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Neuropsych Board Prep > Hypoxic and Ischemic Brain Injury > Flashcards

Hypoxic and Ischemic Brain Injury Flashcards

1
Q

What causes anoxic/hypoxic damage to the brain?

A

It occurs secondary to conditions that affect the cardiac/respiratory systems.

It is defined as the lack of or insufficient supply of oxygen circulating to tissue in the presence of adequate blood flow.

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2
Q

What are prevalence estimates of cognitive impairment following conditions such as cardiac arrest?

A

6-100%. It varies widely due to:

  • Broad range of conditions that can cause damage
  • Multisystem complications that occur and exacerbate encephalopathy
  • Milder cog impairment may not be recognized in hospital setting
  • Varying methodology
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3
Q

Do neurons have the capacity to store energy and oxygen similar to cells in other parts of the body?

A

No. Also, the brain consumes blood, oxygen, and glucose at levels disproportionate to its mass relative to other parts of the body.

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4
Q

What is the partial pressure of arterial oxygen in healthy adults at sea level?

A

95-100mm HG

When this rapidly drops, complex cog processes become impaired

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5
Q

Define anoxia.

A

Complete lack of oxygen in arterial blood, due to a profound and sudden medical event such as cardiac arrest or loss of perfusion pressure.

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6
Q

Define hypoxia.

A

Deficient amount of oxygen available in the blood supply to the brain.

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7
Q

Define hypoxemia.

A

Reduced partial pressure of oxygen in arterial blood (<60mm Hg). Can lead to hypoxia

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8
Q

Define ischemia.

A

Failure of perfusion of blood through the cerebral vessels to tissue.

Ischemia AND anoxia are usually involved in cases of sudden cardiac arrest.

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9
Q

What are acute conditions that cause hypoxic-ischemic brain damage?

A
  • Cardiac arrest
  • Acute respiratory distress syndrome
  • Carbon monoxide poisoning
  • Suffocation, drowning, hanging
  • Massive blood loss d/t trauma
  • Prolonged seizures
  • Anesthesia accidents in surgery
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10
Q

What are chronic conditions that cause hypoxic-ischemic brain damage?

A
  • COPD
  • OSA
  • Asthma
  • Conditions that paralyze the respiratory system such as ALS and myasthenia gravis
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11
Q

What are homeostatic mechanisms that are triggered when PaO2 or perfusion is disrupted?

A
  • Nervous system increases cerebral blood flow up to as much as 400%
  • Autoregulatory response (e.g., dilation of blood vessels to maintain flow)

Beyond a point, protective measures are insufficient to prevent CNS injury.

Brain depletes energy sources w/in several minutes of complete ischemia.

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12
Q

How does the process differ for COPD?

A

This is a more persistent, gradual reduction in arterial oxygen and elevated carbon dioxide.

Arterial oxygen partial pressure gradually declines to levels which, if suffered acutely, produce rapid onset of coma/marked cog impairment

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13
Q

What are neuropathological changes from hypoxia/ischemia?

A

-Brain regions with high metabloic demands and those at the distal end of cerebral arteries are more vulnerable (watershed regions)

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14
Q

What are brain regions that are highly vulnerable to hypoxia/ischemia?

A
  • Neocortx (layers 3, 5, and 6)
  • Hippocampus (pyramidal cells in CA1)
  • Basal ganglia (striatum, GP)-Cerebellar regions (Purkinje cells)
  • Visual cortex
  • Thalamus
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15
Q

Describe the time-dependent neuroimaging findings in hypoxic/ischemic injuries.

A
  • Early studies: loss of distinction btw. white and gray matter in the cortex (but can appear normal)
  • Damage to basal ganglia and neocortex soon after onset
  • Hippocampal damage days or weeks later
  • Diffuse atrophy chronically
  • WM tracts tend to be preserved (but are vulnerable in CO poisoning)
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16
Q

What do reviews of published cases with neuroimaging reveal regarding hippocampal damage in hypoxic injuries?

