A barbiturate-induced coma, or barb coma, is a temporary state of unconsciousness brought on by a controlled dose of a barbiturate drug, usually pentobarbital or thiopental.
Barbiturate comas are used to protect the brain during major brain surgery, such as the removal of arteriovenous malformations or aneurysms. Coma may also be induced to control intracranial hypertension caused by brain injury.
Barbiturate-induced comas are used when conventional therapy to reduce intracranial hypertension has failed. Barbiturate dosing is geared toward burst suppression-that is, reducing brain activity as measured by electroencephalography. This reduction in brain activity has to be balanced against the potential side effects of barbiturates, which include allergic reactions and effects on the cardiovascular system.
One of the greatest hazards associated with brain injury is intracranial hypertension. Brain injury may be caused by an accidental head injury or a medical condition, such as stroke, tumor, or infection. When the brain is injured, fluids accumulate in the brain, causing it to swell. The skull does not allow for the expansion of the brain; in effect, the brain becomes compressed.
If the pressure does not abate, oxygenated blood may not reach all areas of the brain. Also, the brain tissue may be forced against hard, bony edges on the interior of the skull. In either case, the brain tissue may die, causing permanent brain damage or death.
Barbiturates reduce the metabolic rate of brain tissue, as well as the cerebral blood flow. With these reductions, the blood vessels in the brain narrow, decreasing the amount of swelling in the brain. With the swelling relieved, the pressure decreases and some or all brain damage may be averted.
Controversy exists, however, over the benefits of using barbiturates to control intracranial hypertension. Some studies have shown that barbiturate-induced coma can reduce intracranial hypertension but does not necessarily prevent brain damage. Furthermore, the reduction in intracranial hypertension may not be sustained.
Inducing a barbiturate comais usually kept in reserve for cases inwhich conventional treatments for controlling intracranial hypertension have failed. Before coma is induced, intracranial hypertension may be treated by hyperventilation; by facilitation of blood flow from the brain; by decompressive surgical procedures, such as draining excess fluids from under the skull or from the chambers within the brain (ventricles); or by drug therapy, including osmotherapy, diuretic agents, or steroids.
An estimated 25%of barbiturate-induced comas are accompanied by severe side effects. The side effects of barbiturates, especially the depressive effect on the cardiovascular system, can be too risky for some patients. Other side effects include impaired gastrointestinalmotility and impaired immune response and infection. Since barbiturates depress activity in the brain, measurements of brain activity may be unreliable. Careful monitoring of the patient is required to ensure nutritional needs are being met and to guard against complications, such as lung infection, fevers, or deep vein blood clots.
In many patients who do not respond to conventional therapy, barbiturate-induced coma can achieve the necessary control of intracranial hypertension.