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16 Cards in this Set

  • Front
  • Back

What is the no-reflow phenomenon?

A short-lived period of hyperemia is quickly replaced by a longer lasting period of hypoperfusion at the level of the microcirculation after blood flow has been successfully restored

Reperfusion injury is characterized by?

1. Excess free radical formation

2. Nitric oxide toxicity

3. Further glutamate release

The only clinically benficial intervention that has proved to be successful in cases of anoxic-ischemic brain injury?

Hypothermia, which inhibits apoptosis and reduces free radical formation and excitatory neurotransmitters

Areas most susceptible to anoxic-ischemic damage?

1. Area CA1 of hippocampus (Sommer sector)

2. Basal ganglia

3. Thalami

4. Cerebellar Purkinje cells

5. Cortex

Why are the aforementioned areas most susceptible to damage?

1. Presence of receptors for excitatory neurotransmitters

2. High metabolic demands of these neurons

Microscopic evaluation of anoxic-ischemic damage may show what?

Neuronal loss and gliosis of vulnerable areas

Clinical signs that may be promising in a comatose patient after CPR?

1. Localization of a pain stimulus

2. Visual fixation and tracking

Mortality rate for patients who do not receive hypothermic treatment and do not awaken within the first 24 hours?

80% to 90%

Clinical findings that are invariably indicators of a poor prognosis in a comatose patient after anoxic-ischemic damage?

1. Absent pupil responses or corneal reflexes within days 1 to 3

2. Eye movement abnormalities such as sustained upward gaze

3. Myoclonus status epilepticus

Man in the barrel syndrome?

Lack of motor response in the upper extremities after bilateral border zone infarction in the anterior and middle cerebral watershed regions; better outcomes than others with anoxic-ischemic injury

Anoxic injury that affects the watershed region between MCA-PCA, the result may be?

Balint syndrome - asimultagnosia, optic ataxia, ocular apraxia and a transcortical sensory aphasia

Two important factors indicating a very poor prognosis in patients not receiving therapeutic hypothermia?

1. Absent or extensor motor response on day 3

2. Absent pupillary or corneal reflexes on day 3

May be counfounded by multiorgan failure and caution must be advised

Neuroimaging that may be helpful in anoxic-ischemic injury?

MRI with DWI sequences; disappearance of the gray-white junction is associated with failure to awaken

"Malignant patterns" on EEG in anoxic-ischemic injury?

1. Burst suppression

2. Alpha coma with periodic sharp waves and spikes

3. Isoelectric or a markedly suppressed EEG

When would you consider somatosensory evoked potentials in a comatose patient?

Between days 1 and 3 after cardiopulmonary resuscitation; they require stimulation of the median nerve that then results in a potential at the brachial plexus, cervical spinal cord, and bilateral cortex potentials (N20); if both N20 components are absent, the prognosis is poor and will likely never regain consciousness

Possible serum marker for poor outcome in comatose patients after anoxic-ischemic injury?

Serum neuron-specific enolase of >33u/L at days 1 to 3