Coma is a common occurrence in intensive care units.

Epidemiology

• Prevalence
  • Approximately 20% of patients receiving mechanical ventilation
  • 80% of survivors of cardiac arrest are comatose following resuscitation

Pathophysiology

• Brain oxygen is depleted within 20 seconds
• Central nervous system neurons have sufficient glucose stores to support 5 minutes of brain activity
• Prolonged resuscitation or anoxia does not provide adequate circulation to the brain
• Brain becomes ischemic
• Ischemia produces cytoxic cascade with activation of damaging processes to the brain
• Further damage may ensue and result in neuronal death
• These processes may result in permanent brain damage
• In patients who remain comatose >48-72 hours after an anoxic event (eg, trauma, cardiac arrest), outcome assessment is difficult, yet necessary.  Predictive test indicators may be helpful in this assessment process.

Clinical Presentation

• Patient remains unconscious and minimally responsive or unresponsive to stimulation
• Absent brain stem reflexes (pupil, cornea, gag/cough responses); absent motor responses; absent vestibular reflexes (oculomotor - doll’s eyes and cold calorics)
• Seizures

Diagnosis

• Indications for testing: coma >72 hours after anoxic event without evident metabolic or structural etiology
• Laboratory testing
  • Recent reports suggest combining somatosensory evoke potentials (SSEP)  with specific serum neurobiochemical markers
    • Neuron specific enolase (NSE)
      • Enolase isoenzyme is a specific neurobiochemical marker for damage to neuronal brain tissue
        • Elevated in traumatic brain injury
        • Elevated in anoxic brain injury
    • S-100B protein
      • Released into peripheral circulation immediately following primary brain trauma
      • Predictive power of elevated serum S-100B is higher than that of traditional clinical indicators
• Poor outcome prediction is highly likely when (N20) SSEP  is absent and NSE >33 µg/L at 72º post event