Imaging with cranial CT or MRI can be useful in metabolic coma to differentiate between an ischemic infarct, an intracerebral hemorrhage, and a mass lesion involving the cortex or the brain stem. However, these imaging studies are often unremarkable during metabolic coma. Patients in coma who present with cranial nerve deficits and posturing likely suffer from a mass lesion involving the cortex or the brain stem. However, patients in coma with unilateral masses may not initially suffer from transtentorial herniation. In this group, CT and MRI demonstrate horizontal displacement at the level of the pineal body.
In some centers, continuous bedside monitoring of regional cerebrocortical blood flow with laser Doppler flowmetry is employed to follow fluctuations in the cerebral microcirculation in comatose individuals. PET and single positron emission computerized tomography (SPECT) provide an alternative method of imaging that also assesses cerebral function. MRI spectroscopy may provide suggestive evidence of neuronal function through N-acetylaspartate/creati-nine ratios. Blood flow and metabolic studies can also be used as diagnostic aids to differentiate individuals in coma from patients with the "locked-in" syndrome.
Monitoring with EEG is useful in assessing cortical dysfunction since it is sensitive to fluctuations in cerebral blood flow and metabolism. In addition, EEG can detect the presence of occult seizure activity, which reportedly can occur in more than 30% of intensive care patients suffering from metabolic disorders. In patients with overt convulsions, the EEG can also be used to temper anticonvulsant treatment in the comatose patient to prevent or reduce neuronal cell loss. In addition to issues of care, the EEG has been used to assess prognosis. In patients with terminal coma, onset of abnormal EEG changes may sometimes be suggestive of a poor outcome.
Evoked potentials can provide information concerning the functional state of the cerebral cortex and brain stem. Patients with bilateral absence of cortical responses exhibit mortality rates of 73-98%. Others report that motor evoked potentials, although less sensitive than somatosensory evoked potentials during coma, are helpful in directing management. The bilateral absence of motor evoked potentials is suggestive of a poor outcome during metabolic coma. Brain stem auditory evoked potentials correlate with brain stem function and can provide a useful tool for the assessment of brain stem activity. Simultaneous latency increase of all components can be consistent with progressive ischemia of the posterior fossa and a decrease in cerebral perfusion pressure. Loss of the brain stem auditory evoked potentials is usually suggestive of an incumbent deterioration and death. Although brain stem auditory evoked potentials are not usually modified by exogenous factors, brain stem auditory evoked potentials can be falsely altered by hypothermia, anesthetics, and barbiturates.
Treatment of the comatose patient must be directed toward the restoration of respiratory, hemodynamic, and metabolic function. 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, 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 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 thiamine should be given intravenously. Bedside glucose determinations should be employed to identify hypoglycemia. Identification of hyperglyce-mic states is also important since elevated serum glucose may promote ischemic damage in cases of anoxic coma. Naloxone should be administered intravenously in cases of suspected opiate abuse, and flumazenil should be administered in cases of benzo-diazepine-induced coma.
Measurement of the patient's rectal temperature is a vital component of the patient's care. Hypothermia can be due to environmental exposure, near drowning, sedative drug overdose, hypothyroidism, and Wer-nicke's disease. 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. The presence of fever in a comatose patient requires investigation for an underlying infection.
Seizure control is also critical to the management of the metabolic comatose patient. Status epilepticus can result in permanent anoxic brain damage and requires immediate attention. Following airway stabilization, generalized convulsions can initially be treated with diazepam intravenously up to 10-mg total dose. This is to be followed by a phenytoin loading dose of 1000 mg (50 mg/min), but may be increased to 1500 mg if required.
In most cases, coma secondary to infection or sedative drug intoxication carries a low mortality rate. If ventilatory and hemodynamic support are supplied without delay, most individuals experience no residual neurologic impairment. However, complications can include cardiovascular collapse secondary to hypothermia, hypotension, dysrhythmias, myocardial infarction, or pulmonary edema.
In cases complicated by cerebral ischemia, patients can suffer permanent neurologic sequelae if coma duration is at least 6 hr. Individuals with absent pupillary light reflexes usually never regain independent daily function, but the early onset of incomprehensible speech, orienting spontaneous eye movements, or the ability to follow commands can be indicative of a good outcome following the initial insult.
Other factors also play a role in the eventual outcome from coma. Metabolic coma complicated by traumatic lesions, such as subdural hematoma, can have less than a 10% recovery rate. Comatose patients with increased plasma glucose, hypokalemia, elevated serum leukocyte counts, or absent P300 event-related potentials also have a poor prognosis.
In the 17th century, the human body began to be viewed as a system of subunits and independent compartments. This eventually led to the first human anatomical descriptions that mapped the body into different organs and tissues. As a result of this "subunit" or "compartment" theory, the Latin term herniation was employed to describe the protrusion of a portion of an organ or tissue through an abnormal passage.
Brain herniation may result from either supratentorial or subtentorial lesions. Supratentorial masses, such as those that result from lobar hemorrhage, cause brain shifts that can be termed cingulate, central (transtentorial), or uncal herniation. Cingulate herniation refers to the displacement of the cingulate gyrus under the falx cerebri with subsequent compression of the internal cerebral vein. A mass in the cerebral hemisphere that produces cingulate herniation can compress the ipsilateral anterior cerebral artery, producing subsequent vascular ischemia, edema, and progressive mass effect.
Downward displacement of the hemisphere with compression of the diencephalon and midbrain through the tentorial notch results in central hernia-tion. Lesions of the frontal, parietal, and occipital lobes initially can precipitate cingulate herniation that progresses to central herniation. Displacement of the diencephalon against the midbrain produces hemorrhage in the pretectal region and thalamus. The medial perforating branches of the basilar artery rupture during herniation of the midbrain and pons.
Uncal herniation involves shift of the temporal lobe, uncus, and hippocampal gyrus toward the midline with compression of the adjacent midbrain. During this process, the ipsilateral third cranial nerve and the posterior cerebral artery are compressed by the uncus and edge of the tentorium. Both central and uncal herniation can compress the posterior cerebral artery, resulting in occipital lobe ischemia. Further increased intracranial pressure results from compression of the aqueduct. In this instance, cerebral spinal fluid cannot drain from the supratentorial ventricular system, producing a pressure gradient between structures above and below the obstruction. In addition, expansion of the supratentorial volume can yield pressure necrosis of the parahippocampal gyrus.
Supratentorial herniation results in an orderly progression of neurologic dysfunction from the cerebral hemispheres to the brain stem. Exceptions to this observation exist. Massive cerebral hemorrhage can rapidly flood the ventricular system, compress the fourth ventricle, and result in acute medullary failure. Isolated medullary failure can also occur from withdrawal of cerebral spinal fluid by a lumbar puncture in a patient with incipient central herniation from a supratentorial mass.
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