Brain death is defined as the irreversible cessation of function of the entire brain with three specific criteria: 1) coma, 2) absent brainstem reflexes and 3) apnea. In addition to these clinical criteria, there are important prerequisites: 1) NO intoxication or poisoning, 2) NO core temperature greater than 32 degrees Celsius, 3) clinical or neuroimaging evidence of acute central nervous system catastrophe and 4) absence of confounding medical conditions such as severe electrolyte, acid-base, or endocrine disturbances.
Many physicians actively involved in the identification of brain death, if the truth be known, are unable to identify the requisite diagnostic components of brain death, and/or are unable to apply the criteria correctly. A second, or even third opinion should always be sought.
Canadian standards do not test function of the "entire brain"; does not assess subcortical function of structures such as the hypothalamus-pituitary axis. Many patients diagnosed as brain dead have intact neurohumoral control of hypothalamic-pituitary function, demonstrate normal hypothalamic mediated thermoregulatory control, and have intact autonomic function: they do not have hemodynamic collapse, they have physical findings such as bowel sounds, and are reported to have autonomic reflexes (tachycardia and hypertension) at the time of organ retrieval.
Given that current clinical testing does not assess subcortical brain function, ‘whole brain death’ cannot be conclusively identified at the bedside by using clinical criteria, and certainly not on the basis of a paltry CT. A CT scan is useful only in pretty severe cases, such as trauma, and also during the few days after an anoxic (lack of oxygen) brain injury. It’s useful in an emergency-room setting. But if the question is ischemic injury [brain damage caused by lack of blood/oxygen to part of the brain] you want an MRI and PET. For subsequent evaluation of brain injury, the CT is pretty useless unless there has been a massive stroke. In other words, being declared brain dead is a time consuming and detailed procedure, as it should be. It cannot be done in a meager few hours.
Brain death may be described as an esoteric creation of neurologists and neurosurgeons who are seeking to speed up the declaration of death for the purposes of an eye transplant, or a long awaited body part. The general practicing physician does not rely on those esoteric criteria in pronouncing a person dead." He uses the questionable "brain death criteria" based on a paltry CT as a pretext to operate and remove the eyes.
Many patients diagnosed as brain dead have hemodynamic instability. Many of these victims still have physical findings such as spontaneous breathing, including bowel sounds, and are reported to have autonomic (tachycardia and hypertension) in response to painful stimuli at the time of organ retrieval, suggesting a horrific death.
After the diagnosis of brain death, the focus of patient care shifts from interventions aimed at saving the patient's life to interventions aimed at maintaining viability of potentially transplantable organs
Brain death is what happens when ventilator support is discontinued. Condition called cerebral hypoxia or cerebral ischemia, is the direct result of oxygen deprivation to the brain cells. If proper balance is not restored or corrected, the heart and lungs may fail and the brain will literally begin to suffocate.
After several minutes of total oxygen deprivation, the brain may not be able to recover any meaningful function. The autonomic system controlling the heart and lungs fails next, leading to the ultimate cause of death, being oxygen deprivation of the brain cells, akin to "asphyxia".
It is never permissible to take any direct action designed to kill the patient. If a doctor deliberately let a patient die who was suffering from a curable treatable illness, the doctor would certainly be to blame for what he had done, just as he would be to blame if he had needlessly killed the patient. Charges against him would then be appropriate. If so, it would be no defense at all for him to insist that he didn't "do anything". He would have done something very serious indeed, for he let his patient die.
To allow or hasten a patient's demise to cover-up medical error or negligence is reprehensible. It is nothing short of murder since such an act or omission carries the intended consequence of the act or omission and therefore the mens rea or criminal intent. Negligence is where the accused ought to have foreseen the consequences of his actions, or inactions.
There are numerous reports of brain death declaration where the criteria were deliberately misrepresented, or obfuscated in an attempt to retrieve an organ for transplantation. The following is a perfect example.
