Lesson 10, Volume 16—Respiratory Failure in Lung Transplantation

By Juan A. Garcia, MD, FCCP; and Stephanie M. Levine, MD, FCCP

Objectives

1. Know the current opinion regarding lung transplantation in mechanically ventilated patients.
2. Be aware of complications in the immediate posttransplantation period.
3. Know the alternatives in treating perioperative complications related to patients with obstructive physiology.
4. Know the incidence, possible causes, presentation, and treatment options for the pulmonary reimplantation response.
5. Know the management of the common causes of respiratory failure following lung transplantation.

Key words

lung transplantation; mechanical ventilation; posttransplant complications; pulmonary reimplantation response; respiratory failure

Abbreviations

CF = cystic fibrosis; CMV = cytomegalovirus; EBV = Epstein-Barr virus; ECMO = extracorporeal membrane oxygenation; FIO₂ = fraction of inspired oxygen; LT = lung transplantation; NO = nitric oxide; OB = obliterative bronchiolitis; PEEP = positive end-expiratory pressure; PGF = primary graft failure; PRR = pulmonary reimplantation response; PTLD = posttransplant lymphoproliferative disorder; PTX = pentoxifylline; SLT = single lung transplantation

Since the 1980s, lung transplantation (LT) has become an accepted therapeutic option for end-stage pulmonary parenchymal or vascular disease. In 2000, > 1,400 LT procedures were performed worldwide as reported to the Registry of the International Society of Heart and Lung Transplantation.¹ Current survival statistics at 1, 3, and 5 years are 77, 58, and 44%, respectively.¹

This chapter will review respiratory failure in the LT population. The first section will discuss patients who receive a lung transplant while receiving invasive mechanical ventilation. The second section will discuss management of respiratory failure in the immediate postoperative transplant period. The article will then conclude with the presentation and management of some of the many potential complications that can develop after LT that may lead to respiratory failure.

Pretransplant Respiratory Failure

The natural history of the underlying lung diseases is an important determinant of survival on the transplant waiting list. Survival on the waiting list is lower for those patients with interstitial lung disease or primary pulmonary hypertension and better for those with emphysema or cystic fibrosis (CF). However, any of these forms of end-stage lung disease can result in respiratory failure.

In 1997, an international group representing multiple international pulmonary, thoracic surgery, and transplant societies was convened to outline, by consensus, guidelines for LT. Table 1 shows the relative and absolute contraindications outlined by this group.² The guidelines suggested that invasive mechanical ventilation should be a strong relative contraindication to transplantation. Traditionally, ventilator dependency has been considered an absolute or relative contraindication to LT because of concerns about bacterial airway colonization leading to a higher risk of posttransplant pneumonia and infection. Additionally, long-term immobility, often associated with mechanical ventilation, may predispose lung transplant recipients to severe deconditioning and a prolonged recovery time following transplantation. However, there have been several studies reporting series of patients who have undergone transplantation while on receiving invasive mechanical ventilation.

Flume et al³ reported on six patients who received transplants while using mechanical ventilation. Five patients with CF used a ventilator for 7 to 19 days (mean, 10.7 days) prior to their procedure. One patient in this series received ventilation for 115 days preoperatively. None of these patients experienced early complications related to bacterial infection, although one patient remained ventilator-dependent for 27 days after the surgery. The remaining five patients remained intubated for 1 to 19 days after surgery (mean, 7.8 days). The authors concluded that, with the exception of the patient who had required many months of ventilation preoperatively, mechanical ventilation prior to LT did not appear to have a negative impact on the outcome of these patients. The authors suggested that only patients receiving ventilation for a short period of time (< 3 weeks) should be considered for LT. The group also suggested that patients with end-stage lung disease who develop respiratory failure should receive mechanical ventilation only if they have accrued enough time on the transplant list to have a reasonable chance of receiving an organ in < 3 weeks and/or if the indication for mechanical ventilation is potentially reversible.

Low et al⁴ described four patients who received lung transplants while ventilator-dependent. Two of these patients had COPD secondary to a₁-antitrypsin deficiency. One patient had usual interstitial pneumonia and one patient had COPD related to tobacco use. In this study, patients had used ventilation for 7 to 12 days with a mean of 9 days and had no other significant organ damage at the time of LT. The authors compared their ventilator transplant group with nonventilated lung transplant recipients. They found the ischemic time for the second lung implantation was longer and recovery to room air was slower in the ventilator-dependent group. The authors state that the mean time in intensive care and in the hospital, as well as the functional status attained, was similar at 6 weeks posttransplantation in both groups.

