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Definition of brain death and how to declare someone brain dead as established by the AAN.

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

Clinical Observations NOT Evidence of Brain Stem Function

Spinal Movement of Limbs
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
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

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.

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