28

History of Death Policy

Individually, states determine the definition of death, as do countries. In the 1950s, medical advancements that included mechanical ventilation made it possible to keep some vital organs viable. Then, with additional advances in medicine, functioning organs could be transplanted into other individuals, and those patients improved. This established the efficacy of transplanted organs from supported bodies over organs from bodies with no functioning circulation and respiration. The hope delivered by transplant surgeons, because of their ability to restore vital organs to patients dying from similar organ failure, led to brain death as a declaration of death. Death can also be characterized as somatic death, which is the complete cessation of cardiac and respiratory function. In 1970, after 10 years of study, the first statute determining death in all circumstances was passed. In 1978, the National Conference of Commissioners on Uniform State Laws completed the Uniform Brain Death Act. In 1980, the same commission drafted the Uniform Determination of Death Act, which is the basis for the majority of death laws in the United States. The Death Act of 1980 sets the general legal standard for determining death, but not the medical criteria for doing so. The medical profession remains free to formulate acceptable medical practices and to utilize new biomedical knowledge, diagnostic tests, and equipment.1–6

Definition of Death

According to the Death Act of 1980, for death to be declared, “The entire brain must cease to function, irreversibly.” The “entire brain” includes the brainstem and the neocortex. This definition takes into consideration anencephaly, a condition in which an infant is born with the anatomical lack of most cerebral hemispheres but with a functioning brainstem. Such an infant is considered legally alive.7 Although the Death Act of 1980 established the criterion for death, the definition did not address diagnostic tests and specific medical procedures. This gave the medical and legal profession flexibility to develop diagnostic procedures while leaving the door open for disagreement and the need for judicial review. Then in 1981, the President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research developed standards for the determination of brain death, which, with some modifications, are adhered to worldwide.^3,8

The consensus on death declaration by way of lack of brain function must include three mandatory parts: (1) there must be no brain and no brainstem function—the person must be apneic; (2) the etiology must be known and irreversible; and (3) there must be no confounding factors. An example of a state law, the State of California Health and Safety Code, Section 7184, is:

A person who is declared brain dead is legally and physiologically dead. An individual who has sustained either (1) irreversible cessation of circulatory and respiratory functions, or (2) irreversible cessation of all functions of the entire brain, including the brainstem, is dead.

A determination of brain death must be made in accordance with accepted medical standards. In 42 states, one licensed physician is required (in a few states, the physician’s representative can declare brain death); in the 8 other states, two licensed physicians are required. Hospital bylaws usually provide for criteria to pronounce death by means of a neurologic exam and may add qualifications. In most guidelines, the physician who declares a patient dead can be any licensed physician knowledgeable of and comfortable with performing a detailed neurologic exam and familiar with the procedures to declare someone dead. Uniformly, the licensed physician does not have to be a neurologist or neurosurgeon. The only ethical consideration should be that the physician is not the transplant surgeon, because this may appear as a conflict of interest.

In 48 states, family permission is not required prior to performing a brain death exam. Only in New York and New Jersey can families object for religious reasons.⁸

The opposing opinion to the Death Act is that the entire body must not function for the declaration of death. When the heart and lungs are not functioning, which is the criterion for somatic death, a machine can take over until a new heart and lung(s) are transplanted. The result will be an individual who, after recovery, may resume his or her life. However, after the brain ceases to function, there is, as of yet, no machine that can take over until transplantation. In the future, if transplantation were to occur, the result would be a different person lacking the memories and physical abilities, as well as lacking the hope, love, caring, and spirit, that resided in the brain in the unique individual that died. In essence, the other brain that was being transplanted was simply acquiring a new body.

Initial Criteria

There are major criteria that must be met before considering a valid neurologic exam for the purpose of declaring a patient dead. The body should have a systolic blood pressure ≥90 mm Hg. The body core temperature must be above 32.2°C or 90°F. Below 28°C, there is loss of brainstem reflexes.1,4,9 In a trauma center, it is not unusual to see hypothermia in patients, such as snow skiers, the winter homeless, addicts, and cold-acclimatized patients who have ingested opioids, barbiturates, benzodiazepines, phenothiazines, tricyclic antidepressants, and lithium.^10,11 The patient cannot be under the effects of skeletal muscle paralytics. Furthermore, there can be no metabolic abnormalities causing coma or loss of brainstem reflexes and no hypoglycemia.

