Unilateral Pulmonary Edema After Pulmonary Embolism in a Bilateral Lung Transplant Patient

Unilateral Pulmonary Edema After Pulmonary Embolism in a Bilateral Lung Transplant Patient

2086 CASE REPORT ZEGDI ET AL PULMONARY EDEMA AFTER EMBOLISM spill. In view of the two procedures that had been done, the patient was electively vent...

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CASE REPORT ZEGDI ET AL PULMONARY EDEMA AFTER EMBOLISM

spill. In view of the two procedures that had been done, the patient was electively ventilated overnight. Recovery was uncomplicated. At 1 month, the patient and baby were thriving. At 14 months, the mother was entirely well, with a satisfactory result on chest roentgenogram. The resected specimen showed a cavity filled with blood clot and no evidence of fungal infection. Histology revealed necrotizing granulomatous inflammation and caseous necrosis consistent with tuberculosis. No acidfast bacilli were identified.

Comment

FEATURE ARTICLES

The most frequently reported causes of pulmonary hemorrhage in pregnancy are ruptured pulmonary arteriovenous malformations (PAVMs), manifesting as hemothorax or hemoptysis [3, 4], pregnancy being recognized to cause progression and complications of PAVMs [3, 4]. Ference and coworkers [3], reporting 143 patients with PAVM referred with pulmonary hemorrhage, encountered only 1 patient with massive hemoptysis during pregnancy. Management was by emergency cesarean section and embolotherapy [3]. Other rare causes of massive hemoptysis in pregnancy include Takayasu’s arteritis [5]. Hemoptysis due to pulmonary embolus and mitral stenosis are now seldom seen. DePace and colleagues [6] reported “postmortem” cesarean section in late pregnancy after cardiorespiratory arrest due to massive hemoptysis. Both mother and child survived. Further massive hemoptysis was managed by left pneumonectomy, histology not revealing a clear cause [6]. In our province of KwaZulu-Natal, South Africa, said to be the epicenter of the HIV/AIDS pandemic and where tuberculosis is rife, referral of HIV positive patients with significant hemoptysis to our department, the only Public Service Thoracic facility, has become frequent. Nonpregnancy-related infections have been noted to be the most common cause of maternal deaths in South Africa, more than half of these deaths being due to AIDS or tuberculosis, or both [7]. Such deaths are increasing in number. Massive hemoptysis in pregnancy, related to tuberculosis, may well become more common. Following protocol, the patient’s suitability for operation is rapidly determined by history, physical examination, chest roentgenogram, HRCT, blood gas analysis, and a coagulation screen [2]. Sputum is examined for acid-fast bacilli. This patient was eminently suitable for left upper lobectomy as an immediate definitive procedure and would require cesarean section because of the two previous cesarean sections. Bronchoscopy, which may precipitate bleeding, is delayed until surgery, experience having shown that where inflammatory lung disease is localized, that locality is the source of bleeding [2]. Careful screening of the fetus from radiation is mandatory. Where an iodinated compound is used as in BAE, thyroid function can be tested and managed in the newborn. We have found BAE may be definitive in controlling bleeding from a pneumonic tuberculous area, but not so effective in massive hemoptysis with an associated fungal ball, which was initially suspected in this patient. Never© 2007 by The Society of Thoracic Surgeons Published by Elsevier Inc

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theless, the operation having been refused, BAE may well have removed the need for emergency operation in the face of possible ongoing bleeding with all its attendant risks. Its use in controlling massive hemoptysis with pregnancy carried to term has been once reported [8]. Combined cesarean section and lobectomy was here of benefit. With pregnancy at term, it could be assumed a normal infant could be delivered by cesarean, the safest mode of delivery according to local protocol in all women with a history of two cesarean sections. Had massive hemoptysis occurred earlier in pregnancy, it might have been necessary to delay cesarean section until some time after lobectomy.

References 1. Crocco JA, Rooney JJ, Fankushen DS, DiBenedetto RJ, Lyons HA. Massive haemoptysis. Arch Intern Med 1968;121:495– 8. 2. Blyth DF. The management of haemoptysis. S Afr Respir J 1996;2:28 –30. 3. Ference BA, Shannon TM, White RI Jr, Zawin M, Burdge CM. Life-threatening pulmonary hemorrhage with pulmonary arteriovenous malformations and hereditary hemorrhagic telangiectasia. Chest 1994;106:1387–90. 4. Esplin MS, Varner MW. Progression of pulmonary arteriovenous malformation during pregnancy: case report and review of the literature. Ob Gyn Surv 1997;52:248 –53. 5. Rocha MP, Guntupalli KK, Moise KJ Jr, Lockett LD, Khawli F, Rokey R. Massive hemoptysis in Takayasu’s arteritis during pregnancy. Chest 1994;106:1619 –22. 6. DePace NL, Betesh JS, Kotler MN. ‘Postmortem’ cesarean section with recovery of both mother and offspring. JAMA 1982;248:971–3. 7. National Committee for Confidential Enquiries into Maternal Deaths in South Africa. “Saving Mothers Report 1999 –2001.” National Department of Health. 8. Downs TW, Chao CR. Massive hemoptysis in pregnancy treated with bronchial artery embolization. Am J Perinatol 1997;14:51–3.

