Jump to:

1. DISEASE/DISORDER:

Definition

Anoxic brain injury (ABI) is a decline in brain function due to a disruption of the oxygen supply to the brain. This can occur in the presence of absence of adequate blood supply and can be caused by any event interfering with the brain’s ability to receive or utilize oxygen such as drowning, suffocation, cardiac or respiratory arrest, cerebrovascular accident, or carbon monoxide poisoning 1.

Hypoxic ischemic encephalopathy (HIE) is a condition that occurs in infants and is characterized by inadequate oxygenation to the brain either prenatally, intrapartum, or postnatally, that results in abnormal neurologic function 2,3. Neurologic abnormalities resulting from hypoxia and anoxia vary in severity and include seizures, cognitive deficits, and motor impairments 2.

Etiologies of Hypoxia

Diagnosis CauseExample
Hypoxic Inadequate oxygen in environmentChoking, strangulation, hanging, status asthmaticus, near drowning, tracheal injury
Hypemic Inadequate oxygen in blood, adequate oxygen in environmentAnemia, carbon monoxide poisoning
Ischemic Inadequate blood flow to brainCerebrovascular accident, transient ischemic attack, shock, myocardial infarction, cerebral edema, hemorrhage,

Common causes of pediatric anoxic brain injury and primary prevention 4-6

CausePrevention
Near drowning Awareness of pool safety; ensuring pools are barricaded properly and manned, constant toddler supervision, adolescent education regarding dangers of alcohol with diving and swimming.
Carbon monoxide poisoningUse of carbon monoxide detectors, avoid risk-taking behavior with accidental hanging.
Status asthmaticus, cardiac arrest, acute respiratory failureAdequate management of asthma, cardiac disease, and other diseases with risk of secondary cardiac arrest or respiratory failure.
Status epilepticusAppropriate seizure management, early intervention with abortive seizure medications, and escalation of care as needed to prevent respiratory failure or cardiac arrest.

Patho-anatomy/physiology

Prolonged hypoxia induces neuronal cell death by apoptosis. Impaired cell membrane function leads to a decrease in extracellular sodium, chloride, and calcium and an efflux of potassium out of cells into the extracellular space. The influx of calcium triggers apoptotic pathways leading to cell death.  Vulnerable structures in the brain include deep gray matter nuclei, cortices, hippocampi, basal ganglia, white matter and cerebellum 7.

Brain death and disorders of consciousness 8,9

Patients with ABI have variable outcomes depending on length of time of hypoxia, degree of hypoxic injury, duration of impaired consciousness, and duration of post-injury confusion 10.

Brain death:

  • Irreversible cessation of cerebral and brainstem function
  • Lack drive, spontaneous breathing, cranial nerve reflexes, or motor response to any stimulus.
  • Intact spinal reflexes may be seen.

Coma:

  • State of completed unconsciousness during which eyes remain closed and there is no evidence of self-awareness or awareness of surroundings

Unresponsive wakefulness (Also known as post-coma unawareness or vegetative ):

  • Intermittent wakefulness with the presence of sleep-wake cycles
  • Reflexive and autonomous responses to internal stimuli, not to external stimuli
  • No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to external visual, tactile or noxious stimuli
  • No evidence of language comprehension or expression
  • Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and nursing care

Minimally conscious state ():

  • Limited interaction with environment
  • Inconsistent visual tracking across midline
  • Purposeful movements
  • Can include following simple commands or answering yes/no questions with inconsistent accuracy
  • Subdivisions;
    • MCS (-): Lower level responses such as visual pursuit, localization of stimuli, and smile or cry response to emotional stimuli
    • MCS (+): Higher level responses such as command following, verbalizations, and non-functional communication

Emergence from MCS:

  • Recovery of reliable yes/no communication or functional object use
Diagnostic GroupBrain DeathComaUnresponsive WakefulnessMinimally Conscious State (MCS)Emergence from MCS
MCS (-)MCS (+)
Cerebral and Brainstem FunctionAbsentPresent
Wakefulness / Sleep Wake CyclesAbsentIntermittent wakefulness with sleep-wake cycle
Reflexive and Autonomous Responses to Internal StimuliAbsentPresent
Responses to Environment / External StimuliAbsentLower-level responses (visual pursuit, localize noxious stimuli)Higher-level responses (command following, verbalizat-ions)Continued higher-level responses with additional function
CommunicationAbsentNon-functionalReliable yes/no
Functional Object UseAbsentPresent
NotesLack of respiratory drive, cranial nerve reflexes, or motor response to stimuliAlso known as post-coma unawareness or vegetative state.

