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160 Cards in this Set
- Front
- Back
|
Anoxic and hypoxic damage to the brain is secondary to: |
conditions that affect the cardiac and respiratory systems |
|
|
deficient oxygen supply can occur from (2): |
deficient perfusion of blood to the brain
reduced amount or concentration of oxygen in the blood |
|
|
factors which may complicate patterns of neuropathology and cognitive dysfunction due to hypoxic/ischemic conditions: |
broad range of conditions that can cause H/I damage
multisystem complications that occur and can exacerbate encephalopathy
cognitive impairment from milder H/I states may not always be recognized in hospital setting
methodology and operational definitions of key terms such as hypoxia vary across studies |
|
|
partial pressure of arterial oxygen (PaO2) in health adults at sea level: |
95-100 mm Hg |
|
|
Result of arterial oxygen level dropping: |
complex cognitive processes such as memory and judgment become impaired |
|
|
homeostatic protective mechanisms are triggered when PaO2 is disrupted within these parameters: |
increasing cerebral blood flow up to as much as 400%
autoregulartory response to a reduction or loss of perfusion pressure can involve dilation of blood vessels to maintain flow |
|
|
the brain is highly dependent on
|
consistent supply of blood, O2, and glucose and
consumes those at levels disproportionate to its mass in other parts of the body |
|
|
beyond a certain point, protective measures are
insufficient to prevent certain CNS injury |
the brain depletes energy sources within several
minutes of onset of complete ischemia, although conditions like hypothermia can extend that period |
|
|
neuropathological changes from
hypoxia/ischemia are consistent with the mechanism of insult– |
brain regions with high metabolic demands and
those at the distal end of cerebral arteries (in particular, watershed regions) are more vulnerable |
|
|
brain regions that show high vulnerability to
hypoxia/ischemia |
neocortex (layers 3,5,6)
hippocampus (pyramidal cells in CA1) Basal ganglia (striatum, globus pallidus) cerebellar regions (Purkinje cells) visual cortex thalamus |
|
|
neuroimaging also shows time dependent
vulnerability to damage in specific regions |
lesions often evolve over weeks or months
|
|
|
early neuroimaging
|
is variable, sometimes showing loss of
distinction btwn white and gray matter in the cortex, but also often appearing normal basal ganglia and neocortex regions may show damage on neuroimaging soon after onset hippocampal damage may not be evident on neuroimaging for days or weeks diffuse atrophy may appear chronically but is not expected acutely white matter tracts are generally preserved in hypoxia/ischemia but are vulnerable to carbon monoxide poisoning |
|
|
hippocampal damage historically a hallmark of
hypoxic damage, but reviews of published cases w neuroimaging data shows |
1. hippocampal damage is freq not noted |
|
|
the hippocampus was the sole affected structure
in only |
18% of reported cases
|
|
|
hypoxia/ischemia triggers a cascade of neuronal
cell processes that are multifaceted, time dependent, and neurotoxic |
most energy required from neurons is derived |
|
|
a series of secondary toxic processes is also
triggered |
sodium and calcium pumps fail, resulting in
depolarization of the neuronal membrane and release of excessive levels of glutamate glutamate is the most common excitatory neurotransmitter, but at excessive levels it becomes excitotoxic to neurons a further series of toxic events are triggered that involve lactic acidosis from anaerobic metabolism, cytotoxic edema, free cell radical production, and others necrosis and apoptosis become factors as the pathology evolves |
|
|
even if the causal condition is addressed and
circulation is restored, cerebral circulation may not respond effectively |
for reasons that are not well understood but that
may involve edema preventing reflow to small vessels, as well as an inability to remove toxic metabolites that have accumulated |
|
|
carbon monoxide (CO) poisoning shows many of
the same effects as other forms of hypoxia/ischemia but there are some notable differences in the pathological processes |
– CO has a high affinity for binding with
hemoglobin, forming carboxyhemoglobin the effect displaced O2 binding sites in red blood cells, resulting in hypoxia and acidosis once carboxyhemoglobin rises above 20–30% of total hemoglobin in the blood, acute effects are seen levels above 50% cause coma and severe CNS effects not clear whether CO is directly toxic to neurons, and he most sig effects are very similar to what is seen following cardiac arrest CO poisoning often results in delayed neurologic deterioration, which may occur 1–2 weeks after exposure Basal ganglia damage is common, contributing to the extrapyramidal features often seen following severe Co poisoning hippocampal and general brain atrophy ( as measures by ventricle to brain ratio) may be seen months following injury NP deficits may be seen in attn., inform processing, EF, verbal and non verbal memory |