Patients can be declared legally dead if they have ingested drugs; however, the licensed physician has to certify and document that the patient is not toxic on drugs and that the drugs are not preventing brainstem function and are not causing coma. Even in the case of overdose, the pupillary reflex is usually present. However, medications can cause almost any side effects, and there are anecdotal reports that tricyclic antidepressants can mimic brain death. When drug ingestion is suspected, do not rush to pronounce dead; instead, wait and investigate. If the patient is truly dead, he or she will remain that way. Attempt to discover which drug was used, and before proceeding with the neurologic exam, observe the patient for at least 4 or 5 times the excretion half-life, assuming there is no no half-life prolongation due to additional organ dysfunction. Some guidelines provide for specific drugs.1,12 Excessive intake of alcohol would delay the performance of a death-determining exam. Alcohol (EtOH)–valid levels for brain death determinations are <800 to 1500 mg/dL, whereas the legal intoxication level is 80 to 100 mg/dL.¹ With certain suspected drug and medication ingestion, antidotes may be administered. However, if a medication is being prescribed to reduce the cerebral metabolic rate for oxygenation (CMRO₂) or if it is necessary to protect the brain in some form, the benefits of giving the antidote must outweigh the risks, for example, when administering flumazenil 0.2, then 0.3 mg intravenous (IV) for benzodiazepine overdose. When opioid overdose is suspected, administer naloxone 0.2 to 2.0 mg IV. Additional therapeutic cerebral protectant medications are barbiturates, used to reduce increased intracranial pressure (ICP), and CMRO₂ by inhibiting brain activity, placing the patient in a medication-induced coma. The clinical diagnosis of brain death can still be made after stopping the medication if the serum levels are less than the therapeutic range. In most laboratories, the level would be <5 to 15 μg/mL. This is below the level required for burst suppression, 50 μg/mL. When a drug or poison cannot be quantified but seems highly likely from history, one should not make the diagnosis of brain death.

One criterion for death pronouncement is the consideration of altering neurologic status due to drugs’ affect on metabolism. The same consideration of pure systemic abnormalities must also be made; the systemic abnormality must not be causing the coma or loss of brainstem reflexes. Severe abnormalities such as hypoglycemia or hyperglycemia, hyponatremia, hypernatremia, hypothyroidism, panhypopituitarism, or Addison’s disease may decrease the level of consciousness and confuse neurologic examination, but a complete loss of brainstem reflexes is seldom observed. The licensed physician must once again document that the systemic abnormalities are not the cause of coma.¹ The many guidelines state that the patient should not be hypoglycemic.

Brain Death Exam

Only after the initial criteria are met can the licensed physician proceed with the neurologic exam. The exam documents the function of the cerebral hemispheres and the brainstem. When it can be performed, it is as sensitive as any technological test for determining global brain function. It will not assess the entire or specific function of the basal ganglia, thalamus, or cerebral cortices. To assume a lack of functional cerebral hemispheres, the patient must be in a coma. An often touted but rare clinical condition that, by exam, may mimic complete and irreversible lack of entire brain function is a “super” locked-in syndrome, when there is profound damage to the brainstem, with the exception of the ascending reticular activating system (ARAS), and intact cerebral hemisphere function. This circumstance is rare and may be excluded easily in most instances. The history, physical, and radiological and physiological review should argue against this condition. The less severe locked-in syndrome is produced by ischemic or hemorrhagic destruction to the descending motor pathways, the corticospinal and corticobulbar tracts of the basis pontis (ventral pons), and the reticular formation of the pontine tegmentum, sparing the ARAS. It is a pure motor paresis, sparing the sensory pathways. In this somewhat less severe condition, the patient still retains vertical eye and eyelid movements. If there is true concern about either type of locked-in syndrome in which the person is conscious but cannot move or breathe, a simple electroencephalogram (EEG) can be performed to determine the function of the cerebral hemispheres.13

The main test of cortical, basal ganglia function is conscious interaction and conscious reaction to painful stimuli. Pain reaction does occur without consciousness in brainstem and spinal reflexes. Although brainstem reflexes negate death, pronouncement by detailed neurologic exam can occur if spinal reflexes are present. A viable spinal cord is not an exclusion of death; a person could have spinal cord function such as spinal reflexes and still be dead.

