11/4 anoxic and hypoxic brain injury

anoxic brain injury

• injury due to complete absence of oxygen

hypoxic brain injury

• ie. hypoxic ischemic encephalopathy

• occurs over time

• reduction in oxygen supply, can be:

  • environmental

  • due to reduced oxygen in blood

  • due too inadequate blood flow (ischemia)

  • difficulty metabolizing oxygen by brain tissue

oxygen delivery in the brain

• middle cerebral artery (MCA) supplies the most blood

  • exits from lateral fissure

  • superior MCA supplies portions of frontal and parietal cortices above lateral fissure

  • inferior MCA supplies portions of temporal and parietal cortices below lateral fissure

  • also supplies some of inferior surface of frontal lobe and deep structures

• lenticulostriate arteries = deep branches of MCA

  • supply large regions of basal ganglia and internal capsule

• posterior cerebral arteries

  • also supply basal ganglia

what are watershed areas?

• areas where two perfusion areas come together, not much overlap between perfusion territories of arteries

• vulnerable to drops in oxygen and/ or blood pressure because there is very little redundancy in blood supply

• ie. between ACA and MCA, between MCA and PCA

brain structures impacted by H/ABI

• hippocampus

• basal ganglia

• thalamus

• substantia nigra

• cerebral cortex

• cerebellum

• deep white matter

because these are supplied by major arteries and are highly metabolic

bold = most common

cognitive effects of H/ABI

• memory disturbance — hallmark symptom

• personality/ behavior changes

• visuospatial/ visual recognition problems

• expressive language

• attention

• executive functioning

• balance/ gait disturbances

• motor issues

anoxia mechanisms of injury

• cardiac failure (too much time without circulation)

• respiratory failure

• anesthesia

• near drowning

• self-hanging attempts/ asphyxiation

timeline of absence of cerebral blood flow

• 20 seconds = LOC

• 3-5 min = glucose reservoir consumed

• 5-8 min = permanent neuronal lesions

• 10-15 min = death

(assuming normal body temp)

*5 min without blood flow = permanent damage

*very short time interval for serious damage

ABi v. TBI

• ABI pts found to have worse functional outcomes than TBI pts, measured by functional independence measure (FIM)

  • exception = DAI in TBI

  • because white matter tracts and deep structures are usually spared in TBI

hypoxia mechanisms of injury

• chronic obstructive pulmonary disease (COPD)

• sleep apnea

• CO poisoning

• anemia

• high altitude

• smoke inhalation (displaces space for oxygen in lungs)

• toxic substances (ie. cyanide poisoning)

induction of hypothermia (IH)/ targeted temperature management (TTM)

• performed following cardiac arrest to mitigate effects of reperfusion phase

• consists of reducing body temp if consciousness is not regained

• why?

  • much of the damage that occurs due to ischemia is realizing during the reperfusion phase — blood rushing back too quickly. so, want slow reintroduction of blood if possible

  • hypothermia can be protective because:

    • counteracts switch to anaerobic respiration, which leads to increased excitation and cell death

    • stabilizes BBB

    • decreases cerebral metabolism, in turn decreasing need/ hunger for oxygen