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Ann Thorac Surg 1997;64:1459-1461
© 1997 The Society of Thoracic Surgeons

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Case Report

Pulmonary Embolectomy After Single-Lung Transplantation

Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri

Accepted for publication June 18, 1997.

	Abstract

Top Footnotes Abstract Introduction Comment References

 
Single-lung transplantation for pulmonary hypertension results in a significant ventilation/perfusion mismatch with dramatic shift of blood flow, but not ventilation, to the replacement organ. This raises concern that the patient may be precariously dependent on the function of the transplanted lung. We report the successful management of a massive central pulmonary embolus to the transplanted lung in a 43-year-old woman 4 years after single-lung transplantation for primary pulmonary hypertension.

	Introduction

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Single-lung transplantation (SLT) for pulmonary hypertension, in contrast to bilateral pulmonary replacement, establishes a requisite ventilation/perfusion (V/Q) mismatch, which may result in significant cardiopulmonary instability in the early posttransplantation period [1].

Recently, a patient 4 years after right SLT at our institution for primary pulmonary hypertension suffered a massive central pulmonary embolism obstructing almost all flow to her transplant organ. The clinical presentation, evaluation, surgical intervention, and postoperative course are reviewed.

A 43-year-old woman with no evidence of prior pulmonary embolism had undergone uneventful right SLT previously. Her most recent pulmonary function tests indicated a well-functioning graft, and quantitative V/Q scintigraphy demonstrated 90% flow to the transplanted organ without evidence of perfusion defects.

Six days before transfer to our institution, she presented elsewhere with a history of a syncopal episode and acute dyspnea. Physical examination was unrevealing. Chest radiography demonstrated a loculated effusion at the right base. An unmatched defect on the right lung field by V/Q scintigraphy was interpreted to have a high probability of being PE (Fig 1), and echocardiography demonstrated a hypertrophic, dilated right ventricle with severe tricuspid regurgitation and an estimated right ventricular systolic pressure greater than 70 mm Hg. The patient was heparinized and transferred to our institution. Lower extremity noninvasive studies demonstrated no evidence of deep vein thrombosis. At right heart catheterization, her pulmonary artery (PA) pressure was 45/24 mm Hg. Pulmonary angiography (Fig 2) demonstrated a central embolus obstructing flow to the right middle and lower lobes with normal flow to the left lung.

View larger version (143K): [in this window] [in a new window]   Fig 1. . Xenon-133 ventilation and technetium-99m perfusion scans. (1) Preoperative perfusion scan showing no flow to the right middle and lower lobes. (2) Postoperative perfusion scan showing improved perfusion to the right lower and middle lobes. (3 and 4) Preoperative and postoperative ventilation scans showing uniform distribution of ventilation.

View larger version (180K): [in this window] [in a new window]   Fig 2. . Preoperative pulmonary angiogram demonstrating complete obstruction of blood flow to the middle and lower lobes of the transplanted lung.

Postoperatively the patient was kept sedated to maintain low PA pressures. No evidence of reperfusion edema appeared, and the patient was extubated uneventfully 48 hours postoperatively. Her PA pressures remained normal, as did her arterial blood gas determinations. Postoperative V/Q scintigraphy showed the transplanted lung to receive 91% of perfusion with uniform distribution of blood flow. The lower extremity was thought to be the most likely source of the embolism, and a Venotech filter was placed in the inferior vena cava. Upper extremity noninvasive venous studies demonstrated thrombus in the right internal jugular vein. The patient was anticoagulated and discharged home 6 days postoperatively. At 6-week follow-up her pulmonary function test results remained stable and repeat V/Q scan demonstrated normal distribution of blood flow to the transplanted lung.

	Comment

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The incidence of pulmonary thromboembolism after lung transplantation is not well characterized despite its potentially disastrous consequences in this population. In addition to hemodynamic compromise, one might imagine that PA occlusion could result in parenchymal necrosis due to interruption of their bronchial circulation. Kroshus and associates [2] reported 7 cases of PE among 116 recipients of isolated lung or heart-lung transplants (6% incidence), of whom 3 died (43% mortality). Of the 3 patients who received urokinase, 1 died, whereas of 4 patients who received anticoagulation alone, 2 died.

The optimal management strategy for such patients is undefined. The American College of Chest Physician guidelines for management of pulmonary embolus in the general population advocate heparinization in hemodynamically stable patients [3]. Others have argued that optimal long-term results with central emboli are obtained with surgical removal, with an improvement in 5-year survival from 75% to 100% regardless of hemodynamic status at presentation [4]. Clearly lung transplant recipients present a specific case in which concerns for long-term graft function make the case for aggressive intervention stronger.

Although the mortality of surgical embolectomy has been reported by several authors to be as high as 40% [4, 5], multivariate analysis demonstrates preoperative cardiac arrest and associated cardiopulmonary disease as the strongest predictors of operative death [5]. In this regard, our patient's hemodynamic stability, particularly her preserved right ventricular function, suggested that operative risk was not excessive. This reinforced our decision to aggressively intervene in this patient.

This individual's cardiopulmonary stability despite obstruction of almost all blood flow to the transplanted lung is intriguing. Although right ventricular remodeling and regression of hypertrophy have been demonstrated after SLT [1], in this instance her right ventricle was able to acutely accommodate increased pulmonary vascular resistance. This suggests that, despite their early instability after transplantation, patients who have had SLT for primary pulmonary hypertension may be more resilient than had been feared.

We present a case of an acute pulmonary embolus occluding the blood flow to the middle and lower lobes of a transplanted lung. With the loss of the native bronchial circulation in the transplanted lung, we were concerned about the possibility of ischemia and necrosis. In addition, the possibilities of a reperfusion injury raised concerns regarding the postoperative management. It is of interest that we did not observe any of these complications during the perioperative period. We speculate that this may have been due to the presence of a nutritive collateral circulation through chest wall adhesions or redeveloped bronchial arteries.

	Footnotes

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Address reprint requests to Dr Sundt, Division of Cardiothoracic Surgery, Washington University School of Medicine, One Barnes Hospital Plaza, Suite 3108 Queeny Tower, St. Louis, MO 63110.

	References

Top Footnotes Abstract Introduction Comment References

 

1. Davis RD, Trulock EP, Manley J, et al. Differences in early results after single-lung transplantation. Ann Thorac Surg 1994;58:1327–35.[Abstract]
2. Kroshus TJ, Kshettry VR, Hertz MI, Bolman RM III. Deep venous thrombosis and pulmonary embolism after lung transplantation. J Thorac Cardiovasc Surg 1995;110:540–4.[Abstract/Free Full Text]
3. ACCP Consensus Committee on Pulmonary Embolism. Opinions regarding the diagnosis and management of venous thromboembolic disease. Chest 1996;109:233–7.[Free Full Text]
4. Lund O, Nielsen TT, Ronne K, Schifter S. Pulmonary embolism: long term followup after treatment with full dose heparin, streptokinase or embolectomy. Acta Med Scand 1987;221:61–71.[Medline]
5. Meyer G, Tamisier D, Sors H, et al. Pulmonary embolectomy: a 20-year experience at one center. Ann Thorac Surg 1991;51:232–6.[Abstract]

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Seiichi Noda Thoralf M. Sundt, III Sudhir Sundaresan Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Noda, S. Articles by Patterson, G. A. Search for Related Content PubMed PubMed Citation Articles by Noda, S. Articles by Patterson, G. A.