Intracerebral hemorrhage (ICH) is a type of hemorrhagic stroke resulting from blood leaving the vascular system and entering the brain tissue. ICH is associated with significant morbidity and mortality, and constitutes a neurologic emergency requiring swift and organized care by the multidisciplinary team. Despite decades of research aimed at improving outcomes for patients suffering from ICH, care remains largely supportive.
The classification of hemorrhage in the cranial vault is based on the location and the underlying cause. Intracranial hemorrhage includes bleeding into any space within the cranial vault including the subarachnoid, epidural, and subdural spaces. Bleeding into the subdural and epidural spaces is almost always caused by cerebral trauma and is addressed in Chapter 16. Subarachnoid hemorrhage is bleeding into the subarachnoid space and primarily the result of a ruptured cerebral aneurysm or trauma; it is addressed in Chapter 24.
ICH and parenchymal hemorrhage are the terms used to describe spontaneous nontraumatic bleeding directly into the brain substance. ICH is a more general term used to describe bleeding within the brain substance, while parenchymal hemorrhage describes bleeding into the brain tissue as a result of rupture of a small artery, most often a deep, penetrating blood vessel. The term lobar hemorrhage is also used. Lobar hemorrhage is a hemorrhage into a lobe of the brain. Hemorrhage into the intracerebral space may be primary or secondary in nature. Primary ICH includes hemorrhage resulting from hypertension or amyloid angiopathy and comprises 80% of ICH. Secondary causes of ICH include bleeding from vascular malformations or abnormalities, trauma, tumor, and coagulation disorders, and comprise the remaining 20% of ICH.1 In this chapter, the term ICH is used to mean spontaneous nontraumatic ICH. Traumatic ICH is addressed in Chapter 16.
The ventricular system of the brain poses an additional location for hemorrhage. Primary intraventricular hemorrhage (IVH) represents bleeding into the ventricular system without discernable parenchymal hemorrhage and represents less than 5% of ICH.2 ICH of any size may also extend into the ventricular system and is called IVH. Primary IVH most often results from a vascular abnormality such as an arteriovenous malformation (AVM) or aneurysm. The presence of blood in the lateral, third, or fourth ventricles associated with ICH poses additional management risks and issues and will be addressed in this chapter.
Approximately 8% to 10% of all strokes are the result of ICH, translating to approximately 65,000 new ICH strokes per year for Americans. Although ICH represents a smaller percentage of total strokes as compared to ischemic stroke, hemorrhagic stroke is a significant cause of morbidity and mortality in the United States and other countries throughout the world. The incidence for Asians and African Americans is particularly high as compared to Caucasians.3 The mortality rate for patients with hypertensive ICH is approximately 50% with the remaining patients having a varying degree of recovery, if they survive the initial hemorrhage. Only 20% achieve functional independence. With the growing number of older Americans, one can expect an increase in the prevalence of cerebral amyloid angiopathy (CAA)-related ICH, which is discussed later in this chapter.4 In addition, the increased abuse of drugs that can cause hypertensive episodes, and the widespread use of prescription medications that affect coagulation also contribute ICH. The high mortality and morbidity associated with ICH are caused primarily by the blood mass itself (e.g., mass volume) and by the mechanical effects it creates such as increased intracranial pressure (ICP) and herniation.5
ETIOLOGY OF INTRACEREBRAL HEMORRHAGE
Risk factors associated with the development of spontaneous ICH may be divided into nonmodifiable and modifiable influences. Nonmodifiable risk factors include age, race, and gender. Advanced age increases the risk of ICH, as does male gender.6 African American, Latino, and Japanese populations are at a significantly higher risk of developing ICH, although the predisposition to disease development is largely influenced by modifiable risk factor prevalence and control in these groups.7 Modifiable risk factors include hypertension, alcohol consumption, smoking, and cholesterol control.6 Hypertension is the single most important risk factor associated with the development of ICH, particularly, when combined with other risk factors such as advanced age. Lowering of elevated blood pressure is protective against the development of ICH.8 Moderate or heavy alcohol consumption and smoking are associated with the development of ICH. However, the role of smoking in developing ICH is controversial and may be mostly related to the increased rate of hypertension in smokers.6
