4 | Physiological support after brain death

Healthcare Professionals
4.1 Principles of physiological support in brain death

This section of the ODNZ ICU Guidelines provides guidance on maintaining stability during the development of brain death until the donor surgery. Brain death is associated with specific physiological changes which should be treated early to avoid instability.

An ODNZ medical specialist is available 24 hours for advice and assistance and can be contacted through the donor coordinator on call. If there is physiological deterioration outside of the recommended parameters in these guidelines, please contact ODNZ without delay. (09 630 0935).


Why support the physiology of visceral organ systems?
  • To enable brain death to be determined.
  • To preserve the option of donation of the maximum number of organs for transplantation.
  • To ensure that any organs that are donated will be in optimal condition when retrieved and will function well in recipients after transplantation.


How is this done?

By doing well what you normally do for other critically ill patients.


What instrumentation is necessary?
  • Endotracheal tube

  • Nasogastric tube

  • Urinary catheter

  • Multi-lumen central venous line (preferably not femoral)

  • Arterial line (preferably not femoral)

  • One large peripheral IV line (16 or 14 gauge) for rapid fluid infusion


What monitoring is necessary?
  • ECG

  • Pulse oximetry

  • Arterial line

  • Core temperature (not axillary)

  • Urine output


What medications are often required?

ODNZ recommends that these be prescribed with specified doses and indications as appropriate.

  • Desmopressin (Minirin®/DDAVP®) to control diabetes insipidus.
  • Noradrenaline infusion to maintain adequate blood pressure.
  • Insulin infusion to prevent glycosuria (blood glucose <12mmol/L).


What regular laboratory testing is required?
  • FBC, urea, creatinine, electrolytes and blood gases should be measured at least 6 hourly and the results reviewed promptly and therapy altered accordingly.
  • A coagulation screen should be measured at least daily.
  • LFTs should be measured more frequently (6 hourly) if liver function is deranged and liver donation is being considered.
4.2 Temperature maintenance in brain death

Hypothermia can develop easily after brain death due to:

  • reduced heat production (loss of brain metabolism and resting muscle tone)
  • heat loss through exposure and via urine
  • inability to conserve heat by vasoconstriction or generate it by shivering
  • administration of cold fluids.

It is much easier to prevent hypothermia than to treat it in the brain dead patient. It is important to prevent hypothermia developing.


Aim for Core temperature of 36 – 38°C


To achieve this:

  • Cover the patient to provide good insulation.
  • Use a warming blanket if the core temperature is below 36°C.
  • Warm the room to at least 20°C.
  • Warm airway gases by humidifier to greater than 37°C.
  • Prevent heat loss from warm polyuria by quickly recognising and controlling diabetes insipidus with IV desmopressin (Minirin®/DDAVP®) or vasopressin.
  • Use a fluid warmer for high-volume IV fluids (>200mL/hr).


    4.3 Respiratory support in brain death

    Lung function is commonly abnormal in brain dead patients who may have had direct lung injury (aspiration or lung contusion), or pulmonary oedema of any aetiology. Further deterioration can develop due to atelectasis, pneumonia or fluid overload.

    The outcome for lung recipients, especially in the early post-transplant period, is dependent on the degree of lung dysfunction in the donor. It is important to ensure that all aspects of lung function of the donor are as good as possible. Lung donation is sometimes possible even when oxygenation is impaired.

    Irrespective of lung donation, oxygenation and ventilation should be kept normal to preserve the function of visceral organs. If lung function is severely impaired, hypoxaemia is likely to develop before hypercarbia during the clinical examination for the determination of brain death.

    See appendix 9.4 on how to safely maintain oxygenation during the apnoea test.

    Aim for:
    • SpO₂ of 92–95%
    • Normocarbia
    • Plateau pressure <30cmH₂0
    • Clear CXR


    To achieve this:

    • Ventilate the patient with at least 5cm of PEEP and the lowest FiO₂ to achieve SpO₂ of 92%-95%
    • Increase PEEP and FiO₂ as needed for oxygenation.
    • PEEP of ≥10cmH₂O may be required in obese patients and those with abdominal distension.
    • Start with tidal volume of 6–8mL/kg ideal body weight and reduce this as necessary to a minimum of 4mL/kg to ensure plateau pressure remains under 30 cmH₂O.
    • Adjust the rate to ensure normocarbia.
    • Continue regular 2-hourly turns and do not leave the patient supine. Turns should be adjusted appropriately if one lung is worse than the other. The worse lung should be placed uppermost for longer periods.
    • Continue sterile suctioning 2-hourly and as required.
    • Continue chest physiotherapy.
    • Avoid fluid overload. Don’t use resuscitation fluid (eg PL-148 or 0.9% saline) as maintenance fluid.
    • Measure blood gases 6-hourly and make ventilatory changes as appropriate.
    • Repeat CXR if any significant deterioration in lung function looking for ETT position, atelectasis, pulmonary oedema etc. and adjust therapy as appropriate.
    • Consider bronchoscopy and/or proning to improve oxygenation.
    • Start or continue antibiotics for chest infections.
      4.4 Circulatory support before brain death

