Clinical History:

This 61-year-old man, who has a long history of alcohol abuse, was sitting on a bar stool when he was noted to suddenly fall to the floor. He was unable to arise and the paramedics were called. When they arrived, he was able to answer questions and he stated that he had a severe headache. Upon arrival to the hospital the admitting physical examination demonstrated a right hemiparesis. The patient became increasingly somnolent after admission.

Further history:

In spite of supportive care, the patient became comatose and died two hours after admission.

Image 1.1:

This is a CT scan of the patient's head upon admission. What is the probable diagnosis?

The scan shows a large hematoma in the deep basal ganglia on the left with shift of the brain to the right, occlusion of the Foramen of Monro, and enlarged lateral ventricles on the right. This represents an intraparenchymal bleed most likely due to long standing hypertension, although a vascular malformation could have caused a picture similar to this one. Hypertensive hemorrhages are most common in basal ganglia, but may also be seen in pons and cerebellum.

Image 1.2:

This is a coronal section of the brain and midbrain at autopsy. What is the mechanism of death in this case?

The coronal section of the hemispheres demonstrates a large hematoma in the basal ganglia on the left which has pushed the brain to the right. The left medial temporal lobe has been pushed medially and has caused a Duret hemorrhage in the midbrain (from uncal herniation and damage to the small perforating arteries supplying midbrain and pons). The bleeding into the brainstem caused death.

Answers:

1. What are possible causes of this acute incident?

There are several possibilities. Because of the acuteness of the symptoms, one should think of a vascular problem, either due to trauma or to underlying vessel disease. This man could have suffered a skull fracture and epidural hemorrhage upon hitting the floor. Embolic stroke, hypertensive bleed (from long-standing hypertension), or bleed from a vascular malformation are all possible. Bleeding into a tumor is another possibility.

2. What treatment could have prevented this event?

Treatment of hypertension with use of antihypertensive medications will produce a marked reduction in the incidence of hypertensive bleeds in the brain. It is important to do blood pressure screening for hypertension. Hypertension remains a "silent disease" for years, and patients do not know they have it, before enough organ damage occurs to produce clinical signs and symptoms. Hypertensive bleeds of the brain are a major cause of "stroke" that is the third most common cause of death.

The treatment of hypertension depends upon a variety of parameters, including the severity of the hypertension and the presence of other diseases. Persons with "high normal" pressures from 140-159/90-99 mm Hg can be followed to determine if the presence of organ damage or diabetes mellitus warrants pharmacologic therapy. Dietary modifications (reduction in salt intake) and exercise regimens with promotion of lifestyle modifications (stop smoking, lose weight) and having a pet (dog or cat) can aid in normalizing blood pressures in this range.

Persons with pressures above 160/100 mm Hg require drug therapy. Initial therapy typically consists of diuretics and/or beta-adrenergic blockers.

Diuretics aid in sodium excretion to reduce intravascular volume. The most common diuretics block sodium reabsorbtion and include the thiazides which act in the distal convoluted tubule, such as hydrochlorothiazide, and the loop diuretics, such as furosemide that act in the loop of Henle.

The beta blockers work by competitive inhibition of the effects of catecholamines on beta-adrenergic receptors. They can be cardioselective with primarilty beta-1 blocking effects, such as metoprolol, or non-selective with action on beta-2 receptors as well, such as propranolol.

Beta blockers are not indicated for persons who have had a myocardial infarction. Such persons who cannot tolerate beta blockers may benefit from a calcium channel blocker such as diltiazem that causes arteriolar dilation.

For persons with congestive heart failure or with diabetic nephropathy, the angiotensin converting enzyme (ACE) inhibitors such as captopril, are recommended. Angiotensin-II receptor blockers, such as losartan, may be used in persons who cannot tolerate the ACE inhibitors.

Much higher blood pressures, or malignant hypertension, require more aggressive therapies, such as sodium nitroprusside which is a potent direct vasodilator.

3. Is there any treatment after the event occurs?

Evacuation of the blood from a hypertensive bleed in this location is rarely helpful. Hypertensive bleeds into the cerebellum can be life saving, if evacuation is performed before tonsillar herniation and brainstem compression.



4. What happens if the patient does not regain consciousness?

A severe stroke can leave a patient unconscious. After a few days that condition will typically lead to something else: either death, regaining consciousness, or a vegetative state (recovery of brainstem function, including sleep-wake cycles and autonomic functions like breathing, blood pressure and temperature regulation, but no higher cortical functions). A "persistent vegetative state" is defined when a vegetative state lasts more than 3 months.

Since strokes are rarely expected, these decisions are usually make by people who know the patient, but who are not surrogates in the sense of having been named by the patient, and usually do not have any sort of advance directive to help guide their decisions. Yet they may be asked to make life or death decisions, such as whether to stop a ventilator or a feeding tube. They will be asked to use what is known as "substituted judgment" which means to do their best to figure out what the patient would have wanted in this situation. This is a way to indirectly respect the patient's wishes, a sort of substitute autonomy.