Intracerebral Hemorrhage
Author: Eric Anderson, MD, MBA, FACEP, Director of Clinical Operations, Department of Emergency Medicine, Cleveland Clinic; Faculty, Cleveland Clinic Lerner College of Medicine; Faculty, Cleveland Clinic MetroHealth Emergency Medicine Residency Program, Cleveland, OH.
Peer Reviewer: J. Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology, University of Virginia Health System, Charlottesville.
The approach to the stroke patient has changed dramatically in the past several years. In many centers that use thrombolytics for ischemic stroke, stroke is a time-sensitive disease. However, when the patient has a hemorrhagic stroke, administration of thrombolytics can be fatal. This paper reviews hemorrhagic stroke with emphasis on non-traumatic primary intracerebral hemorrhage.
Several medical centers have sought to become Certified Stroke Centers either from their states or through The Joint Commission. Many of the state programs require specific yearly CME education on the topic of stroke for the physicians in the emergency department and in the Stroke Team. This edition of EM Reports should help, at least in part, to fulfill this requirement. The Joint Commission requirements vary depending on the role of the physician. More importantly, the CME requirements of each state will vary as well.
For those of you who have yet to take the 2007 LLSA for ABEM, the topic of hemorrhagic stroke is one of the topics reviewed.
For those readers without a requirement for stroke-specific CME or LLSA, this article should provide a review of a serious type of stroke.
—Sandra M. Schneider, MD, FACEP, Editor
Epidemiology of Intracerebral Hemorrhage
Hemorrhagic stroke accounts for between 10-30% of all strokes.1,2,3 Intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke and accounts for approximately 10% of all strokes with an incidence of 7-17 per 100,000.4 In Asian countries, the percentage of hemorrhagic stroke is higher at 20-30%.1 Intracerebral hemorrhage has the highest mortality rate among all stroke types. The mortality rate for ICH is 30-50%. Data from 1997 of 37,000 Americans who experienced ICH show: 35-52% dead at 1 month (half of those deaths occurring in the first 2 days), 10% were living independently at one month, and 20% were living independently at 6 months.5 The mortality rate at seven days has remained unchanged for the past 10 years.6
The rate of ICH is higher in persons of African, Asian, and Hispanic descent than in Caucasians.1,7 It occurs more frequently in men and in the elderly. The higher incidence in African Americans is felt to be due the excess ICH in deep cerebral and brain stem locations where hypertension is a major risk factor for bleeding.8 Brain hemorrhage causes approximately 90,000 hospital admissions per year in the United States.1 This represents approximately an 18% increase over a 10-year period.9 ICH occurs with an estimated frequency of 37,000 to 52,000 each year in the United States.
Costs of ICH per person over a lifetime have been estimated to be $123,565.3,10 Overall cost of ICH in the United States is $6 billion annually.3 There are other less definable costs to society, industry, and the families.
Etiology
Primary ICH (80-85%) occurs when there is spontaneous hemorrhage from an arteriole or artery that is damaged by chronic hypertension or amyloid angiopathy. Secondary ICH (15-20%) occurs when hemorrhage occurs as the result of trauma, rupture of an aneurysm, vascular malformation, cavernous angioma or coagulopathy, neoplasm, vasculitis, ductal A-V fistula, AVM, cocaine or sympathomimetic drug exposure.3 (See Table 1.) Finally some ischemic strokes can transform into hemorrhagic strokes, either spontaneously or as a consequence of thrombolytic therapy. Such transformations generally present as a sudden deterioration in the patient's condition and are often devastating if not fatal. (See Figures 1 and 2.)