|
|
CO is a
|
gas that is present naturally but also results from
a combustion of man made fuel (gasoline engine and furnace exhaust) |
|
|
incidence
|
not clear, milder cases often unrecognized in a
hospital setting |
|
|
determinants of severity
|
effects vary based on the nature of the
underlying condition that produced the disruption in O2 supply and how rapidly the pathological process can be reversed. |
|
|
if hypoxia is not severe enough to disrupt
consciousness |
CNS damage is unlikely
|
|
|
mild hypoxia that does not lead to LOC (like high
altitude climbing) |
may induce mild cognitive and motor impairment
not expected to have lasting effects, though some studies suggest a possible persistence of mild changes |
|
|
most severe cases
|
result from sudden cardiac arrest or acute
respiratory distress syndrome (ARDS) |
|
|
LOC
|
occurs very rapidly. when the brain is deprived of
O2 for several minutes, damage progresses rapidly and if the underlying cause is not quickly reversed, brain death or a persistent minimally responsive state may result |
|
|
those who emerge from prolonged coma
|
typically have lasting cognitive and functional
disability (varying degree of dementia) and may show extrapyramidal syndromes like Parkinsonianism |
|
|
rapid resuscitation efforts
|
may prevent escalation to permanent damage
|
|
|
COPD
|
examples include emphysema, neuromuscular
weakness, fibrosing lung disease results in persistent respiratory acidosis with reduced arterial O2 sat and elevated carbon dioxide cog deficits may not occur in mild cases that do not produce persistent hypoxia severe COPD often results in cog impairment, lower scores on objective measures compared to less severely affected indiv. positive pressure ventilation with O2 may improve cog Fx but not necessarily better quality of life |
|
|
OSA
|
involves recurrent episodes of blood O2
desaturation due to total or partial breathing cessation Disrupts normal sleep architecture O2 desat may occur up to 100 times an hour neuroprotective vasodilatory response to hypoxia may be lacking |
|
|
severe OSA
|
assoc with greater risk for white matter
hyperintensities and cog imp (learning and mem, EF, psychomotor impairments), but not consistent across studies |
|
|
older adults
|
more vulnerable to sleep disordered breathing
community dwelling elderly women with sleep disordered breathing show increased risk of cognitive impairment |
|
|
CPAP for OSA
|
reduces episodes of breathing dysfunction
reduced O2 desat during sleep improves daytime sleepiness may lead to improvement is select areas of cognition presentation, disease course, and recovery |
|
|
recovery course
|
quite variable
|
|
|
favorable recovery
|
short period of impaired consciousness
regain purposeful motor movements preserved memory within a few hours following resuscitation |
|
|
poor outcome
|
no pupillary response 3 days post injury (68% |
|
|
the following are poor prognostic indicators in
the absence of sedation effects |
coma more than 6 hours
no spontaneous leg movements or localization to pain stimuli prolonged loss of pupillary responses sustained conjunctive eye deviation abnormal eye movements (nystagmus) myoclonic seizures lower cranial nerve dysfunction (such as absent cough and gag reflexes) |
|
|
when evaluating a pt in the acute phase of recovery
|
be mindful of
interventions medications comorbidities that can cause or contribute to encephalopathy, confusing or complicating the presentation |
|
|
recovery curves in pts with severe
hypoxic/ischemic injury |
are fairly flat, and return to independence is
rarely achieved |
|
|
instruments useful for evaluating individuals
early in recovery (acute care or early IP rehab) and that focus on basic functioning: |
GCS
Coma Recovery Scale– Revised Coma– Near Coma Scale Rancho Los Amigos Level of Cog Fx |
|
|
instruments useful for structured basic
assessment of mental status |
MMSE
Orientation Log Cognitive Log MOCA Cognistat with higher cog Fx early in recovery: RBANS |
|
|
For patients recently emerging from minimally
responsive state, out emphasis on: |
frequent reorientation
Est consistent daily routines use short treatment sessions attend carefully to basic physiological needs (nutrition, toileting, sleep) maintain a quiet treatment environment avoid overstimulation |
|
|
as recovery progresses
|
attention deficits, distractibility, severe
anterograde amnesia, and EF dysfunction need to be addressed rehab generally involves teaching compensatory strategies or attempting to directly address areas of cog deficit |
|
|
studies comparing patterns of recovery from
hypoxia/anoxia to TBI have found the following patterns: |
amount of tissue loss is more critical in
