Approach to the Comatose Patient

Michael P. Merchut

Interpersonal communication and cognitive behavior require sufficient wakefulness, arousal, or alertness. Patients in the persistent vegetative state appear conscious or awake at times, but have little to no communicative or cognitive ability. Coma is the unconscious, sleeplike state of patients who are unresponsive to stimuli. Coma may be due to severe, even lethal, brain damage, or to potentially treatable or reversible causes. Comatose patients thus require prompt evaluation, followed by appropriate therapeutic intervention.

Arousal is a function of the ascending reticular activating system (ARAS), a complex pathway from pons to midbrain to intralaminar thalamic nuclei and basal forebrain, with diffuse cortical connections. Single structural lesions, such as an ischemic infarct or tumor, may produce coma by directly disrupting this pathway in the upper brainstem. However, a unilateral cerebral hemispheral lesion does not produce coma unless it creates enough edema and midline shift to adversely affect the ARAS bilaterally, typically at the thalamic level. Coma may also occur from extensive, severe, bilateral cortical lesions, such as multiple hemorrhages, or from metabolic processes suppressing cortical function in a global way, such as drug intoxication or hypoglycemia. If treated immediately, hypoglycemic coma may resolve completely, as may other toximetabolic etiologies. Certain causes of coma, such as fulminant encephalitis, are progressively fatal, and the patient never wakens. In other situations, such as anoxic encephalopathy, the patient may “wake up” after several days of coma, yet remain in a persistent vegetative state with poor or no cognitive recovery.

I. EVALUATION

A. History.

1.Sudden onset of coma is suggestive of the following:

Intracranial hemorrhage (prodromal severe headache may accompany subarachnoid hemorrhage [SAH] from a ruptured intracranial aneurysm, or occur with cerebral hemorrhage).
Critical brainstem infarction or multiple embolic cerebral infarcts.
Significant cerebral hypoperfusion after cardiopulmonary arrest.
Observed or unwitnessed head trauma.

2. Confusion or delirium preceding coma is suggestive of a toximetabolic etiology (organ dysfunction or infection, electrolyte disorder, medicinal or drug toxicity).

3. Important information to obtain immediately consists of the following:

Current medications, especially any diabetic, anticonvulsant, cardiac drugs, or warfarin.
Any history of adverse or allergic medicinal reactions.
Any history of recent head trauma, febrile or other illness, or previous neurological symptoms.
Any use of recreational drugs.

B. Physical examination.

1. A rapid general or systemic examination may provide important clues for the etiology of coma.

Hypertension to an extreme degree may point to causes other than an acute cerebral hemorrhage or infarction, including hypertensive encephalopathy, cocaine abuse, or eclampsia.
Hypotension reflects hypovolemia, cardiogenic or septic shock.
Fever accompanies systemic or CNS infections, as well as malignant hyperthermia, neuroleptic malignant syndrome, or serotonin syndrome.
Hypothermia after cold exposure may even mimic brain death.
Cutaneous bleeding around the eyes or mastoid area accompanies skull fractures. More diffuse hematomas suggest a systemic bleeding disorder. Infective endocarditis may cause “splinter” nailbed or palmar/plantar hemorrhages, producing coma by means of cerebral infarcts or abscesses.
Jaundice and ascites may be noted in hepatic coma patients, as well as hepatosplenomegaly.
An arrhythmia or heart murmur may be clues for cardiogenic shock, cerebral cardioemboli, or infective endocarditis.
Once cervical spine stability is assured, the finding of nuchal rigidity suggests infective meningitis or SAH, but may disappear in deeper stages of coma.
Papilledema evolves a few hours after severe elevation in intracranial pressure. The funduscopic examination may also reveal preretinal “fluid level” hemorrhages from subarachnoid bleeding or retinal hemorrhages from infective endocarditis.

C. Although the neurological examination

in coma is limited, it offers not only a means of localizing the level of neurological deficit, but also serves as a serial measurement of improvement or deterioration. Developed initially for use in trauma patients, the Glasgow Coma Scale is an easy and reproducible scoring system for all medical personnel, as is the more recently developed FOUR Score (see Table 5.1), which also assesses brainstem reflexes and breathing patterns.

1. Motor responsiveness.

Record your observations of the verbal and motor responses from the patient, rather than using brief terms (stuporous, obtunded) with variable meaning.
Verbal responses include oriented conversation, disoriented communication, meaningless words or sounds, to unresponsiveness.
Motor responses include spontaneous limb movements, limb movements on command, limb withdrawal to noxious stimuli, to unresponsiveness.

TABLE 5.1 Coma Scales

Glasgow Coma Scale	Full Outline of UnResponsiveness (FOUR)
Eye response	Eye response
4, eyes open spontaneously	4, eyelids open or opened, tracking, or blinking to command
3, eyes open to command	3, eyelids open but not tracking
2, eyes open to pain	2, eyelids closed but open to loud voice
1, no eye opening	1, eyelids closed but open to pain
	0, eyelids remain closed with pain
Motor response	Motor response
6, follows commands	4, thumbs up, fist or peace sign
5, localizes pain	3, localizing to pain
4, withdraws from pain (flexion)	2, flexion response to pain
3, decorticate posturing to pain	1, extension response to pain
2, decerebrate posturing to pain	0, no response to pain or generalized myoclonus status
1, no motor response
	Brainstem reflexes
Verbal response	4, pupil and corneal reflexes present
5, oriented and converses	3, one pupil wide and fixed
4, disoriented and converses	2, pupil or corneal reflexes absent
3, uses inappropriate words	1, pupil and corneal reflexes absent
2, incomprehensible sounds	0, absent pupil, corneal and cough reflex
1, no verbal response
	Respiration
	4, not intubated, regular breathing pattern
	3, not intubated, Cheyne-Stokes breathing pattern
	2, not intubated, irregular breathing
	1, breathes above ventilator rate
	0, breathes at ventilator rate or apnea