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Cigarette smoking increases the risk of ICH 2.5 times overall.11 In males smoking greater than or equal to 20 cigarettes per day the relative risk was risk was 2.06 [95% confidence interval (CI) 1.08-3.96].12 For females smoking greater than or equal to 15 cigarettes per day the risk was 2.67 [95% CI 1.04-6.9].13
Hypertension is the most common risk factor for spontaneous ICH.14 The role of hypertension and the efficacy of blood pressure control was demonstrated in the Perindopril Protection aGainst REcurrent Stroke Study (PROGRESS). PROGRESS demonstrated a 50% relative risk reduction for ICH in the group treated for hypertension vs. placebo groups after 4 years of study.15 Controlling systemic blood pressure in populations at higher risk is the most important therapy in prevention of ICH.16
In the United States, people of African, Asian and Hispanic ethnicity have a higher incidence of ICH that the white population.3,16
Amyloid angiopathy of the cerebral vasculature increases with age. It is a progressive disease of the elderly. Cerebral amyloid angiopathy (CAA) is the deposition of congophilic material in the media and adventitia of cortical and meningeal vessels, which can lead to necrosis of the vessel wall and result in hemorrhage. The resulting hemorrhage can range in size from microscopic to in excess of 100 ml.16 Due to the progressive nature of CAA, the risk of recurrent intracerebral bleed is increased in survivors of the initial bleed. Genetic predispositions to CAA are being studied since those with e2 or e4 allele of apolipoprotein E had a 2 year recurrence rate of 28% compared to 10% rate in those who did not have the e2 or e4 allele.17 Exploration of the genetic basis of CAA is important since these patients may be predisposed to the development of symptomatic ICH related to anticoagulants or thrombolytics.18
As age increases, so does the incidence of amyloid angiopathy, hypertension, diabetes, and many other conditions that may directly, or via use of therapeutic anticoagulants, contribute to increased risk of ICH. It is no wonder that the incidence of ICH increases as patients age.
Alcohol use is a known risk factor for ICH. Alcohol is believed to impair platelet function and coagulation. It is also thought that alcohol may affect the consistency of the endothelial wall in cerebral blood vessels.16
Chronic anticoagulation with warfarin has been shown to increase the risk of ICH by 2 to 4 fold.19 The antithrombotic benefits far outweigh the increased ICH risk. Risk factors for warfarin associated ICH include intensity of anticoagulation, advanced age, and prior ischemic stroke. The majority of warfarin related ICH occurs at an international normalized ration of < 3.0.20 "Although prior studies have involved warfarin, there is reason to suspect that newer generation antithrombotics such as the direct thrombin inhibitors are likely to be associated with similar risks of ICH."16
Antiplatelet medications increase the risk of ICH. Aspirin therapy was shown to increase the risk of ICH (12 events per 10,000).21 The effect did not outweigh the benefit of reducing the risk of myocardial infarction (137 per 10,000) or of ischemic stroke reduction (39 per 10,000).21 The risk of ICH was significantly increased by the combination of aspirin and clopidogrel compared with aspirin alone when given for secondary prevention of stroke or transient ischemic attack.22 Rates of ICH with other antiplatelet medications alone is less clear.16 To date, increased incidence of ICH with clopidogrel alone has not been reported.
Several authors mention drug use as a risk factor for ICH. The illicit drugs include cocaine and heroin.16 Prescription medications that have been implicated in ICH include ephedrine and phenylpropanolamine.7,16 Phenylpropanolamine has been withdrawn from the market in the United states due to concerns of the risk of hemorrhagic stroke.16
Pathophysiology
ICH preferentially occurs at certain locations that are associated with the specific underlying disease etiology. Basal ganglia and lobar bleeding are associated with hypertension and often are seen in older patients with amyloid angiopathy.7 (See Figure 3.) Hypertensive bleeding typically occurs in the basal ganglia, putamen, thalamus, or caudate nucleus.3 (See Figure 4.) Noncompliance with antihypertensive therapy increases the risk for ICH. Chronic hypertension causes degeneration, fragmentation, and fibrinoid necrosis of small penetrating arteries in the brain, which can eventually result in spontaneous rupture.23 The risk of recurrent bleeding after hypertensive ICH is as low as 2% per year when the blood pressure is well controlled.24
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The second most common source of primary ICH is cerebral amyloid angiopathy (CAA) which accounts for approximately 15% of cases.14 The clinical picture is one of spontaneous lobar hemorrhage in an elderly patient with a history of cognitive decline. The ICH caused by cerebral amyloid angiopathy is typically less severe than that caused by poorly treated hypertension.3 In some cases the lobar hemorrhages are asymptomatic. The risk of recurrence of ICH in patients with probable amyloid angiopathy is 5-15% and is most common in those with many chronic baseline hemorrhages seen on gradient echo magnetic resonance imaging (MRI).25
Early hematoma growth is common and associated with poor neurologic outcome.3,25 Even in the absence of coagulopathy, 38% of patients had an increase in hematoma volume of more than 33% shown by brain CT within 3 hours of onset.3 The location of ICH seems to have no effect on risk of hematoma enlargement.3
Exact mechanisms that affect early growth of hematoma have not yet been identified; however, there may be shear forces, distortion of normal anatomy, and peri-hematoma inflammation that may contribute to the process. Vascular engorgement, the result of impaired venous outflow, early ischemia, and breakdown of the blood brain barrier may all contribute to the process.
