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Ann Thorac Surg 1995;59:1565-1566
© 1995 The Society of Thoracic Surgeons

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Case Report

Donor-Acquired Fat Embolism Causing Primary Organ Failure After Lung Transplantation

Regional Cardiothoracic Centre, Freeman Hospital, New-castle-upon-Tyne, United Kingdom

Accepted for publication October 20, 1994.

	Abstract

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Technically successful bilateral sequential lung transplantation in a 40-year-old man was complicated by the immediate development of pulmonary edema on reperfusion of the allograft. Death resulted within 12 hours and was caused by the fat embolism syndrome confirmed on premortem open-lung biopsy. The donor had satisfied current selection criteria but had sustained a femoral and multiple rib fractures. This case highlights the potential risks of transplanting lungs from traumatic donors and the deficiencies in current methods of donor assessment.

	Introduction

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Acute graft dysfunction remains a significant cause of mortality after technically successful pulmonary transplantation despite increasing expertise with the procedure [1]. Problems with suboptimal tissue preservation have been reduced greatly and thorough bacteriologic assessment of the donor tracheobronchial tree has reduced the problem of donor-transmitted infection. By necessity a large proportion of organ donors are involved in major trauma, but the use of these pulmonary grafts carries the risk of posttraumatic adult respiratory distress syndrome, which may be of delayed onset. We report on an incident of primary organ failure after bilateral sequential lung transplantation that related to occult presentation of the fat embolism syndrome (FES) in the donor.

A 40-year-old man with a 10-year history of primary pulmonary hypertension was admitted for bilateral sequential lung transplantation.

The donor was a 37-year-old man who had fallen 6 m, sustaining a fatal head injury, bilateral rib fractures, and a fractured right femoral shaft. Chest radiography revealed only minor contusion of the right upper lobe. The donor had been ventilated for 60 hours and the last arterial blood gas analysis before retrieval revealed an oxygen tension of 113 mm Hg and a carbon dioxide tension of 41 mm Hg at an inspired oxygen fraction of 0.40 and a tidal volume of 15 mL/kg. These values had remained stable over the preceeding 8 hours. A Gram stain of donor endotracheal secretions was negative, as was subsequent culture of donor bronchoalveolar lavage. On direct inspection the donor lungs expanded fully and were macroscopically normal. The heart and lungs were removed en bloc using a single pulmonary artery flush of modified Euro-Collins solution at 4°C to preserve the lungs.

The lungs were transplanted sequentially without technical difficulty using cardiopulmonary bypass. Reperfusion began after a total ischemic time of 344 minutes. Bypass was discontinued after 290 minutes with difficulty due to systemic hypotension, despite the use of intraaortic balloon counterpulsation and high-dose inotropic and vasopressor support. Intraoperative transesophageal echocardiography was performed and showed good biventricular function.

On reperfusion of the lungs, profound pulmonary edema developed rapidly. Over the next 10 hours, more than 3 L of high-protein fluid was suctioned from the endotracheal tube and 3.5 L drained from the pleural cavities, indicating extensive damage to the alveolar-capillary membrane. The patient's condition gradually deteriorated despite mechanical ventilation with an inspired oxygen fraction of 1.0 and positive end-expiratory pressure of 20 mm Hg, increasing systemic inotropic and vasopressor support, and direct infusion of epoprostenol prostaglandin (E₁) into the pulmonary artery. He died 11 hours after operation.

An open-lung biopsy was performed after implantation to determine the nature of the primary organ failure. The pulmonary vasculature was found to be laden with fat and bone marrow cells (Fig 1). The cause of death was confirmed at postmortem examination to be FES resulting from the femoral fracture in the donor.

View larger version (134K): [in this window] [in a new window]   Fig 1. . Photomicrograph of recipient premortem lung biopsy specimen. (Hematoxylin and eosin; x50 before 51% reduction.)

	Comment

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Although we have not found the mode of donor death to significantly influence early outcome after pulmonary transplantation [3], the above report highlights the potential pitfalls in current donor selection criteria. The classic FES is characterized by the triad of acute respiratory failure (with hypoxia and diffuse pulmonary infiltrates), cerebral dysfunction, and petechial rash developing within 72 hours of injury [5]. However, these criteria are not helpful when assessing the potential organ donor. Radiographic changes may be caused by pulmonary contusion; cerebral dysfunction is impossible to assess, and due to blood transfusion, the patient may be thrombocytopenic with petechiae. However, bronchoalveolar lavage may be used to predict the development of FES.

In a study of 18 patients with long bone fractures, a mean of 63% of lavage cells contained intracellular fat deposits in patients with confirmed FES compared with less than 2% in patients with no FES [6]. The technique described was simple, inexpensive, produced no false-positive results, and provided a result within 3 hours of bronchoalveolar lavage. However, a larger, prospective study of patients with multiple trauma concluded that bronchoalveolar lavage lacked specificity for FES. Fat droplets were found in alveolar macrophages in association with sepsis, multiorgan failure, and even lipid infusions [7]. Bronchoalveolar lavage may be used to predict the development of posttraumatic adult respiratory distress syndrome in the absence of FES. At 48 hours after injury, the total cell count on bronchoalveolar lavage was almost twice as high in patients with adult respiratory distress syndrome and lung contusion compared with those without [8].

Currently, around 30% to 40% of potential lung donors in the United Kingdom will have suffered major trauma (unpublished data). It is therefore impractical to decline all lungs from patients with long-bone fractures. In view of the deficiencies in current assessment, more detailed analysis of donor bronchoalveolar lavage fluid obtained before donation would be desirable, but it is not yet applicable to lung transplantation.

	Footnotes

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Address reprint requests to Mr Waller, Department of Cardiothoracic Surgery, Walsgrave Hospital, Coventry CV2 2DX, United Kingdom.

	References

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1. Sharples LD, Scott JP, Dennis C, et al. Risk factors for survival following combined heart-lung transplantation. Transplantation 1994;57:218–23.[Medline]
2. Stewart S, Ciulli F, Wells FC, Wallwork J. Pathology of unused donor lungs. Transplant Proc 1993;25:1167–8.[Medline]
3. Waller DA, Thompson AM, Wrightson WN, et al. Does the mode of donor death influence early outcome of pulmonary transplantation? J Heart Lung Transplant (in press).
4. Rosendale BE, Keenan RJ, Duncan SR, et al. Donor cerebral emboli as a cause of acute graft dysfunction in lung transplantation. J Heart Lung Transplant 1992;11:72–6.[Medline]
5. Van-Besouw J-P, Hinds CJ. Fat embolism syndrome. Br J Hosp Med 1989;42:304–11.[Medline]
6. Chastre J, Fagon J-Y, Soler P, et al. Bronchoalveolar lavage for rapid diagnosis of the fat embolism syndrome in trauma patients. Ann Intern Med 1990;113:583–8.[Abstract/Free Full Text]
7. Vedrinne JM, Guillaume C, Gagnieu MC, Gratadour P, Pleuret C, Motin J. Bronchoalveolar lavage in trauma patients for diagnosis of fat embolism syndrome. Chest 1992;102:1323–7.[Abstract/Free Full Text]
8. Pison U, Brand M, Joka T, Obertacke U, Bruch J. Distribution and function of alveolar cells in multiply injured patients with trauma-induced ARDS. Intensive Care Med 1988;14:602–9.[Medline]

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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): David A. Waller John H. Dark Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Waller, D. A. Articles by Dark, J. H. Search for Related Content PubMed PubMed Citation Articles by Waller, D. A. Articles by Dark, J. H.