Perspective

Intracranial hemorrhages have different clinical manifestations ranging from subtle to catastrophic. The efforts of the emergency physician (EP) are directed toward identifying the correct diagnosis, confirming the diagnosis by cranial computed tomography (CT) or other diagnostic tests, and providing supportive care. Liberal consultation plus collaboration with specialists is required. Strong evidence of the best course of action regarding basic treatment issues such as blood pressure management and the use of anticonvulsants is lacking. Definitive therapy is most often in the hands of consulting and admitting physicians.

It is tempting to place any intracranial hemorrhage in the diagnostic category head bleed. Different types of intracranial hemorrhage may have different causes, different natural histories, different diagnostic strategies, different treatments, and frequently different prognoses. It is important to delineate the various types of intracranial hemorrhage so that correct diagnostic steps and therapeutic interventions can be performed.

Epidemiology

Estimates of the incidence of intracranial hemorrhage in patients seen in the emergency department (ED) are difficult because the findings include isolated headache, stroke syndromes, and head trauma, but a few generalities may be made. It is estimated that approximately 800,000 strokes occur each year in the United States, with intracranial hemorrhages accounting for 20% of the strokes. About 1% to 2% of patients seek treatment in EDs with a primary complaint of headache, and it is thought that 1% of these patients may have subarachnoid hemorrhage (SAH). If a filter of “worst headache of my life” is used, that estimate increases to up to 12% of patients with SAH. Approximately 500,000 moderate and severe traumatic head injuries occur each year in the United States. One percent to 2% of these patients have epidural hematomas, with estimates of an additional 5% to 25% having acute subdural hematomas.

Pathophysiology

intracranial hemorrhage is the umbrella term used to encompass the many types of bleeding within the cranial vault (Figs. 103.1 to 103.5 and Table 103.1). Intraparenchymal hemorrhage implies blood within the substance of the brain. When the hemorrhage is not clearly secondary to a detectable cause, it is deemed a spontaneous hemorrhage. This term is often used synonymously with the terms hypertensive hemorrhage and, when anatomically appropriate, intracerebral hemorrhage. Intraparenchymal hemorrhages may also occur in the brainstem or cerebellum. SAH literally describes blood in the subarachnoid space, and if nontraumatic, a vascular lesion such as an aneurysm is the implied cause of the bleeding. SAH and intraparenchymal hemorrhage may coexist. Intraventricular hemorrhage means that blood is visualized within the ventricles by cranial CT, and it is most often present with other types of intracranial hemorrhage. intracranial hemorrhages outside the brain substance are referred to as extraaxial hemorrhages and include both subdural hemorrhages and epidural hemorrhages. Although uncommon exceptions exist, extraaxial hemorrhages almost always have a traumatic etiology. The term hemorrhagic stroke might literally describe abrupt symptoms with any of the previously mentioned hemorrhages, but it is sometimes used in a more restrictive sense to describe hemorrhagic changes in an area of ischemic stroke to the point of being visible on cranial CT; this is termed hemorrhagic transformation of ischemic stroke.

Fig. 103.1 Computed tomography scan: supratentorial intracerebral hematoma.

Note the bright white appearance consistent with an acute hemorrhage. The anatomic location is thalamic.

Fig. 103.2 Computed tomography scan: acute subarachnoid hemorrhage.

Blood density is not as dramatic as in Figure 103.13. Hydrocephalus with enlarged temporal horns of the lateral ventricle is present.

Fig. 103.3 Computed tomography scan: acute subdural hematoma.

Note the crescent-shaped hemorrhage extending the length of the left hemisphere. The mottled appearance is consistent with ongoing bleeding.

Fig. 103.4 Computed tomography (CT) scan: acute epidural hematoma with the “swirl” sign.

This is a slice from a repeated CT scan of the patient in Figure 103.10 taken approximately 1 hour later. The marbled density of the clot is consistent with ongoing hemorrhage. Note the lens shape of the hematoma.

Fig. 103.5 Computed tomography scan: hemorrhagic transformation of ischemic stroke.

