Clinical Vignette

A 72-year-old woman with history of hypertension noticed tingling in the right arm. Within 30 minutes, her right leg buckled and she fell. Her husband helped her up and she was able to walk without support. She rested, but within an hour, she developed speech difficulties and more definite right-sided weakness.

She was brought to the emergency department (ED) and was noted to have mild right arm weakness and some word-finding difficulties. Her blood pressure was 140/80 mm Hg. She got up to go to the bathroom, walked approximately 10 ft, and collapsed on the floor. She was then globally aphasic, with left gaze deviation (i.e., paralysis of gaze to the right) and right hemiplegia. Within 10 minutes, she became gradually unresponsive.

She was intubated for airway protection and taken for brain CT scanning, which demonstrated a large left putaminal hemorrhage. Soon thereafter, she had bilaterally dilated fixed pupils. The vestibular-ocular reflexes were lost. Within another 10 minutes, she was determined brain dead.

The preceding vignette demonstrates the classic presentation of a primary intracerebral hemorrhage (ICH with a rapidly evolving focal neurologic deficit). Its progressively increasing size led to increased intracranial pressure with coma from downward herniation of the uncus onto the brainstem and ultimately irreversible neurologic damage. The only means to prevent ICH is appropriate therapy of its major risk factor, hypertension.

There are two forms of intrinsic cerebral hemorrhage, primary ICH, which has a predilection to affect the striatum, thalamus, midbrain, pons, and cerebellum, and subarachnoid hemorrhage (Chapter 57). ICH comprises approximately 10% of all strokes in the Caucasian population and up to 20% in the Asian population. Over the past several years, improved treatment of hypertension has decreased the number of patients experiencing ICH.

Hypertension is a major risk factor for intracerebral hemorrhages in patients between the ages of 40 and 70. A small proportion of intracerebral hemorrhages in patients older than age 60 years is not directly related to hypertension and is primarily caused by amyloid angiopathy. Furthermore, the increased use of oral anticoagulant therapy in the elderly population has led to higher rates of warfarin-associated ICH. Warfarin anticoagulation increases the risk of intracerebral hemorrhage fivefold, and some studies have estimated that 18% of intracerebral hemorrhages admitted to the hospital are related to its use. Of interest is that most bleeds in patients on warfarin occur when the INR is within the recommended therapeutic limits. Secondary, less common causes of intracerebral hemorrhages include primary and metastatic tumors of the brain and in younger individuals cerebral hemorrhage associated with underlying arterial venous malformation or cavernous angioma.

Pathophysiology of Hypertensisve Primary Ich

Intracranial hemorrhage is a rapidly evolving process that may progress over hours or days. The pressure effects of the initial hemorrhage lead to mechanical disruption and tearing of surrounding vessels with subsequent gradual expansion of the hematoma out from the original center. Rebleeding is the most feared early complication of ICH and occurs in approximately 40% of patients. Rebleeding usually occurs within the first 24 hours but, on occasion, has been reported up to a week later. The underlying pathological mechanism of primary hypertensive ICH is attributable to either the formation of miliary microaneurysms or primary arteriolar degeneration (lipohyalinosis and weakening of the blood vessel intima and media wall layers) (Fig. 58-1). The presence of miliary aneurysms is directly related to hypertension but is not necessarily the initial site of bleeding, and cases of hypertensive ICH outside the areas of microaneurysms have been noted. This suggests that degeneration of the arteriolar smooth muscle wall is likely an important factor in the evolution of ICH. Hypertensive intracerebral hemorrhages have a predilection to occur in the basal ganglia and the thalamus. The arterioles in these structures are likely more vulnerable to degenerative changes brought on by diffuse, large pressure pulses over time.

Figure 58-1 Hypertensive Intracerebral Hemorrhage: Pathogenesis.

