[Routine computerized tomography in suspected acute appendicitis?].
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Biomedical subjects
Publications and source records attributed to E Hanisch.
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BACKGROUND: In this study we have analyzed the local immunosuppression with budesonide, a topically selective glucocorticosteroid, in rats after orthotopic liver transplantation. Because of its high first-pass hepatic clearance budesonide can be given orally, achieving high intrahepatic and low systemic concentrations. METHODS: Using an acute rejection model from Dark Agouti (DA) to Lewis rats, the histomorphological degree of rejection was assessed on histological sections at the ninth postoperative day. RESULTS: Livers of the DA to Lewis study group without immunosuppression revealed severe allograft rejection with vast cellular infiltrates, massive endothelialitis, and hepatocyte necrosis. In the three budesonide study groups (250 microg, 500 microg, and 1 mg/kg/day) a moderate to mild liver allograft rejection was seen. Rejection was most prominent in the 250 microg group, whereas the 1 g group showed almost no signs of rejection, similar to the Lewis to Lewis control group. Aspartate and alanine transaminase (sGOT, sGPT) as well as alkaline phosphatase serum levels correlated with the degree of rejection, achieving highest levels in the DA to Lewis group without immunosuppression. Animals treated with 1 g of budesonide had serum levels similar to Lewis to Lewis control animals. CONCLUSIONS: These results implicate a beneficial effect of local immunosuppression with budesonide in rats based on the histomorphological degree of liver allograft rejection.
BACKGROUND: Cholestasis is a complication that occurs during the rejection of liver transplants. The aim of this study was to investigate the association of activated Kupffer cells (KCs) and Na+,K+-ATPase activity for taurocholate cotransport and bile canalicular (BC) Mg++-ATPase activity for hepatobiliary excretion in rat liver allograft. METHODS: Quantitative analyses of KC number and size in relationship to enzyme activity of Na+,K+-ATPase and of BC Mg++-ATPase were conducted in rejected liver after allogenic transplantation and after prevention of rejection using cyclosporine. RESULTS: The animals were examined on the 10th postoperative day. In the rejection group, the number of KCs significantly increased more than fourfold in comparison with the number of KCs in the control livers. Some KCs were found in the sinusoids, but the majority were located in the space of Disse. Na+,K+-ATPase activity vanished from the basolateral plasma membrane, whereas BC Mg++-ATPase activity was restored in the apical domain. With immunosuppression, KCs showed the same behavior as in the control group, and activity of both ATPases was observed as strong electron-dense precipitates in basolateral and apical plasma membrane domains. CONCLUSIONS: In this study, we demonstrate that activated KCs migrate into the donor liver and release cytokines, which leads to the loss of Na+,K+-ATPase activity in the rejection group. BC Mg++-ATPase activity was not influenced by these mediators of activated macrophages. Since Na+,K+-ATPase is the cotransporter for hepatocyte taurocholate uptake, these data may contribute to understanding the mechanisms for cholestasis during hepatic allograft rejection.
For 1 year all patients in the Department of General Surgery who were transferred to the intensive care unit (n = 237) were prospectively studied as to the development of hyponatremia. Relevant hyponatremia developed in 6.3% of the patients. The lowest sodium concentration observed was 121 mmol/l, the mean duration was 1.2 days. In general, hyponatremia is related to hypovolemia and diuretics are often involved. In no patient were there any clinical consequences.
Jaundice in critically ill patients may be difficult to explain. This study analyzes pathophysiologically relevant data, and discusses the prognostic value of hyperbilirubinemia. A total of 1275 patients were prospectively enrolled; 7.6% developed hyperbilirubinemia of at least 2 mg/dl. Mortality in icteric patients was significantly higher (29%) than in the non-icteric group. Sepsis, shock and the number of blood transfusions are very important in hyperbilirubinemia. Nevertheless, in critically ill patients, jaundice per se is not a sign of poor outcome; indeed it only reflects the underlying disease.
BACKGROUND/AIM: This study addresses cholecystokinin (CCK)-receptor alterations in stone-diseased and stone-free human gallbladders using different CCK-fragments. METHODS: Serosa-free muscle strips were mounted in a modified Krebs-Henseleit-solution of 37 degrees C and aerated with carbogen. The following concentrations of CCK-fragments (CCK 26-33, N-Acetyl CCK 27-33 sulf., CCK 26-29 sulf., CCK 25-33 sulf.) were achieved: 0.1 nmol, 0.5 nmol, 2 nmol, 10 nmol, 100 nmol. RESULTS: Stone-diseased gallbladders were classified into two groups based on their in vitro reaction to CCK 26-33 (CCK-octapeptide). Muscle strips not contracting below 10 nmol were assigned to the subcontractor group. Histologically scarification, necrosis and signs of severe inflammation of the mucosa were seen in 76.9% of this group. Those starting contractions at 0.1 nmol (like the control group) were called the contractor group. This group had a shallow mucosa and mild inflammatory signs in 54.5%. The sub-contractor group showed higher spontaneous phasic activity at lower tonic activity than the contractor and control groups. In the sub-contractor group CCK 27-33 caused several times higher contractions than all other fragments. A maximal contraction level in the contractor and control groups was reached by CCK 25-33. CONCLUSIONS: This striking effect of CCK 27-33 in the sub-contractor group favors the view of CCK-receptor structural alteration in a subgroup of patients with cholecystolithiasis.