In examining consciousness, the physician must determine if the patient talks or makes any sound. Next, the physician must determine if the patient will open his or her eyes to name, touch, or painful stimuli. The examiner must then determine if the patient follows commands, localizes to pain, withdraws to pain, or has decorticate or decerebrate response to pain. Simply applying pinpricks to the body is not an appropriate stimulation of pain. Pressure on the supraorbital nerve positioned on the medial aspect of the eyebrow ridge is the best place to test for motor response to pain. It can also be elicited with temporomandibular joint compression. Do not use painful stimuli such as sternal rubbing or twisting of forearm or nipples because of the disfiguring and psychological effect that may have on family members or health care workers. Additionally, peripheral stimulation, such as nail bed pressure, may elicit a spinal reflex instead of a central response, often confusing the exam. A spinal reflex is a stereotypical repetitive, nonsustained movement that is usually monosynaptic. A withdrawal brainstem response is more complex because of additional inputs. The difference between high-level withdrawal response and decorticate reflex or spinal reflex can be determined by applying pain to the medial upper arm. The withdrawal response will usually be to abduct the arm away from the chest, whereas the reflex will be to adduct the arm toward the chest. A nonreflex conscious pain response demonstrates some integrity of the spine–brainstem–thalamus–cortical basal ganglion pathway. If there is decreased input from the cerebral hemispheres, decreased input through the cortical spinal tract, a functioning rubrospinal tract, and motor flexor of the distal limb, inhibition of extensor muscles becomes dominant, resulting in decorticate activity.

If there is disruption between the superior colliculi (anterior quadrigeminal bodies) or the decussation of the rubrospinal pathway, the rostral portion of the vestibular nuclei, pain stimulation becomes the major response of the vestibulospinal tract. This results in extensor tone to motor neurons innervating the neck, back, and limbs, and inhibition of flexion of the trunk and limbs. Since the track is uncrossed, the decerebrate activity occurs on the same side of the lesion. Spinal cord responses in addition to the stereotypical repetitive, nonsustained movement at the site of stimulation may also be seen as a slow response in the extremities, brief flexion of the fingers, or minimal eyelid deviation.

Next, the midbrain to lower pons is tested, investigating the oculovestibu-lar reflex by injecting ice water into the external auditory canal that is known to have an intact unobstructed tympanic membrane. The physician observes the eye movement while stimulating the vestibular system. First, elevate the head to 30 degrees to allow maximum stimulation of the horizontal canal. Then inject 30 to 50 cc of ice water into the external auditory canal and watch 30 seconds or more for the slow movement to the side of the cold-water stimulus. In coma, the quick nystagmus is lost, and the slow component to the side of the cold-water stimulus remains. If there is no brainstem reflex, the eyes will not move. Test one side, wait 5 minutes, then test the other. Testing the other side too soon after the first will inhibit the slow component to the side of the cold-water stimulus. This tests the CN III, VI, and VIII, the medial longitudinal fasciculus (MLF), the paramedian pon-tine reticular formation (PPRF), and the lower pons. Similar information can be obtained during the oculocephalic reflex. However, if spinal cord injury is suspected, do not perform the test. It would be terrible to have someone survive an ordeal to wake up quadriplegic. The oculocephalic reflex is observed while turning the patient’s head. Fast turning of the head to both sides should not produce any eye movement; however, conjunctival swelling sometimes makes this difficult to elicit. This is referred to as the doll’s eyes reflex because the patient’s eyes, like the painted eyes of a doll, stay fixed forward without movement. This reflex tests the similar components of the oculovestibular reflex: CN III, VI, and VIII; MLF; PPRF; and lower pons.

Certain movements are seen in the dead body and do not denote brainstem function. There can be spinal reflex spontaneous movements of the head and limbs; respiratory-like spinal reflex movements of the shoulders, back, and intercostal muscles without tidal volumes; and deep tendon reflexes, superficial abdominal reflexes, triple flexion response, Babinski’s reflex, and other spinal reflexes due to stimulation from acidosis or other means. There can also be spinal autonomic responses such as tachycardia, sudden increases in blood pressure, blushing, and sweating. There does not have to be the need for blood pressure control, nor does diabetes insipidus have to be present.14,15

Irreversibility

Apnea Test

After the final detailed neurologic exam, the hallmark of brain death should be performed: the apnea test. Do not perform it before the first detailed neurologic exam. Instead, the apnea test can be performed with the first of two detailed neurologic exams or with the second. It does not have to be performed twice, even in states where two licensed physicians are required to certify death by detailed exam. When a second exam is required, the physician must verify the results of any previous apnea test. It is often practical to perform the apnea test with the first of two required detailed neurologic exams if there is no additional requirement for a waiting period. However, the apnea test may produce a period of relative hypotension or hypoxia, which, with a condition of uncertainty in which the patient may still be alive, is detrimental. Therefore, optimally, the apnea test should be performed with the second detailed neurologic exam (Table 28–1).