Increased intracranial pressure, the result of bleeding into the closed space of the skull, can result in herniation and is the primary cause of neurological deterioration after the first day.26 The number of patients with neurological deterioration is highest on the first day of the hemorrhage and decreases progressively each subsequent day.26 An inflammatory response induced by the hematoma has been identified in human studies. A hematoma that does not clot secondary to anticoagulant, antifibrinolytic, or a thrombin inhibitor causes less brain swelling and tissue injury in the adjacent brain tissue.3 Plasma that is rich in thrombin and other coagulation end products, released by the clotted hematoma, seeps into the surrounding brain tissue and is the primary trigger of the inflammatory process.3,27 Release of inflammatory mediators, leukocyte recruitment, and breakdown of the blood brain barrier are all implicated in experimental models.3
Therapies directed against early hematoma growth, cerebral edema, and inflammatory response may prove effective in decreasing the morbidity and mortality associated with ICH.
Clinical Features
Intracerebral hemorrhage patients can present with symptoms that vary from mild headache to acute coma. Patients may present with acute neurologic deficits or with migraine-like symptoms. There have been attempts to develop criteria that would accurately distinguish ischemic versus hemorrhagic brain injury as the etiology of the patient's symptoms. These grading scales lack the sensitivity or specificity to be used clinically in emergency practice where brain imaging is still used to differentiate infarct from hemorrhage in patients where thrombolytic therapy is considered.28
Historical clues may help the clinician decide on the likelihood that the patient is suffering from an ICH. The risk factors mentioned in Table 1 should increase the likelihood of ICH.
The physical examination can vary from no specific findings to new focal deficits. The patient may manifest altered mental status or present in a comatose state. The physical examination will not yield a specific diagnosis of intracerebral bleeding. The history and physical examination can lead the physician to suspect this clinical entity; however, at this stage of the emergency evaluation, the diagnosis will not be certain.
Differential Diagnosis
Diagnostic considerations include ischemia stroke syndromes, i.e., transient ischemic attack (TIA), frank ischemic stroke and reversible ischemic neurologic deficit (RIND). Intracranial bleeding conditions like epidural hematoma, subdural hematoma, subarachnoid bleeding, and bleeding around a mass should also be considered.
Infectious causes of altered mental status, headache, or focal neurologic deficits include: subdural or epidural empyema, brain abscess, meningitis, encephalitis, cerebritis, or sepsis.
Hypoglycemia may mimic intracerebral bleeding clinically, and blood glucose level should be obtained in patients who present with acute altered mental status or new focal neurologic deficits.
Intoxication with illicit drugs or therapeutic medications may result in headache and alteration of mental status. The symptoms may also occur as a result of a reaction to the medication. Watch for toxidromes that may present with alteration of mental status and seizures. Patients with sympathomimetic, cholinergic, anticholinergic, or serotonin syndrome may present with alteration of mental status and seizures.29 Alcohol intoxication or withdrawal syndrome may present with similar findings. Keep in mind that alcohol use is a risk factor for ICH.7,16 Behavioral characteristics of an intoxicated person put them at risk for trauma, which may not be obvious on initial evaluation and may not be obtained from the history.
Underlying neurologic conditions such as seizures or the post-ictal state should be considered. Patients with a bad migraine headache or with a migraine variant may present a diagnostic dilemma; however, imaging will help in these patients.
Marked dehydration, hypernatremia, or hyponatremia may manifest with altered mental status.
Psychiatric conditions, catatonia, or psychosis may present as change in mental status. Malingering should also be considered, but it is a diagnosis of exclusion.
Trauma, of course, should be considered, especially when a history is not readily available. (See Table 2 for differential diagnosis of ICH.)
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Diagnostics
The diagnostic approach to these patients takes place after resuscitation airway, breathing, and circulation (ABCs) have been addressed. (See emergency management below.) Measure blood glucose rapidly at the bedside and order blood chemistries and initial plain x-rays as determined by the clinical circumstances. History should include known trauma, fever, bleeding diathesis, and anticoagulant or anti-platelet or use. Physical examination, after ABCs, should include a head and neck examination, a neurological examination to assess for focal deficits in addition to the usual general physical examination. Check for unusual bruising or hematomas on the dermal examination.
