Hemorrhagic cerebrovascular disease includes nontraumatic bleeding that occurs primarily in the brain (intracerebral hemorrhage [ICH]), the ventricles (intraventricular hemorrhage [IVH]), the subarachnoid space (subarachnoid hemorrhage [SAH]), or the subdural space (subdural hematoma [SDH]). Bleeding often simultaneously involves the brain, the ventricles, and the subarachnoid space.
Nontraumatic intracranial hemorrhage (hemorrhagic stroke/cerebral hemorrhage) annually occurs in approximately 75,000 Americans. The 1-month mortality of intracranial hemorrhage is approximately 35% to 50%; most of the deaths happen within the first 24 to 48 hours of the illness. Approximately 10% of patients do not survive long enough to reach a hospital or they die shortly after arriving in an emergency department. Mortality is highest among persons older than 60, those with secondary intraventricular bleeding, and those with severe neurologic impairments (in particular, coma). Only 20% of survivors of intracranial hemorrhages achieve functional independence.
Although the incidence of stroke, including hypertensive hemorrhage, has declined, the rate of SAH, largely due to ruptured intracranial aneurysms, remains stable. The frequency of hemorrhagic stroke may increase in the future as the result of the aging of the American population, an increase in the prevalence of cerebral amyloid angiopathy, increased abuse of drugs that cause hypertensive crises, and the widespread prescription of medications that affect coagulation. Although the chances of hemorrhagic stroke increases with advancing age, intracranial bleeding also occurs in children and young adults. Because ischemic strokes are relatively uncommon among children, adolescents, and persons younger than 45, the relative proportion of hemorrhagic strokes is very prominent in these age groups. The patient’s age also affects the diagnosis of the cause of intracranial hemorrhage. For example, cerebral amyloid angiopathy and hypertension are important causes of bleeding among the elderly, whereas the average age of patient with a ruptured CNS vascular malformation is approximately 30 years. Even when trauma is excluded, hemorrhagic stroke is more frequent among men than among women. The incidence of hemorrhagic stroke is higher among Americans of African or Asian heritage than among those with European ancestry. Intracranial hemorrhage is an especially important cause of death among young African Americans.
I. CAUSES OF HEMORRHAGIC STROKE
Intracranial hemorrhages are secondary to a large variety of diseases (Table 37.1). In most cases, the most likely cause of bleeding can be identified.
A. Occult craniocerebral trauma. Trauma is a potential cause of intracranial bleeding—typical SDH or epidural hematomas or parenchymal contusions. A history of injury may be lacking when a patient is found unconscious and other clues must be sought, such as lacerations or soft-tissue swelling. Conversely, a patient with a primary hemorrhage may suffer secondary trauma.
B. Arterial hypertension. Either acute or chronic arterial hypertension may be a cause of ICH. Chronic hypertension leads to degenerative changes in small penetrating arteries in the deep structures of the brain. Sudden, severe hypertension may overwhelm the autoregulatory responses of the cerebral vasculature and an arteriole may rupture. Acute and severe arterial hypertension may be secondary to acute glomerulonephritis, eclampsia, severe emotional stress, or the use of a sympathomimetic agent. The most common sites for hypertensive ICH are the basal ganglia (putamen), thalamus, brainstem, cerebellum, or lobar white matter. Hypertension should be considered as the likely cause of a hematoma located in deep gray matter structures of the cerebral hemisphere if a patient has a history of hypertension. Other features of chronic hypertension, such as retinopathy, renal dysfunction, or left ventricular hypertrophy, support the diagnosis. Even though hemorrhagic stroke often is attributed to hypertension because of the presence of an elevated blood pressure measured upon arrival to an emergency department, arterial hypertension is common among acutely ill patients with intracranial hemorrhage, and the finding should not automatically lead to the diagnosis of hypertensive hemorrhage.