Specific secondary complications in anoxic brain injury as opposed to traumatic brain injury 11-15

Patients with anoxic brain injury have differences in neuropathology than those with traumatic brain injury, which may contribute to differences in recovery. Some proposed reasons for recovery difference include more global injury (as opposed to focal injury), more neuronal apoptosis (as opposed to axonal injury) that decreases opportunity for plasticity, and overall different mechanisms of competition for neural responses between cognitive and motor recovery.

  • Longer rehabilitation stays
  • More severe impairments
  • Slower rate of recovery as measured by FIM score, with physical recovery slowed than cognitive recovery
  • For those in vegetative states, anoxic brain injury patients improved to minimally conscious states (or better) at a lower rate than traumatic brain injury.
  • Higher mortality

2. ESSENTIALS OF ASSESSMENT

History

  1. History of present illness – Detailed history of event leading up to anoxia; duration of anoxia; details of immediate resuscitation, including effectiveness; use of any medications/drugs- prescribed (e.g., antiepileptics or antidepressants) or recreational (alcohol, heroin etc); history of trauma; 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: specifically include cardiac history, respiratory history, seizure history, or history related to another specific known cause of anoxia for specific patient.
  4. Family history: specifically include cardiac history (sudden death suggesting Wolff Parkinson White syndrome, prolonged QT syndrome); history of epilepsy, or history related to another specific known cause of anoxia for specific patient
  5. Social history: Type of house family lives in, any steps in, who will help care for the child, adults involved in child’s care at this time, educational stage

Physical examination

General Appearance

  1. Level of arousal / consciousness
  2. Circulatory status:
    1. Vital Signs
    2. Capillary refill
  3. Respiratory status:
    1. Regular vs. irregular spontaneous breathing
    2. Intubation: Breathing over vent, at vent rate or apneic?
  4. For infants: anterior fontanelle exam for fullness, assess sutures for separation

Neurologic Examination

  1. Fundal exam: multilayered retinal hemorrhage suggestive of nonaccidental head injury
  2. Extraocular assessment including brainstem function:
    1. Ocular movements
      1. Sustained down/up-gaze, irregular upward nystagmus, ping-pong gaze, periodic lateral gaze associated with poor outcome
    2. Corneal reflexes
    3. Pupillary light reflex 16
      1. Unilateral fixed dilated pupil à suggestive of transtentorial herniation
      2. Acute bilateral fixed dilated pupils à concern for central herniation
    4. Oculocephalic reflexes
  3. Motor exam
    1. Muscle Tone
    2. Motor response to pain
    3. Decorticate and decerebrate posturing
    4. Ability to follow motor commands
  4. Sensory exam
  5. Reflex exam
  6. Coordination exam
  7. Abnormal Movement:
    1. Rigidity, dystonia, chorea, action myoclonus more common in ABI

Musculoskeletal Examination 17

  1. Muscle Bulk
  2. Muscle Tone:
    1. Spasticity, rigidity and dystonia often more severe and generalized in children with ABI compared to TBI
  3. Range of Motion
    1. Common contractures include equinus deformity, hip flexion contracture, and knee flexion contracture.
  4. Hip subluxation/dislocation
    1. Found in 34% of near-drowning children with ABI as early as 1 month after injury
  5. Scoliosis
    1. Found in 18% of children with ABI
  6. Gait:
    1. 70% children with ABI from near-drowning non-ambulatory

Note: Neurologic exam often limited in acute phase of anoxic brain injury due to severe cognitive compromise. PICU clinical assessment often compromised by sedation, neuromuscular blockade, ventilation, hypothermia, inotropic management etc.

