Brain death.

Brain death involves persistent loss of consciousness, sustained spontaneous respiration, and brainstem reflexes; spinal reflexes, including deep tendon reflexes, plantar flexion, and limb withdrawal reflexes (flexor reflexes), may persist.

The concept of brain death arose with the advent of the possibility of maintaining respiration and circulation despite the complete loss of brain activity. Therefore, the definition of human death as the irreversible cessation of brain activity, especially in the structures of the brain stem, is widely accepted in law and society.

At all times there has been no more exciting and mysterious problem for humanity than life, death and the transitional stages between these interconnected and mutually exclusive concepts. States bordering on existence and non-existence have always aroused and continue to arouse great interest: lethargy, some amazing "coma-like" stages of self-hypnosis of Indian yogis, etc. However, at first these phenomena attracted the attention of philosophers and writers more than doctors. It seemed obvious to doctors that a few minutes after the heart and breathing stop, life ceases and death occurs. As early as the 7th century, Democritus wrote that in reality there are no completely convincing signs of death for doctors. In 1896, V. Montgomery claimed that cases of erroneous burial make up at least 2% during epidemics and mass battles. And Edgar Poe’s famous short story “Buried Alive” impressed his contemporaries so much that in 1897 a certain Karnice patented in Berlin an ingenious device for signaling to others about the possible “reanimation of a corpse.”

Since 1927, after the creation of the "iron lung" by Paul Drinker, which laid the foundation for resuscitation aids, the era of active support of fading vital functions has begun. Unprecedented progress in this branch of medicine is associated with the enormous successes of medical technology. The use of forced synchronized breathing, defibrillation, artificial pacemakers, cardiopulsation, artificial blood circulation, controlled hypothermia, hemodialysis, hemosorption and other methods provided seemingly unlimited opportunities for the restoration and long-term artificial support of the main functions of the human body.

In 1959, the French researcher Mollaret was the first in the world to describe 8 patients who were in the intensive care unit on artificial ventilation, who completely lacked all brainstem reflexes, responses to pain stimuli, and pupillary reactions to light. In all patients, cardiac arrest occurred within 7 hours from the moment the described condition was recorded, and autopsy revealed pronounced necrotic changes in the brain matter, including the formation of detritus. The author called this condition an extreme coma.

In 1968, the Harvard criteria for human death based on brain death were published. They postulated the possibility of diagnosing death based on the cessation of brain function and were the first to use the term "brain death".

In recent decades, a specialist in the restoration of impaired functions in patients with urgent intracranial lesions (severe TBI, rupture of a large intracerebral aneurysm, etc.) has increasingly been faced with a very serious moral and legal responsibility - to participate in sanctioning the termination of resuscitation measures and the removal of organs from the deceased for transplantation. Significant advances in transplantology in the artificial engraftment of not only the kidney, but also the heart, liver and other organs make the problem of creating a "donor bank" extremely urgent. The most seriously ill neurological and neurosurgical patients - relatively young and somatically healthy people, according to most researchers - are optimal "donor candidates".

The results of modern research indicate that the pathogenesis of dying and death of the brain is extremely complex and includes reversible and irreversible stages. Until recently, the clinical signs of brain death were considered to be the absence of response to any sensory stimulation, the absence of spontaneous breathing and any spontaneous motor phenomena, the occurrence of bilateral mydriasis with the absence of pupillary response to light, a rapid drop in arterial pressure when artificial circulation is stopped. However, some researchers believe that none of these clinical criteria can be considered a pathognomonic reflection of brain death. On the one hand, spinal reflexes may be present for some time after documented death of the brain, on the other hand, all the signs considered to be undoubted symptoms of brain death cannot in fact be considered as such: they do not always reflect the biological death of a person.

Thus, from the doctor's point of view, human death is not cardiac arrest (it can be restarted and maintained again and again, saving the patient's life), not cessation of breathing (rapid transfer of the patient to forced ventilation restores gas exchange), but cessation of cerebral circulation. The overwhelming majority of researchers around the world believe that if the death of a person as an individual, and not as an organism, is inextricably associated with the death of the brain, then brain death is practically equivalent to the cessation and non-resumption of cerebral perfusion.

Pathophysiological mechanisms of brain death

Severe mechanical damage to the brain most often occurs as a result of trauma caused by sudden acceleration with an oppositely directed vector. Such injuries most often occur in car accidents, falls from great heights, etc. Traumatic brain injury in these cases is caused by a sharp antiphase movement of the brain in the cranial cavity, which directly destroys parts of the brain. Critical non-traumatic brain damage most often occurs as a result of hemorrhage either into the brain substance or under the meninges. Severe forms of hemorrhage, such as parenchymatous or subarachnoid, accompanied by the outpouring of a large amount of blood into the cranial cavity, trigger mechanisms of brain damage similar to traumatic brain injury. Anoxia, which occurs as a result of temporary cessation of cardiac activity, also leads to fatal brain damage.

