Psoas muscle pancreatic pseudocyst: CT--US diagnosis and percutaneous drainage

We present 2 cases of psoas muscle pancreatic pseudocysts. In both cases there was no clinical or laboratory evidence of recent acute pancreatitis. The route of extension for the pseudocyst from the pancreas to the psoas was the perirenal space. In both cases the diagnosis was made on the basis of imaging studies and the pseudocysts resolved with percutaneous drainage only.     

Accuracy of helical computed tomographic angiography for the diagnosis of colonic angiodysplasia

BACKGROUND & AIMS: The diagnosis of colonic angiodysplasia is often challenging and relies on endoscopy or catheter angiography. We investigated whether computed tomographic angiography (CTA) contributes to the diagnosis of colonic angiodysplasia. METHODS: Twenty-eight patients with suspected bleeding from colonic angiodysplasia were prospectively evaluated. Gastrointestinal bleeding was investigated by colonoscopy plus visceral angiography and by CTA. The level of agreement between CTA and the former procedures was determined. RESULTS: CTA images of diagnostic quality were obtained in 26 patients. Eighteen patients were diagnosed with colonic angiodysplasia by colonoscopy plus visceral angiography, and 14 by CTA (kappa = 0.68; P < 0.001). Sensitivity, specificity, and positive predictive values of CTA for detection of colonic angiodysplasia were 70%, 100%, and 100%, respectively. CTA signs including accumulation of vessels in the colonic wall, early filling vein, and supplying enlarged artery were present in 55%, 50%, and 22% of cases, respectively. None of these signs were present in the 8 patients with obscure gastrointestinal bleeding and negative diagnostic investigation of the digestive tract. CONCLUSIONS: CTA is a sensitive, specific, well-tolerated, and minimally invasive tool for the diagnosis of colonic angiodysplasia.     

Outcomes and markers in the assessment of chronic obstructive pulmonary disease.

The clinical presentation of chronic obstructive pulmonary disease (COPD) is highly variable, reflecting the interaction of a complex range of pathological changes including both pulmonary and systemic effects. The consequences of COPD experienced by the patient (i.e. its outcomes) include: symptoms, weight loss, exercise intolerance, exacerbations, health-related quality of life, health resource use and death. No single measure can reflect the variety of pathological effects or adequately describe the nature or severity of COPD. Currently, there are few validated markers for assessing COPD and evaluating the effectiveness of treatment. The forced expiratory volume in one second has been used as a global marker of COPD, but it does not fully reflect the burden of COPD on patients. New markers are needed to better characterise the full clinical spectrum of the disease and to guide the development and assessment of new and more effective therapies. This article considers the distinction between outcomes and markers, the various ways in which markers are used and the need for new markers in the management of chronic obstructive pulmonary disease. The process of marker selection and validation is reviewed and potential new biological, physiological and symptomatic markers for chronic obstructive pulmonary disease are assessed.     

Pulmonary hemodynamics and gas exchange during exercise in liver cirrhosis

We have recently shown that ventilation-perfusion (VA/Q) mismatching at rest in cirrhosis is due to an abnormal pulmonary vascular tone. It has been suggested that in patients with cirrhosis, O2 transfer might become diffusion-limited during exercise. This study examined pulmonary hemodynamics and mechanisms modulating gas exchange during exercise (60 to 70% VO2max) in six patients (41 +/- 5 yr, mean +/- SEM) with cirrhosis but with normal lung function tests. At rest, QT was high (8.4 +/- 0.5 L/min), pulmonary vascular resistance (PVR) was low (0.61 +/- 0.17 mm Hg/L/min), and there was mild to moderate VA/Q mismatching (LogSD Q, 0.79 +/- 0.09; normal range, 0.3 to 0.6). However, hyperventilation (PaCO2, 29 +/- 2 mm Hg) and high QT (thus, high PVO2, 41 +/- 2 mm Hg) contributed to the maintenance of PaO2 within normal values (99 +/- 7 mm Hg). Exercise VO2 (1,278 +/- 122 ml/min) was normal relative to work load, but, contrary to that in normal subjects, QT was higher and PVR did not fall. During exercise, PaO2 showed a trend to decrease (to 90 +/- 5 mm Hg) and PaCO2 to rise (to 35 +/- 2 mm Hg), but the differences failed to reach statistical significance (p = 0.07 each). PVO2 fell significantly with exercise (41 +/- 2 to 33 +/- 0.3 mm Hg, p less than 0.05), but neither AaPO2 (15 +/- 7 to 21 +/- 6 mm Hg) nor VA/Q inequality (LogSD Q, 0.82 +/- 0.11) changed. No systemic difference was noticed between predicted and measured PaO2 values, suggesting no O2 diffusion impairment during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)