Unilateral Pulmonary Edema After Pulmonary Embolism in a Bilateral Lung Transplant Patient Rachid Zegdi, MD, PhD, Nicolas Dürrleman, MD, Paul Achouh, MD, Véronique Boussaud, MD, Romain Guillemain, MD, Catherine Amrein, MD, Alain Deloche, MD, and Jean-Noël Fabiani, MD Assistance-Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Department of Cardiovascular Surgery, and René Descartes University, Paris, France

We report a case of unilateral pulmonary edema due to the decompensation of an asymptomatic ipsilateral pulmonary venous stenosis by a contralateral pulmonary Accepted for publication July 5, 2007. Address correspondence to Dr Zegdi, Hôpital Européen Georges Pompidou, Service de Chirurgie Cardiovasculaire, 20, rue Leblanc, Paris, 75908, France; e-mail: [email protected]

0003-4975/07/$32.00 doi:10.1016/j.athoracsur.2007.07.008

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CASE REPORT ZEGDI ET AL PULMONARY EDEMA AFTER EMBOLISM

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embolism. Emergency surgery included pulmonary embolectomy and refashioning of the stenotic pulmonary venous anastomosis. (Ann Thorac Surg 2007;84:2086 – 8) © 2007 by The Society of Thoracic Surgeons

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ccurrence of pulmonary embolism after lung transplantation is underestimated [1]. Only one case of surgical pulmonary embolectomy has been reported in this context so far [2]. We report a case of severe pulmonary embolism with an atypical clinical presentation that required an emergency operation.

Fig 1. Spiral chest computed tomography scan shows right pulmonary venous anastomotic stenosis (arrow) and ipsilateral lung edema.

Fig 2. Spiral chest computed tomography scan reveals occlusion of the left pulmonary artery (the dashed line represents 1.96 cm).

the vena cava and the ascending aorta, and pulmonary embolectomy was first performed. The left pulmonary artery was occluded by a nonadherent thrombus at the level of the arterial pulmonary anastomosis. The thrombus was removed using a special forceps, then a suction device. The proximal right pulmonary artery was free of thrombus. The right pulmonary vein anastomosis was refashioned. After thromboembolectomy, the patient was anticoagulated with intravenous heparin and subsequently with oral anticoagulant. Postoperatively, a pulmonary infarction developed in the left inferior lobe, which required lobectomy for infection 3 weeks later. The patient was afterwards discharged into a rehabilitation facility. At 6 months, she was doing well.

Comment Unilateral pulmonary edema can be caused by contralateral pulmonary embolism, reexpansion edema, acute mitral regurgitation, bronchial stenosis, or pulmonary venous obstruction. After lung transplantation, ischemia– reperfusion injury as well as pulmonary veins stenosis (PVS) can be causes of unilateral pulmonary edema. Severe PVS is a rather rare complication after lung transplantation. It was reported by Griffith and colleagues [3] in 1 of 60 single-lung recipients and in 1 of 74 double-lung recipients. TEE is considered the gold standard for the diagnosis of PVS in lung transplant patients, although its diagnostic value has not been assessed in large series [3]. TEE has the advantage of detecting PVS in the operating room, thus allowing adequate revision without delay and preventing severe lung damage. PVS is considered severe and can lead to graft failure when the anastomotic diameter is less than 2.5 mm [4, 5]; at between 2.5 and 5 mm, the PVS is considered moderate. In a series reported by Cherqui and colleagues [4], 4 patients with moderate PVS had an uneventful course after lung transplantation. Our patient had an infraclinical right PVS, with a 6-mm anastomotic diameter on CT scan. The embolic occlusion

FEATURE ARTICLES

A 15-year-old girl underwent double-lung transplantation for end-stage cystic fibrosis. The procedure was sequentially performed through a bilateral anterolateral thoracotomy with a femorofemoral extracorporeal circulation. Ischemic times were 4 hours for the right lung and 5 hours for the left lung. Mild graft dysfunction was present on postoperative chest roentgenogram, but weaning from ventilation was possible on postoperative day 1. Postoperative thromboembolic prophylaxis consisted of subcutaneous low-molecular-weight heparin. On day 15, the patient required emergency tracheal intubation and mechanical ventilation for acute respiratory failure. Right pulmonary edema was present on the chest roentgenogram. Transesophageal echocardiography (TEE) showed an increased blood flow velocity (aliasing) in the right pulmonary veins suggesting severe stenosis. A spiral chest computed tomography (CT) scan confirmed the right pulmonary vein anastomotic stenosis (Fig 1). Severe bilateral pulmonary emboli were also diagnosed, with occlusion of the proximal left pulmonary artery (Fig 2). The CT scan did not reveal any thrombus in the inferior vena cava. Venous Doppler imaging of the lower limbs did not show any deep venous thrombosis. The patient underwent emergency operation through bilateral thoracotomies associated with a transverse sternotomy. Cardiopulmonary bypass was initiated between

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CASE REPORT LESHNOWER ET AL ANTERIOR MEDIASTINAL PHEOCHROMOCYTOMA

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Fig 3. (A) Severe size mismatch between the large donor and the small recipient’s pulmonary veins. (B) Venous anastomotic stenosis as a consequence of size mismatch. (C) The venous anastomosis was refashioned using an open technique. The left atrial incision was extended superiorly and inferiorly to accommodate the large donor’s pulmonary veins.