Hypertension is the primary underlying and the most significant cause of ICH. The typical profile of a patient with ICH is an older person with a long history of poorly controlled hypertension. The most common sites of hypertensive ICH are the putamen of the basal ganglia (50%), the thalamus (30%), the pons (10%), and the cerebellum (10%). Hemorrhage results from spontaneous rupture of small penetrating arteries and arterioles deep in the brain. The rupture is primarily the result of chronic hypertension and the degenerative changes that occur over time to cerebral arteries. Hemorrhage generally occurs at small artery penetrating branches originating from larger cerebral arteries.9 The classic theory proposed by Charcot and Bouchard in the 1870s is that small aneurysmal dilations in arteries are the underlying pathology associated with ICH remains debated and unproven.6 The reference to small penetrating arteries mainly includes penetrating lenticulostriate branches of the middle cerebral artery (MCA); anterior perforating vessels of the anterior cerebral artery (ACA); penetrating arteries origination for the anterior choroidal arteries; thalamogeniculate penetrators for the posterior cerebral artery (PCA); and paramedical perforating vessels to the pons, midbrain, and thalamus from the basilar artery.10, 11, 12 Sudden increases in blood pressure and blood flow can also cause rupture of these small penetrating arteries even in the absence of chronic hypertensive changes although this is a less common cause, if ICH.11
CAA is another cause of primary ICH and the leading cause of lobar ICH in the elderly. With aging, a protein substance called amyloid is deposited into the walls of the cortical and leptomeningeal arterioles resulting in vascular fragility and propensity for bleeding.4 CAA can cause lobar hemorrhage, particularly in the frontal and parietal lobes, most commonly at the junction of the white matter and cerebral cortex, which should be considered in patients 75 years and older. Approximately 70% of CAA patients have a history of Alzheimer’s disease, dementia, or cognitive decline.4
A definitive diagnosis of CAA can only be made post-mortem on autopsy. However, a presumptive diagnosis of CAA may be made in patients by combining patient history, clinical presentation, and radiologic information. Hemorrhages at multiple sites or recurrent bleeds are common in patients with CAA. Magnetic resonance imaging (MRI) may be useful in identifying small and potentially unnoticed past ICHs in patients with suspected CAA-related ICH. Several sequences of MRI scanning will detect hemosiderin, a by-product of blood breakdown.13
Oral anticoagulant therapy (OAT): with increased use of OAT as prophylaxis against cardioembolic disease in high-risk patients over the past several decades, the occurrence of coagulopathyrelated ICH has increased as well.14 The therapeutic benefit of most OAT agents depends on maintaining coagulation factors, specifically the international normalized ratio (INR), within a narrow therapeutic range. Risk of cerebral hemorrhage doubles with each point elevation of INR over therapeutic range; an INR greater than 4.5 places the patient at significantly elevated risk of cerebral hemorrhage.14 OAT is itself a risk factor for cerebral hemorrhage. However, when combined with other risk factors including hypertension, advanced age, dementia, and risk for falls, patients on OAT are at significantly elevated risk for ICH.14
Additional etiologies for ICH: additional disease processes may present as a secondary nontraumatic ICH in a minority of patient. Location again helps guide the clinician regarding underlying etiology. When cerebral hemorrhage occurs in the central white matter of the lobes in a younger patient or hemorrhage occurring in a nonhypertensive patient, other causes such as vascular malformations, cocaine or amphetamine abuse, cerebral trauma, hemorrhage into a brain tumor, or hypertensive encephalopathy must be considered.3 Rarely, cerebral vasculitis may result in cerebral hemorrhage. Sympathomimetic illicit drugs including amphetamines, methamphetamines, and cocaine may also cause ICH and should be explored in patients who do not exhibit a traditional risk factor profile for ICH.3
Central venous thrombosis (CVT) results from a thrombus forming in the venous system rather than the arterial system and is a rare cause of stroke.15 While only 1% of all strokes are caused by CVT, 30% to 40% of patients with CVT will experience associated ICH. ICH associated with CVT often results in increased ICP and treatment differs from conventional treatment for either acute ischemic or ICH management. Refer to the ASA guidelines for the management of CVT for additional information.15
Finally, hemorrhage into the ventricular system presents unique management challenges. Extension of hemorrhage into the ventricular system is associated with poor outcomes and death with less than 20% of patients experiencing an IVH recovering to good functional outcome. The mechanisms underlying IVH are similar to those outlined for ICH.16 However, primary IVH, where most or all of the hemorrhage is concentrated in the ventricular system, is more likely caused by a vascular malformation than ICH.2
PATHOPHYSIOLOGY OF INTRACEREBRAL HEMORRHAGIC STROKE
Once a hemorrhage occurs as a result of chronic changes to penetrating vessel walls, rupture of microaneurysms, or abrupt spikes in arterial blood pressure, blood leaks from the small vessels into the cerebral tissue creating a hematoma. A sudden and local pressure effect on the surrounding cerebral tissue occurs as the hematoma expands in volume at its circumference. The high blood pressure in the capillaries and arterioles causes them to rupture.17 Vessels around the periphery of the hemorrhage rupture, thus adding volume to the gradually enlarging hematoma. Caplan11 notes that the gradual addition to the volume of the hematoma at the periphery is similar to a snowball rolling down a hill in that it gathers volume along its circumference. High blood pressure and an enlarging hematoma press against local tissue acting to tamponade the bleeding.