Although hypertension is considered an important risk factor for ICH, studies are inconsistent in estimating the exact risk of ICH in hypertensive patients. It has been noted in some studies that up to 90% of patients with ICH have evidence of hypertension at the time of presentation. Other important risk factors include smoking, alcohol consumption, black race, and low total serum cholesterol levels. The latter is likely to be an anomaly of population studies. Patients with ICH and concomitantly low serum cholesterol levels tend to be older than age 80 years and, on average, have higher diastolic pressures. The effect of lower cholesterol levels, particularly LDL, on increasing the incidence of ICH is likely small and the mechanism remains unclear; whether it is causative or an epiphenomenon of another process warrants further investigation.

Clinical Presentation

Intraparenchymal hemorrhages vary in presentation depending on the site of the bleeding (Fig. 58-2). In approximately 60% of patients, neurologic symptoms develop gradually or stepwise over a period of hours. To some extent, the location and size of the hematoma predict clinical outcome.

Figure 58-2 Intracerebral Hemorrhage: Clinical Manifestations Related to Site.

Headache occurs at presentation in approximately 40% of patients with ICH. Less commonly, headache develops within a few days after the ictus. Intracerebral hemorrhages presenting with headache are often located at the brain surface or within the cerebellum. Depression in the level of consciousness and vomiting occur in 50% of patients, particularly those with large cerebellar bleeds. Seizures occur at onset in up to 10% and are seen most commonly with lobar bleeds in the anterior circulation. There are rare incidences of patients with deep hemorrhages having seizures. The subsequent risk for seizures in ICH patients is up to 29% for those with lobar hemorrhages but only 4% for those with deep hemorrhages. Other symptoms seen in association with ICH include low-grade fever without obvious infection, cardiac arrhythmias, and dysautonomia, especially with pontine bleeds. A description of some of the most common symptoms at different sites of ICH follows.

Infratentorial Hemorrhages

Cerebellar Hemorrhage

Clinical Vignette

A 58-year-old woman with substantial history of arterial hypertension presented to the ED with a 1-hour duration of acute-onset headache, gait unsteadiness, and left arm incoordination. On examination, the patient was alert and oriented but had left-sided dysmetria, gait ataxia, and left CN-VI and CN-VII palsies. Her BP was 200/110 mm Hg. Urgent head CT showed a 3-cm cerebellar hemorrhage with slight compression of the fourth ventricle. Antihypertensive treatment aiming for a MAP of 100–120 mm Hg was initiated.

Within 30 minutes after the CT scan, the patient’s level of consciousness deteriorated, necessitating intubation. She was brought immediately to the operating room for evacuation of the hematoma and responded well. One month later, her examination was remarkable for only mild clumsiness of the left arm and a slightly wide-based gait.

As in the preceding vignette, patients with cerebellar hemorrhages can deteriorate rapidly, even “in front of one’s eyes,” but can still respond exceptionally well with expeditious surgical intervention. Most cerebellar hemorrhages are associated with hypertension. However, approximately 10% of primary cerebellar hemorrhages are caused by AVM, tumors, blood dyscrasias and the use of warfarin anticoagulation. Headache, spinning vertigo, nausea, vomiting, and, most commonly, unsteady gait characterize the typical presentation. Some headaches are occipital, but many involve the orbital and supraorbital areas. The most reliable symptoms of a hemispheric cerebellar hemorrhage include headache, vomiting, nystagmus, ipsilateral limb ataxia with, at times, ipsilateral peripheral CN-VI and CN-VII palsies and horizontal nystagmus.

The less common vermian hemorrhages often resemble a pontine hemorrhage and can progress rapidly to coma, making it difficult to identify specific early clinical signs that can differentiate one from the other. Cranial nerve palsies are related to involvement of adjacent pontine structures or stretching secondary to increased cerebellar pressure. In hypertensive bleeds involving the vermis or the cerebellar hemispheres, the superior cerebellar artery is most often involved.

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

Wilson Disease Major Depression Other Autoimmune CNS Demyelinating Disorders Coma, Vegetative State, Brain Death, and Increased Intracranial Pressure Lumbar Radiculopathy Subarachnoid Hemorrhage

Stay updated, free articles. Join our Telegram channel

Join