Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.

The NASA-TLX is a valid tool to gauge mental workload in LRYGB.

Background: Obstructive Jaundice (OJ) is associated with a significant risk of developing acute renal failure (ARF). The involvement of oxidative stress in the development of cholestasis has been demonstrated in different experimental models. However, its role in the morbidity of human cholestasis is far to be elucidated. The aim of the study was the evaluation of oxidative stress markers in blood from patients with OJ and its relation to complications and benign/malignant evolution of cholestasis. Methods: A prospective cross-sectional study of 105 patients with OJ and 34 control subjects were included. Several markers of liver function and oxidative stress, such as lipoperoxides (LPO), as well as reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were assessed. Results: The patients with OJ showed a marked increase in plasma levels of LPO, SOD and GSH, while GSH-Px levels were decreased. The increase in lipid peroxidation products and the depletion of SOD activity in blood were also related to renal dysfunction. The highest level of LPO was associated with malignant etiology of the disease. The logistic regression analysis showed that the age of the patient and the levels of LPO in blood were predictors of renal dysfunction in OJ patients. Conclusions: This study demonstrates a correlation between oxidative stress and renal dysfunction patients with OJ.

Echinococcal cysts are usually found in liver and lungs, but any other organ can potentially be involved. Extrahepatic disease due to hydatid cyst may develop in the abdominal and pelvic cavity, aside from in other less common locations, which may make both diagnosis and treatment more complex. We present a rare case of extrahepatic echinococcosis in a 70-year old patient with a 4-d history of dull abdominal pain, anemia within the transfusion range and fever. She underwent surgery for left renal hydatid cysts 30 years ago. After non operative treatment, imaging studies showed a calcified hydatid cyst in a retrogastric location communicating with a proximal jejunal loop. En-block resection of the mass together with the adrenal gland was performed including closure of the enteric fistula. Anatomic pathology confirmed the diagnosis of a calcified hydatid cyst of left adrenal origin. Surgery is the treatment of choice and most authors recommend removal of cyst and adrenal gland.

Objective: the alteration of hormones regulating sodium and water status is related to renal failure in obstructive jaundice (OJ).Experimental design: OJ was induced by common bile duct ligation. Samples were obtained from the control (SO) and OJ groups at 24 and 72 hours, and at 7 days. Different parameters related to biliary obstruction, liver and renal injury, and vasoactive mediators such as renin, aldosterone, endothelin-1 (ET-1) and prostaglandin E 2 (PGE 2 ) were studied.Results: bile duct ligation caused an increase in total bilirubin (p < 0.001) and alkaline phosphatase (AP) (p < 0.001). The SO and OJ groups had the same values for diuresis, renin, and creatinine clearance at 24 h. However, animals with OJ had a lower sodium concentration in urine than SO animals (p < 0.01), as well as an increase in aldosterone levels (p < 0.03). ANP levels were moderately increased during OJ but did not reach statistical significance when compared to the SO group. In contrast, OJ animals showed a rise in serum ET-1 concentration (p < 0.001) and increased PGE 2 in urine (p < 0.001).Conclusions: biliary obstruction induced an increase in ET-1 release and PGE 2 urine excretion. These hormones might play a role during the renal complications associated with renal disturbances that occur during OJ. INTRODUCTIONCholestasis is a clinical and biochemical syndrome caused by the impaired bile flow often associated with extrahepatic complications (1). Acute renal failure is a major complication of obstructive jaundice (OJ), with 8% incidence in several series (2). Biliary obstruction was first linked to renal failure in the early study carried out by Clairmont and von Haberer (1910) (3). Several hypotheses have sought to explain the pathogenesis of renal dysfunction in OJ. The depletion of the extracellular compartment (4), myocardial dysfunction, and altered hemodynamic status (5) have been linked to renal failure in biliary obstruction. In addition, severe oxidative stress has been implicated in the renal dysfunction associated to experimental OJ (6,7) as well as other liver diseases (8). Other lines of research have looked at the involvement of vasoactive mediators such as endothelin-1 (ET-1). ET-1 is a powerful paracrine vasoconstrictor that acts by means of specific type-A and type-B receptors. In biochemical terms, it is a 21-amino acid peptide derived from what is known as big ET-1 by the action of the endothelin-converter enzyme. It is synthesized mainly by endothelial cells and to a lesser degree by stellate cells in the liver and biliary epithelium (9,10). ET-1 changes have been related to different human diseases (11). ET-1 both acts on the mesangial cells and causes vasoconstriction in the renal microcirculation, which may contribute -along- Enferm Dig 2009; 101: 408-412.