Pancreas-sparing, ampulla-preserving duodenectomy for major duodenal (D1-D2) perforations.

BACKGROUND: Ideal surgical treatment for acute duodenal injuries should offer a definitive treatment, with low morbidity and mortality. It should be simple and easily reproducible by acute care surgeons in an emergency. Duodenal injury, due to major perforated or bleeding peptic ulcers or iatrogenic/traumatic perforation, represents a surgical challenge, with high morbidity and mortality. The aim was to review definitive surgery with pancreas-sparing, ampulla-preserving duodenectomy for these patients. METHODS: Pancreas-sparing, ampulla-preserving D1-D2 duodenectomy was used for patients presenting with major duodenal injuries over a 5-year interval. The ampulla was identified and preserved using a transcystic/transpapillary tube. The outcomes were recorded. RESULTS: Ten patients were treated with this technique; seven had perforated or bleeding peptic ulcers, two had iatrogenic perforations and one blunt abdominal trauma. Their mean age was 78 (range 65-84) years. Four patients were haemodynamically unstable. The location of the duodenal injury was always D1 and/or D2, above or in close proximity to the ampulla of Vater. The surgical approach was open in nine patients and laparoscopic in one. The mean duration of surgery was 264 (range 170-377) min. All patients were transferred to the ICU after surgery (mean ICU stay 4·4 (range 1-11) days), and the overall mean hospital stay was 17·8 (range 10-32) days. Six patients developed major postoperative complications: cardiorespiratory failure in five and gastrointestinal complications in four. Surgical reoperation was needed in one patient for postoperative necrotizing and bleeding pancreatitis. Two patients died from their complications. CONCLUSION: Pancreas-sparing, ampulla-preserving D1-D2 duodenectomy for emergency treatment of major duodenal perforations is feasible and associated with satisfactory outcomes.

A novel technique for enterotomy closure in stapled laparoscopic intracorporeal anastomosis.

AIM: The proximal edge of the enterotomy in a side-to-side anastomosis has been shown to be the site at highest risk of leakage. Several methods have been described to overcome this vulnerability. The technical challenge of intra-corporeal anastomosis (ICA) is to re-create angles between tissues and instruments, similar to those in an open anastomosis. The axis between the suture line and the needle driver is paramount and this angle should be < 45°. METHOD: The crotch stitch of the enterotomy is difficult because of the narrow space between the loops and the depth of the anastomosis. The usual technique is suturing right-handed, 'out-in and in-out', colonic edge first to small bowel. The risk of suture misplacement (e.g. 'out-in/out-in' or 'out-out') is similar to open procedures but laparoscopically the second bite is challenging, due to the straight needle-driver. This may lead to asymmetrical closure of the corner resulting in a slightly larger angle on the bowel side and a potential postoperative leak/fistula. Rotating the small bowel loop to counterbalance this issue, risks tearing of the staple line. The rationale is that starting with a back-handed stitch and taking the small bowel edge first would allow the necessary acute angled bite to be achieved. Subsequently, mounting the needle right-handed for taking the colonic edge also allows achievement of an acute angled bite. RESULTS: Our novel technique, named the 'back-handed, left-to-right stitch' technique, is intended to achieve symmetrical approximation of the ileal and colonic edges during laparoscopy, with an optimal closure of the deepest extremity of the enterotomy. Such a stitch, used in a series of 10 patients, may be useful to avoid leaving an opening within this angle and/or to avoid potential technical pitfalls when closing the deepest apex of the enterotomy. CONCLUSION: This 'back-handed, left-to-right' stitch described here allows a properly angled closure of the proximal edge of the enterotomy and a safe approximation of the corner of the enterotomy in a side-to-side ICA.

Cardiac output decreases and systemic vascular resistance increases in newborns placed in the left-lateral position.

