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Brain death

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Code of practice

Brain death and care of organ donors

Brain death and the law

  • There is no statutory definition of death in UK
  • Following the proposal of brain death criteria in 1976 and 1979 courts in England and Northern Ireland have adopted these criteria, as part of the law, for the diagnosis of death

Brain death criteria

  • comatose patient unable to breathe spontaneously
  • cause of coma irreversible and untreatable ie potentially reversible comatose states due to drugs, hypothermia, metabolic disturbance excluded. Note that in the 1998 UK guidelines there is a change in emphasis regarding circulatory, metabolic and endocrine disturbances. The presence of disturbances that are thought to be an effect of brain death rather than the cause of coma do not preclude the diagnosis of brain stem death.
  • Persistence of effect of neuromuscular blocking agents should be excluded by eliciting deep tendon reflexes or with the use of a nerve stimulator.
  • all brainstem reflexes absent:
    - pupillary reflexes: no response to bright light (both direct and consensual responses). Size of pupils is irrelevant although they are usually dilated
    - corneal reflexes. Take care to avoid damage to corneas
    - vestibulo-ocular reflexes ie caloric responses. No eye movement in response to slow injection of 50 ml of ice water into one or preferably both ear canals. Clear access to the tympanic membrane must be confirmed by prior inspection with an auroscope and head should be flexed to 30°
    - response in distribution of facial nerve to painful stimulus to any somatic area. Conversely there should also be no limb response to supraorbital pressure.
    - gag and coughing reflexes to pharyngeal, laryngeal or tracheal suction
    - lack of spontaneous breathing when patient has been taken off ventilator after having been ventilated with 100% oxygen for 10 minutes. Whilst disconnected from the ventilator oxygen is supplied via a tracheal catheter at 6 l/min. Patient left disconnected until Paco2 > 6.65 kPa. If facility for administering 5% CO2 in oxygen exists this should be used. Ventilate the patient with 100% O2 for 10 mins, then with 5% CO2 for 5 mins and then disconnect from ventilator for 10 mins. If marked bradycardia or haemodynamic instability occur the test should be discontinued. Ideally the oxygen saturation should not be allowed to fall below 90%. Threshold for PaCO2 needs to be increased in patients with chronic hypercapnia
  • tests should be performed twice by 2 different doctors who have expertise in this field. Both doctors need not be present on both occasions. Neither should belong to transplant team.
  • first test should not be performed until ³ 4 h of coma associated with absent motor activity, cough and gag. In the case of anoxic brain damage this period should be increased to 12h
  • time interval between tests is a matter for clinical judgement but the time should be adequate for the reassurance of all those directly concerned.
  • if there is doubt about the diagnosis or if the preconditions for brain stem testing cannot be met then objective tests of cerebral perfusion may be necessary. Indications include:
    - no clear cause for coma
    - possible drug or metabolic effect
    - cranial nerves cannot be adequately tested
    - cervical vertebra or cord injury
    - cardiovascular instability precludes apnoea testing
  • Acceptable objective tests include cerebral angiography (must examine both anterior and posterior circulations) and radionuclide cerebral perfusion scan

  • EEG is not necessary: activity may be present in brain death and may be absent in patients who subsequently recover
  • NB spinal reflexes may be present despite brain death
  • contrary to popular belief brain death is not always followed by asystole within 0.5-9 days and cases of persistence of cardiac output for over 3 months have been described

Diagnosis of brain death in children

  • caution in diagnosing brain death in children <5 yrs. Based on the assumption that young brain has greater capacity for recovery

Australasian guidelines

  • neonates: waiting period of 7 days after acute injury should elapse before testing
  • <2 months: 2 examinations and an EEG separated by at least 48h
  • 2-12 months: 2 examinations and an EEG separated by at least 24 h. Second examination and the EEG can be omitted if absent cerebral blood flow is demonstrated by radionuclide angiography
  • >1 year: criteria are the same as for adults

UK guidelines

  • >2 months age criteria should be same as in adults
  • 37 weeks gestation-2 months: rarely possible to diagnose brain death confidently
  • <37 weeks gestation: criteria for brain stem death cannot be applied.