The Arlene Berry Case
In this case, the harried and hurried physicians did not rely on those esoteric criteria in pronouncing the patient "dead." They simply used the questionable "brain death criteria" (based on a paltry CT after withdrawal of ventillatory support) as a pretext to operate and remove their patient's eyes while she was still very much alive.
There have been many challenges to the several concepts of "brain death" and the means of their diagnosis worldwide (vide infra). Indeed, it seems that there is now an emerging consensus that "brain death" diagnosed by any of the protocols in current use worldwide is "not death."
As a safeguard in determining brain death a number of tests need to be carried out every 6 hours and recorded, the physicians performing this determination must not be part of a transplantation team. In some cases, 48 to 72 hours is required to evaluate brain death and a repeat examination with observation up to 24 hours is sometime needed. The length of time between serial examinations to declare brain death varies marginally from 6 to 72 hours.
Neurological and neurosurgical intensive care - Google Books Result
Brain Death Mimics
The effects of many sedative and anesthetic agents can closely mimic brain death. All the so-called major tranquilizers can mimic a death-like condition by causing reduced brain wave activity and lack of responsiveness. First, hypothermia may blunt brain stem responses when core temperatures are below 32°C and may mimic brain death below 27°C. Drug intoxication and neuromuscular blockade use are reversible causes of coma that can mimic brain death. Demyelinating polyradiculoneuropathy can also resemble brain death. Encephalopathy with peripheral neuropathy may falsely mimic brainstem death, as can viral encephalitis, brainstem encephalitis, rabies, including Locked-in syndrome
Drug intoxication may cause a deep physiologic depression that resembles brain death, and drug intoxication is the most common cause of coma of rapid onset which may mimic brain death. The examination can be marred by the effects of sedation.
Acute metabolic derangement and endocrine abnormalities can also mimic brain death. There may be other conditions that mimic brain death, or that provide examples of the mistaken diagnosis of brain death. Diabetes is the most common endocrine disorder. Severe hypermagnesemia can mimic brain death.
Some patients in this group have been proceeded to organ harvest with discontinuation of care with no conclusive evidence of permanent and irreversible loss of brain function, usually on the basis of a paltry CT, despite respiratory efforts (breathing spontaneously) and despite physical findings, ie 'bowel sounds' and automic reflexes with tachycardia and hypertension evident (which support normal subcortical functions), which is totally inconsistent with 'whole brain death'. The bald truth is that GBS patients with a spontaneous breathing pattern may require prolonged ventilation.
Fulminant cases of Guillain-Barre syndrome have been reported in which a rapid deterioration evolves to a clinical state "resembling brain death". GBS is one of the few neurological diseases whose clinical manifestations may mimic or appear to be identical to those in brainstem death, illustrating an extreme polyneuropathy.
As a safeguard in determining brain death a number of tests need to be carried out every 6 hours and recorded, the physicians performing this determination must not be part of a transplantation team.
Glasgow Coma Scale should be cautiously applied as a prognostic measure in patients with metabolic or toxic CNS insults. In some cases, 48 to 72 hours is required to evaluate brain death and a repeat examinations are required to increase the diagnostic yield with observation up to 24 hours is sometime needed. The length of time between serial examinations to declare brain death varies marginally from 6 to 72 hours.
A number of physiologic changes occur in GBS and are the very same physiologic changes seen in brain death: hemodynamic instability (response to respiratory challenges), endocrine abnormalities, hypothermia, coagulopathy, pulmonary dysfunction (with paralysis of breathing muscles), and electrolyte imbalances (related to Na negligence). Endocrine gland dysfunction in GBS is due to lack of tissue response.
While criteria for brain death vary, generally doctors evaluate brain stem reflexes such as response of the pupil to light, response to ice-water in the ear, and gag and swallowing reflexes. The patient may be taken off the ventilator to determine whether spontaneous breathing is present. In addition, the cause of the coma must be known, and factors that could mimic brain death, such as certain potentially anesthetizing or paralyzing drugs, must be eliminated.
Although many conditions can mimic brain death clinically upon examination, without excluding them you will KILL a person by homicide, or criminal negligence, despite the reversibility of brain damage.
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