The apnea exam tests the reticular formation of the caudal medulla. The strongest human drive is to breathe, and the living human will breathe if the by-product of metabolism, CO₂, increases above a certain threshold. Only rarely will the individual not breathe at mildly elevated CO₂ levels, such as a minority with chronic obstructive pulmonary disease (COPD) who function normally with increased CO₂. Although the drive to breathe occurs earlier with hypoxia and later with acidosis, the most reliable drive to determine a lack of brainstem function is rising CO₂. Acidosis will drive respiration; however, the blood–brain barrier is not as permeable to hydrogen ions as it is to CO₂ gas. Therefore, the microenvironment of the medulla is most responsive to escalating CO₂ gas, and brain death is determined by apnea due to the rise of CO₂ above the threshold. Brain death is not determined by hypoxemic or acidemic apnea.

Do not perform the apnea test unless the criteria to proceed with death declaration by neurologic examination have been met; there can be no effect of paralytics, no toxic effects of drugs, and, specific to the apnea test, no high spinal cord injury to prevent ventilation. Before performing the last part of the neurologic exam, the apnea test to investigate the reticular formation of the caudal medulla, the patient must meet additional criteria. The patient should be normothermic, with a core temperature ≥35.0°to 36.5°C or 95° to 97°F. The warmer the body, the quicker the CO₂ will rise. If the body is colder, the apnea test will take longer, leading to possible hypoxia or hemodynamic instability. However, do not attempt to make the patient hyperthermic, a condition that will increase CMRO₂ should the patient be alive. There should be no hypotension; the systolic blood pressure (SBP) should be greater than 90 mm Hg, although hypotension using 90 mm Hg is an arbitrary number. Young, small women and smaller children have blood pressures normally <90 mm Hg. To decrease the time required off the ventilator, which increases the chance ofdesaturation leading to O₂ hypotension and cardiac instability, the partial pressure of CO₂ (PCO₂) should be normal, 35 to 45 mm Hg by arterial blood gases (ABG). If COPD is suspected, start with a PCO₂ 60 mm Hg or higher. Before beginning the apnea test, the fluids should be running wide open. Vasopressors should be running or hanging and connected to the IV line and able to be given within seconds. SBP in the average adult should be as close to 120 mm Hg as possible but not < 90 mm Hg. Vasopressors should be increased as necessary. There should be pulse oximetry, and it should be maintained at 100% to start and without hypoxia throughout the test. The blood pressure and vitals should be monitored continuously; however, if no arterial line has been inserted, monitor the blood pressure with a cuff every minute. Monitoring blood pressure less often will only lead to the arrest of cardiac and pulmonary systems, with the resultant prolonged resuscitation of a patient who would have possibly been pronounced dead 10 minutes later. Hypotension is usually due to acidosis from decreased oxygenation or perfusion. Therefore, high temporary concentrations of O₂ and a hypervolemic state are necessary. If hypotension cannot be controlled, a blood gas should be drawn immediately and the remaining time aborted until measures can be taken to control loss of blood pressure.

The apnea test will measure the ability of the body to take a breath in response to increasing blood CO₂ (PCO₂). The PCO₂ will rise 3 to 6 mm Hg per minute depending on circulation and temperature. Some authors state that PCO₂ will rise 2 to 8 mm Hg; however, these are unusual conditions. The target PCO₂ is 60 mm Hg on an ABG test, although some municipalities use 55 mm Hg. When the patient has COPD, not only should the PCO ₂ rise above 60 mm Hg, it must rise at least 20 mm Hg above baseline to prevent any false diagnosis of brain death. To facilitate the levels of CO₂, the ventilator should be adjusted in the COPD patient who is known to be a CO₂ retainer; begin with a PCO₂ of 60 mm Hg before the apnea test. After the increased baseline of 60 mm Hg or higher, the PCO₂ should be allowed to rise at least 20 mm Hg.4,16–20 Additional concerns may be that the patient has absolutely no CO₂ drive, another unusual condition. Under those circumstances, a cerebral blood flow study should be ordered to confirm the complete absence of brain and brainstem blood flow.