Selection of organ donors

- general contraindications to organ donation:

  • age > 70 yrs
  • malignancy except primary cerebral tumours
  • juvenile onset DM
  • IV drug abuse
  • severe multi-organ dysfunction
  • active TB
  • systemic infection

Specific organ donor criteria

Kidney:

- age 2-70
- absent renal disease and hypertension
- avoid use of diuretics

Pancreas

- age 10-45 yrs
- no DM, pancreatitis or alcohol abuse

Liver

- age 1/12 to 65 yrs
- absent liver disease, gall stones or alcohol abuse
- appropriate size matching
- prolonged resuscitation and hypotension (<70 mmHg) for >30 mins contraindication

Heart

- 1/12-60 yrs
- size matching
- MAP >60 mmHg, CVP/PCWP <12, LVSWI >15 g/m
- inotropes <5 mcg/kg/h

Lungs

- 1/12-55 yrs
- non-smokers
- no lung disease, barotrauma, lung contusions, fractured ribs, lung infiltrates, purulent secretions, pulmonary oedema
- mechanically ventilated <4/7
- normal ABG at low FIO2
- good lung compliance
- size matching critical

Eyes

- absent ocular disease and trauma

Care of organ donors

NB sympathetic and tactful handling of relatives important
- brain death usually results in haemodynamic instability requiring intensive management. Precise causes of this response is not known. May involve endocrine disturbance

Catecholamine release

- adrenaline and noradrenaline levels elevated after brain death and "catecholamine storm" has been described during acute development of brain death
- in animal models this is thought to contribute to severe vasoconstriction of coronary circulation. Therefore seems reasonable to include calcium antagonist in the treatment of any ischaemic changes in donor ECG

Thyroid hormone deficiency

- in some animal models of brain death a rapid significant decrease in thyroid hormone levels occurs.
- no evidence that this is occurs to any significant degree in humans
- however some evidence that thyroid hormone administration to donors improves early myocardial graft function

Adrenocortical function

- relatively well preserved
- routine steroid administration not recommended

Hyperglycaemia

- common
- may be exacerbated by administration of steroids and use of glucose containing solutions
- hyperglycaemia may improve hepatic graft function but may have adverse effects on pancreatic graft function
- seems reasonable to tolerated mild hyperglycaemia because of potentially beneficial effect on liver but severe hyperglycaemia may exacerbate hyperosmolar state, for which organ donors are at high risk, and therefore should be treated
- if pancreas but not liver is to be transplanted then "tighter" control of blood glucose may be preferable

Diabetes insipidus

- neurogenic DI common
- results in pure water loss and, if this is not replaced, in a hyperosmolar state
- vasopressin should not be given until diagnosis is confirmed by combination of hypernatraemia, serum hyperosmolarity and relative urine hypoosmolarity
- note that mannitol, frusemide, angiographic dye and hyperglycaemia, all common in organ donors, can also produce a diuresis

Haemodynamic stabilization

- often difficult to achieve
- has not been shown to be a prerequisite for adequate function of the transplanted organ. However adequate organ perfusion as judged by systolic BP thought to be important
- aim for systolic BP > 90 mmHg and MAP > 60 mmHg
- invasive monitoring with arterial, central venous and urinary catheters
- if adequate fluid loading insufficient to achieve target BP inotrope of choice probably dopamine but do not increase dose to levels associated with vasoconstriction. Adrenaline and dobutamine are suitable alternatives
- fluid loading with colloid probably preferable to crystalloid as latter is associated with oedema of pancreas and liver
- cardiac arrest commonly occurs after brain death and does not necessarily preclude organ donation provided that resuscitation is rapid
- bradycardia does not respond to atropine as vagal activity is absent in brain dead patient. Treatment requires use of directly acting agent eg isoprenaline

Respiratory care

- ensure correct positioning of ETT to avoid damage to future tracheal anastamosis site in lung donors
- aseptic technique for tracheal suctioning important

Temperature

- mild degree of hypothermia may offer some organ protection but temp <32 results in dysrythmias, decreased cardiac contractility, vasoconstriction, decreased glomerular filtration, cold diuresis, thrombocytopenia, coagulopathy, left shift in Hb dissociation curve
- hypothermia should be anticipated and heat loss prevented
- core temperature >35.5 pre-requisite to diagnose brain death in some countries

Kidneys

- donor urine output <100 ml/h in hour preceding nephrectomy associated with increased ATN in recipient

Haemostasis

- bleeding diathesis may be due to release of tissue fibrinolytic and plasminogen activators from areas of ischaemic and necrotic brain
- DIC occurs in 28% of brain dead donors. Aetiological factors include shock +/or sepsis
- traditionally considered a contraindication to transplantation but view is changing

References

Oh TE. Brain death. In: Bersten AD, Soni N, editors. Oh's Intensive Care Manual. 5 ed. Edinburgh: Butterworth-Heinemann; 2004. p. 515-9.

Powner DJ, Bernstein IM. Extended somatic support for pregnant women after brain death. Crit.Care Med 2003;31:1241-9.


© Charles Gomersall July 1999, February 2004


©Charles Gomersall, February, 2015 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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