Postanoxic Coma

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.

Epidemiology

Prevalence
- ~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 (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
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
S-100B is 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

Indications for Testing

Helps aid in predicting outcome in coma >72 hours after anoxic event without evident metabolic or structural etiology

Laboratory Testing

Recent reports suggest combining somatosensory evoked potentials (SSEP) with specific serum neurobiochemical markers
- Neuron specific enolase (NSE)
  - Poor outcome prediction is highly likely when N20 SSEP is absent and NSE >33µg/L at 72 hours post-event
- S-100B protein
  - Levels indicating poor outcome not concretely established
  - Level normals are highly variable in children

Tests generally appear in the order most useful for common clinical situations

Test name: Neuron Specific Enolase

ARUP #: 0098198

Methodology: Quantitative Enzyme-Linked Immunosorbent Assay

Use:

Aid in predicting poor outcome in postanoxic coma

Limitations:

Absolute values not established

Follow-up:

Should be ordered with SSEP and used in conjunction with clinical findings

Test name: S-100B Protein, Serum

ARUP #: 2001766

Methodology: Quantitative Enzyme-Linked Immunosorbent Assay

Use: Aid in predicting poor outcome in postanoxic coma

Limitations:

Absolute values not established

Due to the short half-life and rapid decrease of serum S-100B, knowledge of the time of injury is important for accurate interpretation and outcome prediction

S-100B is not specific for brain injury; increased serum concentrations are found in patients with melanoma, liver and renal injury, inflammation and infection

Additional Tests Available

Test name: Neuron Specific Enolase, CSF

ARUP #: 0081226

Methodology: Quantitative Enzyme-Linked Immunosorbent Assay

Comments:

Adjunctive test

Normal CSF NSE concentrations do not rule out neuronal disease

Guidelines

Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S. 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) :203-210.PubMed

General

Grenache, David G., PhD. Medical Director, Special Chemistry at ARUP Laboratories; Associate Professor of Pathology (Clinical), University of Utah

Comprehensive Review: June 2011
Last Update: June 2011

Seizure Disorders