Coma is not an independent disease entity but a reflection of an underlying disease process.
Coma results from bilateral, diffuse cerebral hemisphere dysfunction or brainstem (midbrain or pons) involvement of the ascending reticular activating system, or a combination of the two.
Metabolic or systemic disorders generally cause depressed consciousness without focal neurologic findings.
Proper management of the unconscious patient includes an aggressive pursuit of the medical history.
The goal of the neurologic examination of the comatose patient is to determine the presence, location, and nature of the underlying process creating the decreased level of consciousness and also to determine the prognosis of the patient’s condition.
Following the establishment of an airway with stabilization of respiration and maintenance of circulation, certain laboratory tests and therapeutic measures are undertaken that can occur concurrently with the acquisition of a pertinent history and a neurologic examination.
DEFINITIONS AND CLINICAL SYNDROMES
A discussion of the evaluation and treatment of the comatose patient requires one to define certain terms regarding different states and levels of consciousness and unconsciousness. The examination and diagnostic studies must be carried out in an organized and systematic manner with documentation that is clear to all members of the health team. The definitions of different levels of consciousness are, by themselves, often confusing and misleading. When one physician’s understanding of terms (e.g., lethargy, stupor, or obtundation) differs from that of his or her colleagues, one may think that a patient’s condition has deteriorated, although only the terminology has changed between the observers. It is better to specifically describe a patient’s movements, and reactions to painful stimuli, for example, rather than to categorize the patient as being lethargic, semicomatose, or stuporous.
Consciousness is defined as the awareness of one’s self and the environment. This is a poor definition, however, because one can argue that a sleeping person is unconscious—that is, unaware of himself or herself and his or her environment. Clinically, however, no one regards a sleeping person as unconscious: he or she can be aroused to appropriate physical and mental activity with appropriate, non-noxious stimuli.
Consciousness comprises a continuum from full alertness to deep coma, or total unresponsiveness. Drowsiness or lethargy is characterized by easy arousal with light stimuli. There may be a verbal response or appropriate limb movements to pain. Stupor reflects arousability by persistent or vigorous stimuli only, and the arousal is incomplete. There is little verbal response, but limb movements still may be appropriate to the stimulus. Mental and physical activities are reduced to a minimum. Coma reflects the state in which the patient cannot be aroused to make purposeful responses. This is subgrouped into light coma, in which there may be reflex, primitive, or disorganized responses to noxious stimuli (e.g., decorticate and decerebrate responses), and deep coma, in which there is no response to painful stimuli.
Psychogenic unresponsiveness (hysterical coma) is a psychiatric phenomenon in which the patient appears unresponsive but is physiologically awake. The heart and respiratory rates are usually normal. The patient lies with the eyes closed, and the eyelids are frequently difficult to separate (forced eye closure). Muscle tone is normal. Although there may be little resistance to passive movement, suspending the patient’s hand over his or her face usually results in its falling to the side instead of directly downward. Pupils are equal and reactive unless certain eyedrops have been used. Ice water caloric testing produces nystagmus, a sign seen only in awake patients. The electroencephalogram (EEG) reveals a waking record.
The “locked-in” syndrome is an important condition to recognize. The patient appears to be in a coma but has essentially all higher mental activities intact. The syndrome most frequently is related to pontine infarction due to basilar artery thrombosis or embolism. There is an interruption of the descending corticobulbar and corticospinal tracts, resulting in quadriplegia and paralysis of lower cranial nerves. The patient is unable to talk, breathe, or move his or her extremities. Because the ascending reticular activating system is spared, however, arousability and wakefulness are present. There also is sparing of fibers controlling eye blinking and vertical eye movements, though horizontal eye movements are almost always impaired. Thus, the patient’s only means for communication may be using eye blinks (Morse code). The ramifications of not recognizing this disturbing clinical condition are obvious.
▪ SPECIAL CLINICAL POINT: Every patient, no matter how deep in coma he or she appears to be,should be asked to open and close the eyes and to move them up and down, to assess for the locked-in syndrome.
The vegetative state is somewhat clinically opposite of the “locked-in” syndrome. The patient appears to be awake with intermittent eye opening but is unable to attain higher mental functions. Simply stated, there is arousal but no awareness. There is no language comprehension or intelligible speech nor responses to visual or auditory stimuli. Sleep-wake cycles may return, but there is no return of higher mental activity.