See Table 103.1, Types of Intracranial Hemorrhage, online at www.expertconsult.com

Table 103.1 Types of Intracranial Hemorrhage

TYPE OF HEMORRHAGE	CORRESPONDING FIGURES IN TEXT	FINDINGS IN FIGURES
Intraparenchymal (synonyms: intracerebral, lobar, hypertensive)	Fig. 103.1	Blood within the substance of the brain; thalamic hemorrhage
Subarachnoid	Fig. 103.2	Acute hemorrhage with blood in the subarachnoid spaces
Subdural	Fig. 103.3	Blood external to the brain; crescent-shaped hemorrhage
Epidural	Fig. 103.4	Blood external to the brain; lens-shaped hemorrhage
Hemorrhagic transformation of ischemic stroke	Fig. 103.5	Hemorrhage within a wedge-shaped area of ischemia

Intracranial bleeding may be of either arterial or venous origin. Because of the closed nature of the cranial vault, any increase in intracranial volume from bleeding may result in increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). As a mass expands, some initial compensation occurs in the form of diminished intracranial vascular and cerebrospinal fluid volume. However, at some point the compensatory mechanisms fail and ICP will dramatically rise with a further increase in size of the mass. A key concept is CPP, the effective blood pressure exerted on the intracranial contents. CPP is equal to mean arterial pressure (MAP) minus ICP:

If ICP increases abruptly or if MAP falls, CPP decreases and central nervous system ischemia may follow and exacerbate the neuronal injury.

Hemorrhages also cause injury by direct tissue destruction or compression of adjacent structures. Edema formation around a hematoma may further increase the mass effect. For example, with cerebellar hemorrhages, tissue damage may cause the initial symptoms, but increased ICP and rapid progression to coma result from compression of the adjacent brainstem.

Spontaneous intraparenchymal hemorrhages (e.g., intracerebral hemorrhages, lobar hemorrhages, hypertensive hemorrhages) are most often associated with chronic hypertension. Cerebral amyloid angiopathy is increasingly being recognized as a contributing process in the elderly. Chronic excessive alcohol use is also a risk factor. Hemorrhage usually originates from rupture of small penetrating branch arteries of the vessels at the base of the brain ¹ (Fig. 103.6).

Fig. 103.6 Common sites and sources of intracerebral hemorrhage.

Intracerebral hemorrhages most commonly involve the cerebral lobes, with origin from penetrating cortical branches of the anterior, middle, or posterior cerebral arteries (A); the basal ganglia, with origin from ascending lenticulostriate branches of the middle cerebral artery (B); the thalamus, with origin from ascending thalamogeniculate branches of the posterior cerebral artery (C); the pons, with origin from paramedian branches of the basilar artery (D); and the cerebellum, with origin from penetrating branches of the posterior inferior, anterior inferior, or superior cerebellar arteries (E).

Serial cranial CT demonstrates that many intracerebral hemorrhages expand over the course of several hours.² The initial hemorrhage may infiltrate the white matter with little direct destruction, but continued hematoma expansion, white matter edema, additional hemorrhage from surrounding vessels, and the development of hydrocephalus may all contribute to increased ICP and secondary neuronal injury. The frequency of anticoagulant-associated intracerebral hemorrhage is increasing.³ Warfarin therapy does not appear to increase hematoma volume initially, but it does increase the risk for later hematoma expansion.⁴

SAH literally means “blood in the subarachnoid space.” Trauma is the most common cause. Spontaneous, or nontraumatic, SAH has an entirely different differential diagnosis. About 80% of spontaneous SAHs are caused by rupture of saccular (berry) aneurysms of the intracranial vessels, which are commonly located near intracranial arterial bifurcations of the circle of Willis ^5,⁶ (Fig. 103.7). Aneurysms are often named after the vascular site of origin, such as the anterior communicating artery or middle cerebral artery. Aneurysms that develop following vascular infection from endocarditis are termed mycotic aneurysms. Some aneurysms also cause symptoms without rupture from a mass effect or from emboli originating within the aneurysm. Rupture of an intracranial aneurysm abruptly raises ICP and leads to the onset of symptoms. The bleeding may be confined to the subarachnoid space, or a hematoma may extend into the brain substance and create an intraparenchymal hemorrhage, which in turn may rupture into the ventricles. Vasospasm of the vascular tree related to the aneurysm typically takes hours to develop and may worsen regional ischemia.