TABLE 37.1 Causes of Hemorrhagic Stroke
Occult craniocerebral trauma
Aneurysms
Saccular (berry) aneurysm
Nonsaccular aneurysm
Infective
Neoplastic
Traumatic
Dolichoectatic
Dissection
Vascular malformations
AVM
Cavernous malformation
Developmental venous anomaly
Telangiectasia
Arterial hypertension
Chronic hypertension (Charcot–Bouchard’s aneurysm)
Acute hypertension
Eclampsia
Stress-related
Postoperative hyperperfusion syndrome
Moyamoya disease/syndrome
Drug abuse
Amphetamine/methamphetamine
Cocaine
Tumors
Primary
Metastatic
Cerebral amyloid angiopathy
Vasculitis
Multisystem necrotizing vasculitis
Isolated CNS vasculitis
Bleeding disorders
Hemophilia
Sickle cell disease
Thrombocytopenia
Leukemia
Thrombolytic agents
Antithrombotic agents
Venous thrombosis
Hemorrhagic transformation of ischemic stroke
C. Saccular aneurysm. Rupture of a saccular aneurysm is the most common cause of nontraumatic SAH and it is an important cause of ICH. Approximately 1% to 5% of adults harbor intracranial aneurysms, but a minority of these lesions actually rupture. In general, the risk of rupture is correlated with the size of the aneurysm, with the highest risk found with aneurysms larger than 6 to 8 mm in diameter. Patients with autosomal dominant polycystic kidney disease have a high prevalence of intracranial aneurysms. Approximately 10% of patients have a family history of cerebral aneurysms. Approximately 85% of saccular aneurysms are in the carotid circulation with the most common sites being the junction of the internal carotid artery—posterior communicating artery, the bifurcation of the middle cerebral artery, and the anterior communicating artery. The most common locations in the posterior circulation are the bifurcation of the basilar artery and the origin of the posterior inferior cerebellar artery.
D. Other aneurysms. Infective, neoplastic, and traumatic aneurysms are rare causes of intracranial hemorrhage. These lesions usually are located in peripheral branch pial arteries on the cortical surface of the cerebral hemispheres. They usually are smaller than saccular aneurysms, but they have a relatively high risk of hemorrhage. Dolichoectatic (fusiform) aneurysms are tortuous, elongated arterial enlargements most commonly found in the basilar arteries of patients with extensive atherosclerosis or young men with Fabry’s disease. Hemorrhage is an uncommon complication. Spontaneous or traumatic dissecting aneurysms of intracranial arteries, particularly of the basilar or distal vertebral arteries, are potential causes of atypical SAH.
E. Vascular malformations. Vascular malformations are classified as arteriovenous malformation (AVM), developmental venous anomaly, cavernous malformation, and telangiectasias. They may be located in any part of the brain. Although familial cases, as with hereditary hemorrhagic telangiectasia or familial cavernous malformations, may occur, most are sporadic. The prevalence of vascular malformations is less than that of saccular aneurysms, and most affected persons never have hemorrhage. ICH is the presenting symptoms in approximately 50% of cases. Non-hemorrhagic symptoms include seizures, recurrent and stereotypic headache, or progressive neurologic impairments. Patients with large AVM leading to turbulent blood flow may have pulsatile tinnitus and a cranial bruit may be auscultated.
F. Cerebral amyloid angiopathy. It (congophilic angiopathy) is a leading cause of lobar ICH in the elderly. With aging, amyloid is deposited in the walls of cortical and leptomeningeal arterioles. Presumably, the protein accumulation leads to vascular fragility and bleeding. The hemorrhages, which are most commonly located in the frontal and parietal lobes, usually arise at the junction of the white matter and cerebral cortex. Multiple or recurrent hemorrhages are common. Cerebellar hemorrhages may also develop. Amyloid angiopathy should be considered as the likely cause of lobar ICH among persons older than 75. Because approximately 70% of affected patients also have a history of Alzheimer’s disease, a past history of dementia or cognitive decline increases the likelihood that an ICH in an elderly patient is due to amyloid angiopathy.
G. Vasculitis. Multisystem or isolated CNS vasculitis is a rare cause of intracranial hemorrhage. Bleeding is most often associated with a necrotizing vasculitis, such as polyarteritis nodosa. Vasculitis may be the cause of bleeding among some young patients who have hemorrhagic stroke after the use of a sympathomimetic drug.
H. Bleeding disorders. Intracranial hemorrhage may complicate several inherited or acquired bleeding diatheses, including hemophilia, sickle cell disease, thrombocytopenia, or leukemia. It may also complicate the use of thrombolytic or antithrombotic agents. In general, the severity of bleeding is worse, and the prognosis is poorer among patients with bleeding secondary to a coagulation disorder than among persons with spontaneous hemorrhages. Intracranial bleeding is a side effect of treatment for oral anticoagulants or thrombin inhibitors, and this complication should be considered whenever a patient has acute neurologic symptoms while taking oral anticoagulants even if there is no other evidence of bleeding. The risk of ICH is especially high among the elderly and persons who have leukoaraiosis present on brain imaging studies. Persons with a past history of stroke or poorly controlled hypertension also have a high risk of bleeding secondary to oral anticoagulants. The risk of intracranial bleeding increases when the international normalized ratio (INR) exceeds 3 to 4. The frequency of hemorrhagic stroke is lower with antiplatelet agents than with oral anticoagulants. The combination of aspirin and clopidogrel is more likely to be associated with bleeding than the use of either medication alone especially among persons with a history of stroke. The combination of warfarin and aspirin has a higher risk of bleeding than the administration of either agent alone.
