bill knight on life from death
TRANSCRIPT
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14 June 2016William A Knight IV, MD, FACEP, FNCSUniversity of Cincinnati
Our role in organ donation and death by neurologic criteria
[email protected]@waknight4
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whoever saves a life…it is considered as if he saved an entire world.
-- Mishnah Sanhedrin 4:5 Babylonian Talmud Tractate Sanhedrin 37a
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Where is the soul/life force?
Heart vs. Brain (vs. Liver)
Stethoscope improvements▪ Notion of heart as a fuel pump took some getting used to
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The majority of the patients that proceed to donation are neurologically injured
We are TERRIBLE at accurate prognosis
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• Overall 50.8 % survived• 13.2% had good functional outcome• Bilaterally reactive pupils and GCS 3 = 75% survival
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There are no instances in which physiologically sound resuscitation of the patient will harm organ donation Nor should that matter (in general)
Alignment of parallel intentions Resuscitation of patient
If that fails organ viability
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Good critical care trumps all else
Care for them like any other patient
Do no more, do no less
Good for the brain is good for the body Don’t be confused by rumor and innuendo
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Solid organs:
2 lungs
Heart
2 kidneys
Pancreas
Liver
Small bowel
Tissues:
Heart valves
Skin
Corneas
Bone
Inner ear
Cartilage / tendons
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Organ donation is part of the thought process well before brain death occurs
Any patient in whom we are considering limitation of care should be thought of as a potential donor
Donor management begins and ends with autonomy
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Donation
Brain Death Donation (BDD)
Donation after Circulatory
Death (DCD)
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• Physician role to predict death within 60 – 90 minutes
• Challenging to do well– family is relying on you
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Establish irreversible and proximate cause of coma
Known neurologic process▪ Guillain-Barre, brainstem encephalitis
▪ Hepatic failure, uremia, hyperosmolar coma, hypophosphatemia
No metabolic or electrolyte abnormalities
Absence of hypotension▪ pressors
Core body temperature > 92.5 F (vs 96.5F)
No central nervous system depressants ▪ Intoxication
▪ Medical therapy ▪ Barbiturates, paralytics, narcotics, benzodiazepines, amitriptyline, toxic alcohols
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Are there patients who fulfill the clinical criteria of brain death who recover brain function?
No
What is an adequate observation period to ensure that cessation of neurologic function is permanent?
Insufficient evidence to determine
Are complex motor movements that falsely suggest retained brain function sometimes observed in brain death?
Yes
Wijdicks, Evidence-based guideline update. Neurology 2010
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What is the comparative safety of techniques for determining apnea? Apnea testing is safe but insufficient data to compare different techniques
Are there new ancillary tests that accurately identify patientswith brain death?
Because of a high risk of bias and inadequate statistical precision, there is insufficient evidence to determine if any new ancillary tests accurately identify brain death.
Wijdicks, Evidence-based guideline update. Neurology 2010
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Consequence of raised ICP + herniation
Brainstem ischemia, rostral to caudal
MIDBRAIN▪ Apnea
▪ Bradycardia
▪ Hypotension
▪ Drop in cardiac output (vagal mediation from midbrain ischemia)
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PONS: Sympathetic stimulation superimposed on vagal
▪ Leads to bradycardia with hypertension ▪ Cushing’s reflex
MEDULLA: Vagal cardiomotor nucleus becomes ischemic
▪ Prevents tonic vagal stimulus
Unopposed sympathetic stimulation
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Rise of epinephrine ~ the rate of rise of the ICP
Post storm hypotensive phase secondary to reduced sympathetic flow
Diminished end organ blood flow Further exacerbates prior ischemia if present
Much effort targeted at re-establishing normal CO/CI
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Cardiovascular response Autonomic storm Washout instability
Neuroendocrine Response Autonomic storm Posterior pituitary – vasopressin Anterior pituitary – glycemic control and adrenal function
▪ Usually preserved
Temporal considerations Deregulation will often resolve spontaneously
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“Autonomic storm” of brain death Pulmonary edema End-organ ischemia Profound vasoconstriction
▪ End organ ischemia despite hypertension
Considerable myocardial ischemia▪ Leads to stunned myocardium
This is not unfamiliar physiology: SAH Severe sepsis (EGDT trial, 2001)
Neurogenic pulmonary edema
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PATIENT A
Has severe sepsis Lactate 6.2 mM
MAP 59 mmHg
PATIENT B
Has severe sepsis Lactate 6.2 mM
MAP 105 mmHg
Mortality: 42% Mortality: 61%
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Available evidence does not support the need for immediate procurement after brain death
Taking time to optimize perfusion and allow recovery of cardiac function is appropriate
