Part I. Concepts and Management of Brain Death

95.1 Part I. Concepts and Management of Brain Death

95.1.1 Introduction

Even though before the Modern Era the death of a person was considered unequivocal when related to corporal signs (rigidity, lividity and the beginning of putrefaction), the development of medical concepts have changed this. In the context of the creation of intensive care units (ICUs) and with the development of cardiopulmonary reanimation techniques, concepts about the death of a person have been modified, and now can be related to organs like the heart or lungs. All this leads to the concept of death related to the only essential organ to life: the brain.

Another problem is how to determine the moment of death in patients with severe brain lesions who have previously experienced variable periods of unconsciousness.

95.1.2 Brain Death Concept

Until the 20^th century, the concept of death was related to cardiorespiratory arrest. However, in 19^th century, with Virchow’s tissue theory, death was considered a process in which different organs and tissues (with a different vital potential) progressively ceased to function. This concept is still strongly accepted and is the origin of the requirement for waiting 24 hours before the burial of the cadaver.

It was in 1968, during the 22^nd World Medical Association Meeting, that a declaration about death was elaborated, actualized in later meetings, establishing the responsibility and competence of physicians in the diagnosis and determination of the moment of death.

There are currently three main concepts of brain death: global death, brainstem death, and neocortical death. However, the first two are the most prevalent.

Brainstem death was developed following the criteria established in 1976 in the Conference of Medical Council and their Faculties of the United Kingdom, developing the definition in the document entitled the United Kingdom Code. It is based on the fact that brain death is established when there are lesions in the brainstem with a loss of function. In this case, it is sufficient to perform a clinical examination to make the diagnosis.

Global brain death, a more widespread concept, considers brain death as the summation of brainstem death and neocortical or telencephalon death, i.e., the complete absence of all encephalon and brainstem functions.

Arousal (capacity of consciousness) with loss of awareness (content of consciousness) is considered neocortical death and so the diagnosis should be based on the clinical demonstration of absence of content of consciousness (awareness).

Brain Death Diagnosis

Brain death diagnosis is based on the principle that a patient suffers an irreversible lesion. Therefore, it is essential to know the mechanism of cerebral damage, without which it would be impossible to establish the irreversibility of the process. Determining the irreversibility of the process before performing a clinical diagnosis is mandatory to eliminate the existence of possible factors which could simulate brain death or have an impact on a clinical examination.

Before a diagnosis of brain death can be established, it is mandatory that a patient presents with:

Absence of systemic arterial hypotension. Systemic arterial hypotension can decrease cerebral blood flow, so blood pressure must be normalized prior to the clinical examination, being coherent with age and medical history.
Absence of hypothermia. Accidental or induced hypothermia leads to a general decrease in brain activity and can even alter brainstem reflexes if the body temperature is <28°C. The situation must be reversed and the patient must be explored with a body temperature >32°C.
Absence of effects of neuro-depressant drugs, muscle relaxants and anticholinergics which can mask brain death signs. Among the most frequently used drugs in the ICU is midazolam (benzodiazepine), with a half-life of 1.8-6.4 hours (average, 3 hours). In patients with renal dysfunction this could be more prolonged and may remain for 24 hours. In patients who received benzodiazepines it could be useful to employ antagonist drugs such as flumazenil (dosage of 0.2 mg per minute, with a maximum dosage of 2 mg). Thiopental is another widely used drug, very soluble in fat tissues and low grade of ionization, which allows it to pass easily through the blood-brain barrier. It has a half-life of 3-8 hours after a single injection, but it can be prolonged for 27 hours when administered by continuous intravenous perfusion. As a general rule, authors propose that clinical examination for brain death diagnosis must be postponed until the half-life has elapsed by four times.

Clinical Diagnosis

This diagnosis shows the absence of brainstem function through the absence of reflexes of a given anatomical region. There must be bilateral findings, following a detailed protocol with the next steps.

Absence of direct and consensual pupillary reflex. This is performed with stimulation of a powerful light source, observing in normal conditions pupillary contraction. The pupils can appear round, oval or disc-shaped, medium size or mydriatic, from 4 to 9 mm, and unresponsive to light. There must always be an absence of a consensual reflex. The afferent pathway starts at the retina, continues via the optical nerve until the geniculate ganglion, connecting bilaterally with the Edinger-Westphal nucleus (mesencephalon). The efferent pathway is the parasympathetic portion of the III cranial nerve until the iris muscle constricts. Some drugs (anticholinergics: tricyclics, atropine and adrenergic drugs) produce paralytic mydriasis. So an atropine test must not be done before exploring the pupillary reflex.

