Clinical Evaluation and Management

Imaging studies such as cranial CT or MRI can assist in determining the presence of complications following an anoxic insult. These studies can differentiate between an ischemic infarct, intracerebral hemorrhage, and a mass lesion involving the cortex or the brain stem. A CT without contrast is helpful in suspected cases of cerebral hemorrhage. Within the first 72 hr of intracerebral hemorrhage onset, a cranial CT usually provides greater resolution than a MRI. In addition, CT and MRI are useful to demonstrate cerebral herniation prior to clinical presentation. Both positron emission tomography (PET) and magnetic resonance spectroscopy have also been used to follow cerebral metabolic function in individuals suffering from cerebral anoxic injury. Recently, MRI with the apparent diffusion coefficient of water has become a sensitive tool of neuronal physiology and may represent a reliable indicator of progressive neuronal injury following cerebral ischemia.

The electroencephalogram (EEG) can be useful in assessing cortical dysfunction and identifying the presence of epileptic activity. The EEG is classified in terms of increasing severity in five categories. Grade I

represents normal alpha with theta-delta activity; grade II is theta-delta activity with some normal alpha activity, grade III is dominant theta-delta activity with no normal alpha activity, grade IV is low-voltage delta activity with alpha coma (nonreactive alpha activity), and grade V represents an isoelectric tracing. In individuals suffering postanoxic coma, grade I is compatible with a good prognosis, grades II and III have no definitive predictive value, and grades IV and V are compatible with a poor prognosis and infrequent recovery.

In addition to the EEG, evoked potentials can provide information regarding the functional state of the cerebral cortex following cerebral anoxia. Soma-tosensory evoked potentials determine the functional integrity of the spinal cord posterior columns, brain stem medial lemniscus, thalamus, and frontoparietal sensorimotor cortex. During the loss of bilateral cortical responses despite the etiology of the coma, afflicted individuals can experience a high mortality rate. In anoxic coma, patients who maintain normal responses throughout their illness maintain a good prognosis but may have permanent neurologic sequelae. Brain stem auditory evoked potentials correlate with brain stem dysfunction during coma. A simultaneous latency increase of all components is consistent with progressive ischemia of the posterior fossa and a decrease in cerebral perfusion pressure. Although brain stem auditory evoked potentials are rarely modified by exogenous factors, they can be altered by hypothermia, anesthetics, and barbiturates.

Recovery of the comatose patient is dependent on the rapid treatment of the underlying disorder. Prompt attention must be directed to the restoration of respiratory, hemodynamic, and metabolic homeosta-sis. The respiratory rate and its pattern should be documented prior to therapeutic measures such as intubation and mechanical ventilation. Following initial examination of the respiratory rate, an adequate airway should be obtained. If intubation is required in a comatose patient, one must rule out the existence of a neck fracture prior to hyperextension of the head for endotracheal tube insertion. Arterial blood gases should be obtained to ensure adequate oxygenation (oxygen saturation >90%) and to monitor serum acid/base status.

On the establishment of adequate ventilation, blood should be obtained for determination of serum glucose, routine chemistries, and toxicology. Since patients in coma may have poor nutrition and are susceptible to Wernicke's encephalopathy, initially 100 mg of thiamine should be given intravenously.

Bedside stat glucose determinations should be employed to identify hypoglycemia. In such cases, 50 mg of 50% dextrose should be administered. Although administration of one ampule of dextrose is not detrimental in cases ofhyperosmolar coma, identification of hyperglycemic states is important since elevated serum glucose may promote ischemic damage in cases of anoxic coma.

The hemodynamics of the patient should be closely controlled. Hypertension may be secondary to Cush-ing's reflex with increased intracranial pressure or a result of brain stem ischemia. Hypotension may be indicative of myocardial infarction, hemorrhagic shock, sepsis, or sedative-hypnotic drug overdose. Bradycardia associated with elevated blood pressure suggests brain stem compression or increased intracra-nial pressure. One must note, however, that elevated intracranial pressure does not decrease the heart rate in all instances. Reversible causes of transtentorial hernia-tion, such as subdural hematoma, should be immediately considered before cardiovascular collapse ensues.

