Table of contents
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Bedside Evaluation
- Pupils
- neuromuscular blockade does not affect pupil size/reactivity
- Systemic atropine causes pupil dilation (but remain reactive)
- High-Dose dopamine causes fixed dilated pupils
- If pupils remain non-reactive for > 6-8hrs after resuscitation from an arrest, cahnces of satisfactory neurologic recovery are very poor.
- Ocular Reflex
- Brainstem Evaluation
- Oculocephalic Reflex
- Rotate head from side-to-side
- If lower brainstem is intact --> eyes deviate away from direction of rotation.
- If lower brainstem impaired --> eyes follow direction of motion
- Oculovestibular Reflex
- 50mL of cold saline into external auditory canal
- If brainstem intact --> both eyes deviate towards cold injection
- If brainstem impaired --> conjugate movement lost.
- Sensorimotor Exam
- Clonic Movements?
- Elicit by flextion of hands or feet (asterixis)
- Sign of metabolic encephalopathy
- Focal motor or sensory defect?
- Pain Response
- Injury to thalamus --> painful stimuli provoke flexion of upper extremity
- This is called Decorticate Posturing --> POOR prognosis
- Injury to midbrain and pons --> arms+legs extend and pronate in response to pain.
- This is called Decerebrate Posturing --> VERY POOR prognosis
- Injury to thalamus --> painful stimuli provoke flexion of upper extremity
- Clonic Movements?
Glasgow Coma Scale
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Eye Opening
4 - Spontaneous
3 - To Speech
2 - To Pain
1 - None
Verbal Communication
5 - Oriented
4 - Confused
3 - Inappropriate but recognized words
2 - Incomprehensible sounds
1 - None
Motor Response
6 - Obey Commands
5 - Localizes to pain
4 - Withdraws to pain
3 - Abnormal flexion (decorticate response)
2 - Abnormal extension (decerebrate response)
1 - No movement
- Clinical Applications:
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1. To define coma GCS ≤ 8 2. To stratify severity of head injury 13-15 = MILD
9 - 12 = MODERATE
≤ 8 = SEVERE
3. To identify candidates for intubation GCS ≤ 8 4. To predict likelihood of recovery from coma if GCS < 6 @ 72hrs
= No chance of satisfactory
neurologic recovery
(Edgren et al (1994))
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Brain Death
Irreversible cessation of function in all areas of the brain, with permanent loss of automatic breathing.
- Most often as a result of traumatic head injury, intracranial hemorrhage and cardiac arrest.
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Clinical Diagnosis of Breath Death
1. Irreversible Coma
2. Absence of brainstem reflexes
3. Absence of spontaneous breathing efforts
Two confirmatory evaluations 6-8hrs apart are required
- Apnea Test
- Observe patient for spontaneous breathing in presence of hypercapnia (powerful breathing simulus)
- 100% O2 breathing --> separate from ventilator --> O2 insufflated into ET tube (prevent hypoxemia)
- Patient observed for spontaneous breathing efforts for 8-10min. At that point ABG is obtained + ventilator resumed.
- Arterial pCO2 rises by 2-3mmHg/min of apnea
- If arterial pCO2 increases by > 20 mmHg without breathing efforts --> confirms dx of brain death.
- Note: Apnea test brings hypotension, cardiac arrhythmias (abort if develop this, and test is never repeated once confirmed brain death)
- Note: spontaneous movement bursts head/torso/upperExtremities are "Lazarus' sign", neuronal bursts from C-spine, not manifestations of brain activity.
- May not be possible to diagnose brain death in following:
- Severe facial trauma or C-spine cord injury
- Pre-existing pupillary abnormalities
- End-stage pulmonary disease with high CO2
- Drugs that interfere with evaluation (i.e. paralytics)
- In above cases, may need confirmatory test such as EEG, brain scan with Tc-99m, transcranial doppler, or somatosensory evoked potentials.
Organ Donor
- Measures to maintain organ viability:
- Hemodynamics
- Urine output < 1mL/kg/hr --> give volume to a CVP of 10-15mmHg
- Dopamine 5-15 mcg/kg/min (avoid alpha-adenergic vasoconstriction --> can cause anoxic organ injury)
- Pituitary Failure (50% of brain dead pts)
- Diabetes Insipidus
- Adrenal Insufficiency
- ACTH stim test is not useful
- If suspected due to hypotension --> give IV hydrocortisone 50mg q6h
- Hemodynamics
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