INTRODUCTION
Lung transplantation has gained increased success over the past 20 years owing to improved surgical techniques, refinements in donor and recipient selection, and overall improved postoperative care of the recipients. The perioperative management for lung transplantation has expanded to a global focus of various organ systems. In this chapter, we discuss issues regarding mechanical ventilation, hemodynamic monitoring, the prevention and treatment of infectious pathogens, and the institution of immunosuppressive therapy. These matters are balanced with the prevention of various complications; such as those involving the vascular and airway anastomosis, acute cellular and humoral allograft rejection, primary graft failure, and impairment in the function of other end-organs. For the purposes of this chapter, we will primarily focus the discussion on the first 30 days following lung transplantation.
AIRWAY MANAGEMENT/VENTILATORY SUPPORT
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Standard mechanical ventilation techniques are used to maintain adequate gas exchange while minimizing risk of barotrauma and ventilator-induced lung injury. Some centers use pressure control or pressure-regulated volume control modes to decrease airway pressures. At present, there are no trials to determine the optimal mode of ventilation, but data in literature that focuses on patients with adult respiratory distress syndrome (ARDS) are extrapolated for the lung transplant patients
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Tidal volume adjusted to 6 to 8 mL/kg and respiratory rate to 10 to 16 breaths per minute are recommended to decrease the risk of stretch and tidal trauma, and to decrease the risk of ventilator-induced lung injury.
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Administer the least FiO 2 to maintain adequate oxygenation; the goal FiO 2 is 30% to 40% immediately postoperatively.
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Mode of ventilation and airway pressures should also take into account the physiology of the native lung in single lung transplants; i.e., overly aggressive ventilation of a single lung transplant patient may lead to overdistension of the more compliant native lung in patients with emphysema. This overdistension of a single native lung may lead to development of mediastinal shift towards the allograft in addition to hemodynamic derangements resulting from the development of “auto-peep.”
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Migration of the endotracheal tube into one of the airways can result in barotrauma to the ipsilateral lung, which is due to high airway pressures to a single lung, as well as lung collapse of the contralateral lung.
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Postoperatively, airway secretion clearance becomes ineffective owing to incision pain, decreased cough reflex from lung denervation, and reduced mucociliary function. Bronchoscopy before extubation is generally used for airway clearance; once the patient is extubated, postural drainage with chest percussion therapy is performed. Early patient mobility is also very important in this regard.
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Standard weaning parameters and modes of ventilation are used to allow for early extubation, ideally 24 to 48 hours postoperatively.
CARDIOVASCULAR MANAGEMENT
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With the exception of those transplanted for pulmonary arterial hypertension or for parenchymal lung disease with secondary pulmonary hypertension, most patients are on minimal vasopressors, if any, during the immediate postoperative phase. Theses agents are generally weaned off in the first few hours of admission to the intensive care unit (ICU). Optimization of the preload and afterload is vital for spontaneous hemodynamic compensation. The pulmonary artery (PA) catheter waveforms and values are used to achieve optimization.
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Continued need for or escalation of the vasopressor agents should prompt further investigation into possible sepsis, bleeding, or myocardial dysfunction. If a single lung transplant is performed for emphysema, then dynamic hyperinflation of the native lung may be a contributing factor.
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Although anticoagulation is used during cardiopulmonary bypass, patients are still at risk of developing a thromboembolic event. Owing to the loss of the bronchial circulation, there is a greater degree of hypoxemia if pulmonary emboli occur. In two retrospective single-center studies, 8.6% to 29% of patients developed thromboembolic complications, with 20% occuring in the first month of transplantation.
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Arrhythmias are generally supraventricular in origin owing to the location of the anastomosis in the right or left atrium. Atrial flutter and atrial fibrillation are the most common arrhythmias. They are more likely to occur within 6 weeks of the operation. Some centers provide prophylactic beta-blockers, calcium channel blockers, or amiodarone.
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Pulmonary hypertension can complicate the postoperative course. Although little data exist to support its use, inhaled nitric oxide (iNO), 10 to 40 parts per million, is often used to reduce elevated pulmonary artery pressure (PAP) and to minimize the occurrence of primary graft dysfunction. The goal is to maintain a systolic PAP less than 40 mm Hg with iNO. Most patients tolerate discontinuation of iNO within the first 24 hours. Methemoglobinemia and paradoxical pulmonary hypertension are known adverse events of continued iNO use and during weaning, respectively.
COMMON EARLY COMPLICATIONS IN THE POSTOPERATIVE PERIOD
Primary Graft Dysfunction
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Previously referred to as the reimplantation respose, this is a nonalloimmune process with noncardiogenic pulmonary edema characterized by diffuse parenchymal infiltrates associated with various degrees of hypoxemia ( Fig. 38-1 )
Figure 38-1
A, Chest radiograph shortly after surgery. B, Marked progression several hours later (bilateral consolidation and effusions), which is compatible with primary graft dysfunction.
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Overall incidence has been reported between 10.2% and 25%, with a 30-day mortality rate of up to 42%.
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Chronic obstructive pulmonary disease (COPD) 3% to 9%
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Suppurative lung diseases 10% to 35%
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Restrictive lung diseases 10% to 40%
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Primary pulmonary arterial hypertension 33% to 59%
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Risk factors: lower donor PaO 2 /FiO 2 (P/F) ratio, higher donor age, high inotrope requirement in the allograft recipient, pulmonary arterial hypertension as the underlying disease, and cardiopulmonary bypass requirement. The pathophysiology of pulmonary graft dysfunction (PGD) is thought to be related to cold ischemia time of the allograft, reperfusion lung injury, and other factors leading to an acute lung injury characterized by neutrophyllic infiltration of the lung allograft leading to a capillary leak syndrome.