determining outcome than etiology measures of memory correlate with hippocampal atrophy in both hypoxia and TBI intelligence correlates with whole brain volume in both conditions those with hypoxia have similar lengths of inpatient stay as TBI but show slower progress and poor outcomes those with hypoxic injury more likely to be referred to residential care those with hypoxia perform worse on all measures of fx outcome than TBI and have have lower functional independence measure motor and cognitive gains relative to those w TBI |
|
|
outpatient and post acute brain injury rehab
programs |
are appropriate and may extend treatment
gains from IP setting focus on compensatory strategies, skill acquisition, building independence, and community reintegration family training and support is critical |
|
|
Assessment methods– imaging
|
MRI and CT initially often do not reveal sig
changes follow up studies may reveal white matter changes, corpus callosum atrophy, cortical edema, cerebellar lesions, basal ganglia lesions, thalamic lesions, and/or hippocampal atrophy (OFTEN TAKE WEEKS OR MONTHS TO BE VISUALIZED ON SCANS) |
|
|
NP assessment may serve the following pruposes
|
characterize strengths and deficits and link
such patterns to daily Fx identify target goals for continued rehabilitation identify the presence and severity of psychological disturbance that may impact recovery and rehab determine decision making capacity and need for supervision identify target areas for accommodations for return to school and work |
|
|
outcomes
|
the most catastrophic cases may result in brain
death or persistent minimally responsive states less severe cases show variable periods of coma, marked confusion in early recovery, and lasting significant cog impairment or dementia |
|
|
high percentage of survivors of sudden cardiac
arrest and ARDS show |
generalized cog impairment
a higher percentage show specific/focal deficits in memory, attn., or processing speed |
|
|
changes in memory
|
have been reported in more than 50% of
survivors of severe hypoxia |
|
|
personality changes
|
have been reported in 1/3 of survivors of severe
hypoxia |
|
|
less than 50%
|
of those who require rehabilitation regain full
independence of daily FX, but there is much variability in outcome |
|
|
in mild cases with rapid reversal of pathological
condition |
cog imp may be transient, but some may
experience persistent cognitive deficits |
|
|
expectations for NP assessment results–
IQ/achievement |
overall scores may be reduced due to
impairments in processing speed and efficiency |
|
|
expectations for NP assessment results–
attention/concentration |
gross confusion apparent early
attn. may be a sig prob as rehab progresses and may be a long term issue distractibility is often observed both early in recovery and over the long term |
|
|
expectations for NP assessment results–
processing speed |
often impaired, cognitively and motorically
|
|
|
expectations for NP assessment results–
language |
formal language d/os rarely seen
though cases involving severe watershed damage trans cortical aphasia or other higher order language syndromes may be present |
|
|
expectations for NP assessment results–
visuospatial |
if watershed zones are affected, deficits can be
noticeable cortical blindness and other severe visuospatial imp variants have occurred lower performance on these tests may in part reflect slowed information processing |
|
|
expectations for NP assessment results– memory
|
impairments in storage, capacity, and retrieval
are common in severe cases with bilateral hippocampal damage, a marked amnestic state may be evident a subset of patients have no mem imp but have motor or cog imp in other domains (eg, FX assoc with watershed regions) |
|
|
expectations for NP assessment results–
EF |
may be minimally affected in milder cases, with
the exception of executive aspects of attn. EF deficits common and disabling in severe cases some patients sustain orbitofrontal damage bc this is a watershed region |
|
|
expectations for NP assessment results–
sensorimotor |
the basal ganglia and cerebellum are high risk for
injury severe anoxic injury can cause spastic quadiparesis, ataxia, parkinsonian syndromes, and other motor impairments/dysfunction |
|
|
expectations for NP assessment results–
emotion and personality |
anosognosia (impaired self awareness) is
common early post injury and may persist long term depression commonly observed changes in self regulation of emotion may occur due to medial frontal and frontal systems injury beh dysregulation may be seen in severe cases and may become a chronic feature severe psychiatric issues are common in severe cases, which may incl beh dysregulation and major depression |
|
|
driving
|
prognosis for returning to driving is not good in
severe cases, but may be possible with mild to moderate injuries with good recovery |
|
|
work
|
return to work is unlikely in severe cases, but
