96 <strong>Australasian</strong> <strong>Anaesthesia</strong> <strong>2011</strong>Care of the potential lung transplant donor – optimisation, prevention of decline <strong>and</strong> future prospects. 97ACTIVE DONOR MANAGEMENT PROGRAMSAggressive donor management programs have been trialled throughout the world. A Texan group trialled a programof aggressive lung donor management in 2006. Lungs that were outside the ideal donor criteria, particularly PaO 2 :FiO 2were targeted. This included fluid <strong>and</strong> ventilator management strategies. The donors were kept in negative fluidbalance once resuscitation had occurred. This required diuretics <strong>and</strong> limitation of crystalloid fluid therapy. Ventilatormanagement included 30 degree head up tilt <strong>and</strong> inflated endotracheal cuff pressures (25cmH 2 O) to reduce aspirationrisk, alveolar recruitment manoeuvres <strong>and</strong> elevated positive end expiratory pressure (PEEP) to improve oxygenation(discussed further below). This retrospective review showed an increase in donated lungs particularly in those withmarginal or poor gas exchange. 11An <strong>Australian</strong> review in 1999 showed a similar increase in transplanted lungs from initially sub optimal donorsby aggressive ventilator management <strong>and</strong> physiotherapy. There was no compromise in recipient survival in eitherpaper by the use of donors that were initially classified as poor <strong>and</strong> then brought into the ideal range throughrelatively simple manoeuvres. 12RECOMMENDATIONSTo maintain donor lungs in optimal condition without compromising other potential donor organs, guidelines havebeen developed. In those donors from whom multiple organs are being procured, the management must considerall organs’ care.Once brain death has been confirmed, therapy should be targeted at preventing any further injury or decline.Some therapies in place prior to brain death may be deleterious to the donor. Active cooling should be reversedwith warmed fluids when they are needed, forced air warmers <strong>and</strong> removal of any cooling devices. Similarly, otherneuroprotective strategies such as hypertension, haemodilution <strong>and</strong> hypervolaemia should be ceased with reversalto normal physiological goals aimed at optimising perfusion <strong>and</strong> oxygen delivery to donor organs.The goals of support once brain death has been confirmed <strong>and</strong> consent for donation has been given shouldinclude the following: normovolaemia, normothermia, maintenance of perfusion pressure to target organs, maintenanceof organ function <strong>and</strong> prevention of deterioration. Ideally this should be achieved with the use of minimal inotropicsupport.Correction of coagulopathy could be considered if severe, however attempts should be mindful of the effectsof causing hypervolaemia <strong>and</strong> other adverse consequences of transfusion (e.g. transfusion related lung injury <strong>and</strong>hypothermia).VENTILATOR MANAGEMENTVentilator management hasn’t been the subject of r<strong>and</strong>omised trials, <strong>and</strong> is based on extrapolation of data fromother areas of intensive care medicine. Some aggressive procurement studies have introduced practices aimed atreducing aspiration risk. This included very high endotrachael cuff pressures, 25cmH 2 O, as tracheal mucosal necrosisis of low importance. Donation of the lung block is taken through upper tracheal resection to allow transport ofinflated lungs. Donor anastamosis is done at the bronchial level to reduce stricture formation <strong>and</strong> for improvedanastamotic healing.Those donors hyperventilated as part of intracranial hypertension treatment should have this stopped once braindeath is confirmed in an effort to reduce VALI. Ventilation to normocarbia is acceptable. High minute ventilationprotocols for induced hypocapnea may involve increased shear <strong>and</strong> rapid stretch of the lung parenchyma. Largetidal volumes (>10ml/kg) aren’t necessary <strong>and</strong> will contribute to lung injury. Cyclical opening <strong>and</strong> closing of airwaysin atelectatic lung zones, particularly when continually nursed supine, is also associated with lung injury. This mayalso benefit tissue oxygen delivery if alkalosis has developed correcting the left shift of the oxy-haemoglobin curve.Prevention of atelectasis is ideal in all ventilated