27.1 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. The hope delivered by transplant surgeons, and 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, 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 , ² , ³ , ⁴ , ⁵ , ⁶

27.2 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 alive. ⁷ Although the Death Act of 1980 established the criterion for death, the definition did not address diagnostic tests. This provided the medical and legal profession flexibility to develop diagnostic procedures while leaving the door open for disagreement and the need for judicial review. 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. The following is an example of a state law, the State of California Health and Safety Code, Section 7184:

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 a 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 there is cardiac and pulmonary deterioration, which is the criterion for somatic death, an artificial and mechanical support 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 are no machines 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.

27.3 Initial Criteria

To pronounce a person dead, there must be evidence of irreversible brain damage. The examining licensed physician must personally review the computed tomographic (CT) or magnetic resonance imaging (MRI) scan; it must be consistent with an irreversible condition incompatible with life, such as sustained negative cerebral perfusion pressure, massive stroke, lack of gray–white junction, edema, shift, and multiple other conditions. To proceed with a complete neurologic exam for pronouncing the patient dead, there must be hemodynamic stability; the patient cannot be arresting. It is not unusual for pupils to be fixed and dilated immediately after resuscitation. This nonresponsive brain condition can also be seen during seizures, when abnormal brain activity is impeding functional interaction. To declare death, a patient can be on multiple vasopressors.

There are major prerequisites, outlined by American Academy of Neurology, 2012, that must be met before considering a valid neurologic exam for the purpose of declaring a patient dead. Coma must be irreversible and the cause known. Moreover, neuroimaging should explain the coma. The body should have a systolic blood pressure > 100 mm Hg. The patient cannot be under the effects of a skeletal muscle paralytic (electrical stimulation if paralytics used), and all central nervous system depressant drug effect must be absent (if indicated a toxicology screen must be performed and if barbiturates were given, the serum level must be < 10 micrograms/mL). The body core temperature must be normothermic or mild hypothermic (core temperature > 36°C). 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, or patients on a hypothermia protocol after cardiac arrest. ¹⁰ , ¹¹ Furthermore, there can be no severe acid–base, electrolyte, or endocrine abnormality.

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 preserved. 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 death; instead, wait and investigate. 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 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 1,500 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 for benzodiazepine overdose must outweigh the risks, for example, when administering flumazenil it should be divided, first giving the dose as 0.2 mg intravenous (IV), then giving 0.3 mg. 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’ effect 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 the 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

27.4 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. 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 severe 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, 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, electroencephalography (EEG) can be performed to determine the function of the cerebral hemispheres. ¹³

The main test of cortical, and 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 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. 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.

As the detailed neurologic exam proceeds down from the cerebral cortex and diencephalons, the function of the midbrain and the nuclei of cranial nerve (CN) II and CN III is probed. The physician examines these structures, testing the pupillary reflex using a bright flashlight, first directed into one pupil so that it hits the retina, and then into the other. Dilated pupils are > 4 mm, and asymmetric pupils are > 1 mm different. Pupils that are asymmetrical and small are usually a sign of midbrain or pontine injury in a living person. Always err on the side of caution and on the side of life. If orbital or papillary inspection is hampered, use a magnifying glass. This reflex of sensory and autonomic motor response can demonstrate activity even if the patient has been chemically paralyzed.

The corneal reflex indicates the integrity of the midpons, cranial nerve (CN) V sensory component, and CN VII motor component. It is performed by touching the cornea away from the pupil with a cotton-tipped applicator and observing a blink response. The blink may be slight; however, any movement is an indicator of function and life. For this test, do not use a paper towel, piece of paper, or any material that may be abrasive to the cornea.

Next, the midbrain to lower pons is tested, investigating the oculovestibular 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 pontine 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. 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.

A cough response should be attempted using a suction catheter inserted into the endotracheal tube and advanced to the level of the carina, followed by deep suctioning to test lower brainstem or medulla function. Do not just move the endotracheal tube. The simple stimulation of the gag reflex is a variable test, as it can be blunted by medication and normal physiology. This test, in which there is a cough or sensation, then elevation of the uvula, monitors the function of CN V, IX, and X and the medulla.

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

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