may be possible with mild injury and good recovery for those unable to return to competitive employment, alternative vocational or volunteer placement may be appropriate |
|
|
school/vocational training
|
unlikely, but may be possible with mild injury and
good recovery for students in high school and younger, it is critical to involve the school and educ specialists as early as possible to plan for academic re–entry (important for recovery and legally mandated) |
|
|
capacity
|
for medical and legal affairs will likely be severely
limited early in recovery despite recovery, may remain impaired due to EF and memory imp legal issues vary across jurisdiction |
|
|
medications
|
for attn. and memory may be used– such as:
methylphenidate (Ritalin), other stimulants acetylcholinesterase inhibitors (Aricept) and NMDA receptor antagonists (Namenda) SSRIs or anticonvulsants may be used for mood stabilization evidence for support of the use of these meds in hypoxic injury is more anecdotal than evidence based |
|
|
risk factor modification
|
increased supervision for safety
external and internal structures assistance with decision making (POA, guardianship) family support/training |
|
|
interpersonal relationships
|
can be challenging due to persistent memory
impairment, poor insight, exec dysfunction, and changes in premorbid role Fx |
|
|
functional issues
|
severe injuries often result in dystonia, spastic
hemiparesis, or quadraparesis due to basal ganglia involvement ataxia may persist due to cerebellar involvement many of these patients are unemployable and require attendant care for the rest of their lives |
|
|
rehab considerations
|
compensatory strategy training is critical for
patients with memory or other cog imp emphasis should be placed on errorless learning, procedural learning, attention process training (APT), and evidenced based cognitive rehabilitation Tx |
|
|
pediatric considerations
|
brains of infants and children req a higher
percentage of O2 than adults (over 30% total body O2 consumption from infancy to age 4) impact of hypoxia will depend on developmental period where it occurs neonatal hypoxia may lead to major developmental disorders and impaired cognition, depending on severity and pattern of damage injury to the basal ganglia and thalamus is predominant pattern in neonates assoc with long term outcome congenital heart defects and sleep disordered breathing are also found to have a relationship with cog, academic, and beh Fx some deficits are not noted until a child starts school |
|
|
geriatric considerations
|
older brains less able to recover from an anoxic
injury and will likely suffer more permanent and severe cog deficits due to reduced reserve for many, there are pre–existing MCI and Fx impairment or will have age related impairments |
|
|
acute respiratory distress syndrome (ARDS)
|
severe, often life threatening medical condition
where the lungs are compromised and damaged and are unlikely to supply sufficient O2 to the arterial blood (eg hypoxemia) can result in hypoxic damage to brain as well as many other systemic px |
|
|
apoptosis
|
programmed cell death
part of normal regulation and turnover of cells, but also can result from pathological processes like ischemia |
|
|
ATP (adenosine triphosphate)
|
a chemical compound that provides energy for
cells/neurons under anoxic conditions, becomes less available in the neuron, leading it to catabolize itself |
|
|
glutamate
|
most common excitatory neurotransmitter in the
brain under hypoxic conditions, excessive amounts are released in the synaptic cleft, and it becomes excitotoxic, contributing to deleterious processes in the neuron |
|
|
COPD
|
encompasses several pulmonary conditions, incl
emphysema and bronchitis progressive obstruction of expiration can produce chronic hypoxia and result in cog imp |
|
|
necrosis
|
refers to death of tissue or neurons, typically due
to inefficient blood supply |
|
|
watershed regions
|
in the brain, refers to overlapping border zones |
|
|
anoxic/hypoxic damage
|
results secondary to conditions that affect the
cardiac or respiratory system can result from reduced concentration of O2 in the blood or from deficit perfusion of blood to the brain defined as lack of or insufficient supply of O2 circulating to tissue in the presence of adequate blood flow |
|
|
ischemic–hypoxic encephelopathy
|
terms used together for the purposes of the
chapter b/c in most cases where the brain sustains marked disruption of O2 supply, both processes become involved |
|
|
prevalence of cog imp following cardiac arrest
|
range widely, from 6–100%
|
|
|
several factors complicate attempts to
characterize patterns of neuropathology and cog imp due to hypoxic, ischemic conditions |
a broad range of conditions that cause