A
  • Hippocampal damage is frequently not noted
  • When damage is visible it is in multiple brain regions
  • Watershed regions and basal ganglia are more frequently damaged than the hippocampus
  • Hippocampus was the solely affected structure in 18% of reported cases
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17
Q

Where do most neurons get their energy?

A

Hydrolysis of ATP

The brain has almost no inherent energy stores and is critically dependent on flow of oxygen and glucose. If it does not have this than neuronal death occurs.

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18
Q

What are secondary toxic processes that are triggered by hypoxia/ischemia?

A
  • Sodium and calcium pumps fail which leads to excessive levels of glutamate
  • Glutamate becomes excitotoxic to neurons
  • Additional toxic effects are triggered: lactic acidosis, cytotoxic edema, free radical production
  • Necrosis and apoptosis evolves
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19
Q

Why is carbon monoxide poisoning different from other forms of hypoxic/ischemia?

A
  • It has a very high affinity for binding with hemoglobin & forms carboxyhemoglobin
  • It displaces oxygen binding sites on the red blood cells which leads to hypoxia and acidosis
20
Q

At what levels are acute effects of carboxyhemoglobin seen?

A
  • When it is 20-30% of total hemoglobin in the blood

- Levels above 50% result in coma

21
Q

When does neurologic deterioration typically occur in CO poisoning and what changes are seen in the brain?

A

Delayed deterioration, 1-3 weeks after severe exposure

  • Basal ganglia damage is common
  • Hippocampal atrophy and generalize brain atrophy may be seen months following the injury
22
Q

What are neuropsych deficits of CO poisoning?

A

Deficits in attention, information processing, executive functioning, and verbal and nonverbal memory.

23
Q

If hypoxia does not disrupt consciousness does CNS damage occur?

A

No, it is unlikely. Mild hypoxia that does not lead to LOC may induce mild cog and motor impairment that is not expected to have lasting effects.

24
Q

What causes the most severe cases of hypoxia/ischemic damage?

A

Sudden cardiac arrest or ARDS bc LOC occurs very rapidly

Those who emerge from prolonged coma have lasting cog and functional disability.

25
Q

Describe COPD and hypoxic damage.

A
  • examples of COPD: emphysema, neuromuscular weakness, and fibrous lung disease
  • Results in: persistent respiratory acidosis w/ reduced arterial oxygen saturation and elevated carbon dioxide
  • Severe COPD results in cog impairment
  • Positive pressure ventilation w/ oxygen may improve cog functioning but not QOL
26
Q

Describe OSA and hypoxic damage.

A
  • OSA: recurrent episodes of blood oxygen desaturation d/t total or partial breathing cessation
  • Disrupts normal sleep architecture
  • Oxygen desat occurs up to 100 times an hour
  • Associated w/ greater risk for WM hyperintensities and cog impairment
  • Older adults are more vulnerable
  • Elderly women are at an increased risk
  • CPAP reduced episodes of breathing disruption and oxygen desats,and improves daytime sleepiness and possible cog improvement
27
Q

What are favorable outcomes of a hypoxic/ischemic event associated with?

A

Short period of LOC, regain purposeful motor movements, and have preserved memory w/in a few hours of resuscitation

28
Q

Poor outcome of hypoxic/ischemic events are associated with what?

A
  • No pupillary response on day 3 post-injury (68% prevalence)
  • GCS motor score of 1-3 on day 3 (73%)
  • Alpha coma EEG pattern (66%)
  • Convulsions or myoclonus (74%)
  • Total GCS of 3-5 in first 24 hours (77%)
  • Bilateral absence of somatosensory evoked potential on median nerve stimulation (76%)
29
Q

What are poor prognostic indicators in the absence of sedation effects?

A
  • Coma more than 6 hours
  • No spontaneous limb movements or localization to pain stimuli
  • Prolonged loss of pupillary responses
  • Sustained conjugate eye deviation
  • Abnormal eye movements
  • Presence of myoclonic seizures
  • Lower cranial nerve dysfunction
30
Q

Do those with severe hypoxic/ischemic injuries usually return to independence?

