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
  • Background
  • Lab Tests
  • References
  • Related Topics

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)


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


  • 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
Tests generally appear in the order most useful for common clinical situations. Click on number for test-specific information in the ARUP Laboratory Test Directory.

Neuron Specific Enolase 0098198
Method: Quantitative Enzyme-Linked Immunosorbent Assay

S-100B Protein, Serum 2001766
Method: Quantitative Enzyme-Linked Immunosorbent Assay

S100B, CSF 2013358
Method: Quantitative Enzyme-Linked Immunosorbent Assay


Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S, Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006; 67(2): 203-10. Reaffirmed Oct 2009. PubMed

General References

Berger RP. The use of serum biomarkers to predict outcome after traumatic brain injury in adults and children. J Head Trauma Rehabil. 2006; 21(4): 315-33. PubMed

Filippidis AS, Papadopoulos DC, Kapsalaki EZ, Fountas KN. Role of the S100B serum biomarker in the treatment of children suffering from mild traumatic brain injury. Neurosurg Focus. 2010; 29(5): E2. PubMed

Guzel A, Er U, Tatli M, Aluclu U, Ozkan U, Duzenli Y, Satici O, Guzel E, Kemaloglu S, Ceviz A, Kaplan A. Serum neuron-specific enolase as a predictor of short-term outcome and its correlation with Glasgow Coma Scale in traumatic brain injury. Neurosurg Rev. 2008; 31(4): 439-44; discussion 444-5. PubMed

Korfias S, Stranjalis G, Boviatsis E, Psachoulia C, Jullien G, Gregson B, Mendelow D, Sakas DE. Serum S-100B protein monitoring in patients with severe traumatic brain injury. Intensive Care Med. 2007; 33(2): 255-60. PubMed

Mercier E, Boutin A, Lauzier F, Fergusson DA, Simard J, Zarychanski R, Moore L, McIntyre LA, Archambault P, Lamontagne F, Légaré F, Randell E, Nadeau L, Rousseau F, Turgeon AF. Predictive value of S-100β protein for prognosis in patients with moderate and severe traumatic brain injury: systematic review and meta-analysis. BMJ. 2013; 346: f1757. PubMed

Mondello S, Buki A, Italiano D, Jeromin A. α-Synuclein in CSF of patients with severe traumatic brain injury. Neurology. 2013; 80(18): 1662-8. PubMed

Mondello S, Schmid K, Berger RP, Kobeissy F, Italiano D, Jeromin A, Hayes RL, Tortella FC, Buki A. The challenge of mild traumatic brain injury: role of biochemical markers in diagnosis of brain damage. Med Res Rev. 2014; 34(3): 503-31. PubMed

Nash DL, Bellolio F, Stead LG. S100 as a marker of acute brain ischemia: a systematic review. Neurocrit Care. 2008; 8(2): 301-7. PubMed

Ramaswamy V, Horton J, Vandermeer B, Buscemi N, Miller S, Yager J. Systematic review of biomarkers of brain injury in term neonatal encephalopathy. Pediatr Neurol. 2009; 40(3): 215-26. PubMed

Zandbergen EG, Hijdra A, Koelman JH, Hart AA, Vos PE, Verbeek MM, de Haan RJ, PROPAC Study Group. Prediction of poor outcome within the first 3 days of postanoxic coma. Neurology. 2006; 66(1): 62-8. PubMed

Medical Reviewers

Grenache, David G., PhD, Medical Director, Special Chemistry; Co-Director, Electrophoresis and Manual Endocrinology; Chief Medical Director, Clinical Chemistry at ARUP Laboratories; Associate Professor of Clinical Pathology, University of Utah

Last Update: October 2017