In an attempt to ensure that the apnea test does not lead to cardiac arrest, or that a surviving person does not suffer further injury from hypoxia or ischemia, preoxygenate the patient for 10 minutes with 100% O₂ to eliminate the nitrogen stores, hyperoxygenate tissue to maintain organ viability, and prevent hypotension and cardiac instability. The patient may still develop acidosis during the apnea test from increased CO₂ levels; however, this can be minimized with excellent fluid flow, oxygenation, and blood pressure.

After hyperoxygenation, disconnect the ventilator while maintaining a superadequate O₂ source using a catheter, such as a nasal cannula with the nostril insert cut off, placed at the carina delivering O₂ at 6 L/minute or higher. The alternative is to keep the patient on the ventilator, stopping the breaths administered while maintaining positive pressure support at 10 mm Hg. Be careful: some ventilators have an automatic backup that will deliver 0.5 to 1.0 breath/minute; this fail-safe mechanism must be turned off. Furthermore, the licensed physician must not depend on the ventilator measuring the breaths; instead, he or she must observe the rise and fall of the chest, if present. If using the nasal cannula in the endotracheal tube, verify that both cannulas are at or before the end of the tube. Verify the length before insertion. If the cannulas are too long, they may oxygenate only one lung, and the nasal cannulas may get stuck; neither condition will be known initially. Furthermore, guarantee that there is enough room between the endotracheal tube and the catheter for O₂ to escape so there is no pressure buildup and pneumothorax. Physicians should do no harm, and that includes during the time pronouncing a person dead. The person will be temporarily off the ventilator ~8 to 10 minutes, based on the pretesting PCO₂ level. Under optimal conditions of temperature and blood pressure, after the 10 minutes of apnea multiplied by ~3 mm Hg of arterial CO₂ rise per minute, there should be 30 mm Hg rise from baseline PCO₂ toward the desired target value of 60 mm Hg. During the apnea test, the licensed physician must be present. The apnea test is the last part of the neurologic exam. The physician must observe the abdomen and chest for movements. If there are no movements after 10 minutes, then a new blood gas is drawn. When the arterial blood PCO₂ has reached at least 60 mm Hg, or at least 60 mm Hg plus 20 mm Hg above the patient’s elevated normal baseline, if there is a suspected CO₂ retainer, then the apnea test is positive, and the person is pronounced dead. If the PCO₂ has not reached 60 mm Hg on the ABG test, or has not gone 20 mm Hg higher than the minimum 60 mm Hg starting baseline in the CO₂ retainer, the test must be repeated for longer times.

• Disconnect the ventilator, or turn the ventilator to pressure support only, and disconnect the backup breath.
  
• Start the timer.
  
• Place the nasal cannulas with nasal inserts into the endotracheal tube only up to the end of the tube. Be sure that both nasal cannulas slide into the tube without getting stuck and that air is escaping.
  
• Place one hand on the patient’s chest, observe, and listen for breath.
  
• Check blood pressure readings every minute or continuously by ABG. In the average adult, keep as close to 120 mm Hg as possible.
  
• Check pulse oximetry reading every minute or continuously.
  
• Be able to increase fluids quickly.
  
• Be able to increase vasopressors quickly.
  
• If too hypoxic, abort the test.
  
• If too hypotensive, abort the test.
  
• If there are too many cardiac arrhythmias, abort the test.
  
• After 10 minutes, obtain ABG, place the patient back on the ventilator, and document the time.

