Late Unilateral Pulmonary Edema in Single Lung Transplant Recipients

Late Unilateral Pulmonary Edema in Single Lung Transplant Recipients

Late Unilateral Pulmonary Edema in Single Lung Transplant Recipients Olufemi Akindipe, MD,a Sebastian Fernandez-Bussy, MD,a Edward D. Staples, MD,b an...

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Late Unilateral Pulmonary Edema in Single Lung Transplant Recipients Olufemi Akindipe, MD,a Sebastian Fernandez-Bussy, MD,a Edward D. Staples, MD,b and Maher Baz, MDa In this study we describe 3 single lung transplant recipients who developed unilateral pulmonary edema in the setting of cardiac and renal dysfunction. All 3 patients responded to diuresis with clinical and radiographic improvement. Unilateral cardiogenic pulmonary edema should be considered in the differential diagnosis of dyspnea and unilateral radiographic infiltrates in single lung transplant recipients. J Heart Lung Transplant 2008; 27:1055– 8. Copyright © 2008 by the International Society for Heart and Lung Transplantation.

Three patients, 2 of whom had undergone single lung transplantation and 1 a right lung retransplant after initial left lung transplant, developed pulmonary edema in the setting of cardiac dysfunction and renal insufficiency. Radiographically, each patient presented with a distinct unilateral pulmonary edema pattern. Each patient responded promptly to diuretic therapy with resolution of radiographic infiltrates. We highlight the possible presentation of unilateral pulmonary edema in single lung transplant recipients with heart or renal failure and put forward hypotheses to explain this phenomenon. CASE 1 A 53-year-old woman underwent right single lung transplantation for severe lung disease associated with tuberous sclerosis. During pre-transplant evaluation, mild non-obstructive 2-vessel coronary artery disease with a left ventricular ejection fraction of 35% was found. The patient received metoprolol with an improvement in cardiac function and was accepted for lung transplantation. Her right single lung transplant surgery was uneventful. Two years after transplant surgery, the patient presented with a few days history of exertional and paroxysmal nocturnal dyspnea with pedal edema. She had no cough, fever, chest pain, palpitations or syncopal episodes. Physical exam revealed a soft systolic murmur

From the Divisions of aPulmonary and Critical Care Medicine and b Cardiothoracic Surgery, Lung Transplant Program, University of Florida Health Sciences Center, Gainesville, Florida. Submitted January 25, 2008; revised April 15, 2008; accepted May 21, 2008. Reprint requests: Olufemi Akindipe, MD, Division of Pulmonary and Critical Care Medicine, Lung Transplant Program, University of Florida Health Sciences Center, P.O. Box 100395, Gainesville FL 32610-0395. Telephone: 352-265-8940. Fax: 352-265-8970. E-mail: [email protected] Copyright © 2008 by the International Society for Heart and Lung Transplantation. 1053-2498/08/$–see front matter. doi:10.1016/ j.healun.2008.05.026

best heard over the left sternal border and right basal crackles on inspiration. She had moderate pedal edema up to the knees. Chest X-ray showed hazy opacification of the right hemithorax (Figure 1). Serum creatinine was increased from 1.8 mg/dl a few weeks earlier to 3.3 mg/dl. A 2-dimensional (2D) echocardiogram revealed mild left ventricular systolic dysfunction with a left ventricular ejection fraction (LVEF) of 45%. She had mild mitral insufficiency with no wall motion abnormalities. Our clinical impression was volume overload secondary to declining kidney function in a patient with mild left ventricular systolic dysfunction. Tacrolimus was stopped to assist renal function recovery and she was started on intravenous lasix with prompt symptomatic and radiographic improvement (Figure 2). A post-discharge 2D echocardiogram revealed normal left and right ventricular systolic function. The patient is currently alive and well without dialysis 6 years after lung transplantation. CASE 2 A 62-year-old man underwent right single lung transplantation for chronic obstructive pulmonary disease (COPD). He was seen in the clinic 3 years after the transplant with a history of increased cough with clear sputum. On physical examination, he was tachycardic and tachypneic, but afebrile. Blood pressure was 160/90 mm Hg. Heart sounds were normal and lung auscultation revealed reduced air entry with faint expiratory wheezing. No ascites or pedal edema could be seen. There was an increase in serum creatinine from 1.3 mg/dl 3 months previously to 2.1 mg/dl. Chest X-ray showed right basilar consolidation (Figure 3). The patient received 3 doses of intravenous solumedrol empirically at a dose of 1 g/d. Transbronchial biopsy revealed minimal (Grade A1) rejection. He remained dyspneic while walking short distances. A 2D echocardiogram revealed impaired left ventricular systolic function with LVEF of 35% to 40%. There was global hypokinesia with no evidence of a pericardial effusion. There was moderate mitral and mild aortic 1055