The question of which imaging modality is most efficacious is often raised. Head computed tomography (CT) has been used in the emergency department as the imaging modality of choice because of speed, proximity to emergency departments, and efficacy at identifying fresh bleeding. CT has been used in the main published trials since it remains easier to use and to interpret when facing the possibility of an acute hemorrhage.30 (See Figures 5 and 6.) An MRI study indicated that T2* images can detect micro-bleeds indicative of potential hemorrhage.31 There is conflicting data on the significance of microbleeds and hemorrhagic transformation.32 Considering the time constraints of thrombolytic protocols, head CT will remain the initial emergency imaging modality for patients with acute focal neurologic deficits in the near future.
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There has been much progress made with MR imaging in acute strokes. Echo planar scanners are capable of scanning the entire brain in less than a second.33 Diffusion weighted MR imaging is increasing its sensitivity in detecting acute ischemic strokes.30
MRI is the optimal technique to demonstrate low flow vascular malformations (cavernomas), hemorrhagic tumors, and other vascular pathologies. (See Figures 7 and 8.) CT angiography (CTA) and magnetic resonance angiography (MRA) are the methods of choice to demonstrate dural sinus thrombosis.7 Digital subtraction angiography (DSA) may be used when the ICH is large and may change the hemodynamics of arterio-venous malformations (AVM) to an extent that the malformation cannot be seen on CTA or MRA.7 DSA can be electively performed in consultation with a neuroradiologist.
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Emergency Medical Treatment
Initial assessment of ABCs is important in these patients who present to the emergency department with possible intracranial hemorrhage. Approximately 30% of patients with supratentorial ICH and almost all patients with infratentorial ICH with a decreased level of consciousness require intubation.34 Delays in initially managing the airway may lead to injury secondary to hypoxia, hypercapnia, and aspiration. There are many intubation cocktails and preferred methods of rapid sequence intubation. One of the possible medication sequences includes premedicate with lidocaine 1.0 to 1.5 mg/kg, sedative barbiturate (thiopental 3-5 mg/kg IV is the induction dose; 50-100 mg is the maintenance dose), paralytics nondepolarizing agents: vecuronium 0.1 to 0.25 mg/kg or rocuronium 0.6 to 1.2 mg/kg. Use of nondepolarizing neuromuscular blockade will help to decrease the effect of transient elevated intracranial pressure during the intubation process. After intubation, if the patient's other medical problems permit, the head of the patient's bed should be elevated 30 degrees to help decrease intracranial pressure and reduce the risk of ventilator associated pneumonia.3 The patient should be ventilated to maintain a pCO2 of 28-32 mm Hg.3 The exact level of ventilation (pCO2 level) has been debated and some authors recommend that the pCO2 should be 30-35 mmHg.7
Mannitol may be used to rapidly lower intracranial pressure. This effect is seen within 20 minutes of an intravenous bolus.7 There is some controversy in the use of mannitol: "the benefit of mannitol in deep ganglionic hemorrhage is not known."35 Mannitol (20%) is administered at a dose of 0.75 to 1.0 g/kg IV bolus followed by a dose of 0.25 to 0.5 g/kg every 3-6 hours, depending on the neurologic status, fluid status, and serum osmolality.7 Osmolality will increase with subsequent doses of mannitol and osmolality should be maintained between 300 and 320 mosm/l.7 Complications of mannitol therapy include renal failure and electrolyte disturbances.7
Blood pressure (BP) elevations are common after ICH. Hypertension should be controlled. Patients with a known history of chronic hypertension presenting with systolic BP > 180 mmHg and/or diastolic BP > 105 mm Hg should have a target BP of approximately 170/100 or a mean arterial pressure (MAP) of 125 mmHg.7 In patients without known hypertension who arrive with BP >160 systolic and > 95 diastolic, treat to target blood pressure of 150/90, MAP 110.7 The INTERACT trial demonstrated that early intensive lowering of blood pressure (to systolic of 140 mmHg within 1 hour) resulted in reduced subsequent growth of the hematoma.36 This pilot trial of 203 intensively treated patients and 201 standard therapy patients (target systolic BP 180 mm Hg) needs to be validated by a large randomized trial with outcomes data. Coordination of treatment strategy with the admitting physician is essential.