Confirmatory Test

EEG does not detect brainstem function and cannot be the sole test to pronounce death. Electrocerebral silence does not exclude the possibility of reversible coma; however, multiple EEGs over an extended time, such as 24 hours, in the absence of medication- or metabolic-induced electrocerebral silence do correlate with a lack of cerebral function. EEG is not the gold standard for diagnosis of brain death, and it does not replace the apnea test, but it is used occasionally. When performing an EEG, there should be no electrical activity during at least 30 minutes of recording. The recording must adhere to the minimum technical standards of the American Clinical Neurophysiology Society (ACNS; formerly the American Electroencephalographic Society)21 for EEG recording in suspected brain death. The guidelines include a 16- or 18-channel EEG instrument, with scalp electrodes at least 10 cm apart. The interelectrode impedances should be between 100 and 10,000 ohms. There should be no activity over 2 μV/mm (better determined at 1 μV/mm) for 30 minutes. The high-frequency filter setting should be at 30 Hz, and the low-frequency setting should not be below 1 Hz. There should be no EEG reactivity to intense somatosensory or audiovisual stimuli.22,23 If cerebral angiogram is not performed, and EEG has to be relied on for confirmation of death, then EEG and repeat EEGs should be combined with brainstem auditory evoked responses (BAERs) to at least examine the brain and brainstem. Both electrical tests have characteristics that can lead to misinterpretation.

Transcranial Doppler (TCD) ultrasonography is now being entertained to assist in the confirmation of brain death. The TCD probe should be placed at the temporal bone above the zygomatic arch or the vertebrobasilar arteries through the suboccipital transcranial window. There should be insonation of at least three separate vessels on each side demonstrating the equivalent findings. However, 10% of people have no temporal insonation windows. Therefore, the initial absence of TCD signal cannot be interpreted as consistent with brain death. TCD utilization must produce a signal at all tested vessels demonstrating small systolic peaks in early systole with a lack of diastolic flow. The posterior cerebral artery (PCA) is usually the first to change, with the middle cerebral artery (MCA) being the last. Other criteria include the pulsatility index, which will be above 2.0 globally, indicating very high vascular resistance associated with greatly increased ICP. If the TCD reveals oscillating flow through the intracranial arteries, then brain death is more certain. Except for oscillating flow, all other criteria can be seen in pentobarbital coma. However, TCD does not detect brainstem flow or flow through small vessels, and it must not be used as meeting criteria to pronounce death.^24–28

Single-photon emission computed tomography (SPECT) measures brain uptake activity using radio-labeled amphetamine or radionuclide scan using IV technetium 99m hexamethylpropyleneamineoxime (Tc 99m-HMPAO).²⁹ Tc 99m-HMPAO adequately reflects brain activity and has been used for the determination of brain death. The isotope needs to be injected within 30 minutes of reconstitution and reveals initial dynamic flow images. Then there are important static images of 500,000 counts at several time intervals recorded immediately, between 30 and 60 minutes, and at 2 hours. Tc 99m-HMPAO static images are adequate for demonstrating the posterior fossa and brainstem.³⁰ During evaluation, there should be no uptake of isotope in intracerebral parenchyma; however, there may be activity in the external carotid circulation that will demonstrate a hollow skull. To have a valid test, correct IV injection needs to be confirmed with additional liver images demonstrating uptake. By comparison to conventional technetium agents, Tc 99m-HMPAO is not dependent on bolus quality and allows evaluation of the posterior fossa and brainstem.³¹ The Tc 99m-HMPAO scan is portable, less expensive, and does not require intra-arterial injection.

Brain Death Exam in Children

Before beginning with an examination as part of the declaration of death, the child must meet the initial criteria of irreversibility, no hypothermia, hypotension, or hypoglycemia, and no medications or metabolic changes that would cause coma or loss of brainstem reflexes. The difficult neurologic exam must be completed twice. The nervous system of the newborn is different from the adult because certain physiological functions may not have been developed. However, the same detailed neurologic exam, including the apnea test, must be performed twice. The detailed neurologic exam must be performed before and after the observation period, and the apnea test must be performed only with the second exam.32

Some brainstem reflexes are developed late. In children, the pupillary response to light is obtainable only after week 32 of gestation. The grasp response is obtainable after week 36 of gestation. Most importantly, the last part of the detailed neurologic exam, the apnea response to a PCO₂ stimulus, can only be elicited after 33 weeks of gestation. Therefore, in children there need to be additional criteria mandated for the brain death examination. There is a mandatory observation period in children, and the observation is age-dependent. The complete neurologic exam must be completed before and after the observation period. For children ages 8 days to 2 months, the observation period is 48 hours. For ages 2 months to 12 months, the observation period is 24 hours. For ages 12 months and older, the observation period is 12 hours. An infant must be at least 8 days old to be evaluated for clinical brain death.^32–36

