Brain Death

Brain Death

Brain death occurs when there is an absence of signs of brain stem function or motor response to deep central pain in the absence of pharmacologic or systemic medical conditions that could impair brain function.

For as long as medical practice has existed, the layperson has required of medical practitioners that they be knowledgeable
about death. For cenrunes, lay people and doctors alike have accepted cessation of respiration and heart beat as the classical signs of death. Advances in cardiopulmonary resuscitation and modern mechanical ventilation have made obsolete the traditional clinical definition of death with a small but significant har­vest of irreversibly brain-damaged patients. The worst form of such damage led to the concept of (coma depasse), first defined by Mollaret and Goulon in 1959. As the number of patients with artificially maintained ventilation and circulation increased. they became to be regarded as a potential source of donor organs. These two developments occurred parallel to but independently of each other, and the diagnosis of brain death did not arise because of the need for donor organs.

The presence of an irreversibly damaged brain in a body In

which ventilation and Circulation were being maintained by

artificial means presented a state in need of a definition. Mollaret and Goulon were the first to Investigate this state in their paper Le coma depasse. Many terms for this and other states for which
it has been mistaken have been suggested or used, of which the following are the most commonly encountered: cerebral death, brain stem death, brain death, coma depasse, irreversible coma, cortical death, persistent vegetative state and locked-in syndromeThe high cost of treating patients in intensive therapy units (lTUs) and the premium on such limited resources have con­tributed significantly to the re-evaluation and, management of such states. Nursing and medical staff morale, as well as the emo­tional toll on relatives, are very real considerations. As these patients may now be potential essential organ donors, their care has acquired medico-legal and ethical Significance. The primary task of a doctor is not to provide organs for transplantation, but neither is it to deny patients in need of transplant surgery. Before a patient can be considered as having suffered irreversible brain damage, it is mandatory that a positive diagnosis be made of the pathogenesis of this damage. To produce coma, pathological processes must affect the brain diffusely or encroach upon its deep central structures.

Three major groups of lesions can be differentiated:

supratentorial lesions;

infra tentorial lesions;

metabolic disorders: that widely depress or interrupt brain function, including anoxia, ischaemia, infections, toxins and essential deficiencies

The disintegration of function following progressive hernia­tion will end in cessation of spontaneous respiration, leading to hypoxic cardiac arrest. If ventilation and circulation are maintained artificially, the heart, kidneys and liver may continue to function for some hours or days, but after brain stem death has occurred cardiac arrest will follow within 2 weeks Since Mollaret and Goulon, several committees and reviewers have sought to establish unequivocal and appropriate clinical and EEG criteria for brain stem death, based on retrospective analysis of patients who died. The first was the Harvard group, which included EEG among its criteria. This was later deemed unneces­sary by both the Minnesota and British groups. The current criteria are as follows.

Before diagnosing brain death several preconditions should be satisfied:

There should be no doubt that the patient's condition is due to irremediable brain damage of known aetiology 

The patient should be in a coma on a ventilator because spontaneous respiration has been inadequate or ceased altogether 
Conditions and drugs that simulate brain death have to be excluded and, if necessary, drug levels measured to ensure that there is no reversible cause for coma. Some drugs (e.g. thiopentone) may take days to be cleared from the system.

Potentially reversible circulatory, metabolic and endocrine disturbances must have been excluded as the cause for the continu­ation of unconsciousness. It is recognised that circulatory, metabolic and endocrine disturbances are a likely accompaniment of brain stem death (e.g, hypernatraemia and diabetes insipidus), but these are the effect rather than the cause of that condition and do not preclude the diagnosis

The tests should be performed by two physicians of not less than 5 years' registration who are not members of a transplant team and at least one of whom should be a consultant. The tests are designed to assess brain stern functioning, as it is the reticular activating system in the brain stern that is responsible for activat­ing the rest of the cerebrum

The pupils should be fixed and unresponsive to changes in the intensity of incidental light

 There should be no corneal reflex
 The vestibule-ocular reflexes should be absent. No eye movements should be observed while at least 50 ml of cold water is infused over each eardrum. Clear access to the mem­brane must be established by direct inspiration
 No motor responses within the cranial nerve distribution can be elicited by adequate stimulation of any somatic area.

There is no limb response to somatic pressure, bearing in mind that movements med rared at a spinal level might still be possible  There is no gag reflex to bronchial stimulation by a catheter placed down the trachea.  No respiratory movements appear when the patient is disconnected from the mechanical ventilator. During this test, it is necessary for the arterial CO2 to exceed the threshold for respiratory stimulation, that is the Paco2. should reach 6.65 kPa (49.88 mmHg). This should
Ensured by measurement of the blood gases. The patient
should first be pre-oxygenated with 100%  O2 for 10 minutes
do not correlate with the clinical state. Serum concentrations
(then with 5% CO2 in O2 for 10 minutes, if CO2, is available­
. The ventilator should then be disconnected for 10 minutes while, via a catheter, 61 min" O2, is infused into the trachea

 If no respiratory effort has been detected and other signs of brain stem dysfunction have been demonstrated, the patient may be considered brain dead .