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78% of brain dead donors will develop diabetes insipidus Vasopressin
▪ V1 – vascular smooth musclemediates tone
▪ V2 – renal collecting duct antidiuretic
▪ V3 – anterior pituitarymediates ACTH release
DDAVP is selective V2 with no pressor activity▪ Desmopressin
▪ No effect on graft function or survival
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Large debate
Literature is conflicting
UNOS data supports it
Data adjustment lacking in trial analysis
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Systematic Review and Meta-Analysis of 3 primary donor questions:
• Desmopressin• T3• Ischemic Preconditioning
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Don’t send mixed messages after brain death We are supporting organs, not life Do not examine or talk to the patient after declaration It is acceptable to be sad “Grief teaches the steadiest minds to waver”
Use all hospital supportive resources Chaplains / priests, ODA, Social work, OPO
Set time limits for continued organ support
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Never introduce the topic
Organ Procurement Organization (OPO) should be involved early and available to speak with the family once declared
If family brings up topic
Support they good intentions and let them know the people that can help with that decision are available
Remember an open casket is possible after donation & autopsy
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UCMC, UC Health Policy # II-312, Determination of Death; 2009 American Academy of Neurology, Quality Standards Subcommittee. Practice Parameters: Determining
Brain Death in Adults. Neurology 45:1012-1014; 1995. Wijdicks, EF. The Diagnosis of Brain Death. NEJM 344(16):1215-1221; 2001. Goudreau JL, Wijdicks EF, Eelco FM, Emery S. Complications during apnea testing in the determination
of brain death; Predisposing factors. Neurology 55(7): 1045-1048; 2000. Busl KM and Greer DM. Pitfalls in the Diagnosis of Brain Death. Neurocrit Care 11(2):276-287; 2009. Saposnik, Basile, Young. Movements in Brain Death: A systemic review. Can J Neurol Sci 36:154-160;
2009. Ducrocq, X et al. Consensus opinion on diagnosis of cerebral circulatory arrest using doppler-
sonography. J of Neuro Sci 159:145-150; 1998. Munari et al. Confirmatory tests in the diagnosis of brain death: comparison between SPECT and CTA.
Crit Care Med 33(9):2068-2073; 2005. Excudero et al. Diagnosing brain death by CT perfusion and multislice CTA. Neurocrit Care 11:261-271;
2009. Wijdicks, EF. Evidence-based guideline update: Determining brain death in adults: Report of the
Quality Standards Subcommittee of the American Academy of Neurology. Neurology 74: 1911-1918; 2010.
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Triple flexion Babinski sign Preserved DTRs Abdominal and cremasteric
reflexes Sweating Blushing Respiratory-like movements
without significant TV Shoulder elevation and
adduction Back arching Intercostal expansion
Head turning
Spontaneous movements or with painful stimuli (if no full decerebrate or decorticate response considered to be at spinal level): Brief slow movements of upper
limbs
More complex movements (Lazarus signs) come from spinal cord Stretching of the arms,
followed by crossing or touching of the arms on the chest, and finally falling of the arms alongside the torso.
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Report of the Quality Standards Subcommittee of the American
Academy of Neurology, 1995
Wijdicks, NEJM 2001
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Apnea Test Vitals: Core temperature > 36.5º C or 97º F
SBP > 90mm Hg▪ Can use pressors
Draw a baseline ABG, PCO2 must be ~ 40▪ COPD
Pre-oxygenate with 100% FiO2
Disconnect ventilator, give O2 at 8-12 lpm by tracheal cannula Observe for any respiratory movements
AAN Practice Parameter 1994
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Apnea Test Duration varies Usually 5-10 minutes
▪ General rule: ▪ after 2 minutes off ventilator PCO2 will
increase by 5, then for every additional minute the PCO2 will increase by 2.
Draw post-test ABG and reconnect the ventilator.
The patient has no CNS respiratory drive if PCO2 > 60mm Hg. ▪ Adjust criteria for known CO2
retention▪ 20mm Hg above baseline
During test if patient becomes hemodynamically unstable, stop testing, draw ABG and reconnect the ventilator. ▪ Test is indeterminate if PCO2 <
60mm Hg. ▪ Consider confirmatory studies.
AAN Practice Parameter 2010
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Complications of apnea testing Hypotension Hypoxia Cardiac arrhythmias Death…
Factors associated with complications pH < 7.3 or > 7.5 Plasma Na <120 or >170 Serum potassium <3.0 or >6.0 Calcium <8.0 or >10.5 Pretest hypotension or administration of vasopressors High oxygen requirements
If apnea test is aborted and pCO2 is not ≥60mmHg an ancillary test must be performed
Goudreau et al, Neurology 2000
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Brain death criteria are met if there is no response to any component of the examination.
Confirmatory tests are NOT necessary.
Recommended if unable to assess all cranial nerves.
Options include: ▪ Digital subtraction angiography
▪ EEG
▪ Transcranial Dopplers
▪ Nuclear medicine – brain scintigraphy
Barbiturate levels are required in setting of barbiturate coma▪ ½ life = 15-50 hours
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Systole – brief forward flow
Diastole – abrupt flow reversal
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Artifact Drug effects Sedation Hypothermia Toxic Metabolic
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