I. Drug abuse. Intracranial hemorrhage has been attributed to the abuse of medications such as cocaine or methamphetamine. These agents may lead to bleeding because of sudden increases in blood pressure or because of the development of a vasculitis. Intracranial hemorrhage has also been associated with heavy alcohol use.
J. Moyamoya disease is an uncommon cause of hemorrhagic stroke among young adults and children. The arteriographic hallmark of moyamoya is occlusions of the major arteries of the anterior circulation and the appearance of a mesh of fine blood vessels at the base of the brain. Moyamoya disease is inherited on an autosomal dominant basis and is most common among persons of northeastern Asia. It is also diagnosed when the arteriographic findings occur among patients with a number of acquired disorders. Hemorrhages may be secondary to rupture of an aneurysm (most commonly in the posterior circulation) or rupture of small collateral channels.
K. Venous thrombosis. Occlusion of a cortical vein (cortical venous thrombosis) or sinus (sinus thrombosis) is an uncommon etiology of hemorrhagic stroke. Bleeding is most common among patients with thrombosis of the superior sagittal sinus; in this situation, the areas of hemorrhage are parasagittal in location bilaterally and in a thumbprint pattern. The clinical course of venous thrombosis differs from that of most other hemorrhagic strokes. Most patients have worsening headaches, seizures, altered consciousness, and focal neurologic signs that evolve over a few days. Venous thrombosis often develops in the peripartum period, but it also occurs among persons who are dehydrated, have malignant disease, have undergone a recent cranial operation, or have an otolaryngologic infection.
L. Brain tumors. Hemorrhage may be the initial symptom of a highly vascular primary or metastatic brain tumor, including choriocarcinoma, melanoma, or carcinoma of the kidney, thyroid, liver, lung, or breast. The most common primary tumors are glioblastoma or pilocytic astrocytoma. Patients may have a history of evolving neurologic symptoms such as headache or personality changes before the bleeding event. The presence of extensive brain edema in the first hours after hemorrhages or multiple hemorrhagic lesions should prompt consideration of an underlying brain tumor.
M. Hemorrhagic transformation of an ischemic stroke. Modern brain imaging allows discovery of asymptomatic hemorrhagic changes in the ischemic lesion in a sizable proportion of patients with a recent stroke. A smaller percentage of patients have neurologic worsening secondary to hemorrhagic transformation of the infarction. The risk of this complication is increased with the use of a thrombolytic within the first hours after stroke.
II. MANIFESTATIONS OF HEMORRHAGIC STROKE
The clinical features of hemorrhagic stroke are similar in both adults and children. The symptoms and signs of IVH and SAH may differ from those of ICH in that focal neurologic impairments usually are absent or subtle. Because of the absence of focal neurologic signs, errors in diagnosis are more likely to occur among patients with SAH than among patients with bleeding primarily in the brain.
A. History.
1. Hemorrhagic stroke usually is a sudden, dramatic event. The patient or observers often relate the circumstances surrounding the onset of symptoms. A headache, of any quality and location, usually is described as intense and often is described as the “worst headache of my life.” A headache accompanied by a transient loss of consciousness or one that is of cataclysmic onset is a premier symptom of SAH. Approximately 40% of patients with ICH will complain of severe headache. Other symptoms include nausea, vomiting, prostration, photophobia, phonophobia, and nuchal rigidity. The presence of nausea and vomiting and focal signs suggestive of a stroke in a cerebral hemisphere is predictive of a hemorrhagic event.
2. Disturbances in consciousness are common. Prolonged unresponsiveness (coma) occurs among patients with major hemorrhages. Transient alteration in alertness at the time of bleeding (syncope) may also happen. Disorientation, confusion, or delirium may also occur. Although focal or generalized seizures may develop, recurrent seizures or status epilepticus are uncommon.
3. Focal neurologic signs reflect the location of the hematoma. The most common pattern is a contralateral hemiparesis and hemisensory loss secondary to a hematoma in the basal ganglia. Patients with cerebellar hemorrhage often have a subacute course. They report headache, dizziness (vertigo), disturbed balance, nausea, and vomiting. Signs of increased intracranial pressure (ICP) or brainstem compression subsequently appear, including cranial nerve palsy, motor impairment, and disturbed consciousness. Although most patients with SAH or primary IVH do not have focal neurologic signs, some patients with aneurysms will have focal findings. The most common is a third nerve palsy secondary to a ruptured posterior communicating artery aneurysm.