      There is usually a period of sympathetic hyperactivity as brainstem compression occurs during the development of brain death. This includes marked hypertension (eg MAP >130), tachycardia and sometimes tachydysrhythmias.

      This period may be brief (eg 30 minutes) but it can result in cardiac dysfunction, ischaemia and ECG changes.

      Severe or prolonged hypertension and tachycardia can impair cardiac function severely and preclude heart donation. With appropriate therapy cardiac function can recover in some donors.

      For these reasons it is recommended that the effects of sympathetic hyperactivity should be “blunted” by treatment with short-acting beta-blockade.


      Aim for:

      • An arterial pressure to maintain organ perfusion (eg MAP of 65-90 mmHg)
      • Heart rate within normal range
      • Good perfusion (including peripheral perfusion and resolution of acidosis)
      • Urine output 1mL/kg/hr (acceptable range 0.5–2mL/kg/hr)


      To achieve this:

      • If the MAP exceeds 130 for 30 minutes or heart rate exceeds 160 or a tachydysrhythmia develops (most commonly atrial fibrillation or ventricular tachycardia) use a short-acting beta-blocker, eg esmolol in 10–20mg IV bolus doses and repeat every few minutes as necessary.
      • If hypertension or tachycardia persist, consider an esmolol infusion of 0.05–0.2mg/kg/min (equivalent to 150–600mg/hr for a 50kg person). Alternatively, give 0.5–1mg IV boluses of metoprolol.
      • Titrate the beta-blocker until an acceptable MAP, heart rate and rhythm are achieved. Do not attempt to control these parameters into a strictly normal range or to completely beta-block the patient. A few patients may require a GTN infusion to control hypertension.
      • Tachydysrhythmias that do not respond to beta-blockade might require treatment with potassium or magnesium replacement, amiodarone or electrical cardioversion.
      • Stop the beta-blockade as soon as there are signs that the sympathetic activity is abating as hypotension commonly occurs at this time.


        4.5 Circulatory support after brain death

        When brain death develops, and after a period of sympathetic hyperactivity, there is loss of sympathetic outflow, resulting in vasodilatation affecting both the capacitance vessels (great veins) and the arterial system. This produces relative hypovolaemia and some blood volume expansion with resuscitation fluids (eg PL-148 or 0.9% saline) is usually needed at this time. Even after hypovolaemia has been corrected, inotropic support is usually required to maintain adequate MAP (eg >65 mm Hg) but this is often at low dose (<1 mg/hr noradrenaline in an adult).

        Aim for:

        • MAP of 65–90mmHg (in a patient requiring inotropic support to maintain organ perfusion)
        • Good perfusion (including peripheral perfusion and absence or resolution of acidosis)
        • Urine output 1mL/kg/hr (acceptable range 0.5–2mL/kg/hr)
        • Hb >70g/L consider a higher Hb target if haemodynamically unstable or known coronary ischaemia


        To achieve this:

        • Promptly start a noradrenaline infusion to maintain MAP when it drops at the time of brain death.
        • Give a bolus of resuscitation fluids (eg 500–1000mL of PL-148, 0.9% saline, or 1 unit RBC as appropriate) and repeat until hypovolaemia is corrected.
        • Frequently assess the state of peripheral perfusion and monitor urine output hourly.
        • If the need for inotropic support remains high (eg noradrenaline >1 mg/hr in an adult) search for cardiac dysfunction (eg ECG, echo) sepsis or blood loss and treat appropriately. If inotropic requirements remain high, discuss with the ODNZ medical specialist.
        • If oliguria (<0.5mL/kg/hr) is present, use further volume challenges until it is corrected or early signs of hypervolaemia develop, eg worsening pulmonary compliance or decreasing oxygen saturation.
        • Use 1mL/kg/hr (ideal body weight) of maintenance fluid (5% glucose in water) after hypovolaemia has been corrected. Do not use resuscitation fluids as maintenance fluids as their continued use may lead to oedema and dysfunction of organs that might be able to be donated.
        • Use of resuscitation fluids for maintenance will contribute to the development or persistence of hyperosmolality (hypernatraemia), especially if the treatment of diabetes insipidus is delayed. Donor hyperosmolality has been associated with impaired organ function in some liver recipients.