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Figure 1. Hazy opacification of the right hemithorax with prominent cardiac silhouette.

The Journal of Heart and Lung Transplantation September 2008

Figure 3. Portable chest X-ray film shows right basilar consolidation.

regurgitation. An adenosine myocardial perfusion study revealed moderate dilation of the left ventricle with a reduction in perfusion to the inferolateral and posterolateral wall segments. Rest images showed no change in distribution of blood flow in keeping with no active ischemia. LVEF was estimated at 34%. Cardiac catheterization revealed diffuse but mild coronary artery disease and the patient was treated medically with a betablocker and angiotensin-converting enzyme inhibitor. Diuresis with lasix led to clinical improvement and resolution of the right radiographic consolidation (Figure 4). Tacrolimus was replaced with sirolimus to preserve kidney function. He remains alive and active with stable lung, kidney and heart function 5 years after lung transplant.

CASE 3 A 63-year-old man was hospitalized for fever and cough with yellow-green sputum production. He had undergone left single lung transplant for COPD in 1996 and a right single lung retransplant 6 years later for bronchiolitis obliterans syndrome (BOS). He had a history of chronic renal failure from calcineurin inhibitor therapy with serum creatinine levels between 3 mg/dl and 3.5 mg/dl. On examination, he had a temperature of 38.3°C, with a respiratory rate of 28 breaths/min, blood pressure 140/80 mm Hg and heart rate 104 beats/min. Heart sounds were normal. Lung examanation revealed reduced air entry over both lung fields. Chest X-ray on admission showed a small right-sided pleural effusion and bilateral bronchial stents. The patient was started on intravenous cefepime with resolution of fever and cough within 48 hours. Bronchoscopic examination

Figure 2. Interval improvement in right lower lobe parenchymal disease. Image obtained 72 hours after image from Figure 1.

Figure 4. Single frontal view of the chest demonstrates improved aeration at the right base. Image obtained 48 hours after image from Figure 3.

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Figure 5. Predominantly right-sided air-space disease with patchy consolidation in the right upper lobe.

revealed patent airway stents in the right main stem and bronchus intermedius with small amounts of mucopurulent secretion in the left lower lobe. On Day 4 of hospitalization, he became acutely dyspneic with worsening hypoxemia, audible wheezing, and crackles on lung examination. Chest X-ray revealed diffuse air-space disease predominantly on the right side with patchy consolidation in the right upper lobe (Figure 5). The patient was transferred to the intensive care unit where he required mechanical ventilation. Clinical suspicion of an acute myocardial infarction was bolstered by electrocardiographic changes consistent with ischemia of the anterolateral cardiac wall and elevated cardiac enzymes. A bedside 2D echocardiogram revealed severe LV systolic dysfunction with LVEF of 25% to 30%. There was widespread akinesis and severe stunning of the entire apex with moderate mitral insufficiency. A diagnosis of unilateral pulmonary edema in the setting of an acute myocardial infarction was made and the patient received aspirin, intravenous metoprolol with lasix and dopamine drips. He was liberated from mechanical ventilation after 48 hours with resolution of radiographic pulmonary edema (Figure 6). Left heart catheterization revealed 2-vessel obstructive coronary artery disease involving the distal left anterior descending (LAD) artery and right coronary artery (RCA). Both lesions were treated with balloon angioplasty and insertion of drug-eluting stents, with good revascularization. Kidney function was stable throughout the remainder of the patient’s hospital course. DISCUSSION We have described 3 patients who developed unilateral pulmonary edema in the setting of cardiac and renal dysfunction. Two of the patients had previously received right single lung transplantation for tuberous