B. Examination.
1. General examination. Assessment of the vital signs and the airway, breathing, and circulation (ABCs) of emergency care are the first steps of the examination (Table 37.2). Vital signs are measured frequently, and close neurologic monitoring is required. The airway should be secured for patients with impaired consciousness, seizures, vomiting, or bulbar dysfunction. Patients with severe hemorrhage often have respiratory abnormalities that lead to hypoxia, hypercapnia, or acidosis. Fever is relatively common, and it is especially prominent among patients with IVH. Electrocardiographic abnormalities and cardiac arrhythmias may also be detected. Most patients have elevated blood pressures.
Detection of a bruit over the head or neck suggests an AVM. Multiple areas of ecchymosis or petechiae point to infective endocarditis, recent trauma, or an underlying coagulation disorder. Evidence of cervical spine, facial or cranial injury, such as a Battle’s sign (basilar skull fracture) should be sought. Neck pain or tenderness may represent an associated spine fracture in a patient with craniocerebral trauma and hemorrhage. The neck should not be flexed to check for signs of meningeal irritation until the possibility of cervical spine fracture is excluded.
TABLE 37.2 Examination of a Patient with Suspected Intracranial Hemorrhage
Vital signs
Airway
Breathing and respiratory pattern
Heart rate and rhythm
Temperature
Blood pressure
Cardiovascular examination
Screening for bleeding elsewhere
Petechiae
Ecchymosis
Signs of craniocerebral trauma
Battle sign
Raccoon eyes
Ocular hemorrhage
Scalp laceration
Signs of meningeal irritation
Brudzinski sign
Kernig sign
Ocular signs
Subhyaloid, retinal or conjunctival hemorrhage
Papilledema
Level of consciousness
Glasgow Coma Scale
Other neurologic signs
Cognition and language
Articulation
Motor
Sensory
Cranial nerves
Cerebellar
Meningeal irritation is caused by blood in the subarachnoid space. Nuchal rigidity (Brudzinski’s sign) may not be present in patients with a hematoma restricted to the parenchyma or in comatose patients. A stiff neck is prominent among most patients with SAH, but this sign may take several hours to appear. Ocular hemorrhages (subhyaloid, conjunctival, or retinal) may be detected in approximately 20% of patients; their presence is highly specific for serious hemorrhages. Because the course of the illness usually is short, papilledema is not commonly observed in the first hours of the illness.
2. Assessment of consciousness is the most important component of the neurologic examination because the level of consciousness correlates strongly with the severity of the hemorrhage and prognosis. Although the easily calculated Glasgow Coma Scale score was originally developed to assess patients with head injuries, it is directly applicable to persons with nontraumatic brain hemorrhages. In general, a score of eight or less on the Glasgow Coma Scale correlates with a very poor prognosis.
3. The rest of the neurologic examination is aimed at detecting abnormalities that reflect the location of a hemorrhage within the brain. Depending upon the location of the hemorrhage, motor, sensory, language, or cranial nerve impairments are found.
III. DIFFERENTIAL DIAGNOSIS OF HEMORRHAGIC STROKE
The differential diagnosis is not extensive. The brief duration, clinical severity, and prominent focal neurologic signs are relatively specific.
A. Ischemic stroke. The leading alternative diagnosis is acute ischemic stroke. Although there are no unique features, patients with hemorrhagic stroke generally are more seriously ill than those with ischemic stroke. The symptoms usually are more severe than those that can follow occlusion of a single artery, as in ischemic stroke. Headaches, early depression in consciousness, nausea, vomiting, photophobia, and phonophobia are also more prominent in hemorrhagic stroke.
B. Craniocerebral trauma. Differentiation of trauma from spontaneous bleeding can be difficult when a patient is comatose and no history is available. In general, hemorrhages deep in the brain are not the result of trauma. Conversely, multiple small cortical petechial hemorrhages in the frontal, temporal, and occipital poles usually are secondary to injuries.
C. SAH. In contradistinction to that of ICH, the differential diagnosis of SAH is broad (Table 37.3). Although patients with SAH usually seek medical attention because of the severity of their symptoms, physicians may be misled. The diagnosis of SAH is missed in approximately 15% of cases, most commonly among the least seriously ill patients. Failure to recognize a ruptured aneurysm has serious implications because of the risk of a potentially fatal recurrent hemorrhage and because of the availability of effective therapies that can be administered early. The only way to avoid missing an SAH is to maintain a high index of suspicion. Patients who have the sudden onset of an exceptionally severe headache or a headache associated with loss of consciousness should be evaluated for SAH. The absence of focal neurologic signs or meningeal irritation does not preclude the diagnosis. Atypical symptoms include severe neck, face, shoulder, eye, or ear pain. A ruptured aneurysm in the posterior fossa may produce neck or back pain as a primary symptom.