FEATURE ARTICLES

of the left pulmonary artery redirected most of the cardiac output to the right lung, rendering this right pulmonary vein functionally critical and causing a rapidly aggravating unilateral lung edema. With this case, we report acute decompensation of asymptomatic PVS by contralateral pulmonary embolism in a lung transplant patient. Although TEE was suggestive of severe PVS (increased blood flow velocity), the acute onset of respiratory failure 2 weeks after an uneventful postoperative course led us to consider the diagnosis of pulmonary embolism. The latter was confirmed by CT scan performed before surgery. An undetected pulmonary embolism would have had serious intraoperative consequences: 1. Trying to refashion the venous anastomosis without cardiopulmonary bypass would have been impossible because of the presence of pulmonary embolism. 2. Weaning from bypass would have been difficult, the sole functioning lung being still severely edematous. 3. The risk of pulmonary infarction after pulmonary embolism is high in lung transplant patients owing to the absence of bronchial circulation. Therefore, a surgically untreated pulmonary embolism would have led to left lung infarction and subsequent left pneumonectomy. PVS after lung transplantation usually reflects a technical error. Typically, venous anastomotic stenosis is observed when the donor’s pulmonary vein cuff has not been trimmed enough. This was not the case in our patient, where the anastomotic stenosis was related to a major size mismatch between the large donor and the small recipient’s pulmonary veins (Fig 3). From a technical standpoint, two surgical strategies are possible to avoid anastomotic stenosis in this setting. The first is performing the anastomosis under cardioplegic heart arrest. No lateral clamping of the left atrium is then necessary, allowing a larger and more appropriate venous anastomosis. The second surgical strategy is more complex and consists of anastomosing the right superior pulmonary vein to the left atrium (under lateral cross-clamping), followed by reimplantation of the inferior pulmonary vein into the superior pulmonary vein. This is possible when the donor’s pulmonary veins are larger than the recipient’s. In conclusion, our patient had a secondary decompensation after lung transplantation. In such a case, even in © 2007 by The Society of Thoracic Surgeons Published by Elsevier Inc

the presence of a well-documented PVS, other decompensating factors that might need specific treatment should be ruled out.

References 1. Burns KE, Iacono AT. The prevalence of clinically unsuspected pulmonary embolism in mechanically ventilated lung transplant recipients. Transplantation 2004;77:692– 8. 2. Noda S, Sundt TM, Lynch JP, Trulock EP, Sundaresan S, Patterson GA. Pulmonary embolectomy after single-lung transplantation. Ann Thorac Surg 1997;64:1459 – 61. 3. Griffith BP, Magee MJ, Gonzales IF, et al. Anastomotic pitfalls in lung transplantation. J Thorac Cardiovasc Surg 1994;107: 743–54. 4. Michel-Cherqui M, Brusset A, Liu N, et al. Intraoperative transesophageal echocardiographic assessment of vascular anastomoses in lung transplantation. A report on 18 cases. Chest 1997;111:1229 –35. 5. Huang YC, Cheng YJ, Lin YH, Wang MJ, Tsai SK. Graft failure caused by pulmonary venous obstruction diagnosed by intraoperative transesophageal echocardiography during lung transplantation. Anesth Analg 2000;91:558 – 60.

Management of an Anterior Mediastinal Pheochromocytoma Causing Tracheomalacia Bradley G. Leshnower, MD, Rohinton J. Morris, MD, and Taine T. V. Pechet, MD Divisions of Cardiac and Thoracic Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Thoracic paragangliomas are rare tumors that arise from extra-adrenal chromaffin cells and have the capacity to secrete catecholamines. Surgical excision is the optimal treatment of these tumors as they are resistant to chemotherapy and radiation therapy. Although these tumors are most commonly found in the abdomen, 10% of paraganagliomas are located in the thorax, usually in the posterior mediastinum. Occasionally these tumors present in the anterior mediastinum, which can pose a significant surgical challenge due to the proximity of the great vessels and airway. In this report we describe the treatment of an anterior mediastinal pheochromocytoma that presented Accepted for publication June 13, 2007. Address correspondence to Dr Pechet, 266 Wright Saunders Bldg, 39th & Market Streets, Philadelphia, PA 19104; e-mail: [email protected] upenn.edu.

0003-4975/07/$32.00 doi:10.1016/j.athoracsur.2007.06.036