          4.6 Fluids and biochemistry in brain death

          Diabetes insipidus (DI) due to the loss of anti-diuretic hormone (ADH, vasopressin) occurs in ~85% of brain dead patients. Absence of DI does not mean that brain death has not occurred.

          Untreated DI results in dilute polyuria with urine output typically greater than 2-3mL/kg/hr, sometimes >500 mL/hr.

          Hypovolaemia may also develop with untreated DI. It is very important to recognise and treat DI early. There seems to be little harm associated with early use of desmopressin (DDAVP). However, if DI is not recognised and treated promptly, progressive hypernatraemia can develop quickly. Donor hyperosmolality has been associated with impaired organ function in some liver recipients.

          Hypokalaemia can occur in brain death, especially during polyuria, and contribute to the development of dysrhythmias. Hyperglycaemia can also contribute to polyuria by producing an osmotic diuresis. Occasionally red cell transfusion is necessary.

          Aim for:

          • Na+ 135–150 mmol/L
          • K+ 4.0–4.9 mmol/L
          • Blood glucose < 12 mmol/L
          • Urine output 1mL/kg/hr (acceptable range 0.5–2mL/kg/hr)
          • Hb >70 g/L for stable patient consider a higher Hb target if haemodynamically unstable or known coronary ischaemia

          To achieve this:

          • Measure haemoglobin, haematocrit, serum electrolytes, glucose, urea and creatinine 6-hourly. Review these results promptly and make changes in therapy as appropriate.
          • Use 1 mL/kg/hr (ideal body weight) of maintenance fluid (5% glucose in water) after hypovolaemia has been corrected. Do not use resuscitation fluids (eg PL-148 or 0.9% saline) as maintenance fluids.
          • Measure urine output hourly.
          • Promptly treat DI with IV desmopressin (DDAVP®/Minirin®) 4 to 8 micrograms will be needed to keep urine output between 0.5–2 mL/kg/hr. This dose may need to be repeated in 6-12 hours.
          • If Na >150mmol/L give D5W at 1.5mL/kg/hr. If Na >155mmol/L give 2mL/kg/hr and re-check Na in 2 hours.
          • Use IV potassium carefully (eg 5–10 mmol per hour in the maintenance fluid for 3–6 hours at a time) to keep serum potassium between 4.0–4.9 mmol/L. Potassium may be released from the necrotic brain and renal clearance of potassium may be reduced.
          • Start a low dose continuous insulin infusion (1–2 units/hour) if blood glucose exceeds 12 mmol/L. Adjust as necessary to keep blood glucose around 10 mmol/L and avoid hypoglycaemia.
          • If haemoglobin is <70 g/L search for and stop any easily controllable sites of bleeding and ensure that coagulation abnormalities are also corrected with appropriate blood products.
          • Give vitamin K 10mg IV to all patients with an INR >1.5 to treat or exclude vitamin K deficiency.


            4.7 Donor treatment during organ removal after brain death
            Role of the anaesthetist

            During the donor surgery, the brain dead donor’s physiology is managed in the OT by an anaesthetist.

            When the New Zealand cardiothoracic team is retrieving heart and/or lungs, an anaesthetist is provided by that team. For all other donor surgeries, including heart and lung donation by most Australian cardiothoracic teams, an anaesthetist from the donor hospital is required.

            An anaesthetic technician from the donor hospital is required to assist the anaesthetist for all donor surgeries as per ANZCA Professional Standard 08.

            The anaesthetist should ensure that there is adequate monitoring and intravenous access. The donor coordinator will have requested the ICU to crossmatch 4 units of RBC for the donor surgery.

            The anaesthetist should aim to maintain stability in the donor until aortic cross-clamp. This is to ensure the organs being donated for transplantation are in optimal condition when removed and will function well in recipients following transplantation.

            The anaesthetist will be required to administer intravenous heparin 300 IU/kg immediately prior to aortic cross-clamp. The surgeon will tell the anaesthetist when this is to be given.

            Following aortic cross clamp and commencement of the perfusion fluids, mechanical ventilation ceases, and the anaesthetist is no longer required.


            Spinal movements and sympathetic responses

            It is usual to administer both a neuromuscular blocking drug and a volatile agent, sometimes along with an opioid. These treatments are recommended in the ANZICS Statement and by ODNZ.

            These agents prevent spinal reflex motor responses and ablate spinal sympathetic responses (tachycardia and hypertension) that can occur during the donor surgery. Spinal reflexes in the limbs can be distressing for observers and could potentially lead to contamination of the operative field. Excessive sympathetic responses can also result in myocardial injury or excessive bleeding, with subsequent haemodynamic instability and detrimental effects on graft function.