Massard et al⁵ reported 10 patients with CF who underwent double lung transplants while receiving mechanical ventilation. Nine of the 10 patients were children. Mean time on mechanical ventilation was 7.5 days (range, 3 to 42 days). Only one patient had a multiresistant Pseudomonas cepacia infection, and the others had Pseudomonas aeruginosa in their sputum that was sensitive to at least one antibiotic. The time requiring ventilatory support after the transplant ranged from 1 to 56 days (median, 16 days). The survival rate was 70% at 1 year, but only 35% at 2 years, lower than that of the national registry for that time period.

Most recently, in a two-center study, Baz et al⁶ have described nine patients receiving long-term mechanical ventilation who underwent lung transplantation. The mean duration of mechanical ventilation prior to the transplant was 369 days (range, 13 to 2,160 days). Of the nine patients, four underwent single lung transplantation (SLT) and five bilateral lung transplants, for the following diagnoses: idiopathic pulmonary fibrosis (n = 3), sarcoidosis (n = 2), CF (n = 1), emphysema (n = 1), and bronchiectasis (n = 2). The authors compared the study group with a control population of 65 patients, which consisted of all ventilator-independent patients who underwent LT at the same centers in the calendar year 1997. In the ventilated study group, five of nine patients were colonized with P aeruginosa with drug-sensitive organisms. All the patients in the study group were ambulatory while receiving mechanical ventilation. None of the patients were receiving a fraction of inspired oxygen (FIO₂) of > 60% and the peak inspiratory pressures were < 40 cm H₂O in all of them. The mean number of days required until extubation following LT was significantly longer in the study group, 4l days (median, 16 days) vs a mean of 9 days in the control group. The 1-year survival rates in both groups of patients were comparable, 78% for the mechanically ventilated group and 83% for the control group. Allograft function as defined by FEV₁ at 1 year posttransplantation was comparable in the study and control groups. There was no increased incidence of bronchiolitis obliterans up until 1 year after transplantation in the study group. All study patients were able to perform activities of daily living without assistance and were independent of oxygen at 3 months following transplantation, with the exception of one patient. The authors suggested that transplantation for mechanically ventilated patients should be performed only in very select patients, ie, those who can remain somewhat ambulatory before LT and who have not developed other medical complications.

Sood et al⁷ reported on the outcome of adults with CF requiring ICU admission. The study included 76 patients ranging from 17 to 45 years of age (mean, 27 years). Of this group, 17 of the patients with respiratory failure (40%) went on to receive a lung transplant and 14 were alive 1 year later. Of these 14 patients, one was receiving or had required mask ventilation and 10 received mechanical ventilation via endotracheal intubation for management of the respiratory failure. At the time of transplantation, eight patients were receiving mechanical ventilation (mean, 10.1 days; range, 1 to 17 days) via an endotracheal tube and one via mask ventilation. The 1-year survival for patients who underwent LT while receiving mechanical ventilation was 82%. Four patients received living donor lobar transplants. The authors concluded that ventilatory support should be instituted only when LT is imminent. No data regarding the age and functional status of the patients were provided.

In general, these four articles report on highly selected patients with a predominance of double lung transplants and short ventilatory periods (with the exception of Baz et al⁶). The absence of involvement of other organs and the absence of panresistant bacteria in secretions may be important factors to consider in the selection of mechanically ventilated patients for LT.

Not all transplants performed in ventilator-dependent patients have been so favorable. According to the United Network of Organ Sharing, approximately 3% of lung transplant recipients in the United States have been ventilator-dependent at the time of transplantation.⁸ However, in this group as a whole, there was a reported three-fold increase in 1-year mortality in those patients who were ventilator-dependent at the time of transplantation.⁸

The number of donor organs remains the rate-limiting step for the number of lung transplant procedures performed annually. Currently, the allocation of organs for lung transplantation in the United States is purely by time and therefore the waiting list can be anywhere from 1 to 2 years long. This poses major difficulty in the decision to use mechanical ventilation as a bridge to LT. This has led to the ethical dilemma and debate in the lung transplant community as to whether those patients who have respiratory failure to the degree of requiring mechanical ventilation should receive an organ when donor lungs are in such low supply and high demand.