TABLE 37.3 Differential Diagnosis of SAH
|
Migraine headache |
Tension headache |
|
Sinusitis |
Viral meningitis |
|
Influenza |
Hypertensive crisis |
|
Eclampsia |
Head injury |
|
Cervical spine injury |
Cervical herniated disk |
|
Alcohol intoxication |
Drug intoxication |
IV. DIAGNOSTIC STUDIES
The goals of the emergency evaluation are to confirm hemorrhage as the cause of the neurologic symptoms and to look for acute complications (Table 37.4). These critically ill persons are at high risk for a variety of serious neurologic or medical complications; the most frequent are brain edema, hydrocephalus, increased ICP, and seizures. Medical complications include myocardial ischemia, cardiac arrhythmias, gastrointestinal bleeding, respiratory abnormalities, and fluid and electrolyte disturbances. Before they are moved, obtunded patients with possible craniocerebral trauma should have imaging of the cervical spine to eliminate an occult fracture.
A. CT of the brain. This is the single most important diagnostic test because it is available at most hospitals, relatively inexpensive, noninvasive, and easy to perform. The yield of unenhanced CT is extraordinarily high. When CT is performed within 24 hours of onset, blood density can be detected in almost 100% of patients with ICH and approximately 95% of those with SAH. The presence of a “spot sign” on an early, contrast enhanced CT study/computed tomographic angiography (CTA) predicts those cases that may have enlargement of the hematoma. Sequential CT studies obtained during the first hours after the ictus often shows enlargement of a hematoma presumably as a result of continued bleeding. CT may miss a small collection of subarachnoid blood in a patient with a mild hemorrhage or if the bleeding is restricted to the posterior fossa. If CT is performed several days after the ictus, the yield of the test in detecting SAH decreases because the blood may be been reabsorbed. The location and pattern of blood also predicts the underlying pathology or the site of a ruptured aneurysm. The presence of subarachnoid blood restricted to the perimesencephalic cisterns usually is not due to an aneurysm. CT also detects early complications including brain edema and hydrocephalus. CT provided prognostic information, for example, large amounts of subarachnoid blood are predictive of vasospasm and ischemic stroke after SAH. The presence of IVH complicating either ICH or SAH also forecasts a poor prognosis. Contrast-enhanced CT may detect an AVM or aneurysm. CTA is a valuable method to image the vasculature at the base of the brain and, in particular, to examine the anatomic relations of saccular aneurysms. Because CTA can show three-dimensional images of an AVM, it may be used to help planning for interventions.
TABLE 37.4 Diagnostic Studies of Patients with Hemorrhagic Stroke
Initial emergency studies
CT of the brain
Cervical spine films (if a neck injury is possible)
ECG
Pulse oximetry
CBC and platelet count
Partial thromboplastin time
Prothrombin time (INR)
Serum electrolytes
Blood glucose
CSF examination (if SAH suspected and CT is negative)
Subsequent emergency studies
CTA
MRI of the brain and MRA
Arteriography
Additional studies
Transcranial Doppler ultrasonography
Blood cultures (if infective endocarditis suspected)
Fibrinogen
Sickle cell screen
Erythrocyte sedimentation rate
C-reactive protein
Urine and blood screens for illicit drugs
Brain and meningeal biopsy
B. MRI. This test depicts intracranial bleeding and provides additional data about the likely cause of hemorrhage. Multisequence MRI may be as sensitive as CT in the detection of intracranial bleeding. Although it is more expensive and not as widely available as CT, MRI does have advantages. Because of the changes in the responses of iron in the hematomas of different ages, MRI provides information about the age of the hemorrhagic lesion. A gradient echo sequence is very useful in detecting microhemorrhages, which are a hallmark of amyloid angiopathy. Abnormal flow voids can be found with vascular malformations. Magnetic resonance angiography (MRA) can also be performed to detect aneurysms or vascular malformations.