Children’s Confirmatory Test

Because the complete neurologic and repeat neurologic exams after the appropriate observation period may not be reliable, as the functions tested may not have developed, confirmatory tests are mandatory. A cerebral angiogram is the gold standard. An EEG should be performed in accordance with ACNS21 standards, adjusting the 10 cm inter-electrode distance proportional to the head circumference. Because children <1 year old can survive longer periods of electrocerebral silence without cerebral death, EEGs must be repeated. In children ages 8 days to 2 months, there should be two EEGs and two complete neurologic exams (including an apnea test), 48 hours apart. Two EEGs and complete neurologic exams 24 hours apart or the combination of two complete neurologic examinations 24 hours apart, an EEG showing electrocortical silence, and a Tc 99m-HMPAO radionuclide test showing no cerebral uptake are required in children ages 2 months to 1 year, the rationale being that, in addition to the complete neurologic exams, the radionuclide scan will demonstrate no metabolic brain activity, as well as no electrical activity. Some criteria state that the waiting period is not necessary in children ages 2 months to 1 year if there is a complete neurologic exam, an EEG showing electrocortical silence, and a Tc 99m-HMPAO radionuclide test demonstrating no cerebral uptake. Children’s brains demonstrate an ability to recover substantial function after much more significant damage than do adult brains; therefore, the observation period is longer. It remains questionable why the cerebral arteriogram as the sole test has not been incorporated into published criteria for pediatric brain death.

After the Declaration of Brain Death

Brain death is dead. According to Youngner et al, “First and foremost, brain death is irreversible. Patients who are brain dead have permanently lost the capacity to think, be aware of self or surroundings, experience, or communicate with others.”37

Death must be recorded in the medical record chart when the complete neurologic exam, including the apnea test, is finished. The brain dead patient does not remain alive only to die once the ventilator is removed; the person is dead. There is no need for a physician to return to the body and pronounce the body dead again when the heart stops beating. Death is at the time of the completed full neurologic exam; it is not recorded as the time when the body is removed from the organ-supporting ventilator or when cardiopulmonary function ends.

Health care workers must not state that a patient will be kept alive on the ventilator until organs are recovered. The patient is not alive; only the organs are supported with ventilation. After death is pronounced, the ventilator is turned off if no organs are being donated. The family can visit with the body after removal of the remaining organ support. They should be notified that the patient is dead. The family will naturally ask about the beating heart and should be told that the brain, which contains the memories, activities, joys, love, kindness, and spirit of life, has died and will not return; only the body remains. The heart will continue to beat for an unknown length of time, and most of the organs will function if given support; however, the person is gone. The hospital staff policy must address the length of time that the body can remain in the NICU after the declaration of brain death until a decision about organ donation or until the ventilator is stopped. This short period lasting minutes to a few hours should be offered to allow grieving to begin but should not be so long as to provide false hope. Allowing many hours or, worse, days for out-of-state relatives to visit is not in the best interest of the family. An unusually long length of time only prolongs the family’s agony and inhibits the healing process.

After the declaration of death, when there is no decision to donate organs, the ventilator is discontinued. During this time until minutes after complete cessation of cardiac function, there may be acidosis, ischemia, and a sympathetic surge. This surge can trigger multiple simultaneous muscle contractions leading to opening of the eyes, elevation of the arms, and sitting up. This is called the Lazarus syndrome. Therefore, the family should be counseled should they decide to remain with the body from the time of ventilator discontinuation and extubation until removal to the morgue.

Organ Donation

Sometimes the body remains in the NICU while the family decides if the dead individual had wanted to donate organs. It is best to discuss with the family the gift of organ donation with the organ donation workers prior to death.38–40 The organ donation agency should be contacted anytime the patient has a Glasgow Coma Scale score of 5 or less. The agency could then decide if the individual meets the criteria for donation. If questions from the family arise about organ donation prior to the arrival of organ donation workers, the family may be asked about the wishes of the patient. If the patient is pronounced dead by a complete neurologic exam and the family has consented on behalf of the individual to organ donation, the ventilator continues, and the care of the body should be turned over to the organ transplant agency. The agency coordinators will assume care, write orders, and attempt to maintain the adult parameters of PO₂ ≥ 100 mm Hg, SBP ≥ 100 mm Hg, and PCO₂ 35 to 45 mm Hg.