What is a coma? |

Causes and Symptoms

Consciousness is defined by the normal wakeful state, with its self-aware cognition of past events and future anticipation. Disease or dysfunction that impairs this state usually causes readily identifiable conditions such as coma. The self-aware, cognitive aspects of consciousness depend largely on the interconnected neural networks of the cerebral hemispheres. Normal conscious behavior depends on the continuous, effective interaction of these systems. Loss of consciousness from medical causes can be brief (a matter of minutes to an hour or so) or it can be sustained for many hours, days, or sometimes even weeks. The longer the duration of the comatose state, the more likely it is to reflect structural damage to the brain rather than a transient alteration in its function.

The word “coma” comes from the Greek koma, meaning to put to sleep or to fall asleep. This state of unarousable unresponsiveness results from disturbance or damage to areas of the brain involved in conscious activity or the maintenance of consciousness—particularly parts of the cerebrum (the main mass of the brain), upper parts of the brain stem, and central regions of the brain, especially the limbic system. A wide spectrum of specific conditions can injure the brain and cause coma. The damage to the brain may be the result of a head injury or of an abnormality such as a brain tumor, brain abscess, or intracerebral hemorrhage. Often there has been a buildup of poisonous substances that intoxicates brain tissues. This buildup can occur because of a drug overdose, advanced kidney or liver disease, or acute alcoholic intoxication. Encephalitis (inflammation of the brain) and meningitis (inflammation of the brain coverings) can also cause coma, as can cerebral hypoxia (lack of oxygen in the brain, possibly attributable to the impairment of the blood flow to some areas). Whatever the underlying mechanism, coma indicates brain failure, and the organization of cerebral biochemical systems has been disrupted. Coma is easily distinguishable from sleep in that the person does not respond to external stimulation (such as shouting or pinching) or to the needs of his or her body (such as a full bladder).

Comas are classified according to the event or condition that caused the comatose state. Some of the most frequently encountered types of comas are traumatic coma, alcoholic coma, apoplectic coma, deanimate coma, diabetic coma, hepatic coma, metabolic coma, vigil coma, pseudo coma, and irreversible coma. Traumatic coma follows a head injury. It has a somewhat more favorable outcome than that of comas associated with medical illness. About 50 percent of patients in a coma from head injuries survive, and the recovery is closely linked to age: The younger the patient, the greater the chance for recovery. Alcoholic coma refers to the coma accompanying severe alcohol intoxication, usually more than 400 milligrams of alcohol per 100 milliliters of blood. This coma is marked by rapid, light respiration, usually with tachycardia and hypotension. Apoplectic coma is induced by cerebral, cerebellar, or brain-stem hemorrhage, as well as by embolism or cerebral thrombosis. The term “deanimate coma” refers to a deep coma with loss of all somatic and autonomic reflex activity. The maintenance of life depends wholly upon such supportive measures as assisted respiration, and cardiac arrest will quickly follow if the respirator is stopped; this may be a transient or irreversible state. Diabetic coma is the coma of severe diabetic acidosis. Hepatic coma is the coma accompanying cerebral damage resulting from degeneration of liver cells, especially that associated with
cirrhosis of the liver. “Metabolic coma” is the term applied to the coma occurring in any metabolic disorder in the absence of a demonstrable macroscopic physical abnormality of the brain. Vigil coma is defined as a state of stupor in which the patient is mute and shows no verbal or motor responses to stimuli although the eyes are open and give a false impression of alertness. Pseudo coma refers to states resembling acute unconsciousness but with self-awareness preserved. Irreversible coma, or brain death, occurs when the brain damage is so extensive that the organ enjoys no potential for recovery and can no longer maintain the body’s internal functions without life support.

Treatment and Therapy

Of the acute problems in clinical medicine, none is more difficult than the prompt diagnosis and effective management of the comatose patient. The difficulty exists partly because the causes of coma are so many and partly because the physician possesses only a limited time in which to make the appropriate diagnostic and therapeutic judgment.

Measurements of variations in the depth of coma are important in its assessment and treatment. In less severe forms, the person may respond to stimulation by, for example, moving an arm. In severe cases, the person fails to respond to repeated vigorous stimuli. Yet even deeply comatose patients may show some automatic responses, as they may continue to breathe unaided or may cough, yawn, blink, or show roving eye movement. These actions indicate that the lower brain stem, which controls these responses, is still functioning.

Assessment of the patient in a coma includes an evaluation of all vital signs, the level of consciousness, neuromuscular responses, and the reaction of the pupils to light. In most hospitals, a printed form for neurologic assessment is used to measure and record the patient’s responses to stimuli in objective terms. The Glasgow coma scale also provides a standardized tool that aids in assessing a comatose patient and eliminates the use of ambiguous and easily misinterpreted terms such as “unconscious” and “semicomatose.” Additional assessment data should include evaluation of the gag and corneal reflexes. Abnormal rigidity and posturing in response to noxious stimuli indicate deep coma.

The definitive treatment of altered states of consciousness requires removing, correcting, or halting the specific process responsible for the state to whatever degree possible. Often, accurate diagnosis and specific therapy require time, and the first priority is to protect the brain from permanent damage.

General treatment measures that apply to all patients include the following: assurance of an adequate airway passage and oxygenation; maintenance of proper circulation; intravenous administration of glucose or thiamine if the patient is undernourished; any measures necessary to stop generalized seizures; the restoration of the blood acid-base and osmolar balance; the treatment of any detected infection; the treatment and control of extreme body temperatures; the administration of specific antidotes for situations such as drug overdoses; control of agitation; and the protection of the corneas.

