The process for brain death certification includes
Identification of history or physical examination findings that provide a clear etiology of brain dysfunction.
The determination of brain death requires the identification of the proximate cause and irreversibility of coma. Severe head injury, hypertensive intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage, hypoxic-ischemic brain insults and fulminant hepatic failure are potential causes of irreversible loss of brain function.
The evaluation of a potentially irreversible coma should include, as may be appropriate to the particular case; clinical or neuro-imaging evidence of an acute CNS catastrophe that is compatible with the clinical diagnosis of brain death;
Exclusion of any condition that might confound the subsequent examination of cortical or brain stem function. The conditions that may confound clinical diagnosis of brain death are:
Shock/ hypotension
Hypothermia -temperature < 32°C
Drugs known to alter neurologic, neuromuscular function and electroencephalographic testing, like anaesthetic agents, neuroparalytic drugs, methaqualone, barbiturates, benzodiazepines, high dose bretylium, amitryptiline, meprobamate, trichloroethylene, alcohols.
Brain stem encephalitis.
Guillain- Barre' syndrome.
Encephlopathy associated with hepatic failure, uraemia and hyperosmolar coma
Severe hypophosphatemia.
Performance of a complete neurological examination. Components of a complete neurological examination are:
Examination of the patient-absence of spontaneous movement, decerebrate or decorticate posturing, seizures, shivering, response to verbal stimuli, and response to noxious stimuli administered through a cranial nerve path way.
During the examination spinal reflexes may be present.
Absent pupillary reflex to direct and consensual light; pupils need not be equal or dilated. The pupillary reflex may be selectively altered by eye trauma, cataracts, high dose dopamine, glutethamide, scopolamine, atropine, bretilium or monoamine oxidase inhibitors.
Absent corneal, oculocephalic, cough and gag reflexes. The corneal reflex may be altered as a result of facial weakness.
Absent oculovestibular reflex when tested with 20 to 50 ml. Of ice water irrigated into an external auditory canal clear of cerumen, and after elevating the patients head 30'. Labyrinthine injury or disease, anticholinergics, anticonvulsants, tricyclic antidepressants, and some sedatives may alter response.
Failure of the heart rate to increase by more than 5 beats per minute after 1- 2 mg. of atropine intravenously. This indicates absent function of the vagus nerve and nuclei.
Absent respiratory efforts in the presence of hypercarbia.
Generally, the apnoea test is performed after the second examination of brainstem reflexes.
The apnoea test need only be performed once when its results are conclusive. Before performing the apnoea test, the physician must determine that the patient meets the following conditions:
Core temperature ≥ 36.5°C or 97.7°F
Euvolemia. Option: positive fluid balance in the previous 6 hours
Normal PCO2. Option: arterial PCO2 ≥ 40 mm Hg
Normal PO2. Option: pre-oxygenation to arterial PO2 ≥ 200 mm Hg
After determining that the patient meets the above prerequisites, the physician should conduct the apnoea test as follows:
Connect a pulse oximeter and disconnect the ventilator.
Deliver 100% O2, 6 l/min, into the trachea. Option: place a cannula at the level of the carina.
Look closely for any respiratory movements (abdominal or chest excursions that produce adequate tidal volumes).
Measure arterial PO2, PCO2, and pH after approximately 8 minutes and reconnect the ventilator.
If respiratory movements are absent and arterial PCO2 is ≥ 60 mm Hg (option: 20 mm Hg increase in PCO2 over a baseline normal PCO2), the apnoea test result is positive (i.e. it supports the diagnosis of brain death).
If respiratory movements are observed, the apnoea test result is negative (i.e. it does not support the clinical diagnosis of brain death).
Connect the ventilator, if during testing
the systolic blood pressure becomes < 90 mm Hg (or below age appropriate thresholds in children less than 18 years of age)
or the pulse oximeter indicates significant oxygen desaturation,
or cardiac arrhythmias develop;
Immediately draw an arterial blood sample and analyze arterial blood gas.
If PCO2 is ≥ 60 mm Hg or PCO2 increase is ≥ 20 mm Hg over baseline normal PCO2, the apnoea test result is positive (it supports the clinical diagnosis of brain death).
if PCO2 is < 60 mm Hg and PCO2 increase is < 20 mm Hg over baseline normal PCO2, the result is indeterminate and a confirmatory test can be considered.
When appropriate a 10 min. apnoea test can be performed after preoxygenation for 10 minutes with an Fi02 of 1.0 and normalization of patients PaCO2 to 40 mmHG.
Assessment of brainstem reflexes
Pupils- no response to bright light Size: midposition (4 mm) to dilated (9 mm) (absent light reflex - cranial nerve II and III)
Ocular movement- cranial nerve VIII, III and VI
No oculocephalic reflex (testing only when no fracture or instability of the cervical spine or skull base is apparent)
No deviation of the eyes to irrigation in each ear with 50 ml of cold water (tympanic membranes intact; allow 1 minute after injection and at least 5 minutes between testing on each side)
Facial sensation and facial motor response
No corneal reflex (cranial nerve V and VII)
No jaw reflex (cranial nerve IX)
No grimacing to deep pressure on nail bed, supraorbital ridge, or temporo-mandibular joint (afferent V and efferent VII)
Pharyngeal and tracheal reflexes (cranial nerve IX and X)
No response after stimulation of the posterior pharynx
No cough response to tracheobronchial suctioning
Clinical observations compatible with the diagnosis of brain death:
The following manifestations are occasionally seen and should not be misinterpreted as evidence for brainstem function:
spontaneous movements of limbs other than pathologic flexion or extension response
respiratory-like movements (shoulder elevation and adduction, back arching, intercostal expansion without significant tidal volumes)
sweating, flushing, tachycardia
normal blood pressure without pharmacologic support or sudden increases in blood pressure
absence of diabetes insipidus
deep tendon reflexes; superficial abdominal reflexes; triple flexion response
Babinski reflex
