Brain Death and Organ Donation

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Chapter 38 Brain Death and Organ Donation

Brain death is a clinical syndrome in which there is complete and irreversible loss of cortical and brainstem function. Organ donation by deceased donors requires confirmation of brain death, and is clinically, contextually, and temporally separate from transplantation. Donation takes place after the death of a person in an intensive care unit (ICU), most commonly following an intracranial catastrophe, and it involves the patient’s family and the healthcare professionals who have cared for the patient.¹ Organ donation is thus an integral part of end-of-life care in the ICU.² Intensive care physicians are generally supportive of organ donation³ and are obliged to provide leadership in it⁴ as part of their responsibility for the care of dying patients and their families.

Intensive care physicians must ensure that the processes involved in organ donation are conducted according to the highest standards. These processes include:

• Care of the dying patient and the family (see Chapter 39)

• Determining brain death

• Identifying the potential for organ donation

• Offering the opportunity for organ donation to the family

• Maintaining physiologic stability throughout the time until organ retrieval occurs

• Aftercare for the family of the deceased, irrespective of whether organ donation has taken place.

DIAGNOSING BRAIN DEATH

The syndrome of brain death was recognized soon after the establishment of ICUs and before transplantation was established. Despite a number of guidelines for the determination of brain death,⁵ there remains no single accepted international consensus definition of this syndrome, and codes of practice for the determination of brain death vary slightly internationally, particularly in terms of requirements for repetition and for confirmatory tests (see subsequent material). Nevertheless, all codes of practice contain the following essential common features:

• A known condition that can cause brain death

• An absence of confounding features (e.g., hypothermia or sedation)

• Evidence of persistently absent brainstem function on clinical examination.

Clinical neurologic examination is the standard for the determination of brain death (Table 38-1). This cannot proceed until the following prerequisites are met:

Table 38-1 Clinical Criteria for Brain Death

Clinical criteria for brain death	Coma of known cause
	Absence of motor responses
	Absence of pupillary responses to light
	Absence of corneal reflexes
	Absence of caloric reflexes
	Absence of gag reflex
	Absence of coughing in response to endotracheal suctioning
	Absence of sucking and rooting reflexes
	Absence of respiratory drive at a PaCO2 >8 kPa (60 mmHg) or 2.7 kPa (20 mmHg) above normal baseline values
Interval between two evaluations according to age	0 to 2 months: 48 hr
	2 months to 1 year: 24 hr
	1 to 18 years: optional
	>18 years: optional

From Wijdicks EF: The diagnosis of brain death. N Engl J Med 344:1215-1221, 2001.

• The ruling out of complicated medical conditions that may confound the clinical assessment, particularly severe electrolyte, acid-base, or endocrine disturbances

• The absence of hypothermia, defined as a core temperature of 35°C or lower

• The absence of hypotension

• The absence of evidence of drug intoxication, poisoning, or neuromuscular blocking agents.

A complete clinical neurologic examination includes the documentation of coma, the absence of brainstem reflexes, and apnea. The examination of brainstem reflexes involves the measurement of reflex pathways in the mesencephalon, pons, and medulla oblongata. As brain death develops, patients lose the cranial nerve reflexes in a rostral-to-caudal direction, and the medulla oblongata is the last part of the brain to cease to function.

Some codes of practice require that additional special tests (e.g., electroencephalogram and tests of cerebral blood flow) be performed,⁶ whereas others do not, so brain death should be determined according to locally appropriate codes of practice. When clinical examination cannot be performed (e.g., because of bilateral eye damage) or is confounded (e.g., by prior therapeutic use of high-dose barbiturates), it is necessary to establish that there is no cerebral blood flow by using a confirmatory test such as cerebral angiography, radionuclide cerebral angiography, or a suitably robust alternative method.⁷

Physiologic Changes in Brain Death

Severe hypertension, tachycardia, and sometimes arrhythmias occur during the final phase of brainstem compression prior to brain death, and although these phenomena may cause temporary reduction of cardiac contractility, treatment is usually not required.⁸ Should treatment be necessary, a short-acting intravenous β blocker such as esmolol is recommended. A degree of neurogenic pulmonary edema is common with intracranial injuries and should be managed conservatively, by adequate ventilation, cardiovascular support, and the judicious use of diuretics. Neurogenic pulmonary edema usually resolves within 48 to 72 hours and it will be aided by the diuresis, which occurs if diabetes insipidus (see subsequent material) develops.

Pulmonary edema and myocardial dysfunction do not necessarily preclude good subsequent cardiac graft function. Hypertension is soon followed by hypotension (which may be profound if hypovolemia or cardiac dysfunction is also present) and should be promptly treated by volume expansion and vasopressor support. Diabetes insipidus (see Chapter 32) is common and if untreated will rapidly lead to hyperosmolality, hypernatremia, and hypovolemia. Other hormone alterations^8,⁹ do not have therapeutic implications. Oxygen consumption and carbon dioxide production fall by about 40% during the development of brain death,¹⁰

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