{"id":5132,"date":"2011-07-14T20:23:45","date_gmt":"2011-07-14T20:23:45","guid":{"rendered":"http:\/\/crashtext.org\/misc\/neurologic-criteria-for-death.htm\/"},"modified":"2016-01-15T15:01:29","modified_gmt":"2016-01-15T20:01:29","slug":"neurologic-criteria-for-death","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/intensive-care\/neurologic-criteria-for-death.htm\/","title":{"rendered":"Neurological Criteria for Death (Brain Death Protocols)"},"content":{"rendered":"
New guidelines form AAN (Neurology 2010;74:1911<\/a>)<\/p>\n ———————————-<\/p>\n <\/p>\n Many of the details of the clinical neurologic examination to determine brain death cannot be established by evidence-based methods. The detailed brain death evaluation protocol that follows is intended as a useful tool for clinicians. It must be emphasized that this guidance is opinion-based. Alternative protocols may be equally informative.<\/p>\n <\/p>\n The determination of brain death can be considered to consist of 4 steps.<\/p>\n I. The clinical evaluation (prerequisites).<\/p>\n A. Establish irreversible and proximate cause of coma.The cause of coma can usually be established by history, examination, neuroimaging, and laboratory tests.Exclude the presence of a CNS-depressant drug effect by history, drug screen, calculation of clearance using 5 times the drug’s half-life (assuming normal hepatic and renal function), or, if available, drug plasma levels below the therapeutic range. Prior use of hypothermia (e.g., after cardiopulmonary resuscitation for cardiac arrest) may delay drug metabolism. The legal alcohol limit for driving (blood alcohol content 0.08%) is a practical threshold below which an examination to determine brain death could reasonably proceed.There should be no recent administration or continued presence of neuromuscular blocking agents (this can be defined by the presence of a train of 4 twitches with maximal ulnar nerve stimulation).There should be no severe electrolyte, acid-base, or endocrine disturbance (defined by severe acidosis or laboratory values markedly deviated from the norm).<\/p>\n B. Achieve normal core temperature.In most patients, a warming blanket is needed to raise the body temperature and maintain a normal or near-normal temperature (>36\u00b0C). After the initial equilibration of arterial CO2 with mixed central venous CO2, the Paco2 rises steeply, but then more slowly when the body metabolism raises Paco2.To avoid delaying an increase in Paco2, normal or near-normal core temperature is preferred during the apnea test.<\/p>\n C. Achieve normal systolic blood pressure.Hypotension from loss of peripheral vascular tone or hypovolemia (diabetes insipidus) is common; vasopressors or vasopressin are often required. Neurologic examination is usually reliable with a systolic blood pressure >=100 mm Hg.<\/p>\n D. Perform 1 neurologic examination (sufficient to pronounce brain death in most US states).If a certain period of time has passed since the onset of the brain insult to exclude the possibility of recovery (in practice, usually several hours), 1 neurologic examination should be sufficient to pronounce brain death. However, some US state statutes require 2 examinations.Legally, all physicians are allowed to determine brain death in most US states. Neurologists, neurosurgeons, and intensive care specialists may have specialized expertise. It seems reasonable to require that all physicians making a determination of brain death be intimately familiar with brain death criteria and have demonstrated competence in this complex examination. Brain death statutes in the United States differ by state and institution. Some US state or hospital guidelines require the examiner to have certain expertise.<\/p>\n II. The clinical evaluation (neurologic assessment).<\/p>\n A. Coma.<\/p>\n * Patients must lack all evidence of responsiveness.Eye opening or eye movement to noxious stimuli is absent. Noxious stimuli should not produce a motor response other than spinally mediated reflexes. The clinical differentiation of spinal responses from retained motor responses associated with brain activity requires expertise.<\/p>\n B. Absence of brainstem reflexes.<\/p>\n C. Apnea.<\/p>\n * Absence of a breathing drive.Absence of a breathing drive is tested with a CO2 challenge. Documentation of an increase in Paco2 above normal levels is typical practice. It requires preparation before the test.Prerequisites: 1) normotension, 2) normothermia, 3) euvolemia, 4) eucapnia (Paco2 35\u009645 mm Hg), 5) absence of hypoxia, and 6) no prior evidence of CO2 retention (i.e., chronic obstructive pulmonary disease, severe obesity).Procedure:<\/p>\n * Adjust vasopressors to a systolic blood pressure >=100 mm Hg. \u00a0* Preoxygenate for at least 10 minutes with 100% oxygen to a Pao2 >200 mm Hg.<\/p>\n * Reduce ventilation frequency to 10 breaths per minute to eucapnia.<\/p>\n * Reduce positive end-expiratory pressure (PEEP) to 5 cm H2O (oxygen desaturation with decreasing PEEP may suggest difficulty with apnea testing).