Primary malignant mixed Mullerian tumor arising in the rectosigmoid.
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Biomedical subjects
Publications and source records attributed to C Bloechle.
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BACKGROUND/PURPOSE: Pulmonary hypertension and pulmonary hypoplasia account for the high mortality rate associated with congenital diaphragmatic hernia (CDH). In animal models of CDH, postnatal nitric oxide (NO) inhalation resulted in significantly better survival rates and antenatal glucocorticoid administration in improved lung compliance. The objective of this study was to evaluate the combined effect of prenatal glucocorticoid administration and postnatal NO inhalation on the survival rate of newborn rats with nitrofen-induced CDH. METHODS: Right-sided CDH was induced by maternal administration of a single oral dose (100 mg, intraperitoneally) of nitrofen on day 11.5 of pregnancy. Dexamethasone (DEX, 0.25 mg/kg) was given in groups III and IV by maternal intraperitoneal injection on day 18.5 and 19.5 of pregnancy. Control animals (groups I and II) received vehicle alone. After spontaneous delivery, the newborn animals were exposed to either NO (80 ppm; groups II and IV) or room air (groups I and III). Vitality (Rat-Score), sO(2) and survival were monitored continuously for 12 hours until animals were killed. Hernia size was estimated as percentage of total thoracic content. RESULTS: Right-sided CDH was observed in 392 of 491 newborn rats (81%). Animals with large hernias (>50%) died within 4 hours after birth, irrespective of treatment. Hernias with less than 50% of the thoracic volume were considered clinically relevant hernias. In this category, 12.5% of animals without treatment (group I) survived compared with 63.6% after NO treatment alone (group II; P <.01). Survival rate after DEX treatment alone (group III) was 69.4% (group III v I; P <.01). In group IV (DEX and NO) 95.2% of the animals survived (group IV v I; P <.001). In contrast to DEX alone, NO administration resulted in significantly better sO(2)(group II and IV) compared with group I (P <.05). CONCLUSION: Combination of prenatal maternal glucocorticoids and postnatal NO inhalation significantly improved survival rate of newborn rats with nitrofen-induced CDH.
The aim of surgical therapy in Crohn's disease is to improve quality of life. Surgery does not provide cure with radical resection of inflamed bowel. Therefore strictureplasty has become a useful bowel-preserving surgical technique in the treatment of small-bowel stenosis. To preserve functional bowel we extended the indication of this surgical technique to strictures in large bowel. The aim of this retrospective study was to define the efficacy of strictureplasty and resection in patients with obstructive Crohn's disease of the colon. The results were evaluated in terms of postoperative complications, surgical recurrence, and quality of life. The charts of 58 patients with Crohn's colitis were analyzed retrospectively. Patients were either treated by strictureplasty or resection. Quality of life was evaluated in follow-up examinations using the Inflammatory Bowel Disease Questionnaire. The incidence of postoperative surgical recurrence was 36% in those treated by strictureplasty and 24% in those treated by resection (ns). Postoperative morbidity was 16.1% in the former and 22.3% in the latter. There was no significant difference between the groups in quality of life measures (177 versus 182 points). Strictureplasty in Crohn's colitis is a valuable surgical technique which results in low recurrence rates and in surgical outcome comparable to that in resection without sacrificing functional large bowel length. In our study quality of life after strictureplasty was comparable with quality of life after resection.
OBJECTIVES: In light of evidence suggesting that hemofiltration favorably influences septic diseases by removing sepsis mediators, the impact of different modalities of continuous veno-venous hemofiltration (CVVH) on outcome and immunologic derangements in porcine pancreatogenic sepsis was evaluated. DESIGN: Randomized, controlled intervention trial. SUBJECTS: Forty-eight minipigs of either sex. INTERVENTIONS: Pancreatitis was induced by intraductal injection of sodium taurocholate (4%, 1 mL/kg body weight [BW]) and enterokinase (2 U/kg BW). Animals were allocated either to untreated controls-group 1-or to one of three treatment groups-group 2: low-volume CVVH (20 mL/kg BW), no change of hemofilters; group 3: low-volume CVVH, filters changed every 12 hrs; and group 4: high-volume CVVH (100 mL/kg BW), filters changed every 12 hrs. Survival represented the major parameter of the study. Serum cytokine levels, sepsis-related down-regulation of major histocompatibility complex II and CD14 expression on leukocytes, bacterial translocation, and endotoxemia were further parameters evaluated in the study. MEASUREMENTS AND MAIN RESULTS: High-volume CVVH combined with periodic filter change was significantly superior compared with less intensive treatment modalities (low-volume CVVH, no filter change) in sepsis protection. Long-term survival (>60 hrs) was found in 67% of group 4 and 33% of group 3 animals (p <.05), whereas in controls and group 2 no animal survived. CVVH ameliorated the initial serum tumor necrosis factor-alpha response and prevented sepsis-induced in vitro endotoxin hyporesponsiveness. Down-regulation of major histocompatibility complex II and CD14 expression on monocytes was significantly improved by CVVH. Improved oxidative burst and phagocytosis capacity in polymorphonuclear leukocytes suggested that leukocyte function was stabilized by CVVH. Also, CVVH significantly reduced bacterial translocation and endotoxemia. CONCLUSIONS: Hemofiltration reversed sepsis-induced immunoparalysis in a porcine model of bile acid-induced pancreatitis. Implications for human pancreatitis must be validated in prospective, clinical protocols.
