Patient suffered anoxic brain injury Is the patient comatose?
Yes
No
• Correct hypotension, metabolic acidosis, electrolytes
• Treat cerebral edema
• Reverse sedation or neuromuscular blockade Are confounding factors absent?
• Acute renal failure
• Fulminant hepatic failure
• Cardiogenic or hypovolemic shock
• Sedation or neuromuscular blockade
Is the patient in myoclonus status epilepticus (spontaneous frequent jerks of the limbs, face, and/or trunk) during the first 24 hr following the event?
Wait until 3 days postevent and reassess
Are any of the following true?
• Pupillary responses are absent
• Corneal reflexes are absent
• Extensor posturing to pain
• No motor response to pain
Perform somatosensory evoked potentials
Is the N20 potential absent?
No
No
Yes
Yes
Yes Yes
Based on neurologic criteria alone, the prognosis cannot be determined. If patient remains in comatose or a vegetative state for another 3 mo, then meaningful recoverya is very unlikely.
The likelihood for meaningful recoverya is practically zero, with very rare exceptions.
This information can be relayed confidently to family, friends, and caretakers to help them make appropriate end-of-life decisions including terminal weaning of mechanical ventilation and withdrawal of all medical support.
Assess for brain death
No
Are any brainstem reflexes present?
aMeaningful recovery is defined here as the absence of severe disability requiring constant nursing support, a vegetative state, or death. Many patients, families, and caretakers may consider less severe forms of disability to be outside a desirable state of meaning recovery.
Adapted with permission from Wijdicks EF, Hijdra A, Young GB, et al. Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology.Neurology.2006;67:203–210.
Neurologic Disorders rComa 4 5 1 may show normal sleep–awake cycles but lacks overt signs of conscious, awareness, or responsiveness. If such state lasts for 12 months after brain trauma or 3 months in other cases, the chance for meaningful recovery is minimal. Recent consensus has created other levels of persistent inhibited function such as the minimally conscious state. Brain function is widely distributed and likewise injury can cause a spectrum of residual function. Brain death is a different clinical entity and should not be confused with a type of coma.
S U G G E S T E D R E A D I N G S
Wijdicks EF. Neurologic complications in critically ill patients.Anesth Analg.1996;83:411–419.
Wijdicks EF, Hijdra A, Young GB, et al. Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology.Neurology.2006;67:
203–210.
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56 Declaration of Brain Death
Rajat Dhar
T H E C O N C E P T O F B R A I N D E A T H
Death may be legally determined by either cardiorespiratory or cerebral criteria, the latter (i.e., brain death) emerging as an important concept with the advent of intensive care unit care and artificial ventilation in the 1950s and being first formally delineated in the 1960s.Brain deathis defined as the irreversible cessation of all brain functions, including the brainstem. The specific laws and policies governing determination of death by neurologic criteria vary among countries, states, and different medical institu- tions, albeit based on this overarching concept. The person is declared dead at the time that final determination of brain death has been made. Although it does not require consent of the family or surrogate decision makers, it is always preferable to explain the process explicitly at all stages of testing. Physicians should be sensitive to both religious and ethnic perspectives of the family, as well as allowing them time to process an often sudden catastrophic loss. The diagnosis of (brain) death is an absolute prerequisite for organ and tissue donation, and the role of the intensivist extends to stabilizing the potentially brain-dead patient to both allow safe testing while avoiding further organ injury should the person become an organ donor. Donation should not be discussed with the family prior to determination of death to avoid the appearance of a conflict of interest. The United States and other countries require physicians to contact local organ procurement agencies as soon as a patient is deemed to be a potential organ donor (i.e., any patient with severe brain injury who has lost significant brainstem function), even before the final confirmation of brain death.