Noninvasive ventilation has not been considered to be a contraindication to LT and its use has been reported, particularly in patients with emphysema awaiting LT.

Respiratory Failure in the Immediate Postoperative Period

After LT surgery, the recipient spends approximately 24 to 72 h in the ICU. All lung transplant recipients are intubated and receive mechanical ventilation upon arrival in the ICU. Sedation, pain control, and occasional neuromuscular blockade may be required in the first 24 to 48 h. The ventilator is usually used in either the volume-control or pressure-control mode and airway pressures are maintained as low as possible to potentially avoid barotrauma and anastomotic dehiscence. In general, tidal volumes range from 6 to 10 mL/kg. A low level of positive end-expiratory pressure (PEEP) is often used immediately after lung expansion in the operating room and continued following transplantation.

Certain patient populations may require special ventilator management. For example, patients with primary pulmonary hypertension undergoing SLT can develop severe reperfusion pulmonary edema because the vast majority of perfusion goes immediately to the transplanted lung with low pulmonary vascular resistance, resulting in alveolar flooding. Because the majority of ventilation will go to the native lung, a severe gross ventilation-perfusion inequality can develop acutely. These groups of patients may require prolonged sedation and pharmacologic paralysis for up to 2 to 3 days after surgery. Some centers have recommended that patients receiving an SLT for primary pulmonary hypertension be positioned with the transplanted side up to increase blood flow to the native lung, which is not as severely affected by reperfusion injury.

In those patients with obstructive physiology undergoing SLT, problems can develop if tidal volumes and/or PEEP are high, as acutely there may be preferential ventilation to the more compliant native lung. Significant hyperinflation of the native lung can result in compromise of the new transplanted lung. The use of PEEP and other factors leading to overdistention should be minimized in this select patient group. Early extubation should be strived for. Independent lung ventilation with a double-lumen tube to prevent this disparity may also be required. A double-lumen tracheostomy cannula has also been used.^9,10

Other studies have suggested that acute hyperinflation of the native lung after SLT for emphysema is common radiographically, but of little importance clinically.¹¹ Yonan et al¹² reported on two groups of patients with emphysema who underwent lung transplants. Group 1 consisted of 12 patients who developed native lung hyperinflation after LT. They had a high early mortality—five of the 12 patients (42%) died—compared with the group 2 patients who did not develop native lung hyperinflation. However, on review of the study, three of the five deaths can be attributed to other causes. One patient had a poor donor lung and two other patients developed the pulmonary reimplantation response (PRR).¹²

A significant problem in the immediate postoperative period is PRR or primary graft failure (PGF). It is thought that up to 80% of patients will experience some degree of reimplantation injury, and in 15% of these patients, it can be severe.^13,14 PRR can persist for hours to days after transplantation and is characterized by new radiographic alveolar infiltrates, a reduction in pulmonary compliance, and compromised gas exchange, plus the absence of other factors such as infection, elevated wedge pressure, and rejection. Radiographic findings typically include patchy alveolar consolidation and/or dense perihilar and basilar alveolar consolidation with air bronchograms (Fig 1). The mechanism for PRR remains poorly delineated, but postulated contributing factors are thought to be disruption of lymphatics, bronchial vasculature, and/or nerves as well as lung injury occurring during the preservation period or following reperfusion. PRR is thought to be a form of membrane permeability pulmonary edema. Animal studies have suggested that the severity of PRR may be related to ischemic time as a result of production of toxic oxygen free radicals. It may be minimized by avoiding prolonged ischemic times and optimizing organ preservation.¹³

Figure 1. An anteroposterior radiograph of a 59-year-old woman 6 h after a right SLT for COPD. Note the dense alveolar infiltrate in the lung graft consistent with the PRR.

PRR may be difficult to distinguish from other potential perioperative complications such as acute rejection, cardiogenic pulmonary edema, and/or infection. However, the time course of development, immediately or up to 6 h after transplantation, usually suggests PRR.

