Ferri – Anoxic Brain Injury

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Anoxic Brain Injury

  • Angad Jolly, M.D.
  • Joseph S. Kass, M.D., J.D.

 Basic Information

Definition

Anoxic brain injury occurs when a decrease in either blood flow or oxygen causes cerebral ischemia. The inadequate delivery of nutrients and oxygen to cerebral tissue commonly reflects defects in either cardiac circulation or respiratory function, or defects in both.

Synonyms

  1. Hypoxic-ischemic injury

  2. Anoxic encephalopathy

  3. Cerebral hypoxia

  4. Hypoxia of brain

  5. Perinatal or intrapartum asphyxia (pediatric)

ICD-10CM CODES
G93.1 Anoxic brain damage, not elsewhere classified

Epidemiology & Demographics

Incidence

  1. •

    Variable based on diagnostic criteria

  2. •

    424,000 out-of-hospital cardiac arrests per year in the U.S.

Prevalence

  1. •

    Sequelae of anoxic brain injury may include vegetative state, which varies in prevalence from 40 to 168 per 1 million population, depending on definition used.

  2. •

    Other sequelae may include death from cardiac arrest or loss of whole-brain function (brain death) or progression to either minimally conscious state or dementia.

  3. •

    Recovery is rare after 3 months of vegetative state, with life expectancy of 2 to 5 years.

Risk Factors

Same as risk factors for cardiorespiratory arrest: age, race, HTN, hyperlipidemia, tobacco use, drug or alcohol abuse, and physical inactivity.

Physical Findings & Clinical Presentation

  1. •

    Variable depending on degree of insult

  2. •

    Patient typically initially in coma and then may either recover awareness and wakefulness with variable degrees of cognitive or physical impairment, may progress to a vegetative state or a minimally conscious state, or may die due to cardiopulmonary arrest or loss of whole brain function (brain death).

  3. •

    Coma: eyes-closed state of both unconsciousness and unawareness with loss of sleep-wake cycles

  4. •

    Minimally conscious state: altered state of awareness with normal sleep-wake cycles and intermittent interactivity with the environment; patient may intermittently follow simple commands and maintain visual tracking

  5. •

    Vegetative state (also known as unresponsive wakefulness): altered state of awareness with normal sleep-wake cycles but with complete loss of both cognitive awareness and ability to interact with environment; persistent vegetative state is the term used for vegetative state after anoxic injury of between 1 and 3 months’ duration, and permanent vegetative state is the term used for a vegetative state persisting beyond 3 months. A vegetative state due to traumatic brain injury is permanent only after 12 months.

  6. •

    Brain death: irreversible loss of both cortical and brainstem function manifesting as loss of awareness, cranial reflexes, and motor responses; brain death meets the legal criteria for death in U.S. jurisdictions. EEG is isoelectric; there is no intracerebral blood flow.

Etiology

  1. •

    Ischemia (decreased cerebral perfusion): myocardial infarction, hemorrhage, shock, high intracranial pressure

  2. •

    Hypoxia (decreased oxygenation): drowning, strangulation, aspiration, carbon monoxide poisoning

  3. •

    Fig. E1 shows categories of mechanisms proposed to be involved in the evolution of secondary damage after severe traumatic brain injury in infants and children.

FIG.E1

Categories of mechanisms proposed to be involved in the evolution of secondary

Diagnosis

Differential Diagnosis

  1. •

    Other causes of encephalopathy, including toxic, metabolic, infectious, or neoplastic causes; nonconvulsive status epilepticus; hypothermia

  2. •

    Histotoxic hypoxia, the inability to utilize oxygen despite adequate delivery to cerebral tissue; i.e., cyanide poisoning

Workup

  1. •

    Neurologic examination (coma examination) to ascertain level of encephalopathy

  2. •

    Systemic evaluation for causes of cardiorespiratory failure

  3. •

    Laboratory studies (listed in the following) to evaluate alternate causes of encephalopathy

  4. •

    Imaging studies: MRI of brain or CT of head (if MRI cannot be obtained)

Laboratory Tests

Urine drug screen, serum metabolic profile, ammonia, complete blood count, coagulation panel, finger stick glucose, arterial blood gas, blood alcohol panel, serum neuron-specific enolase (if available)

Imaging Studies

  1. •

    Imaging is usually not revealing within first 24 hr of an anoxic event.

  2. •

    Head CT without contrast (Fig. E2): repeat 24 hr after anoxic event to evaluate for stroke, trauma, hemorrhage, or cerebral edema.

    FIG.E2 

    CT without contrast of a patient 1 day after pulseless electrical activity showing diffuse sulci effacement and loss of gray-white matter differentiation indicating cerebral edema.
    Diffuse white and gray matter hypodensities are also present. The patient remained comatose and life support was eventually withdrawn.
  3. •

    MRI of brain (Fig. E3): obtain if head CT scan unrevealing; may show cortical necrosis and infarcts of the basal ganglia

FIG.E3 

MRI FLAIR (fluid attenuated inversion recovery) of a patient 1 day after pulseless electrical activity showing bilateral multiple cortical, subcortical, gray and white hyperintensities.
The patient remained comatose and life support was eventually withdrawn.

