Coma
Proper evaluation of the comatose patient involves obtaining a history from family and friends, performing a rapid directed physical and neurologic examination, and obtaining certain laboratory studies, while the patient’s airway and vital signs are protected. These tasks often are done simultaneously (e.g., one member of the medical team secures the airway, while another talks to the family). An attempt is made to delineate the cause of coma in hopes of finding a treatable process. Treatable causes of coma include metabolic derangements, ingestions, and at times, supratentorial processes in the brain (e.g., epidural hematoma). Anatomically, coma implies bilateral hemisphere dysfunction; structural, drug-induced, or metabolic, unilateral hemisphere disease with compression of the brainstem (e.g., epidural hematoma); or brainstem dysfunction (e.g., pontine hemorrhage or compression from a posterior fossa mass). If certain basic points are established when examining the comatose patient, the extent of structural central nervous system (CNS) derangement and the cause usually can be determined. One must determine if the patient is comatose or in another state of altered responsiveness (Table 5.1). Comatose patients do not awaken to stimulation of any kind. They may respond with vocalizations, movements, and changes in blood pressure or pulse, but do not interact in any meaningful way with the examiner.
ABCs
Before obtaining a history and physical, make sure the patient’s airway, breathing, and circulation (ABCs) are stable. Draw blood for glucose, and give 1/2 to 1 amp of 50% dextrose intravenously (IV) (for hypoglycemia). Give thiamine 100 mg IV to avoid precipitating Wernicke syndrome in patients with alcoholism. Although traditionally it was considered risky to give glucose before providing thiamine, there are no data to support this supposition. Consider naloxone for narcotic ingestion. Then, proceed with history, physical, and other diagnostic testing. Hypoglycemia is a common and treatable cause of coma.
TABLE 5.1. States of Decreased Responsiveness | ||||||||||||||||||||
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HISTORY
Learn from family or friends whether the patient has a preexisting condition that may explain the coma. Does the patient have diabetes? Is he or she a drug addict or an alcoholic? Does the patient take sleeping pills? Has the patient been depressed? Has the patient sustained recent head trauma? Were there episodes of a similar nature in the past?
If a preexisting medical condition exists, is there a factor that may have exacerbated it, and precipitated the coma (e.g., chronic liver disease, gastrointestinal bleeding, uremia and infection, a seizure disorder, or failure to take anticonvulsant medication)?
A review of all medications, including sleeping pills, and all medical conditions may give hints about the cause of coma.
Review the events leading up to the coma. A prodromal febrile illness may suggest meningitis or encephalitis, whereas a despondent patient may suggest the possibility of an overdose.
EXAMINATION
Observe the patient carefully:
Is there decorticate posturing (arm flexion with leg extension); implying hemisphere or diencephalon dysfunction that may be caused by destructive lesions, or may be secondary to a metabolic derangement?
Is there decerebrate posturing (extension of legs and arms), implying dysfunction of midbrain or upper pons on a structural or metabolic basis?
Is the patient yawning, swallowing, or licking the lips? If so, coma cannot be deep and brainstem function is probably intact.
Are there repetitive, multifocal, myoclonic jerks (brief muscle twitches in varied muscle groups)? These are characteristic of metabolic encephalopathies, such as hypoxia or uremia. Profound multifocal myoclonus may occur after anoxic injury and implies a poor prognosis.
Is there evidence of seizure activity, which sometimes may be as subtle as eye blinking, eye deviation, or facial myoclonus? If so, consider antiepileptic drugs and electroencephalogram (EEG) monitoring. Continued nonconvulsive status may cause irreversible brain injury if not treated.
Does the patient move only one side, suggesting a hemiparesis?Related posts:
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