patients <strong>and</strong> certain strategies may contribute to reducing this.The concepts of optimal PEEP, lung protective ventilation <strong>and</strong> physiotherapy of the brain dead donor are importantin preserving <strong>and</strong> improving lung function. In 2000, the ARDSnet group published a l<strong>and</strong>mark study that wasterminated early due to significant improvements in survival in those lung injury patients treated with protectiveventilation. A tidal volume of 6ml/kg versus 12ml/kg with lower plateau pressures (30 vs 50 cmH2O) showed areduced ventilation time <strong>and</strong> higher survival in patients with ARDS. 13 This practice has carried through into manyareas of anaesthesia <strong>and</strong> intensive care in an attempt to optimise patient lung function <strong>and</strong> reduce VALI. Furtherto this, regular recruitment manoeuvres to lessen alveolar collapse <strong>and</strong> reduce shunting are employed. A recruitmentprotocol developed by the San Antonio group in Texas had a significant effect on lung retrieval rates. Their strategyin poor gas exchange donors involved pressure control ventilation with peak inspiratory pressures of 25cmH2O<strong>and</strong> 15cmH2O PEEP for 2 hours. After recruitment manoeuvres, higher PEEP is necessary for several hours toprevent the cyclical collapse/open injury mechanism. Once PaO2:FiO2 had improved, PEEP was reduced to5cmH2O.The Texan group achieved a 21% increase in lung donation by use of this protocol in donors initially classifiedas poor based on PaO2:FiO2 or radiological infiltrates. 11 Whilst this recruitment protocol isn’t currently recommended,it does demonstrate that active ventilator management can significantly improve the PaO2:FiO2.The avoidance of 100% oxygen after blood gas sampling to maintain PaO2 at or above 80mmHg is recommendedto reduce potential oxygen toxicity <strong>and</strong> adsorption atelectasis.Physiotherapy is also vital to maintaining donor lungs. Two to three hourly percussive physiotherapy, closedcircuit suctioning, 30 degree head up positioning <strong>and</strong> hourly turns are strongly recommended. Without physiotherapy<strong>and</strong> postural drainage, further collapse <strong>and</strong> consolidation are likely with increasing shunt <strong>and</strong> worsening gasexchange. Frequent bronchial toilet with suctioning of secretions after physiotherapy is required.Retrieved secretions should be sent for early microscopy culture <strong>and</strong> staining. Though bacterial infection israrely spread to the recipient, this does allow tailoring of antibiotic therapy if required. Consideration should begiven to broad spectrum antibiotic treatment. Discussion with transplant physicians or donor coordinators isencouraged if doubt exists over management.HAEMODYNAMIC MANAGEMENTAims should be to normalise organ perfusion <strong>and</strong> oxygen delivery. Any form of low output or hypotension shouldbe aggressively managed. Mean arterial blood pressure aim is 60-80mmHg. This can be achieved through preload,afterload, rate, rhythm <strong>and</strong> contractility manipulation.Monitoring should include invasive arterial blood pressure <strong>and</strong> central venous pressure (CVP). Sterility is ascritical in the donor as in the living patient. Recipients will be immunosuppressed; all invasive procedures must betreated as sterile.PRELOADCVP catheterisation should ideally be in a jugular vein as this will be most accurate. Accuracy is relevant in termsof not fluid overloading donors with resultant increases in lung water. Many papers advocate haemodynamicalgorhythms based on pulmonary capillary wedge pressure (PCWP) monitoring. 14 However it is recognised that thisincreases cost <strong>and</strong> complexity of care, often in units unfamiliar with pulmonary artery catheter use. Misinterpretationof data when unfamiliar with a monitoring modality can lead to incorrect changes in therapy. Also, given the presumednormal pulmonary vascular resistance in donor lungs, the accepted deficiencies in using CVP as a surrogate forPCWP <strong>and</strong> hence left ventricular filling are probably insignificant. Preload can be maintained through fluid bolusestaking into account maintenance of a haemoglobin concentration near 10g/L, serum sodium concentration <strong>and</strong>urine output. A target CVP of 6-8 mmHg is the consensus recommendation of the Crystal City Conference