D I A G N O S I N G B R A I N D E A T H
In essence, brain death comprises irreversible coma (of known etiology), accompanied by loss of all brainstem reflexes, and absent respiratory drive. It may result from a variety of severe brain injuries, most commonly cerebral trauma, hemorrhage (subarachnoid, subdural, or intracerebral), and hypoxic-ischemic injury after cardiac arrest. Cerebral edema with raised intracranial pressure resulting from large brain tumors, meningitis or encephalitis, hydrocephalus, or fulminant liver failure may also progress to brain death. The particular etiology for coma should be known in each patient (from history or with adjunctive brain imaging), and brain death should never be diagnosed without a clear cause capable of inducing the observed degree of cerebral dysfunction. Any confounders must be carefully excluded, chief among these are hypothermia and drug
4 5 2
Neurologic Disorders rDeclaration of Brain Death 4 5 3
intoxication. Overdose of a variety of medications (including barbiturates, tricyclic antidepressants, baclofen, and lidocaine) can mimic a brain-dead state with absent brainstem reflexes. The metabolic milieu must also be normalized as much as possible to avoid confounding from systemic disturbances including hypoglycemia, hypoten- sion, severe electrolyte imbalances, or acid–base disorders that could result in cerebral dysfunction. Any sedation or neuromuscular blockade must have been allowed to wear off before testing (the latter can be tested by train-of-four stimulation). Patients in a locked-in state from lesions in the ventral pons may appear unresponsive, are unable to move to stimulation, and lack some brainstem function, but on closer testing are able to respond (with vertical eye movements or blinking) and have reactive electroen- cephalography (EEG) (a somewhat similar picture may be seen with high cervical spine injuries). Severe Guillain–Barr´e syndrome may induce a complete de-afferented state where the patient cannot move, respond, and can even lose brainstem and respiratory functions. Careful history, examination, and sometimes ancillary testing will exclude such confounding cases.
Once confounders have been excluded, homeostasis normalized (temperature, electrolytes, acid-base), and shock resuscitated, then the process of brain death testing can begin (Algorithm 56.1). Remember to document the temperature and blood pres- sure at the time of each examination. First an unresponsive comatose state without motor response should be verified. Central painful stimulation (e.g., supraorbital ridge, temporomandibular joint (TMJ) should elicit neither eye opening nor purposeful or reflexive movements (i.e., posturing of the upper extremities). There should be no spontaneous movements in the cranial nerve territory and no signs of seizure activity.
All brainstem reflexes must then be tested on both sides to verify complete cessation of all brainstem function. This includes absence of midbrain function by lack of pupillary constriction to bright light; pupils should be mid-position or dilated. Pontine function is assessed with corneal reflex and cold water caloric testing of vestibular-ocular reac- tivity. Medullary failure is documented with lack of cough reflex to deep suctioning.
To confirm stable absence of brain function, this whole sequence of testing should be repeated between 1 and 24 hours after the first examination. Short intervals are appro- priate in catastrophic conditions in which devastating injury is clearly seen on imaging and condition has been unchanged before testing (new recommendations suggest one examination may be adequate in such a case). A longer duration is recommended in children and in patients with postcardiac arrest in whom imaging is usually normal and the early examination can fluctuate. Testing should also be deferred till after rewarm- ing from induced hypothermia if utilized in such patients. At some institutions, only certain (“qualified”) personnel can perform either all or parts of the brain death testing.
In complicated cases, regardless, it is advisable to have assistance from a neurologist or neurosurgeon in the determination of death by neurologic criteria.
Clinical confirmation of complete cerebral death requires absence of spontaneous respiratory efforts despite adequate stimuli of hypercapnia and academia. Theapnea testis required to complete determination of death by neurologic criteria, and time of death is set when the patient fails to breath and a blood gas demonstrates ade- quate academia (usually pH<7.28 to 7.30) and hypercapnia (PaCO2above 60 mm Hg and/or rise by 20 mm Hg from baseline). Two things should be done before performing the apnea test. Preoxygenation for at least 10 minutes on 100% FiO2 will minimize the risk of desaturation during testing. A baseline blood gas should be reviewed and ventilator settings adjusted to obtain a PaCO2in the normal range (ideally 40–45 mm Hg) with a pH as close to normal as possible. Proper apnea testing may be impossible in significant CO2retainers or those who are markedly acidotic from
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