FRCA Notes

Brainstem Death Testing

This topic last came up as an SAQ in 2016 (69% pass rate) with a focus on the cardiovascular changes associated with brainstem death, the goals for optimisation and how to acheive them.

Resources

  • Death is the irreversible loss of capacity for consciousness combined with the irreversible loss of the ability to breathe
  • Death by neurological criteria occurs after neurological injury secondary to irreversible damage of the brainstem, though the heart is still beating and the body kept alive by a ventilator
  • Organ donation is managed by NHSBT (NHS Blood and Transplant)
  • Death by neurological criteria requires:
    1. Fulfilment of essential pre-conditions
    2. Exclusion of reversible causes of apnoeic coma
    3. Formal demonstration of coma, apnoea and absence of brainstem reflex activity

  • Tests must be:
    • Performed by two qualified doctors who are competent to perform the procedure
      • One consultant
      • One doctor of at least 5 years' full registration with the GMC
      • Undertaken by the two doctors together and completed successfully on two occasions
    • Performed by doctors not on the organ retrieval team

  1. Patient's condition is due to irreversible brain damage of known aetiology
    • If there is doubt about the nature of the primary diagnosis then an extended period of clinical observation and support may be required

  2. Exclusion of potentially reversible causes:
    • Patient is deeply unconscious, apnoeic and mechanically ventilated
    • No evidence the patient's state is due to depressant or neuromuscular blocking drugs
    • Primary hypothermia has been excluded i.e. core temperature >34°C
    • Circulatory, metabolic and endocrine disturbances

  • Clinicians must be sure a patient's condition does not derive partially or wholly from reversible causes such as:
    • Sedative drugs
    • Endocrine, metabolic or thermal abnormalities
    • Cardiovascular instability

Sedative drugs

  • A variety of approaches are possible, although identification of particular contributory drugs may be difficult (e.g. intentional OD) and their pharmacokinetics complicated by renal or liver dysfunction
  • Examples include
    • Observation for a period 4x the elimination half-life of the drug e.g. propofol, fentanyl
    • Administration of specific antidotes e.g. naloxone, flumazenil
    • Plasma concentration analysis to ensure levels sub-therapeutic e.g. thiopentone, phenobarbital
    • Use nerve monitoring to ensure no NMBA effec
    • Confirmation of a lack of cerebral blood flow e.g. cerebral angiography

Endocrine, metabolic or thermal abnormalities

  • Temperature >34'C
    • <34'C impairs consciousness
    • <28'C causes brainstem areflexia

  • Sodium 115 - 160mmol/L
  • Potassium >2mmol/L
  • Magnesium 0.5 - 3mmol/L
  • Phosphate 0.5 - 3mmol/L
  • Glucose 3 - 20mmol/L

  • Profound hypothyroidism or hypoadrenalism

Cardiovascular instability

  • pH 7.35 - 7.45
  • PaO2 >10kPa
  • PaCO2 <6kPa
  • MAP 60mmHg

Ancillary tests

  • Should be used:
    • When a comprehensive neurological examination cannot be carried out e.g. after severe maxillofacial trauma
    • When the influence of residual sedation cannot be excluded
      • E.g. a thiopentone level of 5mg/L is probably safe
      • One study showed thiopentone levels required to inhibit motor response (12mg/L) and pupillary response (50mg/L) were much higher than this
    • In high cervical cord injury, where a distinction between central apnoea and effects of cord injury cannot be distinguished i.e. use EEG

  • Examples include:
    • Neurophysiology (EEG, EMG)
    • Brain tissue perfusion (SPECT, PET)
    • Cerebral artery blood flow (4 vessel angiography, transcranial Doppler)

  • Formal demonstration of loss of reflex brainstem activity and apnoea should only take place once a patient is established to be fulfilling pre-conditions and reversible causes excluded
  • The apnoea test is performed after the brainstem reflex tests
  • Both tests are performed twice; time of death is the completion of the first set of tests

Brainstem reflex tests

Test/reflex Afferent pathway Efferent pathway Test details Response in brainstem death
Pupillary II III Bright light shone in both eyes
Direct and consensual reflexes sought (Midbrain) 		No pupillary constriction
Corneal V VII Cornea brushed lightly with a swab (Pons) No blinking
Pain V VII Pressure on the supra-orbital ridge (Pons), limbs and trunk No motor response
Oculo-vestibular
(caloric)		 VIII III, IV and VI Tympanic membrane visualised with otoscopy before testing
50ml ice cold saline instilled into external auditory meatus over 1 min
Both sides should be tested although still valid if only one side tested (Pons)		 No eye movement
(Eyes move towards ipsilateral side if reflex intact)
Gag IX X Pharynx is stimulated with spatula or similar (Medulla) No gag or pharyngeal contractions
Cough X X Bronchial catheter is passed to the carina (Medulla) No cough

Apnoea test

  • The aim is to induce an acidaemic respiratory stimulus without hypoxia or cardiovascular instability
  • Should only be performed once brainstem reflex testing is completed
  • After the test is completed the ventilator should be reconnected, to normalise acid-base status before the 2nd set of tests

  • FiO2 increased to 1.0
  • ABG performed to calibrate EtCO2 and PaCO2
  • Reduce minute ventilation until EtCO2 >6.0kPa
    • Perform second ABG to confirm PaCO2 is >6.0kPa and pH <7.40
    • In chronic CO2 retention or IV bicarbonate therapy, allow the PaCO2 to rise to above 6.5KPa to a point where the pH is less than 7.40
  • Maintain saturations >95%; apnoeic oxygenation can be maintained by CPAP or 5L/min oxygen via suction catheter down ETT
  • Observe for respiratory activity for 5 minutes
  • Confirm an increase in of PaCO2 >0.5kPa


Respiratory

  • Neurogenic pulmonary oedema (18%) due to acute blood diversion and pulmonary capillary damage

Cardiovascular

  • There may be initial hypertension and tachycardia from a sympathetic storm due to compression of the cardiovascular centres
  • Equally Cushing's reflex may be present

  • Hypotension (81%)
    • From vasoplegia, hypovolaemia and myocardial dysfunction

  • Arrythmias (25%)
    • Initial raised ICP causes catecholamine storm, which can cause myocardial damage
    • Following this there is loss of sympathetic tone

  • The cardio-respiratory response to brain-stem ischaemia is classically triphasic:
    1. The Cushing reflex of hypertension and bradycardia
    2. A transient phase of severe hypertension and tachycardia that is related to a massive out-pouring of catecholamines
    3. An agonal phase of hypotension
      • Profound and refractory vasodilatation (complete loss of sympathetic tone and adrenoceptor desensitisation)
      • Left ventricular impairment (sympathetic storm)
      • Hypovolaemia (neurogenic pulmonary oedema and diabetes insipidus)

Haematological

  • DIC (28%)
    • Release of tissue thromboplastin from necrotic brain tissue
    • Tissue factor release

Metabolic

  • Metabolic acidosis (11%)
  • Diabetes insipidus (65%) due to loss of ADH release from posterior pituitary
  • There may be reduced T3 levels

  • Hypothermia
    • Hypothalamic damage leads to reduced BMR and loss of heat-generating metabolic processes
    • Vasodilation contributed to heat loss

  • Hypernatraemia and hypokalaemia (diabetes insipidus, diuretic therapy)
  • Hyperglycaemia (insulin resistance, methylprednisolone, administration of 5% dextrose)