Management of PRR includes careful hemodynamic monitoring, diuretics, and inotropic agents. Other authors have described the use of inhaled nitric oxide (NO), independent lung ventilation, and/or extracorporeal membrane oxygenation (ECMO) for severe cases.^15-17 The mechanism of the beneficial effects of inhaled NO in the setting of reperfusion injury is thought to be related to the fact that inhaled NO is delivered to ventilated lung segments only, allowing vasodilatation in these areas with improved ventilation-perfusion matching. In addition, NO has little or no systemic toxicity because inhaled NO is not delivered to the bloodstream.¹⁵

Khan et al¹⁸ examined 56 of 99 lung transplant recipients (57%) who experienced some degree of PRR. The authors found no difference among ischemic times, the presence of pretransplant pulmonary hypertension, the type of lung transplant procedure performed, underlying lung disease, age, or sex of the recipients in comparison with the control group without PGF. This study did note that cardiopulmonary bypass was associated with an increased incidence in severity of PRR. Other significant findings were prolonged duration of mechanical ventilation and a longer ICU stay in those patients who developed PRR. Length of hospital stay was similar in the two groups. One- and 3-year survival rates were comparable between those patients with and without PRR.

Christie et al¹⁴ studied 15 of 100 patients with severe PGF, a severe form of PRR. This complication was associated with a prolonged hospital course, prolonged duration of mechanical ventilation, and poor 1- and 2-year survival rates, 40 and 27% vs 69 and 66%, respectively, in those patients who did not have PGF. The authors tried to determine predisposing risk factors for PGF including age, sex, underlying disease, pulmonary artery pressures, the type of transplant, ischemic time, or use of cardiopulmonary bypass, and found no differences in these parameters between the patients with and without PGF. In those patients with PGF, induction lympholytic immunosuppressive therapy was used less frequently than in those patients who did not develop this complication. ECMO and NO were not used.

Date et al¹⁷ reported on 32 of 243 lung transplant recipients (13.2%) who had developed severe allograft dysfunction with a PAO₂/FIO₂ ratio of < 150. Of this group of patients, 17 received transplants before the widespread availability of NO and 15 received transplants with the use of NO for severe allograft dysfunction. The duration of NO use ranged from 15 to 217 h, with an average of 84 h. The group receiving NO had lower mean pulmonary artery pressures in comparison with the control group with an improved ratio of PAOao₂ to FIO₂, both in the first hour and sustained during NO therapy. The duration of mechanical ventilation was 17 ± 5 days in the control group and 12 ± 3 days in the NO group, although this did not reach statistical significance. Mortality was 24% (4/17) for the control group and 7% (1/15) in the NO group. The authors concluded that NO could significantly improve pulmonary artery pressures and gas exchange without systemic side effects. In addition, there was a trend towards a decreased duration of postoperative mechanical ventilation and improved mortality in those patients receiving NO.

Thabut et al¹⁹ compared 23 patients who received preventive NO and pentoxifylline (PTX) after LT with 23 patients who received transplants just before the use of NO and PTX was implemented. NO (10 ppm) was given right before reperfusion and continued for 8 h. PTX (400 mg) was also given right before reperfusion and was infused for 30 min. The following parameters reached statistical significance in favor of the NO-PTX group: less PRR, improved PAO₂/FIO₂ ratio, fewer days on mechanical ventilation, and lower mortality at 2 months.

The rapid recognition and treatment of PRR may improve survival as reported by Fiser et al.²⁰ These authors used the oxygenation index (mean airway pressure x FIO₂/PAO₂) as an early indicator of significant PRR. When the index was > 30, ECMO was initiated. The survival for patients with an index > 30 when ECMO was started within 2 h was 80% (4/5) vs only 15% (2/13) when ECMO was not implemented within 2 h.

Postoperative Complications

Numerous complications can develop following lung transplantation.²¹ Figure 2 is a temporal outline of some of the common posttransplant complications.²² Any of these complications can potentially result in respiratory failure, some more frequently than others.

Figure 2. A temporal outline of the major complications that can develop after LT. Reprinted with permission from Melo and Levine.²²

Airway complications were once a significant cause of morbidity and mortality after early LT attempts, developing in 20 to 50% of recipients. Airway complications can be divided into the early and late postoperative periods. Typically, early airway complications develop in the first 4 to 8 weeks postoperatively, and patients may present with cough, shortness of breath, and/or a change in contour in the flow-volume loop. Anastomotic dehiscence can also develop. Partial or complete dehiscence may be detected by the presence of mediastinal emphysema on chest radiograph or on CT. An infectious tracheobronchitis may develop at the anastomosis site, primarily because there is no direct revascularization of the bronchial vessels after surgery and thus the anastomosis is subject to ischemia. Infections that develop at the anastomosis are most commonly caused by bacterial organisms, such as Staphylococcus or Pseudomonas, or fungal organisms, primarily Candida and Aspergillus, and appropriate microbial agents should be instituted. Eventual anastomotic stenosis and/or bronchomalacia can develop after resolution of the infection. Therapeutic options at that point include balloon dilatation, stent placement, laser treatment, and occasionally surgery.