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Monitor for PGD from 0 to 72 hours after surgery. A low P/F ratio at 6 hours found to correlate with mechanical ventilation need, length of ICU admission and 30-day mortality
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Grades (mild to severe)
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Grade 0: No chest x-ray study (CXR) abnormality and P/F ratio greater than 300
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Grade 1: CXR abnormality and P/F of 200 to 300
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Grade 2: CXR abnormality and P/F between 100 and 200
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Grade 3: CXR abnormality and P/F < 100
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Treatment options include supportive care, judicious administration of intravenous fluids balanced with adequate perfusion of end organs, and diuresis. Inhaled nitric oxide improves oxygenation for up to 72 hours, but it has not been shown to positively effect the duration of mechanical ventilation requirement or mortality. In severe cases, extracorporeal membrane oxygenation (ECMO) is used. When clinically indicated, early use shows a survival benefit. Late initiation (greater than 7 days after severe PGD) has a 100% mortality rate associated with it. In cases refractory to ECMO support, retransplantation can also be considered in select cases.
Pleural Space Complications
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Exudative, serosanguinous pleural effusions are very common in the early postoperative course. This is due to interruption of the lungs’ lymphatic drainage. Chest tube drainage catheters should remain in place until the output is less than 100 to 150 mL/day. A persistent pleural effusion with high output should prompt the treating physician to consider a pathologic process such as an acute cellular rejection, primary graft failure, infectious process, bleeding, or injury to the thoracic duct.
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Complicated pleural effusions and empyema are not very common, but when they occur, they are associated with a high rate of morbidity and mortality.
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Chylothorax is rare but should be considered in the differential diagnosis of persistent pleural effusions early in the postoperative period.
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Postoperative hemorrhage is more common in patients requiring cardiopulmonary bypass because anticoagulation is required. A re-exploration of the chest may be required to evaluate for a source of bleeding and to evacuate a potential hemothorax.
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Small intermittent air leaks are common early after surgery. A persistent air leak is reported in approximately 10% of patients. It may be due to a donor-recipient size mismatch, but the possibility for the development of a bronchial anastomotic dehiscence should be evaluated via bronchoscope. Bronchial anastomotic dehiscence is rare, but when it is present, it usually occurs within the first month of transplantation because of impaired wound healing. Earlier studies attributed this to high dose corticosteroid use, but subsequent studies have refuted this. The single most effective way to prevent this complication from developing is to place the bronchial anastomosis as distal as possible, thereby preserving as much of the native bronchus and its bronchial circulation. Sirolimus utilization within the first 3 months is associated with a high risk of developing bronchial anastomotic dehiscence and should be avoided in the early postoperative period.
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In double-lung transplantations, the anterior pleural reflection is taken down and there is communication between both hemithoraces. It is not uncommon that if a particular pathology occurs on one side that output or air leaks may be visualized on the contralateral side.
IMMUNOSUPPRESSANT THERAPY
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Immunosuppressive therapy is initiated just before transplantation to prevent rejection of the allograft. Similar to other solid organ transplantation therapy is aimed as a two-phase process: induction and maintenance.
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Induction therapy
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Induction therapy is used in order to prevent the activation and proliferation of alloreactive T cells. Up to 49% of the transplant centers have induction therapy as part of their protocol, but not all centers use induction as part of their immunosuppressive protocol due to lack of data demonstrating efficacy against development of chronic rejection and improved survival. Alloreactive T cells are activated by the interleukin-2 (IL-2) receptor activation with the presence of the T cell–antigen complex. A number of different agents are available that can be used for induction immunosuppression.
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Induction therapy with thymoglobulin antibodies (monoclonal versus polyclonal) (anti-lymphocyte or anti-thymocyte globulins) is used for induction through a complement-dependent cytotoxic methodology. They inhibit alloreactive T cells but also promote regulatory T cells. These agents reduced the rate of acute rejection in the first year compared to no induction or induction with IL-2 antibodies. Major adverse drug effects include hypotension, systemic inflammatory response syndrome, capillary leak syndromes, and an increased risk of post-transplant lymphoproliferative disorder.
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Mouse-human or rabbit-human IL-2 receptor antibodies (daclizumab or basiliximab) have been found to decrease incidence of acute cellular rejection compared with no induction, without an increased risk of CMV infection or malignancy and therefore have gained some favor among centers that do have induction protocols.
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The anti-CD52 monoclonal antibody alemtuzumab has recently been introduced but has not been compared in head-to-head studies with other agents used for induction in lung transplantation.
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Induction therapy does not alter risk of bronchiolitis obliterans syndrome and has not been shown to improve long-term survival outcomes after lung transplantation.
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Maintenance immunosuppressant therapy
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Maintenance therapy may be administered by nasogastric tube, sublingually, or through intravenous routes.
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A high-dose corticosteroid bolus is administered intraoperatively and can then be continued at 125 mg intravenously every 8 hours in the first 24 hours as part of the induction protocol. Prednisone is then administered orally starting at 0.5 to 1 mg/kg daily and tapered on a weekly basis to a maintenance dose of 0.2 to 0.3 mg/kg daily by 6 months if no induction immunosuppression is used. In cases in which induction immunosuppression is used, prednisone therapy can be initiated at the maintenance dose immediately after surgery.
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Approximately 75% of lung allograft recipients are currently receiving a tacrolimus, prednisone, and mycophenolate mofetil combination as a standard triple-drug immunosuppression regimen. Other immunosuppressive agents used include cyclosporine, azathioprine, sirolimus, and on occasion, methotrexate. Sirolimus, however, is not used in the first 3 months owing to the risk of bronchial anastomotic dehiscence and chest wound complications.
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