Loss of Consciousness or Coma

The most benign causes of syncope include syncope brought on by fear or pain, orthostatic hypotension, prolonged standing, or seizure. Dangerous causes of syncope that should concern you include syncope with exertion, because this suggests cardiac outflow obstruction, syncope without warning, suggesting an arrhythmia, syncope while recumbent, which also suggests an arrhythmia, or syncope associated with significant injury.

LOSS OF CONSCIOUSNESS OR COMA

A true coma is a level of unresponsiveness in which the patient cannot be awakened or aroused. This is an extreme form of impaired consciousness, in which there are varying degrees of mentation that do not represent full arousal or full coma. In order to have a coma, the disturbance must be in both cerebral hemispheres or must involve damage to the reticular activating system, which controls arousal. The reticular activating system is located in the pons, midbrain, and posterior diencephalon of the brain.

Causes of coma can be focal ischemia of the reticular activating system, hemorrhage of the same area, hypoxia, hypoglycemia, drug overdose, or uremia. Increased intracranial pressure for any reason can lead to coma plus a secondary risk of brain herniation. Psychiatric causes can look like coma but can be relatively distinguished from a genuine coma by the neurological examination.

Your examination should include an eye examination. The pupils can be mid-position and fixed, unequal, dilated, or pinpoint with a dysconjugate or paralyzed gaze. Examine the blink reflex as well as the oculocephalic reflex, which is the “doll’s eyes” examination, looking for movement in response to head rotation. Breathing and heart rate patterns can be abnormal. Cheyne-Stokes breathing, hypertension, and bradycardia can be present. The motor exam is variable, with completely flaccid muscles, muscle spasticity, myoclonus, decorticate posturing, or decerebrate posturing.

Your diagnostic process includes a neurological examination, urgent imaging of the brain, pulse oximetry, blood glucose measurement, electrolytes, CBC, and a urine drug screen. If there is evidence of increased intracranial pressure, this may have to be

measured. If seizures are suspected, get an electroencephalogram. A lumbar puncture can look for a CNS infection.

Other than a neurological examination, a general physical examination is warranted. Look for signs of trauma to the brain, such as contusions, skull fracture, rhinorrhea, and/or otorrhea. Hypothermia by itself can lead to coma and heatstroke can also lead to a coma. Petechiae or purpura along with systemic findings suggest CNS infection or sepsis. Needle marks can be seen with drug overdoses. Smell the breath for ketoacidosis or alcohol intoxication. The cardiac examination could suggest hypoperfusion of the brain.

The Glasgow coma scale is a standardized way of determining the degree of coma, especially after a head trauma. Figure 4 shows the Glasgow coma scale:

Figure 4.

Motor findings can indicate the severity of the CNS process. The most severely affected patient will have complete flaccidity because the lower brainstem is not responding. Next severe is decerebrate posturing because only the lower brain stem centers are intact. The next most severely affected patient will have decorticate posturing, from cortical injury only. Other findings that are less severe are asterixis and multifocal clonus.

As mentioned, the eye examination is important. Examine the fundi for evidence of papilledema, suggesting increased intracranial pressure. The oculocephalic reflex, if absent, suggests that the oculovestibular pathways are affected or that there is psychogenic unresponsiveness. A cold caloric test can also be done with cold water injected into the external ear. If the brainstem is normal, the eyes will deviate to the side of the irrigation. If the eyes do not move or if the gaze becomes dysconjugate, this is a less favorable prognosis because it means a deeper coma.

Respiratory patterns are also important. Cheyne-Stokes breathing suggest bilateral hemisphere involvement. Hyperventilation is seen with dysfunction of the upper pons or midbrain. Gasping breathing with respiratory pauses mean a pontine or medullary injury, which leads to respiratory arrest.

All comatose patients should have continuous pulse oximetry, bedside glucose measurement, and cardiac monitoring. A comprehensive metabolic panel and CBC, liver function test, and ammonia level should be draw. ABGs and carboxyhemoglobin level should be measured if carbon monoxide poisoning is suspected. Blood and urine testing for culture and toxicology should be done. ECG and chest x-ray may be indicated. The MRI exam or contrast CT scan will detect many intracranial lesions.

Besides supportive measures, including treatment of hypotension, thiamin should be given intravenously if Wernicke encephalopathy is suspected. Naloxone is given if opioid overdose is suspected. Treat all underlying metabolic diseases. Control increased intracranial pressure with propofol sedation, benzodiazepines, hyperventilation, and mannitol as an osmotic diuretic. Corticosteroids are helpful if the problem is vasogenic brain edema.