Most spontaneous hypertensive ICHs develop over 30 to 90 minutes. The dynamic nature of the pathophysiology continues to evolve over the first few days after onset and is best described using the concepts of primary and secondary brain injuries. Primary injury in ICH results from the vessel tearing and leaking blood into the cerebral parenchyma. However, secondary damage caused by multiple metabolic processes and resulting in cerebral edema, oxidative damage, and ischemia occurs for days and even weeks after a hemorrhage.18 Primary injury may be exacerbated by hemorrhagic volume increase, which occurs in up to 30% of all cases. Cerebral edema occurring over the following hours and days continues to add a mass effect and volume to the damaged tissue potentially increasing ICP to dangerously high levels.
The evolving cerebral edema helps to explain why patients with ICH often worsen during the first 24 to 48 hours after their initial symptoms. The pathophysiology of ICH is associated with a rise in ICP, as the volume of the hematoma increases ischemic cellular responses, cerebral edema, compromised cerebral perfusion pressure (CPP), and possible herniation related to an increased ICP. A major ICH with increased ICP can cause midline displacement and herniation syndromes, and has a high mortality rate of 50%. The ventricular system may also be compressed as a result of an ICH. A hemorrhage in the putamen may distort the foramen of Monro, thus causing a dilated lateral ventricle contralaterally, while a thalamic hemorrhage can cause compression of the third ventricle leading to hydrocephalus.11 Secondary injury is mediated by activation of hemeproteins, the platelet system, and leukocytes.18 Macrophages and microglia begin phagocytosis on the hemorrhage at its periphery within 48 hours. After 1 to 6 months, the hemorrhage is generally resolved and appears like a slit-like orange cavity lined with glial scar and hemosiderin-laden macrophages.3
CLINICAL PRESENTATION OF INTRACEREBRAL HEMORRHAGIC STROKE
The clinical presentation of neurologic impairment and decreased level of consciousness associated with ICH is largely dictated by hemorrhage location and size. While hemorrhagic stroke patients are more likely to exhibit rapid decrease in level of consciousness, headache, nausea, and vomiting than patients with ischemic stroke, differentiation from ischemic stroke by clinical signs and symptoms alone is not possible. The location of the hemorrhage and the degree of neurologic impairment guides medical and nursing interventions with larger hemorrhage requiring rapid protection of airway and emergent intervention. Regardless of size or neurologic impairment, ICH is considered a neurologic emergency.
Intracerebral hemorrhagic stroke as a result of chronic hypertension is associated with bleeding into the putamen (part of the basal ganglia) that may extend into the adjacent internal capsule (50%), thalamus (30%), pons (10%), and cerebellum (10%). Each site has distinguishing signs and symptoms which will be discussed. Hemorrhagic stroke occurs rapidly and symptoms develop steady over a period of minutes to hours (1 to 24 hours). A wide range of signs and symptoms and related severity (e.g., mild to severe) depends on the size of the hemorrhage and the subsequent hematoma that forms. The larger the hematoma, the more severe are the signs and symptoms. The hematoma acts as a space-occupying lesion, and can lead to a rapid increase in ICP which progresses to brainstem compression and herniation. Extension of the hemorrhage to compress the ventricular system, results in hydrocephalus. Therefore, the practitioner must not only be able to treat current clinical problems, but also be vigilant for potential developing complications such as hydrocephalus. The following outlines the specific syndromes associated with each of the four sites of ICH.19, 20 See Table 23-1 for a summary of the signs and symptoms related to each location.
