Erysipelas-like inflammation following breast surgery.

Impaired lymph drainage is an inevitable consequence of any form of surgery that disrupts lymphatics, resulting in a degree of lymphoedema that may vary from subtle to dramatic and although classically involving an entire limb, may be more localised, confined to only a small area such as a skin flap. Infection is a well-recognised complication of lymphoedema. However, not all inflammatory episodes occurring in the setting of lymphatic dysfunction can be clearly attributed to infection as this article demonstrates. Five patients presented over a 5-year period with distinctive erysipelas-like inflammation affecting the breast which occurred several weeks following reduction mammaplasty in four patients and breast reconstruction in one patient. No clinical response was obtained with standard antibiotics. This inflammatory problem may represent a previously unreported complication of breast surgery with an incidence of 4% following reduction mammaplasty. Recent research supports the notion that this type of episode is most likely to be due to a non-infective inflammatory process related to lymphatic dysfunction induced by surgery.     

Acute leriche syndrome due to paradoxical embolism.

Paradoxical embolism, describing the passage of venous or right-sided cardiac thrombus into the arterial or systemic circulation through patent foramen ovale, is an uncommon cause of acute arterial occlusion. Here, we report acute Leriche syndrome in a young woman attributable to paradoxical embolism. Ischaemia, patent foramen ovale, and venous thrombosis were the triad of evidence for paradoxical embolism.     

Partial Portal Vein Ligation Plus Thioacetamide: A Method to Obtain a New Model of Cirrhosis and Chronic Portal Hypertension in the Rat

To obtain a new model of chronic portal hypertension in the rat, two classical methods to produce portal hypertension, partial portal vein ligation and the oral administration of thioacetamide (TAA), have been combined. Male Wistar rats were divided into four groups: 1 (control; n?=?10), 2 [triple partial portal vein ligation (TPVL); n?=?9], 3 (TAA; n?=?11), and 4 (TPVL plus TAA; n?=?9). After 3 months, portal pressure, types of portosystemic collateral circulation, laboratory hepatic function tests (aspartate aminotransferase, alanine aminotransferase, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase) and liver histology were studied. The animals belonging to group 2 (TPVL) developed extrahepatic portosystemic collateral circulation, associated with mesenteric venous vasculopathy without hepatic destructurization or portal hypertension. Animals from group 3 (TAA) developed cirrhosis and portal hypertension but not extrahepatic portosystemic collateral circulation, or mesenteric venous vasculopathy. Finally, the animals from group 4 (TPVL?+?TAA) developed cirrhosis, portal hypertension, portosystemic collateral circulation, and mesenteric venous vasculopathy. The association of TPVL and TAA can be used to obtain a model of chronic portal hypertension in the rat that includes all the alterations that patients with hepatic cirrhosis usually have. This could, therefore, prove to be a useful tool to study the pathophysiological mechanisms involved in these alterations.