thataimed to maximise all donor organ utilisation.RATE AND RHYTHMArrhythmias should be aggressively treated as per st<strong>and</strong>ard care. Correction of all electrolytes <strong>and</strong> acid baseabnormalities are first line steps. Indirect acting agents such as atropine will be ineffective post brain stem death.Temporary transvenous pacing may be required for severe bradycardia. Amiodarone <strong>and</strong> beta agonist infusionsmay be required.AFTERLOAD AND CONTRACTILITYPost brain stem death, vasoplegia induced low afterload may render the donor severely hypotensive. Attemptsshould be made to distinguish low cardiac output hypotension from vasoplegic hypotension. Pure alpha1 agentuse to maintain perfusion pressure to tissues may accentuate anaerobic acidosis <strong>and</strong> lactate accumulation ifhypotension is due to a low output state rather than vasodilation. It has however been a mainstay of support <strong>and</strong>organ protection. Throughout Australia <strong>and</strong> <strong>New</strong> Zeal<strong>and</strong>, noradrenaline use is common for donor haemodynamicsupport <strong>and</strong> has not been associated with worsened donor kidney <strong>and</strong> liver graft function though this has not beenreviewed for lung donors. High dose catecholamines are to be avoided as their infusion in the donor causes upregulation of beta receptors in the heart which may m<strong>and</strong>ate the use of higher inotrope requirements in the hearttransplant recipient.Dopamine administration to the donor has been shown to improve function in cadaveric kidney grafts <strong>and</strong> alsoto prolong graft survival. It is also thought that the alveolar membrane is receptive to catecholamine induced sodium<strong>and</strong> water reabsorption. 15 Beta2 stimulation in both the donor <strong>and</strong> recipient can accelerate water clearance fromthe alveolus. This can be achieved with dopamine administration or inhaled beta agonist therapy.A retrospective review has however shown an association between worsened early graft function (PaO 2 :FiO 2 )<strong>and</strong> catecholamine administration. 16 However this paper included those donors receiving high dose alpha 1 agonistswhich may have been an indicator of more severe acute lung injury <strong>and</strong> sympathetic storm.The use of triiodothyronine <strong>and</strong> arginine vasopressin should be considered. These may be combined with lowdose dopamine as needed.Should hypertension (MAP >90mmHg) require pharmacological intervention, it is important to use short actingagents as the haemodynamic status of the donor may change rapidly. Sodium Nitroprusside is ideal. Esmolol mayalso be used, however pure beta antagonism in the face of high afterload may cause heart failure so should becombined with a vasodilator.
98 <strong>Australasian</strong> <strong>Anaesthesia</strong> <strong>2011</strong>Care of the potential lung transplant donor – optimisation, prevention of decline <strong>and</strong> future prospects. 99FLUID MANAGEMENTResuscitation should aim to correct sodium levels to less than 155mmol/L. Hypotonic glucose containing fluidreplacement or even sterile water may be necessary if hypernatraemia, hyperglycaemia <strong>and</strong> hypovolaemia areproblematic. Large volumes may result in hypothermia <strong>and</strong> hyperglycaemia which again should be aggressivelycorrected to within their normal ranges. Ideally all organs should be managed together from a haemodynamicperspective though when specific organs have been rejected, therapy may be more focused on the target organs.If the lungs have been rejected more aggressive fluid loading is acceptable. The debate about colloid versuscrystalloid use is far from complete <strong>and</strong> no clear recommendation can be made.Optimal haematocrit for oxygen delivery should be considered, 30% being acceptable. If transfusion is requiredto achieve this, cytomegalovirus negative blood should be requested.Conventional management of the liver <strong>and</strong> kidney donor favours relative hypervolaemia. Pennefather et alhowever, showed that crystalloid fluid loading to a CVP of 8-12cmH2O had a significantly negative impact on thealveolar to arterial (A-a) gradient. 17A recent publication from Spain challenges this approach to the kidney donor. The effect of aggressive fluidrestriction (target CVP
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