hypoxic/ischemic damage multisystem complications occur and may exacerbate encephalopathy cog imp from milder hypoxic/ischemic states may not be recog. in the hospital setting methodology and operational def of key terms vary across studies |
|
|
the brain is highly dependent on
|
consistent supply of blood, O2, and glucose and
consumes those at levels disproportionate to its mass in other parts of the body |
|
|
oxygenation of the blood is the result of
|
a complex process involving hemoglobin
concentration and O2 saturation |
|
|
partial pressure of arterial oxygen (PaO2)
|
refers to pressure exerted independently by a
specific gas within a larger mix of gases in healthy adults at sea level is typically 95–100 mm Hg when this level rapidly drops, complex cognitive processes such as memory and judgment become impaired |
|
|
homeostatic protective mechanisms are
triggered when PaO2 or perfusion is disrupted, and these are effective w/in certain parameters |
– the nervous system responds to hypoxic states
by increasing cerebral blood flow up to 400% – autoregulatory response to a reduction or loss of perfusion pressure involves several mechanisms, including dilation of blood vessels to maintain flow |
|
|
beyond a certain point, protective measures are
insufficient to prevent certain CNS injury |
the brain depletes energy sources within several
minutes of onset of complete ischemia, although conditions like hypothermia can extend that period |
|
|
processes differ in COPD and other advanced
pulmonary illness characterized by persistent, gradual reduction in arterial O2 levels. |
in such individuals, arterial O2 pressure may
gradually decrease to levels that if suffered acutely produce rapid onset of coma or marked cognitive impairment (similarly, high altitude climbers may acclimate gradually to lower O2 sat, though not necessarily without cog or physiological effects) |
|
|
neuropathological changes from
hypoxia/ischemia are consistent with the mechanism of insult– |
brain regions with high metabolic demands and
those at the distal end of cerebral arteries (in particular, watershed regions) are more vulnerable |
|
|
brain regions that show high vulnerability to
hypoxia/ischemia |
neocortex (layers 3,5,6)
hippocampus (pyramidal cells in CA1) Basal ganglia (striatum, globus pallidus) cerebellar regions (Purkinje cells) visual cortex thalamus |
|
|
neuroimaging also shows time dependent
vulnerability to damage in specific regions |
lesions often evolve over weeks or months
|
|
|
early neuroimaging
|
is variable, sometimes showing loss of
distinction btwn white and gray matter in the cortex, but also often appearing normal basal ganglia and neocortex regions may show damage on neuroimaging soon after onset hippocampal damage may not be evident on neuroimaging for days or weeks diffuse atrophy may appear chronically but is not expected acutely white matter tracts are generally preserved in hypoxia/ischemia but are vulnerable to carbon monoxide poisoning |
|
|
hippocampal damage historically a hallmark of
hypoxic damage, but reviews of published cases w neuroimaging data shows |
1. hippocampal damage is freq not noted
2. when damage is visible, it usually is present in multiple brain regions one review showed that watershed cortex and the basal ganglia were both more frequently damaged than the hippocampus |
|
|
the hippocampus was the sole affected structure
in only |
18% of reported cases
|
|
|
hypoxia/ischemia triggers a cascade of neuronal
cell processes that are multifaceted, time dependent, and neurotoxic |
most energy required from neurons is derived
from hydrolysis of adenosine triphosphate (ATP) the brain has no inherent energy stores (in contrast to other tissue) and thus is critically dependent on uninterrupted flow of O2 and glucose a sudden loss of cerebral perfusion or anoxia/hypoxia causes a critical shortage of the O2 and glucose supply to neurons, and if not rapidly reversed, initiates processes that result in neuronal death |
|
|
a series of secondary toxic processes is also
triggered |
sodium and calcium pumps fail, resulting in
depolarization of the neuronal membrane and release of excessive levels of glutamate glutamate is the most common excitatory neurotransmitter, but at excessive levels it becomes excitotoxic to neurons a further series of toxic events are triggered that involve lactic acidosis from anaerobic metabolism, cytotoxic edema, free cell radical production, and others necrosis and apoptosis become factors as the pathology evolves |
|
|
even if the causal condition is addressed and
circulation is restored, cerebral circulation may not respond effectively |
for reasons that are not well understood but that
may involve edema preventing reflow to small vessels, as well as an inability to remove toxic metabolites that have accumulated |
|
|
carbon monoxide (CO) poisoning shows many of
the same effects as other forms of hypoxia/ischemia but there are some notable differences in the pathological processes |