Absence of oculocephalic reflex. Exploration is done keeping the eyelids open with the index fingers and thumbs, holding the head with both hands, and moving the head horizontally from left to right (or vice versa) in rapid succession. If a reflex is present, it is observed by conjugated ocular deviation opposite to the head movement, returning to the initial position with a temporal lag. In brain death, with the reflex absent, the eyes do not move and follow the head movement. Always exclude unstable cervical spine lesions before exploring this reflex because it could produce spinal lesions which could lead to cardiac or hemodynamic instability due to the suddenness of the motion. The afferent pathway starts at the semicircular channels in the middle ear, continuing via the VIII cranial nerve (statoacoustic) until the vestibular nucleus (bulb-pontine level), continuing by the medial longitudinal fasciculus and reticular parapontine formation, interconnecting with the efferent pathway, that is the III and IV cranial nerves.

Absence of corneal reflex. Corneal stimulation is performed using sterile gauze (having previously gently opened the upper eyelids with the fingers), observing a palpable contraction and tearing in a live patient, and an absence of response in brain death. The afferent pathway is the ophthalmic branch (first branch of the trigeminal nerve) which leads to its sensory nucleus and determines a bulb-pontine level of prosecution. The efferent pathway is through the III and VII cranial nerves.

Absence of oculovestibular reflex. This is explored with the head elevated to 30°. A volume of 50 ml saline is injected at 4°C into the ear canal, while maintaining the patient’s eyes open for 1 minute. In normal conditions, nystagmus is observed with slow components towards the irrigated ear and a fast corrector cortical component in the opposite direction. It is advisable to wait at least 5 minutes before exploring the contralateral reflex. Nystagmus is regular and rhythmic, and lasts <2-3 minutes. In brain death there is no ocular movement. The afferent pathway is the semicircular lymph channels, continuing via the VIII cranial nerve until the medial longitudinal fasciculum and reticular pontine formation. The efferent pathways are the III, IV and VI cranial nerves.

Absence of nauseous reflex. The soft palate, uvula and oropharynx are stimulated using a wooden tongue depressor. A nauseous reflex is observed in normal conditions and no response in brain death. The afferent pathway is through the IX cranial nerve, connected to the ambiguous nucleus and determining the afferent by the X cranial nerve.

Absence of cough reflex. This is explored by introducing a probe through a nasotracheal tube or tracheostomy to produce tracheal stimulation; in normal conditions cough production is observed and no response in the case of brain death.

Absence of response to atropine. The atropine test explores the activity of the X cranial nerve and its brainstem reflexes. Physiological response consists of increasing the cardiac rate by 10% of the basal cardiac rate after injection of 0.04 mg/kg of atropine sulphate intravenously. In brain death there is no response. It must be administered through a vein not shared by any amine which could have a positive chronotropic effect.

Absence of oculocardiac reflex. Normal response (Ascher’s sign) consists of decreasing cardiac rate by 10% and decreasing blood pressure by 35% after applying pressure on the eyeballs. There is no response in brain death. The afferent pathway is the V cranial nerve; the prosecution centre is the nucleus of the V cranial nerve at the bulb level. The efferent pathway is through the X cranial nerve.

Absence of spontaneous breathing demonstrated by the apnea test. Generally, this is the last test because it can generate deleterious systemic and intracranial effects. To perform this test it is recommended that the patient be previously hemodynamically stabilized, with adequate preload, with serum ions and an acid-base balance within the normal range. The respiratory centre is stimulated when the arterial pressure of CO₂ is >60 mmHg or 20 mmHg higher than the usual value (normal arterial pressure, 35-45 mmHg); patients with chronic obstructive pulmonary disease (COPD) often present compensated respiratory acidosis with CO₂ >45 mmHg. Arterial pressure of CO₂ increases 2.5-3 minutes per minute in apnea, so the apnea test must be prolonged until the PaCO₂ is >60 mmHg or >20 mmHg higher than the usual value.

Steps to perform this test:

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