BACKGROUND: Improvement in quality of life is one of the important determinants in the treatment of Crohn's disease. Since there is no cure with radical resection of inflamed bowel, strictureplasty has become a useful surgical technique in the treatment of small bowel obstruction. The scope of this study was to define the results of strictureplasty and resection in terms of quality of life, surgical recurrence and postoperative complications. METHODS: The charts of 67 patients with Crohn's disease of the small bowel were analyzed retrospectively. Patients were treated either by strictureplasty (group A) or resection (group B). Quality of life was evaluated in follow-up examinations using the Inflammatory Bowel Disease Questionnaire (IBDQ). RESULTS: Postoperative morbidity was 14.8% after strictureplasty and 17% after resection (p = 0.8). 50% of the patients treated by strictureplasty and 37% treated by resection developed recurrent disease (p = 0.40). Quality-of-life measurement revealed no significant difference between patients treated by strictureplasty or resection. CONCLUSION: Results after strictureplasty are comparable to those after resection in terms of complications, recurrence and quality of life in the treatment of small bowel strictures in Crohn's disease. In the long run there might be an advantage for strictureplasty because it prevents complications caused by resectional therapy such as short bowel syndrome.
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A case of hepatic complication in a pregnant woman suffering from HELLP syndrome resulting in the need for transplantation is reported, and an algorithm for those instances is suggested. According to the literature, this is the 5th report of hepatic complications in HELLP syndrome necessitating liver transplantation. Since all but one of the transplanted patients survived (as opposed to a high mortality in non-transplanted patients), it is concluded, that a timely decision for transplantation is a safe option in this high risk group.
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OBJECTIVES: To investigate the impact of the long-acting bradykinin B2 receptor antagonist HOE 140 (Icatibant) on survival time in a model of severe porcine pancreatitis. DESIGN: Randomized, controlled intervention trial. SUBJECTS: Thirty domestic pigs of either gender anesthetized by intravenous application of piritramide, midazolam, and pancuronium and mechanically ventilated. INTERVENTIONS: Pancreatitis was induced by an injection of sodium taurocholate (5%, 1 mL/kg body weight [BW]) and enterokinase (10 U/kg BW). Control animals (group 1, n = 10) underwent the spontaneous course of the disease. In two treatment groups, Icatibant was administered either in a low (100 nmol/kg BW; group 2, n = 10) or in a high dosage (5000 nmol/kg BW; group 3, n = 10). MEASUREMENTS AND MAIN RESULTS: Mean survival time was significantly prolonged by Icatibant (controls, 6.6 hrs; group 2, 9.8 hrs; p = .022; group 3, 10.9 hrs; p = .007). Six hours postinduction, the decline of total peripheral resistance (52% of baseline) and cardiac index (92% of baseline) in controls was significantly improved by Icatibant, both in the low (16% and 44%; p < .05) and high (6% and 45%; p < .05) dosage. The concentrations of free, nonreceptor-bound kinin in plasma 6 hrs postinduction were significantly lower in controls than in groups 2 and 3 animals (111+/-50 vs. 208+/-40 and 237+/-52 fmol/mL, respectively). Six hours postinduction, the pretreatment with Icatibant was associated with significantly higher plasma concentrations of phospholipase A2 (controls, +1194%; group 2, +2000%; group 3, +2285% of baseline values) and interleukin-1 receptor antagonist (controls, 1900+/-800; group 2, 3100+/-800; group 3, 3600+/-800 pg/mL). In contrast, the increase of urinary trypsinogen activation peptides indicating local pancreatic damage (589+/-114 nmol/L in controls) was substantially attenuated by pretreatment with Icatibant (group 2, 467+/-102, NS; 352+/-91 nmol/L in group 3; p = .022 vs. controls). Systemic inflammatory reactions, however, as quantified by C-reactive protein and the extracellularly discharged neutrophil cytosolic inhibitor leukocyte neutral proteinase inhibitor were not influenced by the bradykinin B2-receptor antagonist. CONCLUSIONS: Pretreatment with the bradykinin B2 receptor antagonist Icatibant resulted in prolonged survival time and in delayed impairment of major macrocirculatory and pulmonary variables. Icatibant resulted in elevated concentrations of free, circulating kinin. This was associated with increased concentrations of phospholipase A2 and interleukin-1 receptor antagonist, suggesting that circulating kinins strengthen the activation of some mediator cascades, the association of which with the kinin metabolism requires further experimental clarification. Other variables indicating a systemic inflammatory response (C-reactive protein, leukocyte neutral proteinase inhibitor) remained unaffected by Icatibant. Bradykinin antagonism distinctly ameliorated the local pancreatic damage, indicated by increased urinary concentrations of trypsinogen activation peptides. It is concluded that the kinin metabolism plays an important role in the pathophysiology of systemic complications after severe experimental pancreatitis.