            It is important for ICU and OT staff to understand that the patient is not receiving “an anaesthetic” as such. Anaesthesia is not required in patients who are brain dead.

              4.8 Problem solving
              Hypernatraemia or polyuria

              Hypernatraemia occurs when serum sodium is >150 mmol/L.

              Polyuria occurs when urine output is > 2-3mml/kg/hr.

              To manage hypernatraemia or polyuria:

              1. Control diabetes insipidus with DDAVP (4-8 microgram doses IV q6hr prn), aiming for urine output of 0.5–2 ml/kg/hr.
              2. Stop resuscitation fluids (0.9% saline, plasmalyte-148) if these are being given for any reason except treatment of hypovolaemia.
              3. Give 5% dextrose in water; start with 1.5 mL/kg/hr but if serum sodium is >155 mmol/L give 2 mL/kg/hr. (Add insulin infusion 2 units/hr to start if needed to keep blood glucose under ~12 mmol/L. Potassium replacement might also be required if insulin is used). Alternatively, give sterile IV water at the same rates as above, via central venous line only, which might avoid the need for additional insulin.
              4. Monitor urine output hourly, serum sodium, potassium and glucose initially every 2 hours. Point of care blood gas analysis is adequate. If you are interested to see how much free water deficit is likely to be present, use the following formula:

                Free water deficit (L) = (% total body water, fraction) x (Weight, kg) x ([Current Na/Ideal Na] – 1)

                Ideal Na = 140mmol/L

                where % total body water (TBW) is:

              5. The ODNZ medical specialist is always available for advice by calling the donor coordinator.

              To manage hyoptension:

              1. Ensure normovolaemia.
              2. Aim for a perfusing MAP (>65mmHg) commence noradrenaline.
              3. If noradrenaline requirement is rising rapidly consider starting vasopressin.
              4. Control diabetes insipidus with DDAVP (4-8 micrograms IV prn), aiming for urine output of 0.5–1 mL/kg/hr.
              5. Review a 12-lead ECG and look for treatable abnormalities (eg ischaemia, AF).
              6. If AF is present, check potassium and magnesium and correct. Consider amiodarone and/or electrical cardioversion.
              7. If hypotension persists obtain an echo to guide further therapies.
              8. Is there hypovolaemia likely to be present? Look for signs or sites of bleeding, diarrhoea especially after prolonged CPR, gastric or other fluid loss, including untreated or delayed treatment of diabetes insipidus. A normal or elevated haematocrit after brain death suggests that hypovolaemia is likely to be present.
              9. Transfuse to maintain Hb >70g/L. Higher levels may be required in patients who are haemodynamically unstable or have known coronary artery disease. Control bleeding (correct coagulation abnormality and consider possible haemostatic procedures). Discuss active bleeding with ODNZ medical specialist by calling the donor coordinator.
              10. Clinically assess the haemodynamic response to a rapid volume challenge (10-20 mL/kg of 0.9% saline or similar resuscitation fluid over 10-15 minutes). Repeat smaller challenges (5-10 mL/kg) if favourable effects are seen. Monitor acid-base and lactate initially q2hr.
              11. If noradrenaline dose remains high (eg > 1.5 mg per hour) after volume loading, review the 12-lead ECG and perform bedside echo looking for adequacy of ventricular filling, major valvular or other structural problems, globally impaired ventricular function, or regional wall motion abnormality including takatsubo cardiomyopathy.
              12. Discuss other treatments (eg vasopressin, additional or alternative vasoactive agents) with the ODNZ medical specialist by calling the donor coordinator.



              To manage hyopthermia:

              1. Control diabetes insipidus with DDAVP (4-8 micrograms IV prn), aiming for urine output of 0.5 – 1 mL/kg/hr
              2. Ensure that the ventilator humidifier temperature is set as high as possible.
              3. Increase the room temperature if it is cold (<18˚C); if possible to 24˚C.
              4. Cover the patient well with blankets and expose the patient as little as possible.
              5. Actively warm the patient, preferably with a fluid-filled warming blanket initially set to 39˚C placed both below and on top of the patient. Air-warming (eg Bair Hugger) provides good insulation but is much less effective at transferring heat than warm fluid blankets.
              6. If bolus resuscitation fluids are being given, put them through a blood warmer set to 39˚C.
              7. Temperature must be above 35˚C before the 4 hour observation period can begin and must remain above 35˚C throughout the observation period and the clinical examination for determination of brain death.
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