OBJECTIVE: To evaluate the frequency and causes of recurrent biliary colic after successful extracorporeal shock wave lithotripsy of gallstones. METHODS: Follow-up of 77 patients for 2 yr (median) after complete gallstone clearance by lithotripsy and adjuvant oral litholysis. All patients with recurrent biliary colic were examined thoroughly (laboratory data, ultrasonography, gastroscopy); the examination included gallbladder motility testing. If the patients suffered from additional gastrointestinal complaints, further symptom-guided investigations (pH-metry, lactose absorption study, enteroclysis, colonic transit time, colonoscopy) were performed. Patients without documented gallstone recurrence underwent ERCP and sphincter of Oddi manometry. Cholecystectomy was advised for patients in whom gallstones recurred, and patients with sphincter of Oddi dysfunction underwent endoscopic sphincterotomy. If other gastrointestinal disorders were diagnosed, appropriate treatment was initiated. RESULTS: Twenty-seven patients (35%) experienced biliary colic during follow-up. Gallstone recurrence was documented in 17 patients, and 16 of the patients who underwent cholecystectomy became symptom-free again (follow-up: 12 months). Gallbladder hypomotility was revealed in seven of the 17 patients with gallstone recurrence compared to none of the 10 patients without gallstone recurrence (p < 0.05). Microlithiasis was not detected in bile samples from the patients whose gallstones did not recur. Sphincter of Oddi dysfunction was found in four patients, and sphincterotomy cured all of them (follow-up: 9 months). Two of the remaining six patients had functional gastrointestinal disorders (reflux, constipation) and became asymptomatic after specific treatment. CONCLUSIONS: Biliary colic often recurs after successful gallstone lithotripsy. Recurrent gallbladder stones are the main cause, but another cause is sphincter of Oddi dysfunction. Neither gallbladder hypomotility nor microlithiasis seems to cause biliary symptoms in patients without recurrence of gallstones.
INTRODUCTION: The exact source of phospholipase A2 is unknown. In this context the liver is discussed because the secretion of phospholipase A2 could be initiated during an acute phase response. PATIENTS AND METHODS: Three groups of patients were prospectively established: A liver resection (n = 12); B control (n = 22; oesophageal resection, gastrectomy, rectum resection); C sepsis (n = 5). Blood was collected preoperatively, each day postoperatively for seven days and at the day of discharge. Biochemical procedures: Phospholipase A2, PMN-elastase, C-reactive protein, GPT, GOT, GLDH, cholinesterase. RESULTS: Postoperatively phospholipase A2 is unchanged in the liver resection and control group, whereas it increases significantly in septic patients. Only following liver resection GPT, GOT and GLDH increase. C-reactive protein is increased in all groups. DISCUSSION: Unchanged phospholipase A2 after liver surgery despite an acute phase response indicated by C-reactive protein does not support the view of phospholipase A2 being of hepatic origin.
UNLABELLED: This study is to determine the role of nitric oxide (NO), as primary neurotransmitter of the non-adrenergic noncholinergic (NANC) innervation, of stone-diseased and stone-free human gallbladders. Human gallbladder muscle strips were mounted in modified Krebs-Henseleit-solution with atropine (1 microM), guanethidine sulf. (5 microM) and aerated with Carbogen. Electrical field stimulation (EFS, 70V, 0.5 ms, 100 pulses) was used at frequencies of 1, 3, 10 Hz to activate NANC nerves, L-omega-nitro-L-arginine (L-NNA, 100 microM), L-arginine (L-ARG, 120 microM) was used to manipulate the NO-synthase. Gallbladder slices of 3 microns were stained by means of APAAP-method (alkaline phosphatase anti alkaline phosphatase) for histological examination. In the control group (basal tone = 8.94 +/- 1.17 mN) EFS caused a frequency dependent reduction of basal tone (1 Hz = 5.73 +/- 0.81 mN; 3 Hz = 5.18 +/- 0.65 mN; 10 Hz = 4.63 +/- 0.49 mN). Incubation with L-NNA increased the tone (7.63 +/- 0.76 mN). Contractor group (basal tone = 7.79 +/- 0.93 mN) reacted like the control group but frequency independent and additionally with spontaneous phasic contractions. In the non-contractor group (basal tone 4.13 +/- 0.65 mN) EFS only decreased the frequency of spontaneous phasic contractions. L-NNA caused an increase in tone (5.97 +/- 0.84 mN) and frequency, L-Arginine significantly reversed this effect. HISTOLOGY: Contractor group showed wrinkled mucosal membrane and mild grade of inflammation. Shallow mucosa, necrosis and high grade of inflammation were found in the non-contractor group. CONCLUSIONS: 1. In vitro, NANC-relaxation of human gallbladder is NO dependent. 2. Motility of stone-diseased gallbladders is modulated by NO and seems to depend on the degree of scarrification.