Soft tissue sarcomas embrace a wide variety of rare tumours. This often means excision without wide margins, and the unexpected malignancy leads to diversity of postoperative treatment. As a rule all lesions of a soft tissue tumour should be biopsied if persisting for more than 6 weeks. The extent of the biopsy is determined by the tumour characteristics, but should not aggravate later resection of a malignant tumour. Preoperative diagnostic studies should be standardised and include MNR, while the tumour is characterised according to the recent edition of the UICC GTNM system. The primary tumour should be excised in a limb-sparing way with wide margins, if necessary including the neighbouring fascia. Local recurrence should be approached aggressively like primary tumours, with curative intention. In cases of distant metastases, which usually occur in the lungs, a grading-associated approach is necessary. In G3 metastases chemotherapy should be administered before the surgical intervention. Radiation therapy is saved for patients in whom the tumour cannot be resected with wide margins or is larger than 10 cm maximum diameter. In the light of current knowledge, radiation therapy should be given as an adjuvant for patients whose tumour was resected without wide margins and for tumours larger than 10 cm in diameter. The use of palliative chemotherapy is still controversial and identification of new prognostic markers for patient selection is necessary. Since most patients with soft tissue sarcoma die from distant metastases and not the primary or locally recurrent tumour, the need for effective chemotherapy in an adjuvant setting is obvious. Controlled studies with as many enrolled patients as possible are necessary if valid data are to be collected. The management of soft tissue sarcoma patients is in principle multidisciplinary and should be confined to specialised centres.
OBJECTIVES: Tonometry is widely used in the diagnosis of sepsis and splanchnic ischemia. This study was devised to analyze the predictive value of gastric tonometry for outcome of experimental viscus perforation-induced peritonitis. The impact of conventional and laparoscopic intervention on tonometric measurements was the main scope. METHODS: This randomized controlled intervention trial was performed in a University experimental laboratory, using 24 female Duroc pigs. Pigs were subjected to gastric perforation followed by a 12 h interval of peritonitis, and then to either laparoscopic or conventional surgical repair of the defect with peritoneal lavage. Gastric tonometry and cardiocirculatory monitoring were performed. RESULTS: Septic shock associated with peritonitis and subsequent lethal outcome was accurately predicted with gastric tonometry. Changes of gastric mucosal pH correlated significantly with decreases of MAP (r2=0.880; P<0.001) and SVR (r2=0.678; P<0.001), increase of QT (r2=0.486; P=0.013), and mortality (r=0.752; P<0.001). Mortality was significantly higher in laparoscopically treated animals compared to those subjected to the open procedure (78% vs 22%; P<0.045). CONCLUSIONS: Gastric tonometry accurately predicted mortality in experimental peritonitis. The decline of gastric mucosal pH in the laparoscopic group was more than double that of to conventionally treated animals. This finding not only reflected the increase of systemic CO2 due to higher absorption during CO2-pneumoperitoneum, but probably also indicated a more severe form of splanchnic ischemia during laparoscopic surgery. Even though tonometry can be used to accurately predict mortality and separate the high risk group, extreme caution should be applied under conditions associated with severe peritonitis.