Status epilepticus following cardiac arrest can result in progressive anoxic brain damage and requires immediate attention. Following airway stabilization, generalized convulsions can initially be treated with diazepam intravenously in up to a 10-mg total dose. This is to be followed by a phenytoin loading dose of 18 mg/kg (50 mg/min) intravenously. If status epilepticus continues, 20 mg/kg phenobarbital intravenously should be administered. Persistent convulsions at this point require general anesthesia. In the case of generalized convulsions that are not consistent with status epilepticus, phenytoin orally in appropriate daily dose (dependent on body size) should be maintained in individuals with either EEG or CT/ MRI evidence of a persistent epileptic focus (hemorrhage, neoplasm, large ischemic infarct, abscess, etc).

Measurement of the patient's rectal temperature is a vital component of the initial evaluation. Hypothermic patients with temperatures below 34°C(93.2°F) should be warmed slowly to a body temperature higher than 36°C (96.8°F). Since hypothermia below 80°F results in coma, resuscitative measures are indicated in all hypothermic patients even if vital signs are absent. Hypothermic patients have recovered following cardiac arrest, presumably because of the protective effects of low body temperature and depressed cerebral oxygen requirements. In addition, hypothermia has been shown to reduce neuronal death in the hippocampus and caudate putamen in animal models with forebrain ischemia and is currently under investigation in the clinical setting.

Some centers advocate aggressive treatment of raised intracranial pressure to significantly reduce mortality. Measurement of intracranial pressure can be performed through the use of epidural monitoring or through intraventricular pressure measurements. Intracranial pressure monitoring can differentiate between active hydrocephalus and mass lesions requiring surgical intervention. Intracranial pressure monitoring has also been linked to prognosis. Most patients with a maximum intracranial pressure increase of less than 30 mmHg experience good recovery, whereas a pressure increase above 25-30 mmHg represents a great risk for brain tamponade.

E. Clinical Prognosis

Several studies have examined the prognosis of individuals who remain in coma for extended periods following cardiac arrest. Patients can suffer memory impairment if coma duration is at least 6 hr. In some groups of patients, a poor prognosis was evident in individuals who lacked a motor response to pain. Poor recovery has also been associated with the presence of generalized myoclonus status, which can be suggestive of diffuse neocortical damage. More comprehensive studies evaluating individuals in coma following diffuse global ischemia have demonstrated that individuals with absent pupillary light reflexes never regain independent daily function. However, following the initial insult, the early onset of incomprehensible speech, orienting spontaneous eye movements, or the ability to follow commands were indicative of a good prognosis. Individuals with the best chance of recovery have preserved brain stem function following the initial insult. The most favorable sign of a good outcome is incomprehensible speech, such as moaning. At Day 1, the following signs are each associated with at least a 50% chance of regaining independent function: any form of speech, orienting spontaneous eye movements, intact oculocephalic or oculovestibu-lar responses, ability to follow commands, and normal skeletal tone.

II. METABOLIC COMA A. Historical Background

The patient in metabolic coma may be the cause of some of the greatest diagnostic errors ever made. Some historians believe that the description of Jesus resurrecting his friend Lazarus from the dead may represent one of the first reports of an individual in coma that eventually recovered from a metabolic disability. In addition, recent descriptions, documented approximately 150 years ago, discuss the diagnosis of''apparent death'' as a possible synonym for coma secondary to metabolic illness.

B. Etiology

Although levels of attention and alertness are affected in metabolic coma, each disease process also yields a specific clinical picture. For example, severe anoxic ischemia following cardiac arrest will produce coma, whereas alcohol withdrawal will initially result in an agitated delirium. Metabolic encephalopathy is often reversible if the underlying systemic disorder is corrected promptly.