– CO has a high affinity for binding with
hemoglobin, forming carboxyhemoglobin the effect displaced O2 binding sites in red blood cells, resulting in hypoxia and acidosis once carboxyhemoglobin rises above 20–30% of total hemoglobin in the blood, acute effects are seen levels above 50% cause coma and severe CNS effects not clear whether CO is directly toxic to neurons, and he most sig effects are very similar to what is seen following cardiac arrest CO poisoning often results in delayed neurologic deterioration, which may occur 1–2 weeks after exposure Basal ganglia damage is common, contributing to the extrapyramidal features often seen following severe Co poisoning hippocampal and general brain atrophy ( as measures by ventricle to brain ratio) may be seen months following injury NP deficits may be seen in attn., inform processing, EF, verbal and non verbal memory |
|
|
CO is a
|
gas that is present naturally but also results from
a combustion of man made fuel (gasoline engine and furnace exhaust) |
|
|
incidence
|
not clear, milder cases often unrecognized in a
hospital setting |
|
|
determinants of severity
|
effects vary based on the nature of the
underlying condition that produced the disruption in O2 supply and how rapidly the pathological process can be reversed. |
|
|
if hypoxia is not severe enough to disrupt
consciousness |
CNS damage is unlikely
|
|
|
mild hypoxia that does not lead to LOC (like high
altitude climbing) |
may induce mild cognitive and motor impairment
not expected to have lasting effects, though some studies suggest a possible persistence of mild changes |
|
|
most severe cases
|
result from sudden cardiac arrest or acute
respiratory distress syndrome (ARDS) |
|
|
LOC
|
occurs very rapidly. when the brain is deprived of
O2 for several minutes, damage progresses rapidly and if the underlying cause is not quickly reversed, brain death or a persistent minimally responsive state may result |
|
|
those who emerge from prolonged coma
|
typically have lasting cognitive and functional
disability (varying degree of dementia) and may show extrapyramidal syndromes like Parkinsonianism |
|
|
rapid resuscitation efforts
|
may prevent escalation to permanent damage
|
|
|
COPD
|
examples include emphysema, neuromuscular
weakness, fibrosing lung disease results in persistent respiratory acidosis with reduced arterial O2 sat and elevated carbon dioxide cog deficits may not occur in mild cases that do not produce persistent hypoxia severe COPD often results in cog impairment, lower scores on objective measures compared to less severely affected indiv. positive pressure ventilation with O2 may improve cog Fx but not necessarily better quality of life |
|
|
OSA
|
involves recurrent episodes of blood O2
desaturation due to total or partial breathing cessation Disrupts normal sleep architecture O2 desat may occur up to 100 times an hour neuroprotective vasodilatory response to hypoxia may be lacking |
|
|
severe OSA
|
assoc with greater risk for white matter
hyperintensities and cog imp (learning and mem, EF, psychomotor impairments), but not consistent across studies |
|
|
older adults
|
more vulnerable to sleep disordered breathing
community dwelling elderly women with sleep disordered breathing show increased risk of cognitive impairment |
|
|
CPAP for OSA
|
reduces episodes of breathing dysfunction
reduced O2 desat during sleep improves daytime sleepiness may lead to improvement is select areas of cognition presentation, disease course, and recovery |
|
|
recovery course
|
quite variable
|
|
|
favorable recovery
|
short period of impaired consciousness
regain purposeful motor movements preserved memory within a few hours following resuscitation |
|
|
poor outcome
|
no pupillary response 3 days post injury (68%
prevalence) GCS motor score of 1–2 on day 3 (73%) Alpha coma EEG pattern (66%) convulsions or myoclonus (74%) total GCS score of 3–5 in first 24 hours (77%) bilateral absence of somatosensory evoked potential on median nerve stimulation (76%) |
|
|
the following are poor prognostic indicators in
the absence of sedation effects |
coma more than 6 hours
no spontaneous leg movements or localization to pain stimuli prolonged loss of pupillary responses sustained conjunctive eye deviation abnormal eye movements (nystagmus) myoclonic seizures lower cranial nerve dysfunction (such as absent cough and gag reflexes) |
|
|
when evaluating a pt in the acute phase of recovery
|
be mindful of
interventions medications comorbidities that can cause or contribute to encephalopathy, confusing or complicating the presentation |
|
|
recovery curves in pts with severe
hypoxic/ischemic injury |
are fairly flat, and return to independence is
rarely achieved |
|
|
instruments useful for evaluating individuals
early in recovery (acute care or early IP rehab) and that focus on basic functioning: |
GCS
Coma Recovery Scale– Revised Coma– Near Coma Scale Rancho Los Amigos Level of Cog Fx |
