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Taking the history and performing the physical examination suggested in Chapter 25 should help identify almost all significant neurologic or mental disease. Information gathered from the history that would warrant further investigation includes a previous need for postoperative ventilation in a patient without inordinate lung disease,
Although preoperative treatment of most neurologic disorders has not been reported to lessen perioperative morbidity, knowledge of the pathophysiologic characteristics of these disorders is important in planning intraoperative and postoperative management. Thus, preoperative knowledge about these disorders and their associated conditions (e.g., cardiac arrhythmias with Duchenne's muscular dystrophy or respiratory and cardiac muscle weakness in dermatomyositis) may reduce perioperative morbidity. A primary goal of neurologic evaluation is to determine the site of the lesion in the nervous system. Such localization to one of four levels (supratentorial compartment, posterior fossa, spinal cord, peripheral nervous system) is essential for accurate diagnosis and appropriate management. (Disorders accompanied by increased intracranial pressure and cerebrovascular disorders are discussed in Chapter 53 .)
Little is known about specific anesthetic or perioperative or periprocedural choices that alter outcome for a comatose patient, but as for all other conditions, it is imperative to know the cause of the coma so that drugs can be avoided that might worsen the condition or that might not be metabolized because of organ dysfunction. First, the patient should be observed. Yawning, swallowing, or licking of the lips implies a "light" coma with major brainstem function intact. If consciousness is depressed but respiration, pupillary reactivity to light, and eye movements are normal and no focal motor signs are present, metabolic depression is likely. Abnormal pupillary responses may indicate hypoxia, hypothermia, local eye disease, or drug intoxication with belladonna alkaloids, narcotics, benzodiazepines, or glutethimide; pupillary responses may also be abnormal, however, after the use of eye drops. Other metabolic causes of coma include uremia, hypoglycemia, hepatic coma, alcohol ingestion, hypophosphatemia, myxedema, and hyperosmolar nonketotic coma. Except in extreme emergencies, such as uncontrolled bleeding or a perforated viscus, care should be taken to render the patient as metabolically normal as possible before surgery. This practice and documenting the findings on the chart preoperatively lessen any confusion regarding the cause of intraoperative and postoperative problems. However, too rapid correction of uremia or hyperosmolar nonketotic coma can lead to cerebral edema, a shift of water into the brain as a result of a reverse osmotic effect caused by the dysequilibrium of urea concentration.
The physical examination can be extremely helpful preoperatively in assessing the prognosis.[622] [623] [624] [625] [626] Arms flexed at the elbow (i.e., decorticate posture) imply bilateral hemisphere dysfunction but an intact brainstem, whereas extension of the legs and arms (bilateral decerebrate posture) implies bilateral damage to structures at the upper brainstem or deep hemisphere level. Seizures are often seen in patients with uremia and other metabolic encephalopathies. Hyperreflexia and upward-pointing toes suggest a structural CNS lesion or uremia, hypoglycemia, or hepatic coma; hyporeflexia and downward-pointing toes with no hemiplegia generally indicate no structural CNS lesion.
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