Common Prognostic Scales

  1. Modified Pediatric Glasgow Coma Scale
  2. Full Outline of Unresponsiveness (FOUR) Scores 10, including
    1. Eye responses
    2. Motor responses
    3. Brainstem reflexes
    4. Respiration pattern

Intracranial Pressure (ICP) Monitoring

  1. Ventricular catheter placement provides most accurate assessment of ICP, as well as allows for therapeutic CSF drainage
  2. ICP > 20mmHg in comatose patients associated with poor outcome
  3. Look out for increased ICP / herniation syndromes 16
    1. Decerebration pattern
    2. Abrupt pupillary change
    3. Impaired upward gaze
    4. Sudden deterioration of respiration and apnea
  4. Sustained late intracranial hypertension more likely a sign of irreversible brain damage

Electroencephalography (EEG) Monitoring 10, 18-21

  1. Continuous or repetitive EEG monitoring most helpful for evaluation of encephalopathy (EEG background) and seizure detection
  2. Good outcome predictors:
    1. Moderate background activity, sleep patterns, response to auditory and painful stimulations, numerous beta rhythms
  3. Poor outcome predictors:
    1. High voltage, rhythmic delta waves, biphasic sharp waves, “burst suppression” pattern, absence of beta rhythms, generalized suppression, status epilepticus, nonreactivity
    2. Persistently abnormal EEG at 48 hours or more associated with adverse neurodevelopmental outcome

Somatosensory Evoked Potential (SSEP) Monitoring 10

  1. SSEP as neurophysiologic test for assessing integrity of neuronal pathways from peripheral nerve, spinal cord, brainstem and cerebral cortex.
  2. Most reliable evoked potential waveform as median N20 component of SSEP
    1. Median N20 SSEP: first cortical response of SSEP with median nerve stimulation
    2. Bilateral absence of median N20 response on days 1 and 3 or later following CPR accurately predicts poor outcome (reflects widespread cortical necrosis)
  3. Advantage: less susceptible to effects of sedative drugs, metabolic changes and artifact interference compared to EEG monitoring.
  4. Disadvantage: require advanced neurologic training, interpretation limited to specialized centers, low sensitivity

Serum Biomarkers for ABI Prognostication

  1. Serum NSE (neuron-specific enolase)
    1. Isomer of intracytoplasmic lycolytic enzyme enolase found in neuronal bodies, axons, neuroendocrine cells and tumors
    2. NSE peaks in serum and CSF at 72hr after injury
    3. Serum NSE > 33microgram/L at days 1 and 3 associated with poor outcome
    4. Use limited by lack of laboratory standardization, long turn-around time
  2. S100 protein
    1. Calcium-binding protein highly concentrated in glial and Schwann cells
    2. Highest level in first 24 hours after anoxic injury; declines over next 48 hours
  3. CKBB (creatine kinase brain isozyme)
    1. Present in neurons and astrocytes; leaks from cytoplasm of destroyed cells
    2. Peaks around 48-72 hours after injury

Laboratory studies to monitor for complications

TestTo monitor for
Electrolyte imbalancesDiabetes insipidus (DI), Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Creatine phosphokinase (CPK), lactateSpasticity induced rhabdomyolysis, poor outcome when lactate > 16 mmol/lt.
Creatine phosphate (CRP), erythrocyte sedimentation rate (ESR), CBC, urine analysis, tracheal aspirateInfection

Brain Imaging 22

Cranial ultrasound

  1. Ideal for newborn/infants
  2. Suitable for screening and follow-up exam
  3. Generally performed using anterior fontanelle as acoustic window
  4. Posterior fontanelle and mastoid fontanelles can be used as acoustic windows to study posterior fossa and brainstem
  5. Noninvasive and low cost, can be done at bedside
  6. Cons: does not depict white matter signal abnormalities, does not give detailed information on myelination and detect lesions on posterior limb of internal capsule

Head CT

  1. Very limited role in young infants due to high ionizing radiation
  2. Excellent for detecting hemorrhage
  3. Not great for detecting edema/infarction newborn with hypoxic-ischemic brain injury due to high water content in newborn brain

Brain MRI

  1. Superb soft tissue contrast differentiation
  2. Diffusion-weighted imaging (DWI)—uses hydrogen molecules physical property of diffusion: sensitive for detecting cytotoxic edema; white matter lesions; ventricular enlargement vs loss of gyri and sulci causing an ex vacuo effect.

