Pediatric anoxic brain injury

Author(s): Rajashree Srinivasan, MD, Cristina Sanders, DO

Originally published:9/20/2013

Last updated:9/20/2013



Anoxic brain injury (ABI) is a decline in brain function seen after disruption of blood supply leading to inadequate oxygenation of the brain; or low levels of oxygen that cause a decline in brain function in an otherwise adequate blood supply. It can be caused by any event interfering with the brain’s ability to receive or utilize oxygen; classified on severity of impairment.

Name Impairment Cause
Diffuse Cerebral hypoxia Mild to moderate Low oxygen levels
Focal Cerebral Ischemia Moderate to severe Hemorrhagic stroke/ischemic occlusion
Global Cerebral Ischemia Severe (Cognitive and speech impairments, dysphagia, spasticity and seizures) Complete stoppage of blood flow to brain
Massive Cerebral Infarction Severe – affects multiple areas of brain Complete oxygen deprivation due to an interference in blood flow


Diagnosis 1-5 Cause Example
Hypoxic Hypoxia Limited oxygen reduces brain function Choking, Strangulation, Crushed windpipe, Hanging, Severe asthma, Near drowning
Hypemic Hypoxia Inadequate oxygen in blood, adequate oxygen in environment Anemia, carbon monoxide poisoning
Ischemic Hypoxia Inadequate blood flow to brain CVA, TIA, Shock, Myocardial Infarction, Cerebral edema, Hemorrhage, Hydrocephalus

Epidemiology including risk factors and primary prevention

Cause Prevention
Drowning (most common cause in children)2,3 Awareness of pool safety; ensuring pools are barricaded properly and manned, constant toddler supervision, adolescent education regarding dangers of alcohol with diving and swimming.
Asphyxiation Use of carbon monoxide detectors, avoid risk-taking behavior with accidental hanging.
Asthma, Stroke, and Cardiac causes Adequate management of asthma, stroke; monitoring cardiac causes closely.


Prolonged hypoxia induces neuronal cell death by apoptosis. The brain requires 3.3 ml of oxygen per 100g of brain tissue per minute (in adults). In the initial stages of oxygen deprivation, the body will respond by redirecting blood to the brain and increasing cerebral flow. If the oxygen is not sufficient, hypoxia will result. Typically parts of the brain involved include deep gray matter nuclei, cortices, hippocampi, basal ganglia, white matter and cerebellum.6

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Patients with ABI have variable progression depending on arousal states varying from brain death to minimally conscious states. 7-16.

  1. Brain Death- irreversible cessation of cerebral and brainstem function; most severe phase of anoxic brain injury.
  2. No respiratory drive, spontaneous breath, cranial nerve reflexes, or motor response to any stimulus.
  3. Intact spinal reflexes may be seen.

A persistent vegetative state (PVS): a state of wakefulness without awareness. May be permanent or represent progression from coma to recovery. No evidence of awareness of self or environment and an inability to interact with others.

Criteria of persistent vegetative state7

  1. No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, tactile or noxious stimuli
  2. No evidence of language comprehension or expression
  3. Intermittent wakefulness with the presence of sleep-wake cycles
  4. Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and nursing care
  5. Bowel and bladder incontinence
  6. Variably preserved cranial nerve reflexes and spinal reflexes

A minimally conscious state (MCS)– seen as another stage in recovery, used for patients who do not meet criteria for persistent vegetative state.

  1. Severe alteration in consciousness seen
  2. Limited interaction with environment–Visual tracking, following simple commands
  3. Answering yes/no questions occasionally accurately
  4. Intelligent or verbalization or purposeful behavior not evident in persistent vegetative state.

Specific secondary or associated conditions and complications

Associated complications

  1. Aspiration
  2. Seizures
  3. Infections leading to sepsis and multiorgan failure–Respiratory or urinary tract infections common.