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BACKGROUND: Minimal invasive surgery is increasingly used in conditions complicated by peritonitis-e.g., peptic ulcer perforation. This study was devised to assess the effect of a pneumoperitoneum (PP) on the ultrastructural integrity of parietal peritoneum in perforation-induced peritonitis. METHODS: Anesthetized rats were subjected either to standardized gastrotomy simulating gastric perforation (groups Ia-d; IIa-d) or to sham perforation (groups IIIa-d, IVa-d). In group I (a-d) and III (a-d), CO2 was insufflated 12 h after gastrotomy for 60 min (Pia 4 mmHg). Glutaraldehyde was administered intraperitoneally at the end of the PP period while the abdominal wall was still extended (group index a), as well as 30 sec (b), 2 h (c), and 12 h (d) after desufflation. Specimens were taken from the parietal peritoneum of the left diaphragm for scanning electronic-microscopic (SEM) analysis. In groups II (a-d) and IV (a-d), simple puncture of the abdominal cavity was performed, and specimens were taken at corresponding times. RESULTS: In group Ia (gastric perforation with PP), distortion of the mesothelial cell layer with concomittant opening of stomata to the submesothelial tissue was already observed in specimens harvested while the abdominal wall was still extended. Concomitantly, scarce microvilli, which appeared coarse and thickened, were lying flat on top of the mesothelial cells. After desufflation (groups Ib-c), a rapid process of mesothelial disintegration with disruption from the submesothelial layer and vanishing of microvilli occurred. At 12 h after PP (group Id), complete deterioration of mesothelial cell integrity was observed. In groups IIa-c (gastric perforation without PP), microvilli appeared shrunk and coarse, while integrity of the mesothelial cell layer remained intact up to 2 h after the abdominal puncture. At 12 h after abdominal puncture (group IId), the microvilli had nearly completely vanished and the mesothelium was breaking apart into multiple soils. CONCLUSIONS: In SEM analysis of parietal peritoneum, premature distortion, and disintegration of the mesothelial cell layer was observed in animals exposed to increased abdominal pressure in addition to gastric perforation-induced peritonitis.
In patients with implanted pacemaker/cardioverter defibrillator (ICD), the use of electrocautery can lead to serious pacemaker dysfunction. The ultrasonically activated scalpel, however, which has been introduced mainly for the use in laparoscopic surgery, could potentially avoid the outlined problem, since no electrical current flows while in use. This hypothesis was tested in a pacemaker patient undergoing laparoscopic cholecystectomy. During the procedure, no abnormal rhythms or ECG interferences were detected while working in close vicinity to the device. Thus, the ultrasonically activated scalpel provides adequate hemostasis and does not bear the risk of pacemaker dysfunction.
In conclusion, surgical therapy in patients with chronic pancreatitis may be characterized as follows: 1. Independently, several investigators have found intraductal and intraparenchymatous hypertension in patients with chronic pancreatitis. Decompression of the ductal system as the main principle of surgical therapy achieves clinical pain relief in most patients with chronic pancreatitis. The precondition is a consequent drainage of the main pancreatic duct and tributary ducts of second and third order up to the prepapillary region. The presence of an inflammatory tumor in the head of the pancreas or ductal abnormalities in the prepapillary region or a pancreas divisum requires performance of an extended drainage operation (LPJ-LPHE) to achieve pain relief and an improved quality of life. An extended drainage operation effectively manages complications arising from adjacent organs, such as distal common bile duct stenosis, segmental duodenal stenosis, and internal pancreatic fistulas. The extent of decompression has to be tailored to the anatomic and morphologic situation of the patient. 2. In patients with chronic pancreatitis, the main pancreatic duct is usually dilated. A small duct (3-5 mm) is only small for the surgeon. For the sclerosing entity of chronic pancreatitis with a truly small duct, that is, less than 3 mm in diameter ("small duct disease"), a longitudinal V-shaped excision of the ventral pancreas, as opposed to left resection, provides a new perspective for a sufficient drainage. 3. In the presence of segmental portal hypertension, a simple or extended drainage operation does not result in a normalization of the portal venous blood flow; however, how often relevant upper gastrointestinal hemorrhage develops from segmental portal hypertension is unclear. Therefore, the clinical relevance of this special problem needs further evaluation. 4. Postoperative morbidity of LPJ-LPHE is significantly lower in comparison to resectional procedures, such as PD, PPPD, and DPRHP. A lower perioperative mortality rate is not justified anymore as a relevant criterion in favor of drainage procedures because resectional procedures are burdened by a minimal or no mortality in experienced centers; however, PD and PPPD are greatly hampered by a significantly decreased postoperative global quality of life as opposed to the LPJ-LPHE. This is reflected by a significantly lower rate of social and professional rehabilitation. 5. The incidence of exocrine and endocrine organ dysfunction is lower after LPJ-LPHE compared with PD or PPPD, but not compared with DPRHP. Preservation of the gastroduodenal passage and the continuity of the bile duct with its associated feedback mechanisms of exocrine pancreatic secretion and glucose metabolism seem to be responsible for this phenomenon. 6. An early surgical or endoscopic interventional drainage of the hypertensive pancreatic duct system possibly offers the chance to favorably manipulate the natural course of chronic pancreatitis with regard to a delayed onset of exocrine or endocrine insufficiency. 7. Late mortality reflects continued alcohol abuse rather than the effect of an operative procedure.
