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bosis. The examination was otherwise normal. TumourInitial investigations revealed severe hypoxia (Pa 2 43.6 mmHg (5.8 kPa), Pa 2 28.7 mmHg microembolism (3.8 kPa), Fi 2 0.21) and mild elevation of serum alkaline phosphatase. Biochemistry, liver presenting as function tests, cardiac enzymes, and full blood profile were otherwise normal. The chest radio-"primary pulmonary graph was normal. The electrocardiograph showed P pulmonale but no other features of hypertension" right heart strain or hypertrophy. Echocardiography demonstrated moderate right atrial and right ventricular enlargement, with moderate tricuspid regurgitation and an es-M Hibbert, S Braude timated pulmonary artery systolic pressure of 60 mmHg. The left ventricular ejection fraction was normal. A ventilation:perfusion lung scan Abstract revealed a mild global reduction in perfusion Pulmonary tumour microembolism is a with no segmental defects and normal ventrare cause of pulmonary hypertension. A ilation. Pulmonary artery catheterisation concase of rapidly progressive pulmonary firmed severe pulmonary hypertension with a hypertension in a patient with a past pulmonary artery pressure (PAP) of 67/ history of breast carcinoma is presented. 15 mmHg and a pulmonary vascular resistance Despite active consideration and in-(PVR) of 550 dyne s.cm. The patient was vestigation for malignancy as a cause, initially managed with oxygen therapy alone correct diagnosis was only made at with marked symptomatic improvement. necropsy.Further investigations were then undertaken (Thorax 1997;52:1016-1017 to define possible causes of the patient's pulmonary hypertension. Pulmonary angiography Keywords: pulmonary hypertension, tumour microwas normal with no evidence of embolic disemboli.ease. Computed tomographic scans of the chest and abdomen (Siemens Somatom DR2 with Tumour microembolism is a recognised but 8 mm cuts) were also normal with no evidence extremely uncommon cause of pulmonary of metastatic disease. These films were of good hypertension. Even in dyspnoeic patients with quality as the patient was able to breath-hold known metastatic disease, a high index of sus-with supplemental oxygen. Fibreoptic picion is necessary to initiate appropriate in-bronchoscopic examination revealed no vestigations.abnormalities. The patient declined transWe present a case of severe and rapidly pro-oesophageal echocardiography to exclude an gressive pulmonary hypertension in a patient intracardiac shunt. Serological screening for with a past history of mastectomy for breast connective tissue disease was negative. In the carcinoma. Extensive investigations revealed absence of a precipitating cause a provisional no evidence of metastatic disease, nor a cause diagnosis of primary pulmonary hypertension for pulmonary hypertension. The diagnosis was made. An assessment of acute reof adenocarcinomatous microembolism was sponsiveness to vasodilators 1 demonstrated a made only at necropsy. This case demonstrates 10% fall in pulmonary vascular resistance with the extreme difficulty o...

In this series, DAD was the most frequent pathology. The biopsy result was associated with a change in management in a majority of the subjects, most frequently an escalation of prior empiric therapy. Mortality was high.