C. CSF examination. The frequency of examination of the CSF has declined with the advent of brain imaging. If CT shows a hemorrhage, there is little reason to do a lumbar puncture (LP) to search for blood. Conversely, CSF examination is important if SAH is suspected and CT does not show blood. CSF examination may help detect bleeding among alert patients who have mild signs. The risk of neurologic complications, including herniation, is low in an alert patient who does not have focal impairments and no mass found on CT. Determining whether the source of bloody CSF is an intracranial hemorrhage or a traumatic LP (bloody tap) can be difficult. Bloody CSF from SAH generally does not clear in sequentially collected tubes. Xanthochromia (yellowing) of the CSF supernatant after centrifugation is the most reliable sign, but it can take up to 12 hours after SAH to appear. A physician should immediately centrifuge a bloody CSF specimen to check for xanthochromia because a delay of several hours may give a false-positive result. The CSF findings evolve over time, and if the LP is delayed several days, only slightly yellow fluid, an elevated CSF protein level, or an inflammatory response that mimics viral meningitis may be detected.
D. Arteriography. The role of arteriography has declined with advances in the use of MRA and CTA to detect vascular malformations and aneurysms. It usually is not needed for evaluation of older patients with a history of hypertension and a hemorrhage in the basal ganglia or thalamus. It may be useful in detecting small aneurysms or vasculitis. It may also be used to detect vasospasm following SAH. A relatively common scenario for arteriography is its performance as a preliminary step for endovascular treatment for the source of bleeding or before treatment for vasospasm.
E. Other diagnostic studies. Patients should have an electrocardiography and hematologic, coagulation, and biochemistry studies as part of their evaluation. These tests are done to screen for medical complications and to search for a cause of hemorrhage.
V. TREATMENT
A. Prevention. Prevention is the most cost-effective strategy for treatment of patients at a high risk for hemorrhagic stroke. Administration of antihypertensive agents to patients with either acute or chronic sustained elevations of blood pressure may lower the risk of intracranial hemorrhage. Cautious use of thrombolytic, anticoagulant, and antiplatelet agents should also decrease the likelihood of intracranial bleeding. Management of inherited or acquired disorders of coagulation, including the administration of clotting factors, also lowers the risk of hemorrhage. Management of an unruptured AVM or aneurysm often is recommended. Choices include endovascular or direct surgical occlusion of larger aneurysms. Surgical resection, focused radiation, or endovascular therapies are potential therapies for treatment of AVM. However, recent evidence suggests that in some cases the risks of the interventions may be greater than the likelihood of hemorrhage.
B. Referral and admission. Patients with acute hemorrhagic stroke are critically ill. Inpatient care is warranted because intracranial hemorrhage is life-threatening and is accompanied by serious medical or neurologic complications. The facilities and personnel required for successful care of these patients may not be available at most community hospitals. Admission to a specialized treatment facility that has monitoring capabilities or an ICU usually is needed. The high-risk nature of hemorrhagic stroke means that most patients should be referred to centers that have neurologic and neurosurgical expertise.
C. General management. Measures for control of acute medical and neurologic complications are part of emergency treatment (Table 37.5). Endotracheal intubation and ventilatory assistance may be needed. Hypoxic patients should receive supplemental oxygen. Fever should be treated. Access for intravenous administration of medications and fluids is needed, and normal saline solution is infused slowly. Hypotonic solutions generally are avoided because of their potential effects on the formation of edema and because many patients have hyponatremia. Hypoglycemia or hyperglycemia should be managed. Cardiac monitoring to detect serious arrhythmias and frequent measurements of vital signs and the neurologic status are performed. Symptoms such as headache, agitation, nausea, and vomiting warrant treatment. Patients who have had seizures are given anticonvulsants, but prophylactic use of anticonvulsants to patients who have not had seizures is controversial. Because of fears that stress of a seizure may cause rebleeding, many physicians prophylactically prescribe anticonvulsants to patients with ruptured aneurysms.
D. Treatment for arterial hypertension. Elevated blood pressure may worsen intracranial bleeding, promote edema formation, or induce recurrent aneurysmal rupture. It usually declines as pain, agitation, seizures, and vomiting are controlled. The level of blood pressure that mandates medical treatment is not known, but there is a consensus to treat a systolic pressure >200 mm Hg or mean arterial pressure >150 mm Hg. Because an elevated ICP promoted arterial hypertension, special caution is needed when lowering the blood pressure among patients with intracranial hypertension. In general, a goal is to lower the blood pressure by approximately 15% per day. Responses to antihypertensive agents often are exaggerated. Short-acting parenteral medications are preferred because the dosages can be titrated in response to the patient’s blood pressure and neurologic status (Table 37.6). In addition, caution should be exercised when using sodium nitroprusside because its secondary cerebral vasodilatory effects may worsen increased ICP.
