Spontaneous Intracerebral Hemorrhage

Background and Epidemiology

Spontaneous intracerebral hemorrhage is defined as a nontraumatic hemorrhage into brain parenchyma. The clinical significance of intracerebral hemorrhage (ICH), also known as hemorrhagic stroke, can be more clearly understood when it is viewed as a subtype of stroke. According to the National Vital Statistics Report, stroke is the third leading cause of death in the United States, behind only heart disease and cancer, and is responsible for nearly 6% of total deaths on an annual basis. ICH accounts for approximately 10% of all strokes with an annual incidence of between 15.9 and 32.9 per 100,000. A sharp increase in incidence occurs in patients more than 75 years old, and it is even higher in patients older than 85, with reported incidence rates as high as 309.8 per 100,000, nearly 7 times greater than the rate in the general population. Though less frequent than ischemic stroke, the overall mortality of ICH is significantly greater, with 30-day mortality estimated at 44% to 52% and half of all deaths occurring within the first 2 days of hemorrhage. The national cost of first-time strokes has been estimated at $40.6 billion, with more than $6 billion accounting for aggregate lifetime cost. Of the $40.6 billion, only 45% of the cost was attributable to acute stroke care, with more than 47% of the total cost coming from long-term ambulatory and nursing care. Of all patients with ICH, only 20% have been noted to be functionally independent 6 months after their stroke. Although these statistics underscore the significant economic burden of ICH, they fail to emphasize the immeasurable emotional and social impact of ICH. It is essential to note, however, that since 1958, there has been a general annual decline in stroke deaths nationally. Between 2005 and 2006, there was a 6.4% decrease in stroke deaths. This decline is attributable to significant improvements in treatment of modifiable risk factors related to cardiovascular and cerebrovascular health. Still, the rate of ICH is expected to increase in the future, as the world population's average age increases.

Pathophysiology

ICH may be classified as primary or secondary, depending on the etiology of the hemorrhage. Primary ICH most commonly results from chronic arterial hypertension. It occurs in small perforating arteries, typically at bifurcations from larger cerebral arteries where a pressure gradient is transmitted from the larger vessel to smaller, susceptible vessels. Small perforating vessels with diameters of 50 to 700 microns are often the offending vessels and may have multiple sites of rupture. Hypertension is the most important risk factor for ICH, with nearly 60% of patients with ICH in a prospective study having elevated blood pressure. Hypertensive bleeds are noted to occur more frequently within deep gray matter structures, most commonly the basal ganglia, followed by the thalamus, pons, and the cerebellum ( Fig. 22.1 ). Lobar hemorrhages, however, are not infrequent. Of all ICHs, one population study reviewed the locations of cerebral bleeds and noted 49% were deep in location, 35% were lobar, 10% were in the cerebellum, and 6% were in the brainstem.

Classically, hypertensive bleeds have been attributed to the rupture of miliary aneurysms as described initially by Charcot and Bouchard in 1868 from their postmortem analysis of hemorrhage cavities in autopsy specimens. Further research has clarified that the miliary aneurysms described by Charcot and Bouchard are in fact pseudoaneurysms or weaknesses in the perforating arteriole walls where extravasated blood and accumulated fibrin have existed. Pathologic analysis of vessels in ICH specimens and in patients with chronic hypertension has more clearly demonstrated the process of lipohyalinosis in which chronic hypertensive damage gives rise to intimal hyperplasia, fibrin deposition, and focal accumulation of fat-filled macrophages, ultimately leading to necrosis in the vessel walls. These vessel changes are more commonly seen at sites of hemorrhages than miliary aneurysms and thus are believed to be the source.

After the inciting hemorrhage, blood disperses along surrounding fiber tracts in the parenchyma. In an estimated 10% to 15% of cases, blood decompresses from the parenchyma into the ventricular system, creating an intraventricular hemorrhage. Ultimately, the hemorrhage is self-contained by tamponade from the parenchyma adjacent to the bleed site and by activation of hemostatic pathways. Regions of brain surrounding a hemorrhage are often characterized by extensive inflammation, edema, apoptosis, and necrosis that may contribute to the neurologic deficit. Moreover, increased intracranial pressure and herniation secondary to mass effect occur with particularly large-volume hemorrhages. The rate of expansion of a hemorrhagic lesion is also an important variable to consider. Rapidly expanding lesions cause greater direct injury to axons and tissues and therefore result in greater damage to adjacent neural structures than slowly expanding lesions.

Secondary ICH results from underlying lesions such as aneurysms, vascular malformations, coagulopathies, tumors, hemorrhagic conversion of ischemic infarcts, cerebral amyloid angiopathy, and drug-related hemorrhages. Common metastatic tumors that are prone to hemorrhage include melanoma, choriocarcinoma, and renal carcinoma. Lung and breast cancer should also be considered due to their high incidence in the population. Primary brain neoplasms associated with ICH include glioblastoma multiforme, oligodendroglioma, and ependymoma. Although secondary ICH is less common, it is important to consider these etiologies in the differential diagnosis and work them up appropriately, as they place patients at risk for recurrent hemorrhage with the potential for extensive morbidity and mortality.

Etiology