The most common syndrome seen in about 50% of patients with ICH is caused by a hemorrhage and a hematoma into the putamen of the basal ganglia. A small posterior hemorrhage includes mild weakness, some sensory loss, hemianopsia, limited visual pursuit to the opposite side, aphasia, if the dominant side affected, and anosognosia, if the nondominant side affected.20 With a moderatesize hemorrhage confined to the anterior segment of the putamen, the hemiplegia tends to be less severe and clears more rapidly. In addition, there are abulia, motor clumsiness, and unilateral neglect. If the dominant side is affected, aphasia and dysgraphia are noted.
In a large putaminal hemorrhage, the hemorrhage may extend into the adjacent internal capsule. The interruption of internal capsule pathways results in hemiplegia from a medium to a large hematoma. Vomiting and headache are findings in about half of the patients. With the development of symptoms over time, the patient lapses into a stuporous state, the face sags to one side, the arm and leg weaken and progress to flaccidity and hemiplegia, the eyes deviate away from the side of the paretic limbs, and speech becomes slurred or aphasic, if the dominant side is involved. If deterioration continues, signs and symptoms of increased ICP and neurological deterioration to herniation develop and include signs of upper brainstem compress (e.g., dilated pupil, coma) to lower brainstem compression so that decortication, decerebration, abnormal respiratory patterns, and vital sign changes are noted.20
TABLE 23-1 SIGNS AND SYMPTOMS OF MAJOR SYNDROMES IN INTRACEREBRAL HYPERTENSIVE STROKE
SIGNS AND SYMPTOMS (DEVELOP OVER MINUTES TO HOURS)
Putaminal Hemorrhage with extension into internal capsule
Confusion to coma
Small hemorrhage (posterior putamen)
Mild weakness, some sensory loss, hemianopsia, limited visual pursuit to opposite side
Aphasia, if dominant side affected, or anosognosia, if nondominant side affected
Moderate hemorrhage (anterior putamen)
Hemiparesis to hemiplegia, abulia, motor clumsiness, and unilateral neglect
Aphasia and agraphia, if dominant side affected.
Large hemorrhage with internal capsule involvement
Vomiting and headache, decreased LOC to stupor, hemiparesis that becomes hemiplegia (flaccid)
If dominant side involved, slurred speech to aphasia, eyes deviate away from the side of hemiplegia
Possible ventricular compression that leads to hydrocephalus
Later signs and symptoms:
Increased intracranial pressure with downward deterioration toward herniation (dilated pupil, coma, decortication, decerebration, abnormal respirations, deterioration of vital signs).
Confusion to coma
Severe contralateral hemisensory deficits
Dominant side hemorrhage-aphasia
Nondominant side hemorrhage-contralateral neglect
Deficits with vertical and lateral gazes
Unequal nonreactive pupils
Compression of third ventricle can result in hydrocephalus
Possible locked-in syndrome
Deficits in lateral eye movement
Small (pinpoint) reactive pupils
Stupor to coma
Occipital and sometimes cervical headache
Lateral gaze preference
The most prominent clinical feature in thalamic hemorrhage is severe sensory loss on the entire contralateral side of the body from the lesion. Hemorrhages that are moderate to large in size, result in hemiparesis or hemiplegia due to compression or destruction of the adjacent internal capsule. A lesion on the dominant side results in fluent aphasia while lesions on the nondominant side lead to contralateral neglect. Because of the location of the thalamus in the midbrain region, a number of ocular deficits may be noted such as homonymous hemianopsia that usually clears in a day or two; weaknesses of the extraocular muscles resulting in palsies of vertical and lateral gazes, or one or both eyes turn inward and downward, or a forced deviation of the eyes downward; unequal and nonreactive pupils to light; ipsilateral ptosis and miosis; loss of convergence; and retraction of the upper eyelids. Compression of the adjacent third ventricle can lead to hydrocephalus which may require temporary CSF drainage.20
The grave syndrome of hemorrhage into the pons is characterized by deep coma that develops almost immediately, small (1 mm) reactive pupils, total paralysis, and decerebration. Patients may exhibit ocular bobbing or lack of horizontal gaze.21 Pontine hematomas resulting from hypertension are generally devastating and most often result in death. Rarely, pontine hemorrhage may be caused by vascular malformation, for which prognosis is slightly improved.21 Pontine hemorrhages often extend into the fourth ventricle, resulting in hydrocephalus. A pontine hemorrhage of greater than 2 cm is associated with poor outcome.21 For many patients, death usually occurs within a few hours.20
Although symptoms usually develop over a period of an hour or more, loss of consciousness associated with hemorrhage into the cerebellum at onset is not unusual. Patients typically experience nonspecific symptoms such as dizziness, nausea, vomiting, unsteady gait, and occipital or cervical headache. They may show signs of dysarthria, ataxia, and nystagmus.22 Vomiting is common, accompanied by occipital headache. In the early stages, signs and symptoms can be varied and may include slight ipsilateral facial weakness and lateral gaze paresis, although vertical eye movement is intact. Edema and mass effect from cerebellar hemorrhage may obscure CSF flow through the fourth ventricle, and extension of hemorrhage into the ventricular system is also common, both resulting in hydrocephalus. As time passes, the patient can become stuporous and then comatose. With brainstem compression, the usual signs and symptoms of increased ICP and possible herniation develop.