Other Studies

  1. •

    EEG: to assess for non-convulsive status epilepticus

  2. •

    Somatosensory evoked potentials (SSEP; aka, N20 response): obtain 24 to 72 hr after anoxic event

Treatment

Nonpharmacologic Therapy

  1. •

    Hypothermia: evidence suggests that inducing hypothermia 32° to 34° C for 24 hr following anoxic brain injury reduces metabolic demand and may improve prognosis for recovery. However, recent meta-analysis suggests that the true risk-benefit of therapeutic hypothermia is unclear and is a topic of debate.

  2. •

    Complications from hypothermia include bradycardia, hemodynamic instability, coagulopathy, infection, hyperglycemia, and hypokalemia.

  3. •

    Contraindications for hypothermia: active hemorrhage, hemodynamic instability, sepsis, or trauma

  4. •

    Indication for hypothermia: patients who have been resuscitated from a cardiac arrest with VF/VT as the presenting rhythm

  5. •

    Hyperbaric oxygen is used in carbon monoxide poisoning.

Acute General Rx

  1. •

    Supportive care: ABCs, secure airway, cardiopulmonary support in the critical care unit

  2. •

    Control seizures with antiepileptic medications (may need midazolam or propofol drip for severe, uncontrolled seizures).

  3. •

    Treat myoclonus with clonazepam 8 to 12 mg daily in divided doses; levetiracetam and divalproate may be used for myoclonic status epilepticus. Treatment of myoclonus due to cardiac arrest does not change neurologic prognosis.

Chronic Rx

  1. •

    Maintain adequate nutrition, normothermia (if not utilizing therapeutic hypothermia) infection precautions; provide DVT and gastric ulceration prophylaxis.

  2. •

    Physical, occupational, and speech therapy as indicated per prognosis and patient ability

  3. •

    May consider withdrawal of critical care and implementation of palliative care per prognosis, family consultation, and respect for autonomy and dignity of the patient

Prognosis

  1. •

    Out-of-hospital cardiopulmonary resuscitation (CPR) for cardiac arrest has a success rate of <10%.

  2. •

    There is no standardized battery of testing to quantify anoxic injury and reliably predict outcomes.

  3. •

    Anoxia time, duration of CPR, and cause of cardiac arrest are related to poor outcome after CPR but not sufficient for prognosis.

  4. •

    Strong predictors of poor outcome (evidence level A or B) (assuming patient did not undergo therapeutic hypothermia) are the following:

    1. ○

      Presentation with myoclonus status epilepticus within the first 24 hours following injury

    2. ○

      Absence of bilateral cortical SSEPs (N20 response) anytime

    3. ○

      Absent papillary or corneal reflexes, or absent or extensor motor responses after 72 hours following injury

    4. ○

      Serum NSE levels >33 μg/L 24 to 72 hours following injury

  5. •

    Neuroimaging and EEG are sensitive but not specific predictors of outcome.

  6. •

    Burst-suppression pattern or flat-line EEG carries bad prognosis, while reactive EEG to noxious stimuli predicts favorable outcome. Refer to Table E1 for predictors of good prognosis.

    TABLEE1 Predictors of Good Prognosis
    Time from Onset of Anoxic Event Clinical Exam
    Initial exam Pupils react to light (reflex present), motor response flexor or extensor, and eye movements spontaneous roving conjugate or orienting
    24 hr Motor response withdrawal or better, and eye opening improved at least 2 grades
    72 hr Motor response withdrawal or better and normal spontaneous eye movements present
    1 wk Follows commands
    2 wk Normal oculocephalic response
  7. •

    The prognostic value of these findings and the timing of exam changes after therapeutic hypothermia. Timing should, at a minimum, be factored from the time the patient was fully rewarmed rather than from the time of initial cardiopulmonary arrest. The window for concluding poor prognosis based on examination after hypothermia may be extended further based on future studies. Furthermore, the reliability of NSE post-hypothermia has been called into question.

Disposition

Varies per extent of insult from long-term care facility to acute rehabilitation to return to home

Referral

Referral to a neurologist is appropriate for definitive prognostication.

Pearls & Considerations

Comments

When assessing prognosis, use caution if patient is being treated with anesthetic agents or other depressants of consciousness, including anticonvulsants. Thus serial neurologic exams are integral to best-practice care. When examining patients and determining prognosis, account for medications and illicit drugs that may depress consciousness and awareness as well as metabolic derangements that may affect the metabolism of pharmacologic agents or illicit drugs.

Prevention

CPR, risk factor modification, induced hypothermia

Patient/Family Education

Consult with family members regularly and provide accurate assessment of prognosis.

Suggested Readings

  • American Academy of Neurology: AAN summary of evidence-based guideline for clinicians: prediction of outcome in comatose survivors after cardiopulmonary resuscitation . http://aan.com/professionals/practice/guidelines/coma_clinician.pdf. Accessed February 19, 2013.

  • American Academy of Neurology: AAN summary of evidence-based guideline for patients and their families: prediction of recovery from coma after CPR . http://aan.com/professionals/practice/guidelines/coma_patient.pdf. Accessed February 19, 2013.

  • J. Arrich, et al.: Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev. 15 (2):CD004128 2016

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