▪SPECIAL CLINICAL POINT: The vegetative state occurs in the setting of severe cortical dysfunction with relative brainstem sparing, such as in patients who survive a cardiopulmonary arrest with consequent severe cerebral anoxia. The term “persistent vegetative state” implies that the patient has been in a clinical vegetative state for more than 30 days.
▪SPECIAL CLINICAL POINT: The minimally conscious state is seen in patients with marked impairment of consciousness but who have evidence of any awareness of the environment.
Patients in the minimally conscious state can exhibit some deliberate or cognitively mediated behavior. This may be manifested by the ability to follow very simple commands, show some purposeful behavior, or have minimal verbalization.
It is not uncommon for patients with acute onset of global aphasia to be diagnosed initially as being in coma. The patient is indeed unable to comprehend, communicate, or carry out simple verbal commands. The diagnosis may be established by noting that the patient appears to be awake and alert, often with deviation of the eyes to the left with a right hemiplegia.
COMA
Anatomy
In the evaluation of the comatose patient, it is necessary to consider the physiologic and anatomic abnormalities that result in decreased level of consciousness.
▪ SPECIAL CLINICAL POINT: Coma results from bilateral, diffuse cerebral hemisphere dysfunction or brainstem (midbrain or pons) involvement of the ascending reticular activating system, or a combination of the two.
Coma is unusual with unilateral cerebral hemisphere disease unless there is a dysfunction of the other hemisphere or secondary pressure or destruction of brainstem structures. Most large cerebral hemisphere infarctions will result in a slightly decreased level of consciousness, but the patient still can be aroused to elicit some purposeful movements or higher mental activity. Rare exceptions may be patients with large, acute lesions affecting the dominant cerebral hemisphere. In contrast, profound coma may result from very small infarctions in the brainstem affecting the ascending reticular activating system.
A unilateral hemispheral mass lesion, such as a tumor, abscess, or expanding hemorrhage, frequently will present with unilateral focal neurologic symptoms and signs. On continued enlargement of the mass, there may be a compression of the contralateral cerebral hemisphere or a downward herniation of the ipsilateral temporal lobe, creating distortion and compression of the brainstem (transtentorial herniation). At this point, coma will ensue. There is also the suggestion that horizontal displacement of the brain at the level of the pineal body may correlate more closely with levels of consciousness than downward displacement with brainstem compression.
Metabolic processes usually affect both brainstem and cerebral hemispheres to produce coma. This likely reflects a direct interference of the metabolic activity of the neurons. Initially, the patient is drowsy, but coma ensues as the metabolic process worsens.
ETIOLOGY
▪ SPECIAL CLINICAL POINT: Coma is not an independent disease entity but a reflection of an underlying disease process.
The causes of coma can be divided into two main categories: (1) those of primary central nervous system (CNS) disease and (2) those of metabolic or systemic depression (Table 6.1). The latter group contains the more common causes of a depressed level of consciousness.
TABLE 6.1 Common Causes of Coma
Cause
Comments
Coma Secondary to Primary Brain Injury or Disease
Infection
Bacterial meningitis
Nuchal rigidity; CSF shows pleocytosis, increased protein; glucose may be decreased; meningeal enhancement on MRI
Viral encephalitis
May have focal findings; CSF shows increased lymphocytes, increased protein, normal or slightly decreased glucose; positive PCR for HSV; possible focal abnormalities on MRI
Abscess
Focal findings; positive CT or MRI scan; history of ear or sinus infection or HIV or endocarditis; CSF shows mildly increased protein, increased cells, negative cultures
Tumor
Primary or metastatic
Focal findings; progressive course; may have papilledema
Cerebral infarction
Basilar occlusion or bilateral internal artery occlusion
Usually no coma unless bilateral or acute, large dominant hemisphere, or involving brainstem reticular activating system
Primary central nervous system disorders may or may not produce focal abnormalities on examination.
▪ SPECIAL CLINICAL POINT: Metabolic or systemic disorders generally cause depressed consciousness without focal neurologic findings.