It has been shown that if blood completely stops flowing into the cranial cavity for 30 minutes, this causes irreversible damage to neurons, the restoration of which becomes impossible. This situation occurs in 2 cases: with a sharp increase in intracranial pressure to the level of systolic arterial pressure, with cardiac arrest and inadequate indirect cardiac massage during the specified period of time.

Pathophysiological mechanisms of brain death

Clinical criteria for brain death

To make a medical conclusion about brain death, it is necessary to establish the cause of organic or metabolic brain damage, exclude the use, especially independent, of anesthetic and paralyzing drugs. Hypothermia below 32 "C should be corrected and epileptic status should be excluded. Dynamic studies over a period of 6-24 hours are necessary. The study should include determination of pupillary response, oculovestibular and oculocephalic reflexes, corneal reflexes and an apneic oxygenation test. To confirm the absence of brain activity and as additional evidence for family members, it is possible, but not necessary, to use EEG.

There are no known cases of recovery after adequate diagnosis of brain death. Even under artificial ventilation conditions, asystole usually occurs after a few days. Termination of artificial ventilation is accompanied by the development of terminal arrhythmia. During terminal apnea, spinal motor reflexes may occur: arching of the back, turning of the neck, tension of the leg muscles and flexion of the upper limbs (the so-called Lazarus sign). Family members who wish to be present at the termination of artificial ventilation should be warned about this.

Guidelines for Determining Brain Death in Individuals Over One Year of Age

To establish brain death, all 9 requirements must be met.

1. Possible attempts have been made to notify relatives or other close people.
2. The cause of coma is known and is quite capable of leading to irreversible cessation of brain function.
3. Excluded: the possibility of the action of muscle relaxants and substances that depress the central nervous system, hypothermia (<32 °C) and arterial hypotension (SBP <55 mm Hg)
4. All observed movements can be carried out due to the activity of the spinal cord.
5. Cough and/or pharyngeal reflexes are absent
6. Corneal reflex and pupillary response to light are absent
7. There is no reaction in the caloric test with irrigation of the eardrum with ice water through the external auditory canal
8. An apneic oxygenation test for at least 8 minutes does not reveal respiratory movements against the background of a proven increase in PaCO2 >20 mm Hg above the initial pre-test level

Methodology: The test is performed by disconnecting the ventilator from the endotracheal tube, where oxygen is supplied through a cannula at a rate of 6 l/min. Passive growth of PaCO2 stimulates respiration, but spontaneous respiratory movements do not appear within 8-12 minutes of observation.

Note: The risk of hypoxia and hypotension should be minimized during the test. If BP drops significantly during the test, the patient is placed back on the ventilator and an arterial blood sample is taken to determine whether PaCO has risen above 55 mmHg and whether it has increased by >20 mmHg relative to the pre-test level. These values confirm the clinical diagnosis of brain death.

9. At least one of the following four criteria is met.

A. Positions 2-8 have been confirmed twice in studies at least 6 hours apart

B. Positions 2-8 are confirmed AND the EEG shows no electrical activity in the cerebral cortex. The second study was conducted at least 2 hours after the first, which confirmed positions 2-8.

B. Items 2-8 are confirmed AND intracranial blood flow is not detected on arteriography. The second study is performed at least 2 hours after the first study that confirmed items 2-8.

D. If confirmation of any of the items 2-8 is prevented by injury or condition (e.g., extensive traumatic injury to the face prevents caloric testing), the following criteria are used. Confirmation of items available for assessment No evidence of intracranial blood flow

The second study is carried out 6 hours after the first one, which confirmed all positions available for assessment.

SBP - mean arterial pressure; PaCO - partial pressure of CO in arterial blood. From the Guidelines of the American Academy of Neurology (1995), with changes.

Brain death - clinical criteria

Instrumental methods confirming brain death

There are many problems in diagnosing clinical criteria for brain death. Often, their interpretation is insufficient to diagnose this condition with 100% accuracy. In this regard, already in the first descriptions, brain death was confirmed by the cessation of bioelectrical activity of the brain using EEG. Various methods that allow confirming the diagnosis of "brain death" have received recognition throughout the world. The need for their use is recognized by most researchers and clinicians. The only objections concern the diagnosis of "brain death" based only on the results of paraclinical studies without taking into account the data of a clinical examination. In most countries, they are used when it is difficult to conduct a clinical diagnosis and when it is necessary to reduce the observation time in patients with a clinical picture of brain death.

Brain Death - Diagnosis

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