JRSM >
Volume 98, Number 7 >
Pp. 313-314
Department of Cardiology, Birmingham Heartlands and Solihull Hospital NHS Trust, Bordesley Green East, Birmingham B9 5SS, UK
Correspondence to: Dr Faizel Osman E-mail: f.osman{at}bham.ac.uk
Meigs' syndrome consists of benign ovarian tumour with ascites and pleural effusion that resolve after resection of the tumour.1 A variant with pericardial effusion has not to our knowledge been reported.
CASE HISTORY
A woman of 58 was admitted after two weeks of increasing breathlessness and pleuritic chest pain. On examination she was tachycardic and tachypnoeic, with raised venous pressure and signs of bilateral pleural effusions. She was in sinus rhythm. Breast and abdominal examinations were unremarkable and she had no lymphadenopathy. On the electrocardiogram there was non-specific T-wave inversion in the inferior leads, and arterial blood gas analysis (on air) pointed to type 1 respiratory failure. Cardiomegaly and bilateral pleural effusions were seen on chest radiography, and an echocardiogram showed pericardial thickening with a 2 cm global pericardial effusion but no evidence of cardiac tamponade. CT of the thorax and abdomen confirmed the pericardial and pleural effusions (Figure 1) and also revealed ascites and a 9 cm right ovarian mass (Figure 2); the chest, abdomen and pelvis were otherwise disease-free. CT pulmonary angiography excluded significant pulmonary embolism, and on cardiac catheterization pulmonary artery and capillary wedge pressures were normal. There was no evidence of a constrictive process. The coronary arteries were normal as was left ventricular function; a pericardial biopsy, obtained by thoracoscopy, showed no histological abnormality.
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COMMENT
The association of pleural effusion with benign pelvic tumours was reported by Salmon in 1934,2 and 3 years later Meigs and Cass followed with their report on seven patients with ovarian fibroma, pleural effusion and ascites.3 In 1954 Meigs, by now chief of gynaecology at the Massachusetts General Hospital, proposed that his syndrome should be confined to benign solid ovarian tumours in association with ascites and pleural effusion and that resolved without recurrence when the tumour was removed.1 This syndrome occurs with only 1-2% of ovarian 'fibromas'; histologically, the tumour may be a fibroma, thecoma, cystadenoma or granulosa cell tumour. Since the original description by Meigs, ascites and hydrothorax have been reported in other gynaecological conditions including fibroids, degenerative ovarian changes, mature cystic teratomas, and ovarian hyperstimulation syndrome; such variants have been termed pseudo-Meigs' syndrome.4 The reason for the fluid accumulations is unknown. Since fibromas are commonly oedematous, Meigs suggested they might be due to leakage from or pressure on the surface lymphatic vessels.1 He showed that the hydrothorax generally results from movement of the ascitic fluid into the pleural space through congenital defects in the diaphragm.1 Newer work indicates the involvement of inflammatory cytokines in the formation of hydrothorax and ascites.5
The development of a pericardial effusion in our patient seems a novel finding. Such effusions do not seem to have been looked for in patients with true Meigs' syndrome. The possibility of an ovarian lesion needs to be explored in any woman with unexplained pericardial effusion.
Acknowledgments
We thank Mr S W Hall, consultant obstetrician and gynaecologist, for his contribution to the management of this patient.
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