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Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary arterial hypertension that affects predominantly post-capillary pulmonary vessels. A major concern with PVOD is the poor response to available therapies and the risk of pulmonary oedema with continuous intravenous epoprostenol. The present authors hypothesised that alveolar haemorrhage may be a characteristic feature of pulmonary veno-occlusive disease, as compared with other forms of pulmonary arterial hypertension that predominantly involve pre-capillary pulmonary arteries. This paper reports a series of 19 patients with either PVOD (n = 8) or idiopathic pulmonary arterial hypertension (IPAH; n = 11) who underwent bronchoalveolar lavage. Cytological analyses were performed and differential counts were made on Perls-stained preparations. The Golde score was used to assess alveolar haemorrhage. As compared with IPAH, PVOD was characterised by a higher percentage of haemosiderin-laden macrophages (40+/-37 versus 3+/-6%), resulting in elevated Golde scores (81+/-88 versus 4+/-10). It was concluded that occult alveolar haemorrhage is a common feature of pulmonary veno-occlusive disease. Detecting occult alveolar haemorrhage may be of interest in the diagnostic approach of pulmonary veno-occlusive disease.

The diseases concerning the small pulmonary vessels are difficult to diagnose. Pathologic findings are rarely limited to the small vessels, and a continuum between the involvement of small and large vessels is frequent. Moreover, small vessels can be affected by various disease entities with overlapping radiologic features and a wide spectrum of clinical manifestations. Nevertheless, these various entities can be easily separated into two different groups by imaging techniques, particularly by computed tomography: obstructive and inflammatory diseases. Radiologic findings of obstructive diseases are relatively constant, dominated by the manifestation of pulmonary hypertension. In contrast, radiologic manifestations of inflammatory diseases are often florid and nonspecific. After a recall of the classification of small vessel diseases and the imaging techniques, we show the computed tomography features of the principal diseases involving the small pulmonary vessels by classifying them in these two principal groups.

To correlate pretherapeutic thin-section computed tomographic (CT) findings in patients with pulmonary hypertension with the risk of fatality with treatment with epoprostenol.Seventy-three consecutive patients with severe pulmonary hypertension treated with epoprostenol were retrospectively separated into two groups. The first group included 12 patients who had a fatal outcome with epoprostenol therapy. The second group (n = 61) was a reference group of patients with epoprostenol-induced clinical improvement. Pretherapeutic thin-section CT scans of each patient were reviewed.Poorly defined nodular opacities (P =.003), septal lines (P =.04), pleural effusion (P =.01), and adenopathy (P =.009) strongly correlated with a risk of clinical worsening with treatment. In six patients in group 1, postmortem examination of the lung revealed either pulmonary veno-occlusive disease or pulmonary capillary hemangiomatosis.On pretherapeutic thin-section CT scans, poorly defined nodular opacities, septal lines, pleural effusion, and adenopathy should raise suspicion for pulmonary veno-occlusive disease or pulmonary capillary hemangiomatosis and provoke possible further evaluation before epoprostenol therapy.

In pulmonary sarcoidosis, vascular involvement is usually limited to the small and medium-sized vessels. Enlarged hilar lymph nodes are usually considered to be soft and hence unlikely to cause pressure on adjacent bronchi or blood vessels.We report a rare symptomatic compression of a major pulmonary artery by lymphadenopathy in a case of sarcoidosis. Our patient presented with exertional dyspnoea, with enlarged hilar lymph nodes responsible for segmental pulmonary arterial hypertension, without other thoracic abnormalities. The symptoms and lymphadenopathy regressed with corticosteroid therapy.Enlarged hilar lymph nodes can compress major pulmonary arteries and cause segmental pulmonary hypertension. The prognosis can be grave in the absence of treatment.

International audience; This study was carried out to compare ultrasonographic findings on patients after transobturator tape (TOT) and tension-free vaginal tape (TVT) procedures to evaluate displacement of tapes up to a 2-year follow-up and to test the correlation between bladder outlet obstruction and the tape position. Forty-nine patients had a transvaginal ultrasonographic evaluation after TOT (n=31) or TVT (n=18) procedures. Twenty-one patients from the TOT group and 12 from the TVT group had ultrasonographic evaluation both at 1 and 2 years follow-up. Tape position was evaluated with a complete sagittal view, and the width of the tape and the distance between the middle of the tape and the bladder neck were measured. Statistical analysis was performed using a t test. After clinical evaluation, stress test, and uroflowmetry with residual measurement, the tapes were compared on ultrasound with regard to clinical and urodynamic results: success in stress incontinence vs failure, bladder outlet obstruction vs no obstruction, and de novo urgencies vs no urgencies. No difference was found between TOT and TVT in the midurethral tape placement. The distance between the middle of the tape and the bladder neck at rest was similar at both 1 and 2 years after both TOT and TVT and was unchanged after coughing or Valsalva. The width of the tape was similar after TOT and TVT at both 1 and 2 years after the procedure. There was no difference in the distance between the middle of the tape and the bladder neck between cured patients, failure, bladder outlet obstruction, and de novo urgencies after both TOT and TVT. Transvaginal ultrasound examination showed no significant difference in the tape position between TOT and TVT. No correlation was found between ultrasonographic findings and postoperative voiding troubles for both techniques.

To describe the CT findings of pulmonary veno-occlusive disease.Pre-therapeutic CT of 15 patients suffering from pulmonary veno-occlusive disease were retrospectively reviewed. Pathologic evaluation of pulmonary veno-occlusive disease was obtained after post mortem examination or pulmonary transplantation. CT protocol always included intravenous helical CT and high resolution CT.The most frequent CT-findings in pulmonary veno-occlusive disease were the following: ground glass opacity with poorly defined nodular opacities (73%), septal lines (93%), and adenopathy (80%). Pericardial (60%) and pleural effusions (27%) were also noted. Other parenchymal findings were unusual.HRCT must be systematically included in the initial CT evaluation of pulmonary hypertension. Combination of poorly defined nodular opacities, septal lines, and adenopathy are indicative of pulmonary veno-occlusive disease.

We present a case of pulmonary embolism which resulted from the migration of an oesophageal variceal sclerosing agent. Despite its frequency, this complication is rarely described in the literature.

A 66-year-old man with a history of primary hypertension and peripheral arteritis was admitted to the intensive care unit with multiple organ failure including shock, lactic acidosis, Escherichia coli bacteriemia, acute renal failure, respiratory failure, and confusion after 12 hours of abdominal pain and diarrhea. Owing to the severity of the clinical picture, a computed tomographic scanning of the abdomen with intravenous contrast medium was performed. This showed gas in the intrahepatic portal venous system (Fig. 1), in the portal vein (Fig. 2), in the mesenteric vein, and in the wall of the small bowel (Fig. 3), demonstrating the presence of diffuse acute enteritis. The patient was considered too seriously ill to undergo surgery and died a few hours later. No postmortem examination was performed. Non-occlusive ischemic enterocolitis was consistent with the patient’s presentation, despite the associated risk factors. Indeed, the patient did not have a previous history of intestinal angina. The role of severe hypovolemia, vasoconstriction, shock, and systemic sepsis can be suspected. Intramural gas, either linear or bubble shaped, and gas in the portal venous system—an ominous sign—are the radiographic hallmarks required for the diagnosis in adults of ischemic bowel disease and in the premature newborn of necrotizing enterocolitis [1]. In general, plain radiography of the abdomen and ultrasonography may be sufficient for premature