Neuropsychological Evaluation 5, 23

Neuropsychological deficits often pronounced in pediatric survivors of anoxic brain injury due to diffuse and often more severe nature of cerebral involvement.

Exact impairments depend on nature and duration of anoxic event, associated neuronal degeneration, age at injury, and selective vulnerability of different brain regions (eg, hippocampus, globus pallidus, thalamus, putamen, caudate nucleus, parieto-occipital cortex, substantia nigra and cerebellum.)

Common neuropsychological impairments seen in anoxic brain injury:

  • Memory deficits
  • Learning difficulties
  • Attention deficits
  • Decreased visuospatial abilities
  • Generalized intellectual impairment
  • Behavioral problems
  • Dysexecutive syndromes
  • Personality changes

Early predictions of outcomes 24

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, chronic unresponsive wakefulness, or death. If patient is in chronic unresponsive wakefulness at time of discharge, life expectancy is approximately two to five years. Absent motor responses, extensor motor responses, absent pupillary reflexes, or absent corneal reflexes on third day after injury are associated with poor outcomes.

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

Social role and social support system

The patient, family, and/or caregiver(s) should be asked about who lives at home;  adults who can help with care; structure and accessibility of home, including bathroom setup, doorway sizes, stairs to enter and stairs inside home; transportation options for the patient, including vehicle(s), public transportation, and school transportation; and current school setting.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

There are no specific published treatment guidelines at this time.

At different disease stages

Disease Progression

For pediatric patients with disorders of consciousness, amantadine has been shown in a pilot study to help recover consciousness 25.

Patients with anoxic brain injury often initially have flaccid musculature. Initial flaccidity can change to hypertonicity with spasticity, rigidity, or dystonia

Spasticity can be effectively treated using oral, intrathecal, or injectable pharmacologic agents. Oral medications commonly include, but are not limited to (all have been shown to reduce muscle spasms). Spasticity can also be treated with interventional chemodenervation, using botulinum toxins in muscles and/or ethanol or phenol in muscles. It is important to begin treating early to prevent contracture development. Dystonia is difficult to treat pharmacologically; enteral carbidopa/levodopa, enteralbromocriptine, botulinum toxin injections, and intrathecal baclofen via pump have all shown promise during

Dysautonomia, characterized by fever, tachypnea, tachycardia, hypertension, and/or dystonia, is more common in anoxic brain injury than in traumatic brain injury 28. Empirical pharmacologic treatment with morphine, benzodiazepines, clonidine, propranolol, other antihypertensives, bromocriptine, or baclofen can be helpful 26, 27.

Early pump placement for intrathecal baclofen dosing has been shown to be effective in treating both hypertonicity and dysautonomia 28.

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.

Rehabilitation treatment/interventionDetails
Medical care/nursingOngoing 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 therapyRange of motion, stretching, strengthening, standing, transfers, evaluation for splints/braces and equipment evaluation
Occupational therapyRange of motion, evaluation of activities of daily living, visuospatial and visuoperceptual deficits, assistive devices
Speech therapyEvaluation of swallow function, cognition, speech, memory assessment
NeuropsychologyCognitive evaluation – thinking, processing information, strategies to deal with behavioral problems, evaluation of intellectual function
Child life/dietary/care coordinationReintegration 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, therapies required, social needs, and required equipment (including mobility or other assistive devices, and orthoses).

