In the approach to the comatose patient, stabilization, diagnosis, and treatment actions overlap and are often performed simultaneously. Examination, laboratory procedures, and neuroimaging allow determination of the cause of coma in almost all patients in the ED. As with any patient, airway, breathing, and circulation issues need to be immediately addressed. Reversible causes of coma should always be considered. Hypoxia, hypoglycemia, hypo- and hypertension, and hyperthermia are readily diagnosed entities. Hypoglycemia is a frequent cause of acute coma. Rapid bedside determination of glucose may obviate the empiric administration of intravenous dextrose.

The paradox in evaluation of the comatose patient is that history often holds the key to diagnosis but the patient cannot verbally relate that history. Exploit all possible historical sources. EMS personnel frequently have valuable information about the scene including medication history or the possibility of poisoning or trauma. Caregivers, family, or witnesses may provide valuable information. Medical records may be of immense value if promptly available.

Knowing the tempo of onset of the coma is of great value. Abrupt coma suggests abrupt CNS failure with possible causes of trauma, catastrophic stroke, or seizures. Cardiac causes may also cause abrupt loss of consciousness. A slowly progressive onset of coma may suggest a progressive CNS lesion such as tumor or subdural hematoma. Metabolic causes such as hyperglycemia may also develop over several days.

The physical examination of the comatose patient presents other challenges. General examination and vital signs (including oxygen saturation and temperature) should receive special attention following stabilization and resuscitation. General examination may reveal signs of trauma or suggest other diagnostic possibilities of the unresponsiveness. For example, a toxidrome may be present that suggests diagnosis and therapy, such as the hypoventilation and small pupils found with opioid overdose.

Neurologic testing deviates from the standard examination. Fine tests of weakness in the alert patient, such as testing for pronator drift of the outstretched upper extremities, are not possible in the unresponsive patient. However, assessment of cranial nerves through pupillary examination, corneal reflexes, and oculovestibular reflexes may suggest focal CNS lesions. Abnormal extensor or flexor postures are nonspecific for localization or etiology of coma but suggest profound CNS dysfunction. Again, asymmetric muscle tone or reflexes raise the suspicion of a focal lesion. The goal of the physician is to rapidly determine if the CNS dysfunction is from diffuse impairment of the brain or if signs point to a focal (and perhaps surgically treatable) region of CNS dysfunction.

CT scanning is the neuroimaging procedure of choice. Acute hemorrhage is readily identified, as are midline shifts. No clear high-yield criteria for ordering CT scanning have been developed for the comatose patient. Because exceptions to the guideline for clinical assignment of patients to structural or nonstructural coma are frequent, CT is often obtained even in situations where the pretest probability is low. For example, detection of a clinically occult subdural hematoma might radically change management from supportive medical care to aggressive surgical intervention.

The medical community expects the emergency physician to stabilize the patient and to take initial diagnostic and therapeutic steps. The etiology of coma is discovered or strongly suspected in most patients during the ED evaluation. The system depends on the emergency physician to distribute the comatose patient to appropriate specialty services.

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