Treatment of coma involves identification of the etiology of the brain failure and initiation of specific therapy directed at the underlying cause. Brain-saving procedures must be performed while diagnostic steps are taking place. Again, stabilization with attention to airway, ventilation, and circulation assume priority. Attention should be paid to readily reversible causes of coma such as hypoglycemia and opioid toxicity. Management steps are summarized in Tab.'® .2.2.1-9..

The "coma cocktail" that was routinely given to all comatose patients has come under scrutiny. Certainly, hypoglycemia is common, but with rapid glucose determinations, empiric administration of dextrose is not always necessary. It has been axiomatic that thiamine should be administered before glucose administration. This may remain reasonable in a patient with a suspected history of alcohol abuse or malnutrition, but there is no empiric evidence that the administration of thiamine must precede glucose administration in any acute setting. Naloxone, an opiate antagonist, should be given with known or suspected opiate overdose. While administration of opiate antagonists need not be routine, anecdotal reports of opiate reversal when the condition was masked or unsuspected abound. Routine use of flumazenil in unknown coma is not recommended.22

Several rapid decisions face the emergency physician. An early decision involves assigning the patients to probable traumatic or structural coma etiology or to a toxic-metabolic etiology. History and physical examination allow that initial categorization with many patients but maintaining a low threshold for CT scanning is encouraged because exceptions to the tentative clinical diagnosis are frequent. Further, consultants will invariably request this investigative modality except when the emergency clinician misses an obvious reversible cause. However, patients should be stable prior to obtaining this test, and causes such as carboxyhemoglobinemia and hypothermia, conditions easy to overlook at times, should also be sought.

If history, physical, or neuroimaging suggests increased intracranial pressure, specific steps may be indicated to reduce or ameliorate any further rise in ICP. In the intubated patient, hyperventilation with PaCo2 to roughly 30 mmHg will reduce cerebral blood volume and transiently lower ICP. Any noxious stimulus including "bucking" the ventilator will increase ICP. Paralysis and sedation should be readily used. Osmotic diuretics such as mannitol (0.5 to 1 g/kg) will decrease intravascular volume and brain water and may transiently reduce ICP. In cases of brain edema associated with tumor, steroids such as dexamethasone will reduce edema over several hours. Data to recommend specific therapy is lacking, and preferences among individuals and institutions vary greatly; early communication is encouraged with consultants and admitting physicians. Management of ICP is discussed in detail in Chap...247,

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