A multidisciplinary team is best utilized in this situation. Team members include: physiatry, social work, physical therapy, occupational therapy, speech therapy, neuropsychology, nursing, recreational therapy, and child life specialist. Additional team members, such as wound care team or an orthotist, may be required depending on the individual patient

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

Patient & family education

Families should be trained regarding deficits, new care needs, and new equipment. They should be educated about use of current medications, ongoing therapy requirements, and potential course of recovery.

Families benefit from care management and social work to learn about available resources and how to navigate new health care systems. Families should be educated regarding funding and resource programs available to them.

Community integration should be individualized based on a patient’s level of function. This can include return to school, social activities, or recreational activities. It can also include, providing caregiver assistance, education regarding physical and cognitive deficits, counselling services for patient and family for coping strategies, and involvement with support groups.

Professional Issues

Parents and families need support and understanding from the treatment team. At times, the treatment team may not agree with a family’s understanding of a condition or choices for a patient.  . It is important to be non-judgmental and family to make decisions that help the patient and align with the patient’s/family’s values and goals.

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

  1. Families should be given anticipatory guidance about risks for anoxic brain injury, particularly in children with medical conditions that increase risk (cardiac disease, severe respiratory disease, epilepsy)
  2. Aggressive management of spasticity is helpful, particularly early after emergence of increased tone.
  3. Dysautonomia can be treated with a variety of pharmacologic options, including analgesics, benzodiazepines, antihypertensives, or early baclofen pump placement.
  4. Family training and education is paramount during early phases of recovery from anoxic brain injury.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

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 29.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Use of hyperbaric oxygen therapy, including what protocol may be useful, is controversial. Some studies show promise, but sufficient evidence for integration into clinical care is still lacking 30.

