Interact CardioVasc Thorac Surg 2009;9:350-351. doi:10.1510/icvts.2008.201640
© 2009 European Association of Cardio-Thoracic Surgery
Brief communication - Cardiac general |
The risk of fatal re-expansion pulmonary oedema in poor left ventricular reserve
Manish Chowdhary,
Edward W.K. Peng* and
Pradip K. Sarkar
Department of Cardiothoracic Surgery, Northern General Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield S5 7AU, UK
Received 5 January 2009;
received in revised form 9 April 2009;
accepted 14 April 2009
*Corresponding author. Tel.: +44 (0) 114 2434343; fax: +44 (0) 114 2610350.
E-mail address: edwkpeng{at}gmail.com (E.W.K. Peng).
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Abstract
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Re-expansion pulmonary oedema (REPO) is an uncommon complication which may be encountered following drainage of pneumothorax, pleural effusion or haemopneumothorax. Treatment is usually supportive and some patients may require positive pressure ventilation. We provide a novel description of the mechanism of a fatal REPO in a patient with a small and non-compliant left ventricle (LV). We urge for an extreme caution when performing thoracocentesis in patients with poor LV reserve.
Key Words: Pleural effusion; Pulmonary oedema; Hypertrophic cardiomyopathy; Thoracocentesis
Re-expansion pulmonary oedema (REPO) is a rare form of pulmonary oedema even after a large-volume thoracocentesis [1]. It is more commonly reported following thoracocentesis in spontaneous pneumothorax [2]. A 67-year-old gentleman with a history of hypertrophic cardiomyopathy presented with shortness of breath five weeks following a mechanical mitral valve replacement and septal myectomy. The preoperative echocardiography showed a moderate mitral regurgitation with systolic anterior motion (Fig. 1a), left ventricle outflow tract (LVOT) obstruction (peak systolic gradient 50 mmHg), moderate left ventricle (LV) hypertrophy, an asymmetrical septal hypertrophy (IVSd 2.0 cm, normal range <1.2 cm) with small LV cavity (2.8 cm, normal range 3.7–5.6 cm) (Fig. 1b) – features of which were consistent with hypertrophic obstructive cardiomyopathy. Postoperative transoesophageal echo showed no obstruction at the LVOT, well seated prosthetic mitral valve with minimal para-prosthetic leak.
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Fig. 1. (a) Transoesophageal echocardiography showing systolic anterior motion of the mitral valve with turbulent flow across LV outflow tract. (b) Transoesophageal echocardiography showing septal hypertrophy with a small LV cavity. (c) Initial chest radiograph showed a large left pleural effusion. (d) Chest radiograph obtained after chest tube placement showed evidence of acute pulmonary oedema.
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On re-admission, he was in fast atrial fibrillation and chest radiograph showed a large pleural effusion (Fig. 1c). He was resuscitated and commenced on amiodarone. A chest drain was not initially inserted due to high INR. In view of increasing shortness of breath, an intercostal chest drain was subsequently placed after correction of his INR. An estimate of 2 l of pleural fluid was evacuated instantaneously under tension before a clamp could be placed. He became severely hypoxic with frothy sputum and lost his cardiac output following thoracocentesis. A chest radiograph showed a confluent opacity consistent with REPO (Fig. 1d). He developed recurrent cardiac arrest and died 6 h later despite maximal inotropic support and cardiopulmonary resuscitation.
Although REPO is often linked with large volume thoracocentesis, this complication remains uncommon. In one recent study, 185 patients who required thoracocentesis of >1 l of pleural fluid (mean 1.67, range 1–6.55 l), 0.5% developed clinical REPO and 2.2% had radiographic REPO with no fatal outcome [1]. Increased capillary permeability secondary to a chronically collapsed lung may be associated with development of REPO [3]. A small LV cavity and non-sustained ventricular tachycardia leading to low output failure have been shown to be a mechanism of syncope in hypertrophic cardiomyopathy [4]. In this patient, a rapid fluid re-distribution into the pulmonary extravascular space in the presence of a small, non-compliant LV is postulated to be the mechanism of rapid cardiovascular collapse. A significant fluid shift in the re-expanded lung due to severe pulmonary oedema critically reduced the ventricular filling volume with a poor LV reserve. Furthermore, a hypertrophic LV is dependent on atrial contraction during diastolic LV filling and therefore, tolerated poorly to fast AF.
In clinical practice, drainage of no more than 1.5 l is usually advocated. However, in the study by Feller-Kopman and colleagues, very few patients actually developed clinical REPO following a large volume thoracocentesis, despite not limiting the amount of drainage in the majority (over 70%) of their cohort of patients [1]. Therefore, a resulting fatal outcome will be extremely unusual without a pre-disposing mechanism as seen in our patient. The safe limit of what one can drain at a time requires further evidence. Nevertheless, thoracocentesis for a large pleural effusion, especially in the presence of an adverse risk factor such as poor LV reserve, must be performed with extreme caution.
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References
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- Matsuura Y, Nomimura T, Murakami H, Matsushima T, Kakehashi M, Kajihara H. Clinical analysis of re-expansion pulmonary edema. Chest 1991;100:1562–1566.[CrossRef][Medline]
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- Nienaber CA, Hiller S, Spielmann RP, Geiger M, Kuck KH. Syncope in hypertrophic cardiomyopathy: multivariate analysis of prognostic determinants. J Am Coll Cardiol 1990;15:948–955.[Abstract]
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