Definition  summary of brain death

• Electroencephalography (EEG)activity may persist even when brain death is diagnosed

• No case of recovery from prolonged coma ever fulfilled all the criterio

of brain death

• No patient in whom brain death has been diagnosed has ever achieved neurological recovery

It is imperative that conditions simulating brain death be excluded  
Conditions that may mimic some features of brain death

• Drug intoxication

• Hypothermia

• Electric shock injury

• Brain stem encephalitis

Drug intoxication

CNS-depressant drug poisoning may cause total loss of cerebral function and electrocerebral silence for more than 50 hours, fol­ lowed by complete recovery. Self-induced drug poisoning often involves several drugs, frequently in combination with alcohol.
toxicology screening is not always available and frequently levels do not correlate with the clinical state serum
concentrations often lag behind brain concentrations

 hypothermia the core of temperature tends to drops when brain stem ceases to function that hypothermic may cause an isoelectric electroen­cephalogram is a theoretical rather than a practical issue. What is important is that hypothermia should be excluded as the cause rather than the result of the coma. No patient should be declared dead until warm and dead.

Electrical injury

This may be an important cause of coma, apnea and fixed pupils. Full recovery following resuscitation and ventilation can be achieved.

Brain stem encephalitis

This is a rare form of encephalitis characterized by rapid ophthal­moplegia, ataxia and areflexia with apnoea and coma in severe cases. Although the clinical state may suggest brain death, these patients do not comply with the basic prerequisite of an incontro­vertible diagnosis and the physician should be concerned with diagnostic and therapeutic measures rather than speculating about irreversible coma

Ancillary tests

Ever since the concept of brain death arose, efforts have been made to establish the diagnosis electrophysiologically the reason being to seek an objective, non-clinical mode of diagnosis free of error or bias. These tests are not available in all hospitals, and those that have proved to be indisputable indicators of brain stem death have usually been used in patients in whom the diagnosis was never in doubt. They are listed for completeness and not because they replace clinical testing


scalp electromyograms

evoked potentials

brain stem auditory-evoked potentials

somatic-evoked potentials; lower oesophageal contractility; arteriovenous oxygen difference; cerebral blood flow

ocular microtremor

There is strong evidence that EEG silence for greater than 12 hours in a normothermic and drug-free patient is not compatible with neurological recovery
Note that an electroencephalogram does not measure brain­ stem function. Drugs may cause coma with reversible true elec­terocerebral silence. Cessation of cerebral blood flow in patients with raised ICP  It is a significant indicator of brain death, particularly when CT scanning is not available. It caused by ICP rising above the MAP  and by progressive vascular obstruction caused by aurolysis in respirator brain
ocular microtremor is one of three fixational movements measued using the isoelectric stains gauge 

Clinical Examination. A neurologist, neurosurgeon, or intensivist generally performs the clinical brain death exam. Two ex­ams consistent with brain death 12 hours apart, or one exam consis­tent with brain death followed by a consistent confirmatory study is generally sufficient to declare brain death . Hospital reg­ulations and local laws regarding documentation should be followed closely.
Establish the absence of complicating conditions before beginning­  the exam. The patient must be normotensive, euthermic, and oxygenating well. The patient may not be under the effects of any sedating or paralytic drugs.
Documentation of no brain stem function includes the follow­
ing: nonreactive pupils; lack of corneal blink, oculocephalic (doll's eyes), or oculovestibular (cold calories) reflexes; and loss of drive to breathe (apnea test). The apnea test demonstrates no spontaneous breathing even when PaCO2 is allowed to rise above 60 mm Hg
Deep central painful stimulus is provided by forceful twisting
pinch of the sensitive skin above the clavicle. Pathologic responses such as flexor or extensor posturing are not compatible with brain death. Spinal reflexes to peripheral pain, such as triple flexion of the lower extremities, are compatible with brain death

Confirmatory Studies. Confirmatory studies are performed after a documented clinical exam consistent with brain death. A study consistent with brain death may obviate the need to wait  hours for a second exam. This is especially important when the patient is a potential organ donor. as brain dead patients often have progressive hemodynamic instability. Lack of cerebral blood flow consistent with brain death may be documented by cerebral an­ giography or technetium radionuclide study. A "to-and-fro" pattern
On transcranial Doppler (TCD) ultrasonography indicates no net forward flow through the cerebral vasculature, consistent with brain death. An electroencephalogram (EEG) documenting electrical si­lence has been used, but is generally not favored because there is often artifact or noise on the recording. This can confuse the situa­tion and be especially difficult for families to understand


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