OBJECTIVE: To examine the impact of continuous venovenous hemofiltration (CVVH) on the course of experimental pancreatitis in pigs. SUMMARY BACKGROUND DATA: The activation of different mediator cascades is assumed to trigger multiple organ dysfunction or failure during necrotizing pancreatitis. CVVH has been suggested to be beneficial in those instances by eliminating several inflammatory mediators released in the circulation. METHODS: Pancreatitis was induced by a combined intraductal injection of sodium taurocholate and enterokinase. Control group animals received no treatment after induction. A second group underwent "therapeutic" CVVH after a 20% decline of mean arterial pressure. In the third group, "prophylactic" CVVH was started simultaneously with the induction of pancreatitis. The concentrations of tumor necrosis factor-alpha, transforming growth factor-beta1, kinin, and phospholipase A2 were measured at different time points in blood (pre- and postfilter) and in the hemofiltrate to calculate the respective sieving coefficients that reflect most accurately the plasma clearance of mediators by CVVH. RESULTS: Survival time was significantly prolonged both by therapeutic and prophylactic CVVH; it was more pronounced in the latter. CVVH did not influence the increase in transforming growth factor concentrations. However, 6 hours after induction, the increases of plasma concentrations of tumor necrosis factor, phospholipase, and kinin were significantly weakened by CVVH compared with controls. In the treatment groups, the plasma concentrations of tumor necrosis factor and phospholipase showed a significant negative correlation with the respective sieving coefficients, which decreased in the later course of the experiments. CONCLUSIONS: Experimental necrotizing pancreatitis was associated with a tremendous increase of plasma concentrations of tumor necrosis factor, phospholipase, and kinin. The effective removal of these mediators by CVVH resulted in significantly improved survival time. Animals that received prophylactic CVVH had a longer survival period than those in which CVVH was started after clinical impairment. The decreasing efficiency of CVVH in eliminating inflammatory mediators in the later course of the experiments suggested that the filter membranes were compromised by long-term application. These findings provide further evidence that CVVH offers therapeutic options even in the absence of conventional indications for blood-purifying treatments.
Recent epidemiologic evidence suggests that patients with chronic pancreatitis (CP) have an increased risk of developing pancreatic carcinoma (PCA). In spite of numerous similarities in both diseases, mechanisms for progression from CP to PCA are poorly understood. We hypothesized that enhanced angiogenesis might play a pivotal role in the etiology and histopathology of both CP and PCA, and thus form a possible link between precancer and carcinoma. In surgical specimens of 18 patients with CP, 10 with PCA, and 18 controls, absolute numbers of blood vessels and relative blood vessel density were assessed after immunostaining of endothelial cells for von Willebrand factor and PECAM-1 (platelet/ endothelial cell adhesion molecule-1). Furthermore, the expression of cell adhesion molecules ICAM-1 (intercellular adhesion molecule-1) and VCAM-1 (vascular cell adhesion molecule-1) and of VEGF (vascular endothelial growth factor) was investigated in all specimens. Both CP and PCA exhibited areas of high vascular density ("hot spots"). The mean number of blood vessels in these areas in PCA was 132.2+/-16.8 per mm2, and in CP, 99.2+/-7.4 per mm2. The mean vessel count in controls was 25.1+/-5.1. Relative vessel density was increased in both PCA (41.3+/-3.5%) and CP (30.6+/-2.6%) versus controls (8.0+/-0.8%). Both absolute vessel count and relative vessel density were significantly higher (p<0.05) in PCA than in CP. Enhanced expression of ICAM-1 in CP and PCA was seen in ductal cells in CP and cancer cells. In controls, ICAM-1 and VCAM-1 were expressed only at low levels in endothelial cells. VCAM-1 was strongly expressed in acinar cells as well as in ductal cells. In CP and PCA, VEGF was strongly expressed in ductal cells in CP as well as in cancer cells. We show for the first time that angiogenic activity is increased in both CP and PCA. Based on this study, we suggest that antiangiogenesis might be a novel target for prevention or therapy in chronic pancreatic diseases.