  1. History of present illness – Detailed history of event; length of arrest and resuscitation; use of any medications – prescribed (e.g., antiepileptics or antidepressants) or recreational (alcohol, heroin etc). History of trauma. Any allergies to medications.
  2. Birth and developmental history, including gestational age; type of delivery – vaginal vs Cesearean section; any anoxia at birth; baseline developmental history information
  3. Past medical/surgical history: Cardiac history, control status of asthma, including hospitalizations for the same, seizure disorder
  4. Family history: Cardiac problems; sudden death suggesting Wolff Parkinson White syndrome, or prolonged QT syndrome.
  5. Social history: Type of house family lives in, any steps in, who will help care for the child, educational stage

Physical examination

Examine child in the seated, supine, and prone positions.


  1. Hyporeflexia – Decreased/absent reflexes; may indicate sensory deficit
  2. Intact/increased during hypotonic stage prior to hypertonicity in CNS damage

Tone(side to side comparison)

  1. Hypotonia can indicate myopathy, cerebellar involvement or lower motor neuron lesion
  2. No resistance felt with PROM–baby is floppy, limp
  3. Hypertonicity can indicate corticospinal or basal ganglion damage. Spasticity, dystonia and/or rigidity can be seen.

Range of motion

  1. Active and passive


  1. Manual muscle testing useful in children 5 years and above


  1. Observe for purposeful movement
  2. Gross/fine motorfunction: may have central movement disorder secondary to parietal lobe dysfunction, decreased proprioception
  3. Visual tracking across the midline
  4. Cranial nerve assessment


  1. Evaluate:
    • Persistent asymmetrical tonic neck reflex (ATNR) past 6 months
    • Evidence of scissoring after 2 months of age?
    • Extension, plantar flexion
    • with/without gravity
  2. Developmental Reflexes
    • Moro/rooting/sucking/tonic neck reflex/Palmar grasp/plantar
    • Children with ABI may regress to primitive reflexes that would normally be absent at specific developmental stages
    • Developmental milestones

Sensory Exam (dependant on the child’s cognition)

  1. Pinprick/Light touch assessment of sensory dermatomes
  2. Withdrawal from stimulus
  3. Impaired sensory function
    • damage to parietal lobe
    • poor spontaneous function, neglect

Functional assessment

Depending on the severity of injury, global delays may be seen. The Glasgow Coma Scale (GCS) and Ranchos Los Amigos Scale provide baseline and symptomatic assessment of recovery in anoxic brain injury. The Ashworth and Modified Ashworth Scale will aid in the classificiation of spasticity.

Laboratory studies

Test To monitor for
Electrolyte imbalances Diabetes insipidus (DI), Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Creatine phosphokinase (CPK), lactate Spasticity induced rhabdomyolysis, poor outcome when lactate > 16 mmol/lt.
Creatine phosphate (CRP), erythrocyte sedimentation rate (ESR), CBC, urine analysis, tracheal aspirate Infection


  1. Chest x-Rays: for extent of pulmonary involvement
  2. Cranial ultrasound: helpful in infants with open fontanelles.
  3. Magnetic resonance imaging (MRI): diffusion weighted imaging–evidence of deep white matter lesions; ventricular enlargement vs loss of gyri and sulci causing an exvacuo effect.

Early predictions of outcomes

Indicators of recovery include: presence or absence of spontaneous movements; response to voice, light touch, and painful stimuli; pupillary size, response to light; cranial nerve function: corneal and oculovestibular reflexes; respiratory pattern.

A Glasgow Coma Scale (GCS) score of ≤4 within the first 48 hours has been associated with poor outcome, such as coma or death. Absent corneal or pupillary light reflexes at 24 hours, and absent motor responses at 24 or 72 hours, have been associated with severe disability/death.

Based on clinical data, the typical outcome in ABI is recovery, PVS, or death. If patient is in PVS at time of discharge, life expectancy is approximately two to five years. There is a 100% specificity indicating poor outcome if patient has absent or extensor motor response, or absent pupillary or corneal reflexes, on the third day of injury.

Children who sustain ABI demonstrate worse outcomes than children with traumatic brain injury (TBI), cognitively and motorically, especially if unconscious more than 60 days18,19.