Acute rejection can develop in up to 50% of patients in the first postoperative month and in as many as 90% of patients in the first postoperative year. The most common time period for the development of acute rejection within 10 to 90 days of LT. Clinically, patients may present with cough, shortness of breath, and/or fever. Occasionally, the patient can be asymptomatic and rejection is suggested only by a reduction in pulmonary function. Physical examination may be unremarkable or may reveal rales or wheezing. The utility of the chest radiograph for aiding diagnosis is variable. In the first postoperative month, there may be radiographic changes such as a perihilar haze or small pleural effusion. Usually, beyond the first month, there are minimal chest radiographic changes. Bronchoscopy with transbronchial biopsy is performed when acute rejection is suspected. The characteristic pathology for acute lung transplant rejection is a lymphocytic vasculitis. On occasion, acute rejection can progress to respiratory failure requiring mechanical ventilation. However, in general, acute rejection is easily treated with augmentation of immunosuppression, usually methylprednisolone.

Obliterative bronchiolitis (OB) is a leading cause of morbidity and mortality beyond the first year posttransplantation. This is the sine qua non of chronic rejection in LT. The incidence of OB ranges from 35 to 50%. OB typically develops 16 to 20 months after transplantation, but can be reported as early as 3 months. The greatest risk factors for OB appear to be uncontrolled and/or persistent acute rejection and possibly cytomegalovirus (CMV) infection. The presentation of OB is nonspecific and may consist of symptoms like those seen with upper respiratory tract infection. Pulmonary function tests show worsening obstructive dysfunction. The chest radiograph is typically unchanged from baseline or may show some hyperinflation. Hyperinflation, air trapping, and bronchiectasis may be confirmed by high-resolution CT scan. Diagnosis can be made with transbronchial biopsy, but as the bronchiolar area is difficult to sample accurately, bronchoscopy is primarily performed to rule out other possible etiologies for worsening pulmonary function. The classic pathologic finding is a constrictive bronchiolitis. Because it is so difficult to consistently obtain adequate transbronchial specimens, the International Society of Heart and Lung Transplantation has established a staging system for bronchiolitis obliterans syndrome based on the change in pulmonary function from the best postoperative baseline.²³ OB is usually of insidious onset and slow progression, so respiratory failure develops late. Treatment for these patients includes augmented immunosuppression that usually has minimal or no response. However, augmented immunosuppression predisposes these patients to recurrent and opportunistic infections, which can then lead to respiratory failure.

The incidence of infection in lung transplant recipients is higher than that reported in other solid organ transplants. There are several postulated reasons why this happens including a diminished cough reflex due to denervation, poor lymphatic drainage, decreased mucociliary clearance, and/or infection harbored by the recipient. On occasion, infection can also be transferred with the donor organ.

Early on in the first several weeks after LT, bacterial pneumonia is a common life-threatening infection, which can progress to respiratory failure and multiorgan system failure. The incidence of bacterial pneumonia may be as high as 35% in the first 2 weeks postoperatively. Typical organisms include Staphylococcus and/or P aeruginosa. Bronchoscopy with transbronchial biopsy may aid in an infectious diagnosis.

Of the viral infections, CMV is the most common to infect the lung transplant recipient. The usual time period is 1 to 6 months after transplantation. The incidence of illness, which includes both infection and disease, may be as high as 50%. Those patients who are CMV-negative and receive a lung from a CMV-positive donor are at the highest risk of CMV infection, with an incidence that may be as high as 85%. The spectrum of presentations of CMV infection is variable, from asymptomatic shedding to an acute pneumonic process requiring mechanical ventilation for respiratory failure. Treatment includes ganciclovir and CMV hyperimmunoglobulin. Since the advent of prophylactic and preemptive anti-CMV treatment, this problem has become easier to manage.

