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25 terms

Brain Death

Definition of brain death and how to declare someone brain dead as established by the AAN.
STUDY
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Brain Death
Irreversible loss of clinical function of the entire brain including the brain stem.
Causes of Brian Death
Severe head injury, aneurysm, hypoxia/ischemia, fulminant hepatic failure, brain tumors.
Mechanics of Brain Death
Swelling of the brain against the skull causes compression that pushes the brain downward. This causes herniation of the brain stem, which cuts off blood flow to the brain. 10 minutes of absence of cerebral blood flow is incompatible with brain function.
Prerequisites to Brain Death Testing
- Evidence of acute CNS catastrophe compatible with BD.
- Exclusion of complicating medical conditions (severe electrolyte, acid/base, or endocrine imbalance).
- Absence of drug intoxication/poisoning.
- Core temp of >32.2°C or 90°F
Cardinal Findings of Brain Death
- Coma or Unresponsiveness = no cerebral response in all extremeties
- Absence of Brain Stem Reflexes = no cough, gag, corneal, pupillary, oculocephalic, or oculovestibular reflex.
- Apnea = absence of spontaneous respiration 2° to increasing pCO2
Clinical Exam
Response to pain (nail bed, supraorbital nerve)
Corneal (swab)
Pupillary (light)
Oculovestibular (cold calorics)
Cough/Gag/Bradyarrhythia (suctioning)
Oculocephalic (doll's eyes)
Apnea Test Prerequisites
Core Body Temp ≥ 36.5°C or 97°F
SBP ≥90 mmHg
DI under control (positive fluid balance for past 6 hours)
pCO2 must be normal (arterial ≥40 mmHg)
Pre-oxygenation up to arterial pO2 ≥ 200 mmHg
Apnea Test Procedures
Ensure prerequisites are met.
Draw baseline ABG
D/C the vent
Deliver passive O2 via ETT at the carina at 6 l/min >8 min
Monitor for respiratory movements and changes in vital signs
pCO2 rises 3-4 mmHg/minute
Draw ABG and reconnect vent.
Interpretting Apnea Test Results
A pCO2 of ≥ 60 mmHg or an increase of ≥ 20 mmHg over a normal baseline with no respiratory effort supports a positive apnea test and is consistent with brain death.
Confirmatory Tests
4-Vessel Angiography/Conventional Angio/Cerebral Angio
Brain Flow Study/Nuclear Med Scan/Radioactive Isotope Angio
EEG
TCD
SSEP
Clinical Observations NOT Evidence of Brain Stem Function
Spinal Movement of Limbs
Sweating
Blushing
Tachycardia
Normal BP
Absence of DI
Conditions That Interfere with BD Diagnosis
Sever facial trauma
Pre-existing pupillary abnormalities
Toxic levels of drugs or medications
Sleep Apnea or chronic CO2 retention (COPD)
CNS depression 2° renal or hepatic failure
Neurologic States that Mimic BD
Locked-In Syndrome
Hypothermia
Guillain-Barre Syndrome
BD Testing in Children
≤ 7 Days = BD testing not valid
7d-2m = 2 clinical exams and 2 EEG's 48 hours apart
2m-1y = 2 clinical exams and 2 EEG's/flow 24 hours apart
> 1 year = 2 clinical exams 24 hours apart, EEG and flow optional
Documenting Brain Death
Etiology and irreversibility of condition
Absence of BS reflexes
Absence of motor response to pain
Absence of respirations with pCO2 > 60 mmHg
Justification of confirmatory tests with results
Repeat neuro exam (if required)
3 Key Factorrs in Definition
Irreversible
Includes brain stem
Clinical Diagnosis
MajorCauses of Problems after Brain Death
Catecholamine Storm
Endocrine derangment/inhibition of aerobic pathways
What Happens During Brain Death?
1)Vagal Response, resulting in bradycardia, hypotension and decreased CO.
2)Sympathetic response become uncontrolled releasing catecholamines into circulation ->
3)Tachycardia and elevated CO
Consequences of Catecholamine Storm
1) Vasoconstriction increases SVR => systemic hypertension
2)Left Atrial pressure and PCWP increase => increase in myocardial workload => increased oxygen consumption and demand
What causes neurogenic pulmonary edema?
Failing myocardium may cause backflow of blood into the pulmonary circuit, rupturing pulmonary capillaries
Results of Brain Death
1)Central regulatory mechanisms are destroyed, vagal response ends, catecholamine response ends
2)Hypothalmus no longer controls body temp or regulates ADH, fluid and electrolyte balances are affected
3)Loss of pituitary function and lack of intrinsic ADH causes DI
Signs of DI
1) Spec Gravity <1.005
2)Na >150
3)Increased UOP
Temp regulation
Hypothermia leads to increased HR, CO and O2 consumption.
Cardiac sensitivity to K and Ca increased
Release of Plasminogen Aactivator
Brain Dead tissues release plasminogen activator into circulation, leads to coagulopathy, possible DIC
Hormone Loss
Loss of ADH => renal filtrate is not concentrated
Loss of glucocorticoid hormones leads to loss of cell membrane stability, cardiac contractility and CO, loss of vasomotor tone.