|
|
instruments useful for structured basic
assessment of mental status |
MMSE
Orientation Log Cognitive Log MOCA Cognistat with higher cog Fx early in recovery: RBANS |
|
|
For patients recently emerging from minimally
responsive state, out emphasis on: |
frequent reorientation
Est consistent daily routines use short treatment sessions attend carefully to basic physiological needs (nutrition, toileting, sleep) maintain a quiet treatment environment avoid overstimulation |
|
|
as recovery progresses
|
attention deficits, distractibility, severe
anterograde amnesia, and EF dysfunction need to be addressed rehab generally involves teaching compensatory strategies or attempting to directly address areas of cog deficit |
|
|
studies comparing patterns of recovery from
hypoxia/anoxia to TBI have found the following patterns: |
amount of tissue loss is more critical in
determining outcome than etiology measures of memory correlate with hippocampal atrophy in both hypoxia and TBI intelligence correlates with whole brain volume in both conditions those with hypoxia have similar lengths of inpatient stay as TBI but show slower progress and poor outcomes those with hypoxic injury more likely to be referred to residential care those with hypoxia perform worse on all measures of fx outcome than TBI and have have lower functional independence measure motor and cognitive gains relative to those w TBI |
|
|
outpatient and post acute brain injury rehab
programs |
are appropriate and may extend treatment
gains from IP setting focus on compensatory strategies, skill acquisition, building independence, and community reintegration family training and support is critical |
|
|
Assessment methods– imaging
|
MRI and CT initially often do not reveal sig
changes follow up studies may reveal white matter changes, corpus callosum atrophy, cortical edema, cerebellar lesions, basal ganglia lesions, thalamic lesions, and/or hippocampal atrophy (OFTEN TAKE WEEKS OR MONTHS TO BE VISUALIZED ON SCANS) |
|
|
NP assessment may serve the following pruposes
|
characterize strengths and deficits and link
such patterns to daily Fx identify target goals for continued rehabilitation identify the presence and severity of psychological disturbance that may impact recovery and rehab determine decision making capacity and need for supervision identify target areas for accommodations for return to school and work |
|
|
outcomes
|
the most catastrophic cases may result in brain
death or persistent minimally responsive states less severe cases show variable periods of coma, marked confusion in early recovery, and lasting significant cog impairment or dementia |
|
|
high percentage of survivors of sudden cardiac
arrest and ARDS show |
generalized cog impairment
a higher percentage show specific/focal deficits in memory, attn., or processing speed |
|
|
changes in memory
|
have been reported in more than 50% of
survivors of severe hypoxia |
|
|
personality changes
|
have been reported in 1/3 of survivors of severe
hypoxia |
|
|
less than 50%
|
of those who require rehabilitation regain full
independence of daily FX, but there is much variability in outcome |
|
|
in mild cases with rapid reversal of pathological
condition |
cog imp may be transient, but some may
experience persistent cognitive deficits |
|
|
expectations for NP assessment results–
IQ/achievement |
overall scores may be reduced due to
impairments in processing speed and efficiency |
|
|
expectations for NP assessment results–
attention/concentration |
gross confusion apparent early
attn. may be a sig prob as rehab progresses and may be a long term issue distractibility is often observed both early in recovery and over the long term |
|
|
expectations for NP assessment results–
processing speed |
often impaired, cognitively and motorically
|
|
|
expectations for NP assessment results–
language |
formal language d/os rarely seen
though cases involving severe watershed damage trans cortical aphasia or other higher order language syndromes may be present |
|
|
expectations for NP assessment results–
visuospatial |
if watershed zones are affected, deficits can be
noticeable cortical blindness and other severe visuospatial imp variants have occurred lower performance on these tests may in part reflect slowed information processing |
|
|
expectations for NP assessment results– memory
|
impairments in storage, capacity, and retrieval
are common in severe cases with bilateral hippocampal damage, a marked amnestic state may be evident a subset of patients have no mem imp but have motor or cog imp in other domains (eg, FX assoc with watershed regions) |
|
|
expectations for NP assessment results–
EF |
may be minimally affected in milder cases, with
the exception of executive aspects of attn. EF deficits common and disabling in severe cases some patients sustain orbitofrontal damage bc this is a watershed region |