A

No, and recovery curves are fairly flat

31
Q

What instruments are useful for evaluating individuals early in recovery?

A

GSC
Coma recovery scale
Coma-Near Coma Scale
Rancho Los Amigos Level of Cognitive Functioning

32
Q

What are instruments that are used for structured basic assessment of mental status?

A 
MMSE
Orientation Log
Cognitive Log
MoCA
Cognistat
33
Q

Those in acute recovery may experience confusion and agitated behavior. What should one emphasize during this time?

A

Frequent reorientation
Establishment of consistent daily routines
Use of short treatment sessions
Attending carefully basic physiological needs
Maintaining a quiet treatment environment
Avoiding overstimulation

34
Q

What are patterns of recovery in comparing hypoxia/anoxia to TBI?

A
  • Amount of tissue loss is more critical in determining outcome than etiology in both
  • Measures of memory correlates with hippocampal atrophy in both
  • Intelligence correlates with whole brain volume in both
  • Those w/ hypoxia have similar lengths of inpatient stay compared to TBI but show slower progress with poorer outcomes
  • Individuals with hypoxia are more likely to be referred to residential care
  • Those w/ hypoxia perform worse on all measures of functional outcome
  • Individuals with hypoxia have lower FIM motor and cog gains relative to those with TBI
35
Q

What purpose does neuropsych assessment serve after a hypoxic/ischemic injury?

A 
Characterize strengths and deficits.
Help identify target goals for rehab.
Identify psychological disturbance.
Determining decisional capacity.
Identify areas for accomodations in school/work.
36
Q

What are typical outcomes following hypoxic/ishcemic injuries?

A
  • Most catastophic cases:brain death or minimally responsive state
  • Less severe cases: coma, confusion in early recovery phase, and lasting sig cog impairment/dementia
  • > 30% of survivors of cardiac arrest and ADRS show generalized cog impairment
  • Changes in memory are reported in 50% of survivors of severe hypoxia/anoxia, and personality changes in 1/3
  • Mild cases: cog impairment may be transient
37
Q

What are expectations for neurospych assessment results?

A
  • Intelligence: Overall scores may be reduced d/t impairments in processing speed but hold tests are not typically affected
  • Attention/concentration: Impaired as recovery progresses and may be longstanding issue
  • Processing speed: impaired
  • Language: formal language disorders are rare
  • Visuospatial: if watershed zones affected deficits can occur. Cortical blindness has occurred.
  • Memory: impairments in storage, capacity, and retrieval are common. Amnestic states can occur
  • Executive functions: minimally effected in milder cases but common and disabling in more severe cases
  • Sensorimotor: Severe injury can cause spastic quadriparesis, ataxia, parkinsonism syndromes
  • Emotion/personality: anosognosia is common, depression is also common
38
Q

What medications can be used to help in treatment of those with hypoxic and ischemic brain injury?

A
  • Methylphenidates, acetylcholinesterase inhibitors, and NMDA receptor antagonists may be used to improve memory and attention
  • SSRIs or anticonvulsants may be used for mood stabalization
39
Q

What should be emphasized in rehabilitation?

A

Errorless learning, procedural learning, and attention process training

40
Q

What percentage of total oxygen consumption does the brain of infants/children require?

A

30% from infancy to 4 years

41
Q

Injury to what structures has been found to be most strongly associated with long-term outcome in neonates?

A

Basal ganglia and thalamus

42
Q

What is acute respiratory distress syndrome?

A

A severe, often life-threatening medical condition in which the lungs are compromised or damaged and unable to supply sufficient oxygen to the arterial blood.

43
Q

What is apoptosis?

A

Programmed cell death.

44
Q

What is ATP (adenosine triphosphate)?

A

A chemical compound that provides energy for cells/nuerons.

45
Q

What is necorsis?

A

Death of tissues or neurons typically due to insufficient blood supply.

Neuropsych Board Prep (32 decks)

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