Other Locations of Hemorrhage: Lobar Hemorrhage
When bleeding occurs in areas other than the four areas addressed above, other causes of hemorrhage rather than chronic primary hypertension are considered. In lobar hemorrhage, subcortical white matter of a lobe of the cerebral hemisphere is affected with a hemorrhage that appears spherical or ovoid in shape although multiple hemorrhages in the lobe are common. The possible causes of lobar hemorrhage include hemorrhage from anticoagulation drugs or thrombolytic therapy, acquired coagulopathies, craniocerebral trauma, AVM, and CAA in the elderly. The clinical presentation depends on the lobe involved.
To treat a stroke optimally, the healthcare provider must first identify the correct underlying mechanism. Several diagnostics are helpful in determining the type of stroke, which then determine treatment options (see Table 23-2). Early treatment for ischemic stroke includes thrombolytic therapy, which is contraindicated if hemorrhagic stroke is present. Therefore, differentiating between ischemic and hemorrhagic strokes is critical to treatment decisions. The current standard for differentiating ischemic from hemorrhagic stroke is a noncontrast CT scan of the brain. Hemorrhage is visible on a noncontrast CT scan within the moments of occurrence, whereas ischemic stroke takes hours to be visible. Recent evidence points to the benefit of CT angiography in a selected group of patients at risk for rapid hemorrhagic expansion. Patients with ICH may exhibit the “spot sign” when contrast is administered during CT angiography.23 The presence of the spot sign indicates active contrast extravasation into brain parenchyma, and therefore, active hematoma expansion. The presence of the spot sign is associated with hematoma expansion over the following 48 hours as well as increased in-hospital and overall mortality.24
TABLE 23-2 DIAGNOSTIC PROCEDURES FOR INTRACEREBRAL HEMORRHAGIC STROKE
Computed tomography (CT) scan
Goals of emergency evaluation are to confirm hemorrhage as the cause of the neurological symptoms and to identify acute complication.
CT without contrast is the most important single diagnostic test to determine cerebral hemorrhage; high reliability and validity when performed within 24 hrs of onset; blood density clearly visible in almost 100% of ICH and 95% of subarachnoid hemorrhage.4
Critical to differentiation between ischemic and hemorrhagic strokes because thrombolytic therapy used for ischemic stroke is contraindicated in hemorrhagic stroke.
CT scan is useful to monitor enlargement of the hematoma over time as a result of continued bleeding.
Useful to identify complications related to stroke such as cerebral edema and hydrocephalus.
Magnetic resonance imaging (MRI)
Provides information about the probable cause and age of the hemorrhage.
Useful to find multiple micro-hemorrhages as seem in cerebral amyloid angiopathy.
Computed tomography angiography (CTA)
May be ordered if there is a question of small aneurysms or vasculitis
Generally not necessary for primary intracerebral hypertensive stroke
Magnetic resonance angiography (MRA)
May be ordered if there is a question of small aneurysms or vasculitis
Generally not necessary for primary intracerebral hypertensive stroke
Hematology and biochemistry studies: complete blood count (CBC), electrolytes, and blood glucose.
Screen for medical complications and need to be corrected
Coagulation studies: platelet count, prothrombin time, partial thromboplastin time, and international normalized ratio (INR).
Screen for other causes of hemorrhage
Screen for cardiac dysfunction that is either pre-existing or a complication of hemorrhage