E. Halting continued bleeding. Recombinant factor VIIa was used to treat ICH, but a recent trial showed that it did not improve outcomes. Patients with intracranial hemorrhage secondary to a defect in coagulation should receive the appropriate antidotes including protamine, vitamin K, clotting factors, or platelets.
F. Increased ICP and brain edema. Management of increased ICP is important. Monitoring of ICP may be used to guide treatment for critically ill patients. Impaired venous return, agitation, fever, hypoxia, hypercapnia, and hypoventilation aggravate increased ICP and should be managed. Early measures include elevation of the head of the bed, modest fluid restriction, and avoidance of potentially hypo-osmolar fluids. Corticosteroids are not helpful. Intubation and hyperventilation are prescribed when a patient’s condition is deteriorating. Hyperosmolar therapies, which often are prescribed with seriously elevated ICP, include 20% mannitol or hypertonic saline.
G. Emergency surgical management. An early decision involves the need for surgical evacuation of a hematoma that is causing mass effects or increased ICP. A ventricular catheter may be used to drain CSF if the patient has secondary hydrocephalus; it may lower ICP and forestall the need for a craniotomy. Removal of a large hematoma may be a lifesaving procedure. Choices include an open craniotomy, minimally invasive surgery, and endoscopic aspiration. Administration of thrombolytic agents to add aspiration of the hematoma including an IVH has been attempted. The location and size of the hematoma and the patient’s neurologic status, course, and general health affect such a decision (Table 37.7). In general, surgery is recommended for the treatment of a large cerebellar hematoma that is compressing the brainstem or obstructing CSF outflow. Patients with lobar hematomas within 1 cm of the cortical surface can be considered for surgery. However, patients with small-to-moderate-sized hematomas of the cerebral hemisphere usually do not need surgery. Patients with hemorrhages in the thalamus and basal ganglia usually are not treated with surgery. There is no evidence that surgical evacuation of such hematomas improve outcomes. There are no data about the utility of decompressive craniectomy to improve outcomes after intracranial hemorrhage.
TABLE 37.5 Emergency Management of Hemorrhagic Stroke
ABC of life support
Frequent measures of vital signs and blood pressure
Frequent assessments of neurologic status
Cardiac monitoring
Control fever
Supplemental oxygen if hypoxia is present
Intravenous access with slow infusion of normal saline
Control pain, nausea, vomiting, and seizures
H. General inpatient care. Emergency management is continued after admission to an ICU. Bed rest is maintained until the patient’s status has stabilized. Careful nursing care, monitoring, and regular assessments of the patient’s condition and vital signs are continued. To decrease the risk of aspiration and pneumonia, liquids and food are not given by mouth until the patient’s ability to swallow safely has been confirmed. If the patient cannot take fluids by mouth, a nasogastric tube should be placed. Care in avoiding pulmonary complications is part of general management. Modest fluid restriction is continued for patients who have a large hematoma. Management of intravenous fluids should emphasize maintaining normal electrolyte levels. Some patients will have hyponatremia secondary to cerebral salt wasting, and these patients will need hypertonic fluids. Incontinence often mandates placement of an indwelling bladder catheter. Because of the risk of urinary tract infection, the catheter should be removed as soon as possible. Because bedridden patients have a high risk of deep venous thrombosis that may lead to pulmonary embolism, they are treated with alternating pressure devices and antiembolism stockings. Low doses of heparin can be prescribed after the risk of continued bleeding has abated. When the patient’s condition has stabilized, increased activity, mobilization, and rehabilitation begin.
TABLE 37.6 Emergency Management of Arterial Hypertension
If systolic blood pressure >200 mm Hg or mean blood pressure >150 mm Hg
Aggressive lowering of blood pressure with intravenous infusion
Monitor blood pressure every 5 min
If systolic blood pressure >180 mm Hg or mean blood pressure >130 mm Hg and evidence of increased ICP
Reduce blood pressure with intermittent or continuous medications
Keep cerebral perfusion pressure >80 mm Hg
If systolic blood pressure >180 mm Hg or mean blood pressure >130 mm Hg and no evidence of increased ICP
Modest reduction of blood pressure
Intermittent or continuous infusion of medications
Choices of medications
Labetalol
Intermittent—5–20 mg every 15 min
Continuous—2 mg/min (maximum 300 mg in 1 d)
Nicardipine
Continuous—5–15 mg/hr
Esmolol
Intermittent—250 µg/kg push loading dose
Continuous—25–300 µg/kg/min
Enalapril
Intermittent—1.25–5 mg every 6 hr
Hydralazine
Intermittent—5–20 mg every 30 min
Continuous—1.5–5 µg/kg/min
Nitroprusside
Continuous—0.1–10 µg/kg/min
Nitroglycerine
Continuous—20–400 µg/min
TABLE 37.7 Indications for Emergency Surgical Evacuation of Hematoma
Surgery indicated
Cerebellar hematoma 0.3 cm in diameter with compression of brainstem or development of hydrocephalus
Hemorrhage with a structural lesion (aneurysm or AVM) that can be managed surgically
Moderate-to-large lobar hematoma close to the cortical surface
Surgery not indicated
Small hematoma or minimal impairment
Large, deep hematoma
Patient with very severe impairment
VI. CAUSE-SPECIFIC TREATMENT
Management of the cause of bleeding is a key component of the overall treatment for patients with intracranial hemorrhage.