Social role and social support system

The Patient/Patient Guardian should be asked about who lives at home; family members/friends who can help; about structure and accessibility of home, transportation options for the patient (including wheelchair and school setting); bathroom setup; size and accesibility of doorways; school setup should be explored.

Professional Issues

Families in denial need a lot of support and understanding from the treatment team, which may not agree with the family choices. It is important to be non-judgmental and help in making the right choice.


Available or current treatment guidelines

There are no specific published treatment guidelines at this time.

At different disease stages

Disease Progression
Rigidity/dystonia is commonly seen in children with ABI. Initial flaccidity changes to spasticity, which can be effectively treated using oral, intrathecal, or injectable pharmacologic agents such as Baclofen, Tizanidine, Clonidine and Diazepam (all have been shown to reduce muscle spasms). It is important to begin treating spasticty early to prevent contracture development. Dystonia is difficult to treat pharmacologically; carbidopa/levodopa, bromocriptine, and Intrathecal Baclofen Pump have all shown promise during treatment.

Physical, occupational, and speech therapies are beneficial immediately after injuries, and should be involved in all phases of recovery. Passive range of motion exercises, splinting , or bracing benefit the brain-injured child, depending largely upon the presentation of tone.17

Rehabilitation treatment/intervention Details
Medical care/nursing Ongoing monitoring of medical issues–infection, electrolyte imbalance, dehydration, thrombosis, spasticity management, monitor for altered mental status, monitor vital signs, intake output, recognize any change in status
Physical therapy Range of motion, stretching, strengthening, standing, transfers, evaluation for splints/braces and equipment evaluation
Occupational therapy Range of motion, evaluation of activities of daily living, visuospatial and visuoperceptual deficts, assistive devices
Speech therapy Evaluation of swallow function, cognition, speech, memory assessment
Neuropsychology Cognitive evaluation – thinking, processing information, strategies to deal with behavioral problems, evaluation of intellectual function
Child life/dietary/care coordination Reintegration into community, coping strategies, support to child and family, nutritional stability, coordinate care with funding source

Coordination of care

Discharge planning begins on admission. An initial evaluation by team members should be communicated to patient, family and funding source to coordinate adequate care with regard to medical care, equipment and assistive devices needs, orthotic needs.

A multidisciplinary team is best utilized in this situation. Team members include: physiatry, social work, physical therapy, occupational therapy, speech therapy, neuropsychology, nursing, wound care team (if applicable), and child life specialist.

At time of discharge, information should be conveyed to primary care physician and outpatient therapy team to ensure seamless care.

Patient & family education

Families will need to be set up with social worker/case manager to help navigate the heath care system.

Patients and families should be trained regarding deficits, risk-taking behaviors, to be an advocate for themselves. Educate them regarding programs that are state- and federally funded to avail them of services.

Depending on the extent of involvement, community reintegration includes return to school and friends, providing caregiver assistance, education regarding physical and cognitive deficits, counselling services for patient and family for coping strategies, involvement with support groups.

Emerging/unique Interventions

Various etiologies make it difficult to come up with treatment outcomes. Data indicates poor outcomes but there is lack of systematic analysis and no comparison of rehabilitation methods. The Glascow Coma Scale and Ranchos Los Amigos scale are good predictors of overall improvement. The Functional Independence Measure (FIM) is a useful measurement for rehabilitative recovery. The Gross Motor Function Classification System (GMFCS) can help predict ambulatory ability18,21.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  1. Anticipatory guidance regarding pool safety, use of carbon monoxide detectors, risk-taking behaviors.22
  2. Promote healthy lifestyle–addressing obesity, increased activity, healthy eating, smoking cessation where applicable.
  3. Aggressive management of spasticity.