<\/p>\n * If pulse oximetry oxygen saturation remains >95%, obtain a baseline blood gas (Pao2, Paco2, pH, bicarbonate, base excess).<\/p>\n * Disconnect the patient from the ventilator.<\/p>\n * Preserve oxygenation (e.g., place an insufflation catheter through the endotracheal tube and close to the level of the carina and deliver 100% O2 at 6 L\/min).<\/p>\n * Look closely for respiratory movements for 8\u009610 minutes. Respiration is defined as abdominal or chest excursions and may include a brief gasp.<\/p>\n * Abort if systolic blood pressure decreases to <90 mm Hg.<\/p>\n * Abort if oxygen saturation measured by pulse oximetry is <85% for >30 seconds. Retry procedure with T-piece, CPAP 10 cm H2O, and 100% O2 12 L\/min.<\/p>\n * If no respiratory drive is observed, repeat blood gas (Pao2, Paco2, pH, bicarbonate, base excess) after approximately 8 minutes.<\/p>\n * If respiratory movements are absent and arterial Pco2 is >=60 mm Hg (or 20 mm Hg increase in arterial Pco2 over a baseline normal arterial Pco2), the apnea test result is positive (i.e., supports the clinical diagnosis of brain death).<\/p>\n * If the test is inconclusive but the patient is hemodynamically stable during the procedure, it may be repeated for a longer period of time (10\u0096-15 minutes) after the patient is again adequately preoxygenated.<\/p>\n How to Safely Perform Apnea Testing with CPAP:\u00a06 L\/min via a tracheal insufflation catheter, and 2) connected a 20 cm of H2O CPAP valve to the end of the endotracheal tube (APNEA TESTING FOR BRAIN DEATH IN SEVERE ACUTE RESPIRATORY DISTRESS SYNDROME: A POSSIBLE SOLUTION Hocker S; )<\/p>\n <\/a><\/p>\n III. Ancillary tests.In clinical practice, EEG, cerebral angiography, nuclear scan, TCD, CTA, and MRI\/MRA are currently used ancillary tests in adults (see appendix 1). Most hospitals will have the logistics in place to perform and interpret an EEG, nuclear scan, or cerebral angiogram, and these 3 tests may be considered the preferred tests. Ancillary tests can be used when uncertainty exists about the reliability of parts of the neurologic examination or when the apnea test cannot be performed. In some protocols, ancillary tests are used to shorten the duration of the observation period.The interpretation of each of these tests requires expertise. In adults, ancillary tests are not needed for the clinical diagnosis of brain death and cannot replace a neurologic examination. Physicians ordering ancillary tests should appreciate the disparities between tests and the potential for false-positives (i.e., the test suggests brain death, but the patient does not meet clinical criteria). Rather than ordering ancillary tests, physicians may decide not to proceed with the declaration of brain death if clinical findings are unreliable.<\/p>\n IV. Documentation.The time of brain death is documented in the medical records. Time of death is the time the arterial Pco2 reached the target value. In patients with an aborted apnea test, the time of death is when the ancillary test has been officially interpreted. A checklist is filled out, signed, and dated (appendix 2). Federal and state law requires the physician to contact an organ procurement organization following determination of brain death.e4,e5<\/p>\n <\/p>\n ———————————-<\/p>\n <\/p>\n CTA seems to be as good as formal angio for brain death (J Trauma 2010;68:553)<\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/a><\/a><\/p>\n <\/p>\n I take the patient completely off the ventilator after sticking a small oxygen conduit (like a nasal O2 tube) down the E-T tube to provide oxygenation without ventilation. The pCO2 rises 4 torr the first minute and 3 torr every minute thereafter.\u00a0 You know where the pCO2 started. Do the math.\u00a0 The pO2 maintains well over 200 for the entire 5 minutes or so it takes to get to a pCO2 of > 60.\u00a0 I’ve never had a sudden unexpected cardiac arrest with this procedure and I’ve been doing it for over 15 years.\u00a0 During that 5 minutes or so, i simply eyeball the patient. If they show any hint of movement of any kind, they instantly flunk and the brain death test is over.\u00a0 If they don’t make any kind of effort with a pCO2 over 60, that’s the end of the story.<\/p>\n <\/p>\n The diagnosis of brain death (NEJM 2001;344(16):1215)<\/p>\n no reversible cause temp>32 normotension exam: coma absence of motor absence of pupillary response (should be 4-6mm) absence of calorics absence of gag absence of coughing to trach suction absence of resp drive atPaCo2 of 60 or 20 above baseline do calorics with head tilted to 30 degrees <\/a><\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n unusual movements in the braindead (neurology 1984;34:1089)<\/p>\n <\/p>\n apnea test-why not give pt CO2 instead of the miserable way we do it now (Neurocritical Care 2004;1:)<\/p>\n <\/p>\n Streat’s Groups Review of Lit<\/a><\/p>\n<\/span>PRACTICAL (NON-EVIDENCE-BASED) GUIDANCE FOR DETERMINATION OF BRAIN DEATH<\/span><\/h2>\n
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