Coma

I. Background
Coma is a sustained period (>1 hour) of unconsciousness that is distinguished from sleep by the inability to arouse the patient (1,2).
II. Pathophysiology
Coma is a nonspecific manifestation of central nervous system (CNS) impairment that may be due to any number of insults. There is a large differential of possible causes that may be subdivided into focal (e.g., stroke) versus nonfocal (e.g., hypoxia), traumatic versus nontraumatic, or CNS versus systemic causes. The end result is that there is a global dysfunction of both the cerebral hemispheres or the ascending brain stem and diencephalon activating systems (2).
III. Evaluation
The history and physical examination can often elicit the potential causes of coma.
A. History
After ensuring the stability of the airway, breathing, and circulation (ABCs), it is essential to gather pertinent history from friends, family members, and any medical personnel. A sudden loss of consciousness would suggest causes such as intracerebral hemorrhage, seizure, cardiac arrhythmias, or drug overdose. A slower progression implies a much larger list of differential diagnoses.
B. Physical examination
The examination should pay particular attention to the following:
  • Motor responses Are there any purposeful movements? Is there withdrawal from pain? Any posturing? Are the movements symmetric? Asymmetry may imply a structural lesion or a more focal cause. Flexor or extensor posturing implies an impairment of the cerebral hemispheres possibly from metabolic causes, brain stem lesions, or transtentorial herniation. Patients with flexor posturing generally have a better prognosis.
  • Respiration Is there a respiratory effort? If so, what pattern (Cheyne-Stokes, cluster breathing, hyperventilation)? Cheyne-Stokes respiration is more likely with transtentorial herniation, upper brain stem lesions, or metabolic causes. Cluster breathing may be associated more with posterior fossa lesions or elevated intracranial pressure. Hyperventilation is more likely due to metabolic acidosis, hepatic encephalopathy, or analgesic drugs.
  • Pupillary response Are the pupils equal? Are they reactive? Anisocoria implies a structural cause. Pinpoint pupils may be from pontine hemorrhages or drug toxicity. Fixed dilated pupils may follow anoxic or ischemic injury.
  • Eye movements Are the eyelids open? Does the patient blink? Do eye movements conjugate or do they deviate? Do the eyes move with the passive movement of the patient's head (oculocephalic or doll's eye maneuver)(1)?
  • Temperature Is it low, normal, or elevated? Low temperature would suggest drug intoxication, hypoglycemia, hypothyroidism, or environmental exposure (3). A fever suggests infectious causes, heat stroke, neuroleptic malignant syndrome, status epilepticus, or anticholinergic overdose (2).
C. Testing
The imaging of the head using either a computed tomography (CT) scan or a magnetic resonance imaging (MRI) should be done as quickly as possible to rule out structural causes and to guide emergent treatment (e.g., hemorrhage or herniation). Laboratory testing should include an arterial blood gas, a complete blood count, a comprehensive metabolic profile, toxicology (including ethanol, commonly abused drugs, acetaminophen, and salicylates), ammonia, and lactate. Blood and cerebrospinal fluid should also be cultured. An electroencephalogram (EEG) should be performed to look for unrecognized seizures. The EEG can also give clues to the cause and the prognosis (2).
IV. Diagnosis
A. Differential diagnosis
The differential diagnosis of coma is broad but is usually established based on history, physical, laboratory findings, EEG, and imaging. The differential diagnosis, subdivided based on normal versus abnormal CT scan or MRI, includes:
  • Normal CT scan or MRI
    • Drugs/overdose: alcohol, sedatives, opiates
    • Metabolic: anoxia, electrolyte disturbances, glucose abnormalities, thyroid disorders, hepatic coma
    • Severe infections: pneumonia, meningitis, encephalitis, sepsis
    • Shock
    • Seizure-related conditions
    • Severe hypothermia or hyperthermia
    • Concussion.
  • Abnormal CT scan or MRI
    • Hemorrhage or infarction
    • Infection: abscess, empyema
    • Brain tumor
    • Traumatic injuries
    • Others (3).
B. Clinical manifestations
The patient lacks self-awareness and makes no purposeful movements. Vital signs, including the ability to maintain respiratory function may be impaired; so, immediate attention to ensuring stable ABCs is essential. Coma must be distinguished from other similar clinical entities such as vegetative state, catatonia, severe depression, neuromuscular blockade, or akinesia plus aphasia (1,2).
References
1. Burst JCM. Coma. In: Rowland LP, ed. Merritt's neurology, 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2005:20–28.
2. Michelson DJ, Ashwal S. Evaluation of coma and brain death. Semin Pediatr Neurol 2004;11(2):105–118.
3. Ropper AH. Acute confusional states and coma. In: Braunwald E, Hauser SL, et al. eds. Harrison's principles of internal medicine, 15th ed. Philadelphia, PA: McGraw-Hill, 2001:132–140.