|
|
expectations for NP assessment results–
sensorimotor |
the basal ganglia and cerebellum are high risk for
injury severe anoxic injury can cause spastic quadiparesis, ataxia, parkinsonian syndromes, and other motor impairments/dysfunction |
|
|
expectations for NP assessment results–
emotion and personality |
anosognosia (impaired self awareness) is
common early post injury and may persist long term depression commonly observed changes in self regulation of emotion may occur due to medial frontal and frontal systems injury beh dysregulation may be seen in severe cases and may become a chronic feature severe psychiatric issues are common in severe cases, which may incl beh dysregulation and major depression |
|
|
driving
|
prognosis for returning to driving is not good in
severe cases, but may be possible with mild to moderate injuries with good recovery |
|
|
work
|
return to work is unlikely in severe cases, but
may be possible with mild injury and good recovery for those unable to return to competitive employment, alternative vocational or volunteer placement may be appropriate |
|
|
school/vocational training
|
unlikely, but may be possible with mild injury and
good recovery for students in high school and younger, it is critical to involve the school and educ specialists as early as possible to plan for academic re–entry (important for recovery and legally mandated) |
|
|
capacity
|
for medical and legal affairs will likely be severely
limited early in recovery despite recovery, may remain impaired due to EF and memory imp legal issues vary across jurisdiction |
|
|
medications
|
for attn. and memory may be used– such as:
methylphenidate (Ritalin), other stimulants acetylcholinesterase inhibitors (Aricept) and NMDA receptor antagonists (Namenda) SSRIs or anticonvulsants may be used for mood stabilization evidence for support of the use of these meds in hypoxic injury is more anecdotal than evidence based |
|
|
risk factor modification
|
increased supervision for safety
external and internal structures assistance with decision making (POA, guardianship) family support/training |
|
|
interpersonal relationships
|
can be challenging due to persistent memory
impairment, poor insight, exec dysfunction, and changes in premorbid role Fx |
|
|
functional issues
|
severe injuries often result in dystonia, spastic
hemiparesis, or quadraparesis due to basal ganglia involvement ataxia may persist due to cerebellar involvement many of these patients are unemployable and require attendant care for the rest of their lives |
|
|
rehab considerations
|
compensatory strategy training is critical for
patients with memory or other cog imp emphasis should be placed on errorless learning, procedural learning, attention process training (APT), and evidenced based cognitive rehabilitation Tx |
|
|
pediatric considerations
|
brains of infants and children req a higher
percentage of O2 than adults (over 30% total body O2 consumption from infancy to age 4) impact of hypoxia will depend on developmental period where it occurs neonatal hypoxia may lead to major developmental disorders and impaired cognition, depending on severity and pattern of damage injury to the basal ganglia and thalamus is predominant pattern in neonates assoc with long term outcome congenital heart defects and sleep disordered breathing are also found to have a relationship with cog, academic, and beh Fx some deficits are not noted until a child starts school |
|
|
geriatric considerations
|
older brains less able to recover from an anoxic
injury and will likely suffer more permanent and severe cog deficits due to reduced reserve for many, there are pre–existing MCI and Fx impairment or will have age related impairments |
|
|
acute respiratory distress syndrome (ARDS)
|
severe, often life threatening medical condition
where the lungs are compromised and damaged and are unlikely to supply sufficient O2 to the arterial blood (eg hypoxemia) can result in hypoxic damage to brain as well as many other systemic px |
|
|
apoptosis
|
programmed cell death
part of normal regulation and turnover of cells, but also can result from pathological processes like ischemia |
|
|
ATP (adenosine triphosphate)
|
a chemical compound that provides energy for
cells/neurons under anoxic conditions, becomes less available in the neuron, leading it to catabolize itself |
|
|
glutamate
|
most common excitatory neurotransmitter in the
brain under hypoxic conditions, excessive amounts are released in the synaptic cleft, and it becomes excitotoxic, contributing to deleterious processes in the neuron |
|
|
COPD
|
encompasses several pulmonary conditions, incl
emphysema and bronchitis progressive obstruction of expiration can produce chronic hypoxia and result in cog imp |
|
|
necrosis
|
refers to death of tissue or neurons, typically due |
|
|
watershed regions
|
in the brain, refers to overlapping border zones |