A. Vascular malformations. Patients with a ruptured vascular malformation may be treated to prevent a second hemorrhage. Because the risk of early rebleeding is relatively low, treatment usually is delayed until the hematoma has reabsorbed. The options for treatment include surgical resection, endovascular administration of vascular occlusive materials, or focused radiation. Decisions are influenced by the size and location of the malformation and the number and caliber of the feeding arteries. Lesions in neurologically eloquent areas and those that are deep in the brain may not be surgically approachable. A high-flow malformation is also a problem because a postoperative state of hyperperfusion leading to hemorrhage or severe brain edema can follow resection. A staged series including both endovascular and surgical procedures can also be performed. Small and deep vascular malformations may be managed with focused, high-intensity radiation that leads to secondary fibrosis and gradual occlusion of the vessels. Some patients with very large malformations may not be treatable with any of the currently available modalities.
B. Aneurysms. Patients with ruptured aneurysms are vulnerable to recurrent hemorrhage and ischemic stroke (Table 37.8). Rebleeding is a largely fatal event that peaks during the first 24 hours, when the risk is approximately 4%. The overall risk of recurrent hemorrhage during the first 10 days approaches 20%. The symptoms of rebleeding are similar to those of the initial hemorrhage, and a CT will show more blood. The most effective measures to forestall rebleeding are direct surgical obliteration of the aneurysm by clipping or endovascular occlusion of the aneurysm by inserting coils. In general, the goal is to treat the patient as quickly as possible. The selection of endovascular or direct surgical treatment is influenced by the patient’s condition, the location of the aneurysm, the presence of serious comorbid diseases, or the presence of vasospasm. Recent studies suggest that the morbidity associated with endovascular treatment is less than that accompanying surgical clipping.
Vasospasm is an arterial process that occurs almost exclusively in association with aneurysmal SAH. It is most likely to occur among patients with extensive subarachnoid blood found on CT. The progressive arterial narrowing peaks at 7 to 10 days after SAH. Thereafter, vasospasm gradually abates. The arterial narrowing causes hypoperfusion, which leads to brain ischemia. The symptoms of vasospasm are worsening headache, altered consciousness, and focal neurologic signs that wax and wane. Transcranial Doppler ultrasonography may detect alterations of flow velocities in major arteries before the clinical signs appear. These studies often are performed at regular intervals during the period of highest risk. Arteriography can be used to confirm the arterial narrowing. Nimodipine is efficacious in improving outcomes after SAH presumably by lessening the ischemic effects, and it is unclear whether the medication has any effect on vasospasm.
TABLE 37.8 Management of Patients with Aneurysmal SAH
Prevention of recurrent hemorrhage
Surgical treatment—clipping
Endovascular placement of coils or balloon
Antihypertensive agents
Brief course of antifibrinolytic therapy
Prevention of vasospasm and ischemic stroke
Avoidance of dehydration, hyponatremia, and hypotension
Avoidance of use antifibrinolytic agents
Reduction of increased ICP
Nimodipine
60 mg by mouth or nasogastric tube every 4 hr
Hypervolemic hemodilution and drug-induced hypertension
Intra-arterial administration of vasodilator medications
Angioplasty
Hypervolemic hemodilution and drug-induced hypertension (3-H therapy) are prescribed to patients in whom ischemic symptoms develop. Although no controlled trials have shown the efficacy of this regimen, several studies report success with 3-H therapy. The regimen is rigorous and monitoring is critical because myocardial ischemia, congestive heart failure, and pulmonary edema are possible adverse experiences. The regimen can also promote recurrent aneurysmal rupture if the aneurysm has not been treated. Angioplasty or intra-arterial infusions of vasodilators have been used to treat patients with vasospasm who have not responded to other interventions.
Recommended Readings
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