Australasian Anaesthesia 2011 - Australian and New Zealand ...

96 Australasian Anaesthesia 2011Care of the potential lung transplant donor – optimisation, prevention of decline and 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 and ventilator management strategies. The donors were kept in negative fluidbalance once resuscitation had occurred. This required diuretics and limitation of crystalloid fluid therapy. Ventilatormanagement included 30 degree head up tilt and inflated endotracheal cuff pressures (25cmH 2 O) to reduce aspirationrisk, alveolar recruitment manoeuvres and 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 Australian review in 1999 showed a similar increase in transplanted lungs from initially sub optimal donorsby aggressive ventilator management and physiotherapy. There was no compromise in recipient survival in eitherpaper by the use of donors that were initially classified as poor and 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 and removal of any cooling devices. Similarly, otherneuroprotective strategies such as hypertension, haemodilution and hypervolaemia should be ceased with reversalto normal physiological goals aimed at optimising perfusion and oxygen delivery to donor organs.The goals of support once brain death has been confirmed and consent for donation has been given shouldinclude the following: normovolaemia, normothermia, maintenance of perfusion pressure to target organs, maintenanceof organ function and 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 and other adverse consequences of transfusion (e.g. transfusion related lung injury andhypothermia).VENTILATOR MANAGEMENTVentilator management hasn’t been the subject of randomised trials, and 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 and 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 and rapid stretch of the lung parenchyma. Largetidal volumes (>10ml/kg) aren’t necessary and will contribute to lung injury. Cyclical opening and 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 and certain strategies may contribute to reducing this.The concepts of optimal PEEP, lung protective ventilation and physiotherapy of the brain dead donor are importantin preserving and improving lung function. In 2000, the ARDSnet group published a landmark 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 and higher survival in patients with ARDS. 13 This practice has carried through into manyareas of anaesthesia and intensive care in an attempt to optimise patient lung function and reduce VALI. Furtherto this, regular recruitment manoeuvres to lessen alveolar collapse and 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 25cmH2Oand 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 and adsorption atelectasis.Physiotherapy is also vital to maintaining donor lungs. Two to three hourly percussive physiotherapy, closedcircuit suctioning, 30 degree head up positioning and hourly turns are strongly recommended. Without physiotherapyand postural drainage, further collapse and consolidation are likely with increasing shunt and worsening gasexchange. Frequent bronchial toilet with suctioning of secretions after physiotherapy is required.Retrieved secretions should be sent for early microscopy culture and 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 and 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 and contractility manipulation.Monitoring should include invasive arterial blood pressure and 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 and 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 and 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 andurine 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 standard care. Correction of all electrolytes and 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 and 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 and lactate accumulation ifhypotension is due to a low output state rather than vasodilation. It has however been a mainstay of support andorgan protection. Throughout Australia and New Zealand, noradrenaline use is common for donor haemodynamicsupport and has not been associated with worsened donor kidney and 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 mandate 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 and alsoto prolong graft survival. It is also thought that the alveolar membrane is receptive to catecholamine induced sodiumand water reabsorption. 15 Beta2 stimulation in both the donor and 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 )and 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 and sympathetic storm.The use of triiodothyronine and 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.