In these instances, the clinician does not expect to find unequal pupils, signs of weakness on only one side, or asymmetric reflexes. A previous neurologic injury, however, may render certain neurons more susceptible to a metabolic insult and accentuate clinical signs related to the older injury. A metabolic encephalopathy in a patient with an old stroke that had fully resolved thus could produce a reemergence of the former weakness in a focal pattern, even though the cause of the current coma is a metabolic one. With correction of the metabolic abnormality, the focal signs would be expected to disappear again, unless there was further focal damage superimposed.
HISTORY AND EXAMINATION
A history should be taken, but unfortunately this is often incomplete, nonexistent, or misleading. A search for “less likely” causes for coma is necessary when treatment for the “obvious” cause from the history obtained does not change the patient’s clinical status.
▪ SPECIAL CLINICAL POINT: Aggressive management of the unconscious patient includes an aggressive pursuit of the history.
For example, metabolic abnormalities most often are associated with subacute onset of coma, whereas a history of a more rapid course is suggestive of cardiac or cerebrovascular cause or drug overdose.
There should be a search for evidence of trauma. Battle’s sign (purple and blue discoloration of the mastoid skin area), blood in the external auditory canal, or blood noted behind the tympanic membranes may signify a temporal bone or basal skull fracture. Raccoon eyes (purple discoloration of the eyelid and orbital regions) may signify orbital or basal skull fractures. Cerebrospinal fluid rhinorrhea or otorrhea also suggests a skull fracture.
One should check carefully for nuchal rigidity, but several factors must be considered in doing so. If there is any suspicion of a cervical neck fracture, there should be no manipulation of the neck. In deep coma, nuchal rigidity may be lacking despite its presence in a lighter level of consciousness. Finally, some patients with a CNS infection or subarachnoid hemorrhage may not manifest nuchal rigidity initially in the course of their illness.
The odor of the patient’s breath may indicate the cause for the coma. Alcohol gives its characteristic smell; hepatic coma is often associated with a musty odor; and a fruity or acetone smell is characteristic of ketoacidosis.
After a screening, general physical examination, an orderly, systematic neurologic examination, is undertaken.
▪ SPECIAL CLINICAL POINT: The goal of the neurologic examination is to determine the presence, location, and nature of the underlying process creating the decreased level of consciousness and also to determine the prognosis of the patient’s condition.
Respiratory patterns yield information regarding the activity of different cerebral areas. When one develops bilateral cerebral hemisphere dysfunction (essentially, functioning at the diencephalic level), Cheyne-Stokes respiration may occur. This respiratory pattern is associated with periods of hyperpnea alternating with periods of apnea. There is a regularity to the respirations: first a gradual buildup of respirations to the level of hyperpnea and then a gradual tapering off of respirations to apnea. The periods of apnea may last up to 30 seconds or more and may be accompanied by decreased responsiveness and miosis. It is believed that Cheyne-Stokes respiration relates to an abnormal response of carbon dioxide-sensitive respiratory brain centers. There is an increased ventilatory response to carbon dioxide stimulation, creating hyperpnea. After the concentration of carbon dioxide drops below the level at which the centers are stimulated, the apnea phase appears and continues until the carbon dioxide reaccumulates and the cycle repeats itself. Because sleep induces further cerebral- depressing mechanisms, Cheyne-Stokes respiration may be seen in some patients during sleep, whereas they exhibit normal breathing patterns while awake. Cheyne-Stokes respiration is, by itself, not a serious prognostic sign. Although it can be seen in focal primary CNS problems, it also can be seen early in many metabolic and systemic problems.
Central neurogenic hyperventilation appears when lower brain centers are involved; it is noted with dysfunction at the midbrain or the upper pons and often is associated with pulmonary edema. There are continuous, regular, and rapid respirations up to 40 or 50 times per minute. Arterial blood gases reveal a respiratory alkalosis with decreased Pco2 and increased pH. The Po2 must be greater than 70 or 80 mm Hg. If the Po2 is not higher than that level, it raises the possibility of an extracerebral cause (hypoxemia) for the respiratory problem. In reality, most cases of sustained hyperventilation in comatose patients are not central neurogenic hyperventilation. Cardiac, pulmonary, and metabolic (e.g., diabetes, uremia, hepatic, salicylates) problems must be ruled out as possible causes of the hyperventilation.
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