REFERENCES

  1. Cerebral Hypoxia Information Page – National Institute of Neurologic Disorders and Stroke. 2019 3-27-2019 [cited 2019 July 23]; Available from: https://www.ninds.nih.gov/Disorders/All-Disorders/Cerebral-Hypoxia-Information-Page#disorders-r1.
  2. Allen, K.A. and D.H. Brandon, Hypoxic Ischemic Encephalopathy: Pathophysiology and Experimental Treatments. Newborn Infant Nurs Rev, 2011. 11(3): p. 125-133.
  3. Fatemi, A., M.A. Wilson, and M.V. Johnston, Hypoxic-ischemic encephalopathy in the term infant. Clin Perinatol, 2009. 36(4): p. 835-58, vii.
  4. Hopkins, R.O. and E.D. Bigler, Neuroimaging of anoxic injury: implications for neurorehabilitation. NeuroRehabilitation, 2012. 31(3): p. 319-29.
  5. Thaler, N.S., et al., Neuropsychological profiles of six children with anoxic brain injury. Child Neuropsychol, 2013. 19(5): p. 479-94.
  6. Fitzgerald, A., et al., Anoxic brain injury: Clinical patterns and functional outcomes. A study of 93 cases. Brain Inj, 2010. 24(11): p. 1311-23.
  7. Busl, K.M. and D.M. Greer, Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms. NeuroRehabilitation, 2010. 26(1): p. 5-13.
  8. Bruno, M.-A., et al., From unresponsive wakefulness to minimally conscious PLUS and funtional locked-in symdromes: recent advances in our understanding of disorders of consciousness. J Neurol, 2011. 248(7): p. 1373-1384.
  9. Giacino, J.T., et al., Practice Guideline Update Recommendations Summary: Disorders of Consciousness: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology; the American Congress of Rehabilitation Medicine; and the National Institute on Disability, Independent Living, and Rehabilitation Research. Arch Phys Med Rehabil, 2018. 99(9): p. 1699-1709.
  10. Nguyen, K.P.L., et al., Prognostication in Anoxic Brain Injury. Am J Hosp Palliat Care, 2018. 35(11): p. 1446-1455.
  11. Cullen, N.K., C. Crescini, and M.T. Bayley, Rehabilitation outcomes after anoxic brain injury: a case-controlled comparison with traumatic brain injury. PM R, 2009. 1(12): p. 1069-76.
  12. Schmidt, J.G., J. Drew-Cates, and M.L. Dombovy, Anoxic encephalopathy: Outcome after inpatient rehabilitation. Journal of Neurologic Rehabilitation, 1997. 11(3): p. 189-195.
  13. Kriel, R.L., L.E. Krach, and C. Jones-Saete, Outcome of children with prolonged unconsciousness and vegetative states. Pediatr Neurol, 1993. 9(5): p. 362-8.
  14. Kriel, R.L., et al., Outcome of severe anoxic/ischemic brain injury in children. Pediatr Neurol, 1994. 10(3): p. 207-12.
  15. Adams, J.H., D.I. Graham, and B. Jennett. The neuropathology of the vegetative state after an acute brain insult. Brain, 2000. 123 (7): p. 1327-1338.
  16. Seshia, S.S., et al., Nontraumatic Coma in Children and Adolescents: Diagnosis and Management. Neurologic Clinics, 2011. 29(4): p. 1007-1043.
  17. Abrams, R.A. and S. Mubarak, Musculoskeletal consequences of near-drowning in children. J Pediatr Orthop, 1991. 11(2): p. 168-75.
  18. Suominen, P.K. and R. Vahatalo, Neurologic long term outcome after drowning in children. Scand J Trauma Resusc Emerg Med, 2012. 20: p. 55.
  19. Chang, T. and A. du Plessis, Neurodiagnostic techniques in neonatal critical care. Curr Neurol Neurosci Rep, 2012. 12(2): p. 145-52.
  20. Chandrasekaran, M., et al., Predictive value of amplitude-integrated EEG (aEEG) after rescue hypothermic neuroprotection for hypoxic ischemic encephalopathy: a meta-analysis. J Perinatol, 2017. 37(6): p. 684-689.
  21. Cheliout-Heraut, F., et al., [Cerebral anoxia in near-drowning of children. The prognostic value of EEG]. Neurophysiol Clin, 1991. 21(2): p. 121-32.
  22. Liauw, L. Hypoxic-Ischemic BI in Young Infants. Ann Acad Med Singapore, 2009. 38: p. 788-794.
  23. Pierro, M.M., et al., Anoxic brain injury following near-drowning in children. Rehabilitation outcome: three case reports. Brain Inj, 2005. 19(13): p. 1147-55.
  24. Levy, D.E., et al., Predicting Outcome from Hypoxic-Ischemic Coma. Jama-Journal of the American Medical Association, 1985. 253(10): p. 1420-1426.
  25. McMahon, M.A., et al. Effects of Amantadine in Children with Impaired Consciousness Caused by Acquired Brain Injury: A Pilot Study. Am J Phys Med Rehabil, 2009. 88(7): p. 525-532.
  26. Kirk K.A., et al. Dysautonomia after pediatric brain injury. Dev Med Child Neurol, 2012. 54: p. 759-764.
  27. Baguley, I.J., et al. Pharmacological management of Dysautonomia following traumatic brain injury. Brain Inj. 2004 18(5): p. 409-417.
  28. Turner, M.S. Early use of intrathecal baclofen in brain injury in pediatric patients. In: Katayama Y. (eds) Neurosurgical Re-Engineering of the Damaged Brain and Spinal Cord. Acta Neurochirurgica Supplements, vol 87; 2003. Springer, Vienna.
  29. Davidson, J.O., et al. Therapeutic Hypothermia for Neonatal Hypoxic-Ischemic Encephalopathy – Where to from Here?. Front Neurol, 2015. 6: 198.
  30. Ostrowski, R.P., et al. Hyperbaric oxygen modalities are differentially effective in distinct brain ischemia models. Med Gas Res, 6(1): p. 39-47.

Original Version of the Topic

Rajashree Srinivasan, MD, Cristina Sanders, DO. Pediatric Anoxic Brain Injury. Original Publication Date: 09/20/2013

Author Disclosure

Andrew Collins, MD
Nothing to Disclose

Priya Bolikal, MD
Nothing to Disclose

SheanHuey Ng, MD
Nothing to Disclose