Hypoxia

Question 1

Definition

Answer 1

Ischemia: insufficient blood supply to the brain and organs due to interruption or reduction of blood delivery

Anoxia: the absence or near complete absence of oxygen in the arterial blood supply to an organ or tissue

Hypoxia: diminished availability of oxygen to tissues

Hypoxemia: condition where there is reduced oxygenation in the blood

Apnea: total breathing cessation or hypopnea which is partial breathing cessation

Question 2

Neuropathology

Answer 2

Cascade of pathophysiological processes that result in cell death

Have biochemical changes: increased intracellular calcium due to ionic pump failure - leads to cell death and apoptosis

Energy depletion, glutamate and aspirate are released in large quantities causing damage (excitotoxic-induced neuronal damage)

Reoxygenation and reperfusion injury occurs (oxygen radicals)

Nitric oxide expressed in inflammatory cells

Question 3

Risk factors

Answer 3

Medical conditions: cardiac arrest, carbon monoxide poisoning, drowning, suffocation, massive blood loss, prolonged seizures, OSA, asthma

Congenital heart disease
Sleep-disordered breathing

Question 4

Determinants of severity

Answer 4

Extent of brain abnormalities may be markers for prognosis following hypoxia brain injury

Cerebellar atrophy correlates with low GCS, profound acidosis, and EEG abnormalities

Severity of hypoxia / apnea

No pupillary response on day 3 post injury
GCS motor score of 1-3 on day 3
Alpha coma EEG pattern 
Convulsive or myoclonus 
GCS of 3-5 in first 24 hours 
Coma more than 6 hours
Sustained conjugate eye deviation 
Lower cranial nerve dysfunction (e.g., absence gag reflexes)

Question 5

Presentation

Answer 5

OSA: hippocampal atrophy is a common finding - also atrophy in fornix (major output pathway to the hippocampus to the mammillary bodies) and Cingular

Near drowning: similar to deficits found in carbon monoxide poisoning - diffuse cerebral atrophy and basal ganglia lesions

Hypoxia: cortical edema or atrophy, cerebellar lesions, basal ganglia, and hippocampal atrophy - thalamic lesions are less common

Carbon monoxide positioning: affinity for binding with hemoglobin - displace oxygen binding sites resulting in hypoxia and acidosis (delayed neurological deterioration that may take 1-3 weeks after exposure) - NP findings are attention, information processing, EF, and memory

Question 6

Course

Answer 6

During acute period following hypoxia brain injury, MRI and CT may be normal or only see subtle changes

See white matter abnormalities within 7 days of hypoxia brain injury.

Some deficits may not be revealed until later developmental periods

Question 7

Recovery

Answer 7

As recovery progresses, attention deficit, distractibility, severe anterograde amnesia, and executive dysfunction often emerge

Lower functional independence measure (FIM0

Amount of tissue loss is more critical in determining outcome than etiology (e.g., anoxia vs. TBI)

Question 8

Treatment

Answer 8

Serial assessment of responsiveness
Teaching compensatory strategies
Follow up MRI

PT and OT often due to motor impairment from damage to cerebellar and basal ganglia structures

Speech-language therapy focus on pragmáticos and cognitive abilities

Question 9

Neuroimaging and vulnerable areas

Answer 9

End arteries are most vulnerable (watershed areas) - neocortex, hippocampus, basal ganglia, cerebellar purkinje cells, primary visual cortex, and thalamus

Lesions of the basal ganglia and cortex will see in the first few hours following hypoxia but won’t see damage to the hippocampus for days to weeks (delayed apoptosis)

White matter changes and atrophy in the corpus callosum - in carbon monoxide poisoning and generally preserved in hypoxia/ischemia

Question 10

Neuropsychological findings

Answer 10

Language: disorders rarely seen
EF: minimally affected in milder cases but common and disabling in more severe
Attention: distractibility early and long term
Visuospatial: watershed zones affected - cortical blindness or other severe visuospatial impairment
Emotions: anosognosia (impaired self-awareness) is common early post injury, depression, and changes in self-regulation and behavioral dysregulation
Memory: impaired storage and retrieval - amnestied state with bilateral hippocampal damage
Adaptive: often not back at baseline and functional issues that can be debilitating
Processing speed impaired both cognitively and motorically
IQ: not affected
Motor sensory: basal ganglia and cerebellum are high risk injury - spastic quadriparesis, ataxia, Parkinsonism syndromes, etc.