpha Activity
- Beta Blockers, Beta-1 Selective
- Vasodilators
- Calcium Channel Blockers
- Angiotensin-converting Enzyme Inhibitors
- Angiotensin Receptor Blockers
- Diuretics, Thiazide
- Diuretics, Osmotic Agents
- Analgesics, Other
- Hemostatics
- Blood Components
- Antidotes, Other
- Vasopressin-Related
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