Under physiologic conditions, glucose is the brain's only substrate and crosses the blood-brain barrier by facilitated transport. Each minute, the normal brain requires 5.5 mg (31 mmol) of glucose per 100 grams of tissue. However, one of the most significant complications of exogenous insulin therapy is hypoglycemic coma. If there is hypoglycemia, defined in adults as a blood glucose concentration of less than 40 mg/dl, loss of cortical function ensues secondary to cerebral cortex and brain stem dysfunction. Neurologic presentation during hypoglycemia can be variable. Some patients will present with focal motor or sensory deficits, whereas others become comatose.

A significant proportion of cases of metabolic coma are a result of drug ingestion, with at least half of the afflicted individuals administering multiple drugs. Proper diagnosis relies heavily on the physical examination since an accurate or complete history may be unobtainable from the patient. Toxic drug screens of blood and urine will assist in the diagnosis. Excessive barbiturate consumption results in hypothermia, hypotension, and possible apnea. An individual's pupils remain small but reactive with intact ciliospinal reflexes.

Alcohol ingestion may be indistinguishable from other metabolic disorders, such as depressant drug intoxication or hypoglycemia. In addition, progressive loss of consciousness may be complicated by underlying cerebral trauma such as a subdural hematoma. Evidence of "alcohol on the breath'' provides insight into the etiology of the coma but does not distinguish between pure alcohol intoxication or a "cocktail" of alcohol, sedative, and hypnotic drugs. A blood alcohol level and drug screen should be determined in individuals with alcohol and/or multiple drug abuse who present with coma.

Benzodiazepines can result in stupor or coma without respiratory depression. Clinical trials have studied treatment with the benzodiazepine antagonist fluma-zenil. Flumazenil is also considered to have a diagnostic value in cases of mixed-drug intoxication.

Opiate and heroin overdoses occur by either par-enteral injection or sniffing of the agent. Neurologic impairment secondary to opiate abuse is currently on the rise despite a reduction in use during previous years. Systemic complications include hypothermia, hypotension, bradycardia, respiratory slowing, and pulmonary edema. Coma does not require chronic administration and can result following an initial injection of the opiate. Opiate coma is characteristically associated with pinpoint pupils reactive to bright light.

Toxicity from cocaine administration has systemic, psychiatric, and neurologic manifestations. Neurologic complications of cocaine use range from benign headaches to coma. Focal neurologic manifestations include subarachnoid hemorrhage, anterior spinal artery syndrome, lateral medullary syndrome, transient ischemic attacks, and cerebral infarction. Although the exact mechanism of cocaine-related cerebral vascular disease is unknown, adrenergic stimulation and surges in blood pressure may play a significant role.

Overmedication with prescription agents can also lead to coma. The most notable neurologic manifestations of tricyclic antidepressants are seizures and coma. Lithium toxicity can progress to seizures, lethargy, and coma. Treatment consists of supportive care with artificial ventilation, fluid, and electrolyte infusions in conjunction with hemodialysis. Valproate can lead to coma during excessive drug levels or during carnitine insufficiency. Amantadine, an antiviral agent employed in the therapeutic regimes for Parkinson's disease and fatigue syndromes, has been reported to induce coma in the presence of end-stage renal disease. Ibuprofen, a popular over-the-counter analgesic agent, is rarely associated with nervous system toxi-city, but abuse of this agent can result in metabolic acidosis and lead to coma.

In addition to drug administration, other metabolic mechanisms that lead to coma should be considered. For example, endocrine dysfunction that occurs with severe hypothyroidism or renal insufficiency can result in coma. Infectious processes, such as cerebral malaria and meningitis, lead to increased intracranial pressure and subsequent coma if allowed to progress without treatment. Less common causes of coma, such as ciguatera food poisoning and hyperammoniemia, should also be considered when the diagnosis appears obscure.

Defeat Drugs and Live Free

Defeat Drugs and Live Free

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