Pharmacologic agents used to treat hypertension in patients with ICH include adrenergic inhibitors, vasodilators and diuretics. Labetalol has alpha-1, beta-1, and beta-2 receptor antagonist activity. The dose of labetalol is 20-80 mg bolus every 10 minutes up to 300 mg. Labetalol infusion rate is 0.5-2.0 mg/min. Onset of action is 2-6 minutes, and the duration of action is 2-6 hours. Side effects of labetalol include hypotension, bradycardia, congestive heart failure, and bronchospasm. Labetalol is contraindicated in acute decompensated heart failure. Esmolol is a beta-1 receptor antagonist. The dose of esmolol is 250 to 500 mcg/kg/min x 1 min. followed by an infusion of 50-200 mcg/kg/min. If the blood pressure response to a given esmolol rate is insufficient, then the patient needs to be rebolused prior to starting the new higher infusion rate.37,38 The onset of action of esmolol is one to two minutes, and the duration of action is 10-30 minutes. Side effects of esmolol are: hypotension, bradycardia, congestive heart failure, and bronchospasm. Contraindications for esmolol include bradycardia, AV block, acute decompensated heart failure, and bronchospasm.7
Vasodilators include nicardipine, an L-type calcium channel blocker (dihydropyridine); enalaprilat, an angiotensin-converting enzyme inhibitor; and hydralazine. The nicardipine dose is 5-15 mg/hr infusion. The onset of action is 5-10 minutes, and duration of action is 0.5 to 4 hours. The side effect of nicardipine is hypotension. Contraindications for nicardipine are severe aortic stenosis and myocardial ischemia.3 Enalaprilat's dose is 0.625 mg IV bolus then 1.25 to 5 mg IV every 6 hours. Enalaprilat's onset of action is 5-10 minutes and duration of action is 2-6 hours. Hypotensive responsive may be dramatic in high rennin states.3
Hydralazine is a direct arterial vasodilator whose dose is 10-20 mg bolus. The onset of action is 10-20 minutes and duration of action is 1 to 4 hours. Side effects include elevated heart rate in response to vasodilation.
Nitroprusside is a direct vasodilator, arterial and venous. The initial dosage is 0.25 mcg/kg/min infusion that can be titrated to the desired blood pressure response. Nitroprusside's onset of action is within seconds of initiation of infusion. The duration of action is 2-5 minutes. Side effects include thiocyanate and cyanide toxicity when used for days at a time. Contraindications include elevated intracranial pressure.3
Seizures occur more commonly in lobar ICH.3 Thirty-day risk of clinically evident seizures is approximately 8%.34 Status epilepticus may be seen in 1-2% of patients with development of subsequent epilepsy in 5-20%.39 A prospective study, using continuous electroencephalography (EEG) monitoring, showed nonconvulsive seizures or status epilepticus in 28% of comatose or obtunded patients with ICH and in 6% of patients with ischemic strokes.40 Bedside EEG may help determine if status epilepticus is causing the coma. Some physicians debate the clinical significance of this since many of these patients are paralyzed and intubated anyway. Treat acute seizures initially with lorazepam 0.05 to 0.1 mg/kg IV. Treatment with fosphenytoin 15-20 mg/kg PE IV or phenytoin 15-20 mg/kg IV (infuse phenytoin no faster than 50 mg/min) should be initiated for maintenance or persistent seizures. If seizures persist, phenobarbital 15-20 mg/kg IV may be used. Valproic acid 15-45 mg/kg is another alternative.3
Patients with ICH may benefit from prophylactic antiepileptic therapy; however, no randomized trial has addressed the efficacy of this approach.3 Some centers prophylactically treat patients with large supratentorial hemorrhages and low consciousness during the first week, based on evidence that this practice reduces the frequency of seizures from 14% to 4% during the first 7 days after severe traumatic brain injury.41 In 1999 the American Heart Association guidelines recommended antiepileptic treatment in selected patients for up to 1 month after which therapy should be discontinued if there were no seizures.5 There was an observational study that found a low frequency of seizures in patients with lobar ICH given prophylactic antiepileptic drug therapy.39
Early surgical hematoma evacuation of intracerebral hemorrhage was not found to be effective in a large randomized clinical trial (STICH).42 Early neurosurgical evaluation is still needed in these patients since an urgent ventriculostomy may be needed to help relieve increased intracranial pressure. Neurosurgical intervention may be needed to treat associated subdural hematoma.
Approximately 30% of ICH occurs in patients on antithrombotic medication.43 Certain medications may ameliorate the effects of these medications. Hematoma size and oral anticoagulant use have been associated with decreased survival from ICH. (See Table 4.) Compared with traumatic ICH, spontaneous ICH was associated with a higher mortality rate both-in hospital (32%) and at 3 month follow-up (53%).43 The Antiplatelet group's death rate went from 42% deaths in-hospital to 62% deaths at 3 month follow-up (a 77% relative increase). The oral anticoagulant group's death rate went from 42% deaths in-hospital to 64.1% deaths at 3 month follow-up (a 51% relative increase).43 Other factors known to increase the risk of death in ICH patients are listed in Table 4.