Fungal infections also are more common in the lung transplant recipient than in other solid organ transplant recipients and the incidence may be as high as 10 to 22%. Usually, fungal infections develop in the first several months after transplantation. One of the most feared organisms to affect the lung transplant patient is Aspergillus. Aspergillus may invade blood vessels and present with pulmonary infarcts and/or hemoptysis. The radiographic appearance is variable and can include focal lower lobe infiltrates, a bronchopneumonia-like pattern, single or multiple nodules with or without cavitation, or opacification of the entire lung graft. High-resolution CT may show a typical halo sign thought to be pathognomonic for invasive fungal infections. Treatment includes amphotericin or a liposomal amphotericin agent. Many LT programs now institute prophylaxis with azole agents, usually itraconazole. Of the infectious etiologies, Aspergillus may be the most common to progress to respiratory failure.

Posttransplant lymphoproliferative disorders (PTLDs) are reported more frequently in LT patients than in other solid organ transplant groups. PTLDs are heterogenous groups of lymphoproliferations of variable clonality. The most frequent form of PTLD is a B cell non-Hodgkin’s lymphoma and its development is strongly associated with Epstein-Barr virus (EBV). The incidence of PTLD after LT has been reported to range between 4.6 and 9.4%. EBV-negative recipients of an EBV-positive organ are most likely to develop this complication. Children tend to be at higher risk because they are often EBV-negative. The clinical presentation of PTLD includes development in the first posttransplant year, usually involvement of the allograft, and radiographic findings of solitary or multiple pulmonary nodules. Disseminated disease affecting the CNS, skin, and other extrapulmonary sites has been reported. Treatment for PTLD includes a reduction in immunosuppression, antiviral therapy, radiation and/or chemotherapy as would be appropriate for lymphoma, and adoptive immunotherapies extrapolated from the bone marrow transplant population. PTLD and/or its treatment can lead to respiratory failure in the lung transplant population.

Other post-LT complications that can cause or contribute to respiratory failure include transient or permanent diaphragmatic paralysis and venous thromboembolism. The latter has been reported to have an incidence of 12% in lung transplant recipients.

Noninvasive Ventilation

The role of noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation has recently been examined by Antonelli et al.²⁴ Of 238 patients receiving solid organ transplants, 51 were treated for acute respiratory failure, and the authors randomized treatment for 40 patients. Twenty patients received noninvasive ventilation and 20 received the standard treatment of supplemental oxygen administration. The median time from transplantation to requiring noninvasive ventilation was 18 days; causes of respiratory failure included pneumonia, cardiogenic pulmonary edema, ARDS, atelectasis, and pulmonary embolism. The outcomes examined included endotracheal intubation and mechanical ventilation, new complications, duration of ventilatory support, length of hospital stay, and ICU mortality. Standard exclusion criteria for noninvasive ventilation included hemodynamic instability, decreased levels of consciousness, respiratory failure caused by neurologic disease, two new organ failures, tracheostomy, facial deformity, and recent oral, esophageal, or gastric surgery. Of this group of 40 patients, four lung transplant recipients were included in the noninvasive ventilation group (reason for LT: CF, n = 2; bronchiectasis, n = 1; a₁-antitrypsin deficiency, n = 1) and two in the standard treatment group (CF, n = 2). There were no differences in demographics between the patient groups. In the two groups examined as a whole, 14 patients in the noninvasive-ventilation group (70%) and five patients in the standard group (25%) improved their PAO₂/FIO₂ ratio with statistically significant sustained improvement in 12 patients in the noninvasive-treatment group (60%) and five in the standard-treatment group (25%). Noninvasive ventilation was associated with a significant reduction in the rate of endotracheal intubation (20 vs 70%), the rate of fatal complications (20 vs 50%), length of stay in the ICU by survivors (5.5 vs 9 days), mean number of days in ICU by survivors (5.5 vs 9 days), and ICU mortality (20 vs 50%). Hospital mortality did not differ between the two groups. The authors suggested that noninvasive ventilation be considered in the treatment of acute respiratory failure in recipients of solid organ transplants, including lung.

Conclusion

In conclusion, respiratory failure can develop at any time during the course of LT. In the pretransplant period, patients with end-stage lung disease may require mechanical ventilation for respiratory failure. Although this is still considered a strong relative contraindication to transplantation, a select group of patients who are maintaining some degree of mobility or who have been intubated for short periods of time may be candidates for lung transplantation. In the perioperative period, newer strategies for managing PRR can be used. After transplantation, numerous infectious and noninfectious complications may develop, all of which can lead to respiratory failure. Noninvasive mechanical ventilation may have a role in the management of respiratory failure in the lung transplant population.

References

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