Postanoxic Coma - Anoxia

Acquired brain injury (ABI) is caused by a variety of insults, including trauma, stroke, tumor, infection, and hypoxia. A portion of ABI patients suffer from postanoxic coma.

Diagnosis

Indications for Testing

Predict outcome in coma >48 hours after anoxic event without evident metabolic or structural etiology and in conjunction with clinical presentation

Laboratory Testing

  • Recent reports suggest combining somatosensory evoked potentials (SSEP) with specific serum neurobiochemical markers
    • Neuron specific enolase (NSE)
      • Poor outcome prediction highly likely when N20 SSEP is absent and NSE >33µg/L at 72 hours post event (Mondello, 2014)
      • Not specific – false positives in the setting of central nervous system (CNS) injury combined with shock or hemolysis
    • S-100B protein (Mercier, 2013)
      • Levels indicating poor outcome not concretely established
      • Level normals are highly variable in children
        • Concentrations tend to be inversely correlated with age
      • Not specific for brain injury – increased serum concentrations are found in patients with melanoma, liver and renal injury, inflammation, and infection
    • Alpha-synuclein
      • Higher levels correlated with death (Mondello, 2013)

Background

Epidemiology

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

Pathophysiology

  • Brain oxygen depleted within 20 seconds
  • Central nervous system (CNS) 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, producing cytoxic cascade that activates brain-damaging processes
    • Further damage may ensue and result in neuronal death
    • These processes may result in permanent brain damage
  • S-100B involved in signal transduction and found in glial cells
    • Released into peripheral circulation after neural injury
    • Considered surrogate marker of CNS injury

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

ARUP Lab Tests

Primary Tests

Use as a tumor marker for evaluation of neuroendocrine tumors

Useful as a biomarker of various central nervous system (CNS) pathologies and as a tumor marker for malignant melanoma

May be useful as a biomarker of various CNS pathologies

Related Test

Use as a nonspecific marker of neuronal damage

Medical Experts

Contributor

Genzen

Jonathan R. Genzen, MD, PhD

Associate Professor of Clinical Pathology, University of Utah

Chief Operations Officer, Medical Director of Automated Core Laboratory and Farmington Health Center Clinical Laboratory, at ARUP Laboratories

References

Additional Resources