In the absence of the gag reflex, regurgitation and aspiration are potential problems. Tube feeding, if necessary, must be done slowly and with the head of the bed raised during the feeding and for about half an hour later. Absence of the corneal reflex can inhibit blinking and natural moistening of the eye. The cornea cannot be allowed to dry, since blindness can result; therefore, artificial tears are instilled in the eyes to keep them moist.

Once the cause of the comatose state has been determined, the appropriate steps should be taken to minimize or eliminate it whenever possible. For many causes of coma, rapid intervention and treatment can mean recuperation for the patient, such as in the cases of diabetes, removable hematomas, and drug overdose.

Comatose patients are predisposed to all the hazards of immobility, including impairment of skin integrity and the development of ulcers, contractures and joint disabilities, problems related to respiratory and circulatory status, and alterations in fluid and electrolyte balance. All these factors must be taken into consideration when dealing with the comatose patient.

The outcome from severe medical coma depends on its cause and, with the exception of depressant drug poisoning, on the initial severity and extent of neurologic damage. Depressant drug poisoning reflects a state of general anesthesia, and, barring severe complications, almost all patients who survive drug intoxication can recover physically.

The clinical tests most valuable for estimating the capacity for recovery after medical coma are identical to those used in making the initial diagnosis. Within a few hours or days after the onset of coma, many patients show neurologic signs that can differentiate, with a high probability, the future extremes of either no improvement or the capacity for good recovery. After a period of about six hours (except for patients on drugs), certain neurological findings begin to correlate with the potential for neurologic recovery and can predict the outcome of about one-third of patients who will not recover. By the end of the first day, tests can predict the two-thirds of the patients who will do well. With each successive day, the signs develop greater predictive power. Persistence of coma in an adult for more than four weeks is almost never associated with later complete recovery.

Perspective and Prospects

Attempts to define “coma” must give at least brief consideration to the concepts of consciousness. Consciousness involves not only the perception of stimuli but also the emotional implications of such stimuli, as well as the construction of intricate mental images.

Since the days of the ancient Greeks, people have known that normal conscious behavior depends on intact brain function and that disorders of consciousness are a sign of cerebral insufficiency. The range of awake and intelligent behavior is so rich and variable, however, that clinical abnormalities are difficult to recognize unless there are substantial deviations from the norm. Impaired, reduced, or absent conscious behavior implies the presence of severe brain dysfunction and demands urgent attention if recovery is to be expected. The brain can tolerate only a limited amount of physical or metabolic injury without suffering irreparable harm, and the longer the failure lasts, the narrower the margin between recovery and the development of permanent neurologic invalidism.

Since such researchers as Pierre Mollaret and Maurice Goulon first examined the question in 1959, many others have tried to establish criteria that would accurately determine that the brain is dead or about to die, no matter what therapeutic measures one undertakes. In 1968, the Harvard Medical School Ad Hoc Committee to Examine the Definition of Brain Death established criteria for determining irreversible coma, or brain death. These criteria are often used to complement the traditional criteria for determining death. All other existing guidelines, such as the Swedish, British, and United States Collaborative Study Criteria, include nearly identical clinical points but contain some differences as to the duration of observation necessary to establish the diagnosis as well as the emphasis to be placed on laboratory procedures in diagnosis.

Techniques such as computed tomography (CT) scanning, electroencephalography (EEG), and functional magnetic magnetic resonance imagery (fMRI) have transformed the process of diagnosis in clinical neurology, with technology sometimes replacing clinical deduction. The art of diagnosis, however, is to comprehend the whole picture—where the lesion is, what it comprises, and above all, what it is doing to the patient.

Advances in resuscitative medicine have made obsolete the traditional clinical definition of death, that is, the cessation of heartbeat. Cardiac
resuscitation can salvage patients after periods of asystole lasting up to several minutes. Cardiopulmonary bypass machines permit the patient’s heartbeat to cease for several hours with full clinical recovery after resuscitation. While respiratory depression formerly meant death within minutes, modern mechanical ventilators can maintain pulmonary oxygen exchange indefinitely. Such advances have permitted many patients with formerly lethal cardiac, pulmonary, and neuromuscular disease to return to relatively full and healthy lives. Abundant clinical evidence, however, demonstrates that severe damage to the brain can completely destroy the organ’s vital functions and capacity to recover, even when the other parts of the body still live. The result has been to switch the emphasis in defining death to a cessation of brain function. Brain death occurs when brain damage is so extensive that the organ has no potential for recovery and cannot maintain the body’s internal functions. Countries worldwide have adopted the principle that death occurs when either the brain or the heart irreversibly fails in its functions. In the United States, the time of brain death has been accepted as the time of the person’s death in legal terms.

The determination of whether a comatose patient is brain-dead or can possibly recuperate is extremely important. Issues such as organ transplant programs that require the donation of healthy organs and the economic and emotional expense involved in the treatment and care of a comatose patient make it critical to know when to fight for life and when to diagnose death.

In carrying out the many details of the physical care and assessment of the comatose patient, health care personnel must not lose sight of the fact that the patient is a fellow human being and a member of a family. One cannot always be sure exactly how much the patients are aware of what is being said or done as care is given. Whatever the level of awareness and response, comatose patients should be told what will be done to and for them, as they deserve the same respect afforded alert and aware patients.

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