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ICH in patients treated with heparin is related to the level of anticoagulation induced by the heparin. Protamine sulfate inactivates heparin. Protamine sulfate is used at a dose of 1 mg per every 100 units of heparin.16 Possible adverse reactions to protamine sulfate include bronchospasm, anaphylaxis, angioedema, bradycardia, hypotension, paradoxical hemorrhage, and heparin rebound. Fresh frozen plasma contains antithrombin III that may be bound by circulating heparin molecules and prolong the anticoagulation status of the patient. Therefore, the use of fresh frozen plasma in reversing the action of heparin is contraindicated.16
Vitamin K is used to reverse the effects of warfarin. Vitamin K can be administered orally, subcutaneously, or IV. The IV route of administration provides a rapid, reliable, and more efficacious reversal of anticoagulation than the oral or subcutaneous route.15 Vitamin K's dose is 1-2 mg IV or subcutaneously. Possible serious side effects of vitamin K include anaphylaxis and shock. Cardiac or respiratory arrest can occur in patients with first-time vitamin K exposure. Dilute injection and avoid rapid infusion. Restrict IV infusion to cases where the risk is justified.
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Fresh frozen plasma can be used to reverse the effects of warfarin. The dose is 5 to 10 cc per kg. Complications of fresh frozen plasma include transfusion reactions and can lead to pulmonary edema.16
"There are no proven therapies that are used for patients with ICH in the setting of oral antiplatelet agents; however, in those with documented platelet dysfunction, there is a potential role for the transfusion of platelets and use of desmopressin acetate."16 Use of platelets is of questionable efficacy and carries risks of blood product transfusion complications.
Desmopressin (DDAVP) dose 0.3 mcg/kg IV should be used only for documented platelet dysfunction, i.e., mild to moderate von Willebrand's disease (type1) or Hemophilia A (factor VIII deficiency). Use of DDAVP can lead to a decrease in osmolality, which may result in seizures or coma.16
Recombinant factor VIIa (rFVIIa) promotes hemostasis at sites of vascular injury where tissue factor is expressed and activated platelets are found. It promotes localized thrombin generation and fibrin clot formation and is currently approved for hemophilia patients with inhibitors to factors VIII or IX.44 In Europe, rFVIIa is also licensed for use in patients with acquired hemophilia, FVII deficiency, and Glanzmann's thrombasthenia.45 Various treatment regimes of rFVIIa have been used to treat ICH and results are promising. Dosage has varied from 5 mcg per kg to 80 mcg per kg. Complications of treatment include pulmonary embolism, myocardial ischemia, deep venous thrombosis, and cerebral ischemia.45 The FAST trial did not show benefit of rFVIIa. The FAST trial was a phase 3 study that assessed the efficacy of rFVIIa in decreasing the primary endpoints of mortality and severe disability at 90 days. There was no difference in the two trial rFVIIa regimes and placebo in those primary endpoints.46 Further study is needed to determine the appropriate dosage regime and appropriate use in emergency patients since rFVIIa showed significant complications and side effects in the FAST trial.
Disposition
Consultation should be sought with neurosurgery or neurology, as dictated by local practice patterns, during the emergency department evaluation and stabilization of the ICH patient. Serial head CTs may be requested to evaluate for early hematoma expansion and to assess the effectiveness of treatment. These patients require admission, preferably to a neurointensive care unit, since these patients generally have better outcomes when treated in a neuro-specialty unit.3,7
Summary
Intracranial hemorrhage is the most lethal of the stroke syndromes. It carries a mortality rate of 30-50%. The rate of hematoma expansion within the first three hours of symptom onset is 38%.3 Modifiable risk factors for ICH include hypertension, cigarette smoking, alcohol consumption, and illicit drug use. Other risk factors include advanced age, amyloid angiopathy, race, and AVM. Emergency medical care should include medical stabilization, neuro-imaging, and assessment for ICH risk factors and possible trauma. Prompt attention should be given to the airway, blood pressure control, and coagulation status. Early neurosurgical or neurology consultation and admission of these patients to a neurointensive care unit, if available, will provide the best possible outcomes.
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