Cutting edge concepts and practice

Therapeutic hypothermia, or “cooling,” is a process by which core body temperature is purposely lowered to 32-34 degrees celsius in order to prevent ischemic injury or death. This treatment is showing the most success for the treatment of Hypoxic Ischemic Encephalopathy. Recent research has shown that therapeutic hypothermia reduces the outcome of death or long-term neurodevelopmental disability at 18 months.20


Gaps in the evidence-based knowledge

Use of hyperbaric oxygen therapy is controversial. Although it has been proven effective in the management of carbon monoxide poisoning and in wound care, it has not shown any benefit in the treatment of ABI.

Early use of Intrathecal Baclofen pump in the treatment of spasticity is now gaining acceptance.


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2. Brooks KE. Are you a hypoxia expert? Approach. 2005 (May). U.S. Navy Naval Safety. Accessed Feb. 8,2007.

3. Cerebral hypoxia information page. NINDS. 2007;2. U.S. National Institutes of Health. Retrieved 2013-02.

4. Ferro JM, et al. Diagnosis of transient ischemic attack by the non-neurologist. A validation study. 1 PMID 8969785; 1996;27(12):22225-2229.

5. Easton JD, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from AHA/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anedthsia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. Stroke. 2009;40(6):2276-2293.

6. Butterworth RF. Hypoxic encephalopathy. In: Siegel GJ et al, eds. Basic Neurochemistry: Molecular, Cellular, Cellular and Medical Aspects, 6th ed. Philadelphia, PA:Lippincott Williams & Wilkins; 1999.

7. Laureys S, Owen AM, Schiff ND. Brain function in coma, vegetative state, and related disorders. LancetNeurol. 2004;3:537.

8. Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet. 1975;1:480.

9. Levy DE, Bates D, Caronna JJ, et al. Prognosis in nontraumatic coma. Ann Intern Med. 1981;94:293.

10. Medical aspects of the persistent vegetative state (2). The Multi-Society Task Force on PVS. NEJM. 1994;330:1572.

11. Luauté J, Maucort-Boulch D, Tell L, et al. Long-term outcomes of chronic minimally conscious and vegetative states. Neurology. 2010;75:246.

12. Estraneo A, Moretta P, Loreto V, et al. Late recovery after traumatic, anoxic, or hemorrhagic long-lasting vegetative state. Neurology. 2010;75:239.

13. Giacino JT, Ashwal S, Childs N, et al. The minimally conscious state: definition and diagnostic criteria. Neurology. 2002;58:349.

14. Voss HU, Uluç AM, Dyke JP, et al. Possible axonal regrowth in late recovery from the minimally conscious state. J Clin Invest. 2006;116:2005.

15. Whyte J, Katz D, Long D, et al. Predictors of outcome in prolonged posttraumatic disorders of consciousness and assessment of medication effects: A multicenter study. Arch Phys Med Rehabil. 2005;86:453.

16. Zandbergen EG, de Haan RJ, Stoutenbeek CP, et al. Systematic review of early prediction of poor outcome in anoxic-ischaemic coma. Lancet. 1998;352:1808.

17. Dubowitz V, Dubowitz L. The neurological assessment of the preterm and full term infant. Clin Dev.Med. 1982;79.

18. Kriel RL, et al. Outcome of severe anoxic/ischemic brain injury in children. Pediatric Neurology. 1994;10:207-212.

19. Alexander M, Matthews D. Pediatric Rehabilitation. Principles and Practices. 4th ed.Demos Medical Publishing, New York, NY. 4th edition (September 15, 2009)

20. Ballot DE. Cooling for newborns with hypoxic ischemic encephalopathy. RHL commentary. rev.1 October 2010). WHO Reproductive Health Library. Geneva: World Health Organization. Accessed March 24, 2013.

21. Rehabilitation Measures Database. Rehabilitation institute of Chicago. Accessed 2013-03-24.

22. Web-based injury statistics query and reporting systems (WISQARS). CDC, National Center for Injury Prevention and Control. Updated Sep 17, 2012. Accessed April 5, 2013.

Author Disclosure

Rajashree Srinivasan, MD
Nothing to Disclose

Cristina Sanders, DO
Nothing to Disclose


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