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sclerosis and emphysema, respectively, whereas the third patient had a right single lung retransplant for bronchiolitis obliterans syndrome 6 years after receiving a retained left lung allograft. All 3 patients responded promptly to heart failure management including diuretics with resolution of radiographic infiltrates. To the best of our knowledge, unilateral pulmonary edema due to cardiac or renal dysfunction has not been described previously in single lung transplant recipients. Unilateral pulmonary edema is an uncommon manifestation of heart failure or renal dysfunction, which may be difficult to distinguish from other conditions causing unilateral infiltrates on chest X-ray, such as acute rejection or pneumonia. In the non–lung transplant population, unilateral cardiogenic pulmonary edema is rare but has been described in isolated case reports.1,2 It has been described in patients with cardiac failure with prolonged rest on one side3 and in patients with mitral insufficiency in which the direction of regurgitant blood flow is toward the central right pulmonary veins.4,5 Cases 2 and 3 in our series did have moderate mitral insufficiency and, in Case 2, the mitral regurgitant jet was directed toward the right pulmonary veins. Perfusion imbalance between the lungs is thought to be another source of acute unilateral pulmonary edema with the degree of edema being proportional to the degree of perfusion. Thus, pulmonary edema has been described after pulmonary artery compression from aortic dissection,6 and in pulmonary venous obstruction from mediastinal fibrosis7 and in unilateral pulmonary disease such as Macleod’s syndrome,8 unilateral pulmonary agenesis and acquired pulmonary artery hypoplasia.9 Lung allografts may have an increased propensity to accumulate extravascular water. Studies have shown that, after single lung trans-

Figure 6. Single semi-erect portable view of the chest taken 48 hours after image from Figure 5 shows resolution of predominantly rightsided parenchymal abnormalities.

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plantation, most of the perfusion is shifted toward the transplanted lung.10,11 Although perfusion scans were not performed at presentation in any of our patients, it is likely that increased venous pressure from cardiac dysfunction coupled with fluid overload from renal dysfunction manifested as unilateral edema in the more perfused vascular bed. The role of bronchial lymphatics disrupted at the time of transplant surgery in the development of pulmonary edema is uncertain. Although impaired lymphatic drainage is often given as one explanation for reperfusion injury in the immediate post-transplant period,12 animal studies by Ruggiero et al have suggested that lymphatic drainage after lung transplantation is re-established as early as Week 2 postoperatively.13 In 2 of our patients, alternative diagnoses, such as pneumonia or acute rejection, were excluded by negative transbronchial biopsies and microbial cultures, absence of fever, and a prompt clinical and radiographic response to diuresis. Our third patient (Case 3) was hospitalized with symptoms thought to indicate pneumonia and appeared to improve clinically with resolution of fever before the development of hypoxemic respiratory failure requiring intubation. Elevated cardiac enzymes, electrocardiographic and echocardiographic evidence of cardiac ischemia and a clinical response to pre- and after-load reduction by mechanical ventilation, beta-blockade and diuresis were all consistent with a clinical picture of acute cardiogenic pulmonary edema. In conclusion, we have described 3 single lung transplant recipients who developed unilateral pulmonary edema as a complication of cardiac failure and renal dysfunction. Unilateral pulmonary edema should be considered in the differential diagnosis of single lung transplant recipients with unilateral infiltrates on the allograft.

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