Models of evaluation in therapeutic management pathways (practice guidelines, clinical algorithms) are demanded today, both by public health research and health policy. However, practical achievements are lacking. To overcome this controversy, the Lucerne Study Group on Sepsis Research was founded to develop guidelines in accordance with a series of official groups. It was shown that there was no agreement between the providers and the daily users. However, every surgeon has a firm, personal view about sepsis.
BACKGROUND: Multiple organ failure (MOF) is becoming the most common cause of death in patients in surgical intensive care units. In this respect, a multicenter study in four different groups of patients in surgical intensive care units was done to evaluate the role of phospholipase A2 (PLA2) in comparison with C-reactive protein (CRP) and polymorphonuclear (PMN) elastase. STUDY DESIGN: A total of 223 patients entered the study: 73 patients with multiple injuries, 46 patients with diffuse peritonitis, 52 patients with sepsis, and 52 patients in a control group who were at a higher risk for postoperative sepsis after defined surgical interventions. The patients underwent a daily monitoring of PLA2, CRP, and PMN elastase for seven days. RESULTS: Phospholipase A2 activity remained within the normal range in patients with multiple injuries and patients in the control group, indicating that this parameter is not influenced by the postaggression metabolism. In contrast, in patients with peritonitis, high PLA2 values were found from the beginning. The efficiency for predicting a lethal MOF was 85 percent for PLA2 (cut-off 80 U/L) in patients if determined at the day of operation. A comparably favorable efficiency (84 percent) was demonstrated for PMN elastase in patients with multiple injuries (cut-off 205 micrograms/L) measured at day one. CONCLUSIONS: These efficiency rates of PLA2 in peritonitis and PMN elastase in multiple injuries were comparable or even better than multifactorial scoring systems used in the study. C-reactive protein did not contribute to an early estimation of the prognosis in all groups analyzed. Therefore, the measurement of PLA2 in patients with diffuse peritonitis and PMN elastase in patients with multiple injuries, as single parameters, is recommended to estimate the individual risk for the occurrence of lethal MOF.
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There is as yet no agreement about a conservative surgical strategy in the therapy of acute necrotizing pancreatitis. This report describes our experience with "open packing" laparostomy. This procedure is only performed when renal and pulmonary insufficiency is proceeding, despite optimal conservative treatment. Since 1986 twenty-two patients were treated in this manner. Three compartments are established: an upper compartment (stomach, liver, spleen covered by the omentum majus, which is dissected from the colon transversum); a lower compartment (small bowel covered by the left colon) and the mid compartment that permanently opens the bursa omentalis and the left retrocolic space. Initially a careful necrosectomy is performed, followed by a tamponade. At the intensive care unit changing of the tamponade and lavage of the bursa omentalis was done every day. So far three patients (13.6%) have died pursuing this therapeutic regimen.
In general, balloon tamponade is still part of the therapy of bleeding esophageal varices, despite effective sclerotherapy. Four case reports demonstrate that the application of balloon tamponade may be associated with severe complications. Moreover, a critical analysis of the literature shows a very different handling with respect to volume of gastric balloon, duration of blockade and traction to the tube. To prevent serious side effects, a safe way is described in detail when using balloon tamponade.
To investigate whether there is a permanent translocation of Thorotrast in the body, the liver of male Lewis rats was removed 4 weeks after injection of Thorotrast (300 microliters) and replaced by a donor liver. In half of the animals the spleen was removed as well. Measuring the 232Th content in the donor liver at different times after implantation demonstrated a permanent transport of 232Th into the surrogate organ. After 231 days a 232Th depot of about 1.1 mg was found, representing about 3% of the total body burden. The additional removal of the spleen resulted in a significantly lower transport of 232Th into the implanted liver. Histological examinations of the donated livers revealed increasing local concentration of Thorotrast granules, leading to the development of conglomerates. A comparable translocation of Thorotrast was verified in two humans who required liver transplantation more than 40 years after Thorotrast injection.
Liver transplantation (LTX) in the rat is a frequently used transplantation model. In the present study we give a detailed description of the suture technique for all anastomoses, except the bile duct, with arterialization of the transplanted liver over an aortoceliac segment to the recipient's aorta. Using this technique, we finally achieved survival rates of 80%. During the development stages, the main cause of death was an exceedingly long anhepatic time (> 20 min); later on, complications occurred only from insufficient anastomoses. The advantage of the suture technique over the cuff technique is that a more physiological anastomosis is obtained with less trauma to the recipient when using rearterialization. Despite the complicated suture technique, the anhepatic time can be well reduced to below 20 min.