OBJECTIVE: The objective of the study was to study the effect of short-term left-lateral position on cardiovascular parameters in hemodynamically stable newborns. STUDY DESIGN: Cardiac output (CO), stroke volume (SV), systemic vascular resistance index (SVRI) and heart rate (HR) were measured by electric velocimetry in hemodynamically stable newborns without respiratory support in the supine, left-lateral and back-to-supine positions, each kept for 10 min. RESULTS: Thirty-two newborns were enrolled, birth weight 2134 (1818 to 2460) g, gestational age 34.5±2.4 weeks. CO and SV decreased significantly from supine to left-lateral position (CO supine: 193.4 (168.0 to 229.6) ml kg-1min-1; CO left-lateral: 172.0 (154.9 to 201.6) ml kg-1min-1, P<0.0001; SV supine: 3.0 (2.7 to 4.0) ml; SV left-lateral: 2.7 (2.4 to 3.2) ml, P<0.0004). Conversely, SVRI increased in left-lateral position: SVRI supine: 18865±9244 dyns cm-5 m-2; SVRI left-lateral: 21203±10059 dyns cm-5 m-2, P<0.0001). All variables returned to the initial value when infants were back in the supine position. HR and blood pressure did not change. CONCLUSION: In stable infants, CO and SV decrease and SVRI increases, in left-lateral position.

Malondialdehyde-acetaldehyde-protein adducts increase secretion of chemokines by rat hepatic stellate cells.

Findings obtained from our recent studies have demonstrated that malondialdehyde, a product of lipid peroxidation, and acetaldehyde can react together with proteins in a synergistic manner and form hybrid protein conjugates, which have been designated as malondialdehyde-acetaldehyde (MAA)-protein adducts. These adducts have been detected in livers of ethanol-fed rats and are immunogenic because significant increases in circulating antibody titers against MAA-adducted proteins have been observed in ethanol-fed rats and more recently in human alcoholics. Although immunological factors may tend to perpetuate liver injury, little is known about the direct functional consequences of MAA-adducted proteins on the different cellular populations of the liver. Hepatic stellate cells (HSCs) have been shown to be pivotal in the pathogenesis of fibrosis and in the amplification and self-perpetuation of the inflammatory process. The present study was conducted to determine the effects of MAA-adducted proteins on the function of HSCs. Rat HSCs were exposed to various amounts of MAA-protein adducts and their unmodified controls, and the secretion of two chemokines, monocyte chemoattractant protein (MCP)-1 and macrophage inflammatory protein (MIP)-2, that are involved in the chemotaxis of monocytes/macrophages and neutrophils, respectively, was determined. We observed that bovine serum albumin-MAA induced a dose- and time-dependent increase in the secretion of both of these chemokines. These findings indicate that MAA-adducted proteins may play a role in the modulation of the hepatic inflammatory response and could contribute to the pathogenesis of alcoholic liver disease.

Chronic ethanol ingestion impairs TGF-alpha-stimulated receptor autophosphorylation.

The effects of chronic ethanol feeding on the binding of transforming growth factor-alpha (TGF-alpha) and TGF-alpha-stimulated receptor autophosphorylation were investigated in isolated rat hepatocytes. When hepatocytes were isolated from rats that were fed an ethanol liquid diet for 6-8 weeks, these cells exhibited a marked impairment of TGF-alpha-stimulated autophosphorylation of the receptor that binds this growth factor compared with hepatocytes from the pair-fed controls. This impaired autophosphorylation of receptor tyrosine residues was accompanied by significant decreases in the amount of surface-bound TGF-alpha. Immunoanalysis indicated no changes in receptor number, indicating that decreased receptor content was not responsible for decreased TGF-alpha binding in the hepatocytes from the ethanol-fed rats. In conclusion, chronic ethanol feeding reduced TGF-alpha binding to hepatocytes with a concomitant decrease in the ability of the receptor tyrosine kinase to autophosphorylate its tyrosine residues. These changes were not accompanied by decreased receptor protein content. These defects could lead to altered signal transduction and to impaired reparative and regenerative processes in the liver.

Effects of chronic ethanol administration on the endocytosis of cytokines by rat hepatocytes.

The effects of chronic ethanol administration on the endocytosis of three representative cytokines were investigated in isolated rat hepatocytes. When hepatocytes were isolated from rats that were fed an ethanol liquid diet for 12 to 13 weeks, these cells exhibited a decreased ability to internalize and degrade transforming growth factor-alpha, tumor necrosis factor-alpha and interleukin-6, compared with hepatocytes from the pair-fed controls. This impaired endocytosis of all three cytokines was accompanied by significant decreases in the amount of hepatocyte surface-bound cytokine. Changes in cytokine binding to surface receptors and reduced rates of receptor-cytokine complex internalization into the cells seem to be major contributors to defective endocytosis in hepatocytes from the ethanol-fed rats. Impaired hepatocyte endocytosis could lead to altered steady-state levels of cytokines in the liver and modified physiological responses to cytokines. These changes could affect homeostasis among the various cell types in the liver and could contribute to liver dysfunction and injury.