Transanal endoscopic surgery is effective and safe after endoscopic polypectomy of potentially malignant rectal polyps with questionable margins.

AIM: To determine the percentage of residual lesion observed in the pathology study of transanal endoscopic surgery (TEM) specimens after endoscopic polypectomy of malignant rectal polyps with questionable margins, and the need for further surgery. Secondary aims: to determine the morbidity and mortality associated with this procedure and to identify the percentage of recurrence after excision by TEM. METHODS: Observational study with prospective data collection of all patients undergoing TEM after endoscopic polypectomy for malignant rectal polyps or non-invasive high-grade neoplasia, from January 2004 to December 2016. An en bloc full-thickness wall excision of the scar was performed. Variables recorded: histology of TEM specimen, 30-day morbidity and mortality according to the Clavien-Dindo classification, need for salvage surgery and recurrence. RESULTS: Fifty out of 690 patients undergoing TEM during the study period (36 adenocarcinomas, five non-invasive high-grade neoplasias and 9 neuroendocrine tumors) were included. Post-surgery histology showed residual lesion in 21 (42%) patients: 7 neuroendocrine tumors, 10 adenomas and 4 adenocarcinomas (two pT1, one pT2 and one pT3). The pT2 and pT3 patients (4%) underwent salvage surgery. No recurrence was observed, and mean follow-up was 29.1Â ± 21.6 months. The 30-day morbidity rate was 14%, but 4/7 with Clavien-Dindo grade I. CONCLUSIONS: After endoscopic polypectomy of malignant rectal polyps with questionable margins, the presence of residual lesion in the pathology study of transanal resection specimens is high. TEM with full-thickness resection of these lesions is an appropriate treatment, allowing disease control and achieving minimal morbidity.

Variation among endoscopy units in the achievement of the standards of colonoscopic performance indicators.

BACKGROUND/AIMS: To assess the achievement of quality standards of colonoscopy at six endoscopy units. METHODOLOGY: Three indicators were used to assess the quality of 1056 colonoscopies performed at six hospitals: cecal intubation; adequate colon cleansing; and removal and recovery of all detected polyps. Analyses were performed on the total number of colonoscopies and on colonoscopies in which polyps were actually detected. The accomplishment of each indicator and a global compound index of all three indicators, named the Problem Rate, were analyzed. Results from each endoscopy unit were compared to previously established standards. RESULTS: Adequate colon cleansing was the most frequent problem for quality in all centers; adequate colon preparation was 67% (range 50 to 84%). The cecum was reached in 84% of all colonoscopies (range 76 to 90%). 75% of all patients (range 28. 79%) had all polyps excised and recovered. All centers had rates below standard for one or several indicators (p<0.01, all cases). Two of the participant hospitals had an overall problem rate above the estimated standard (p<0.01). CONCLUSIONS: There is a significant variation in the achievement of quality standards of colonoscopy between endoscopy units. Colon cleansing is the most frequent quality problem for colonoscopy.

[Sedation in digestive endoscopy. Results of a hospital survey in Catalonia (Spain)]. / Sedación en la endoscopia digestiva. Resultados de una encuesta hospitalaria en Cataluña.

INTRODUCTION: The need for sedation is increasing in digestive endoscopy units (DEU). There are no data on the use of sedation in DEU in Catalonia (Spain). OBJECTIVE: To evaluate the use of sedation in DEU in Catalonia. MATERIAL AND METHOD: A questionnaire on the practice of sedation was designed and sent to the heads of medical and nursing staff of the DEU of 63 public and private hospitals in Catalonia. Two mailings were sent with an interval of three months between each. The questionnaire included 62 items on the characteristics of the hospital and the DEU, number of explorations, frequency of sedation use, drugs employed, participation of an anesthesiologist, use of monitoring, and complications. RESULTS: Forty-four DEU (70%) corresponding to 31 public hospitals and 13 private hospitals completed the questionnaire. Evaluation of sedation patterns was based on 105,904 explorations performed in the various DEU (56,453 gastroscopies, 47,278 colonoscopies and 2,173 endoscopic retrograde cholangiopancreatographies (ERCP) in 2001. Sedation, sedation-analgesia or anesthesia was used in 17% of gastroscopies, 61% of colonoscopies and 100% of ERCP. Sedation was administered by an anesthesiologist in 7% of gastroscopies, 25% of colonoscopies and 38% of ERCP. Anesthesiologist administration was more frequent in private than in public centers (gastroscopies: 25% vs. 2%; colonoscopies: 57% vs. 9%, p < 0.001). No deaths associated with the use of sedation were reported. Eighty-nine percent of the DEU complied with standard recommendations for the practice of sedation. CONCLUSIONS: In Catalonia, the use of sedation is highly variable, depending on the endoscopic procedure and the DEU. Use of sedation in infrequent in gastroscopy, fairly widespread in colonoscopy and routine in ERCP. Anesthesiologist administration is significantly more frequent in private hospitals. Most DEU follow standard sedation practices.

Ethanol feeding aggravates morphological and biochemical parameters in experimental chronic pancreatitis.

BACKGROUND AND AIMS: Instillation of trinitrobenzene sulfonic acid (TNBS) into the rat pancreatic ducts induces morphological changes resembling human chronic pancreatitis. In humans, alcoholism is commonly associated with chronic pancreatitis, but ethanol feeding fails to induce pancreatitis in experimental animals. We hypothesized that ethanol would manifest its pathogenetic effects on a duct-injured pancreas. METHODS: Chronic pancreatitis was induced in rats by instillation of TNBS into pancreatic ducts. Thereafter, rats were fed a normal chow diet with or without ethanol supplementation. Control rats received vehicle and a normal diet. A separate group of vehicle-treated rats were also fed with ethanol. At 2 and 4 weeks pancreata were excised and processed for morphological examination or for biochemical assays. From crude homogenates, protein and hydroxyproline were quantified. After sonication, homogenates were also assayed for amylase and DNA. An oral glucose tolerance test was performed on the fourth week. RESULTS: TNBS induced chronic fibrogenic pancreatitis that was associated with a reduction in pancreatic weight, DNA, protein and amylase as compared to control rats. Ethanol feeding to TNBS-treated animals slowed weight gain, increased fasting glucose and impaired glucose tolerance test. Larger areas of gland atrophy were observed with a striking disruption of the normal architecture of the islets. Ethanol accelerated pancreatic involution and collagen deposition as measured by total amylase, protein, DNA and hydroxyproline content. CONCLUSIONS: In TNBS chronic pancreatitis, active fibrogenesis is associated with progressive atrophy of glandular elements. Morphological and biochemical parameters are aggravated by sustained ethanol intake.

Acute pancreatitis as a triggering factor for thrombotic thrombocytopenic purpura.

Thrombotic thrombocytopenic purpura (TTP) constitutes a poorly understood multisystemic disease of vascular origin that may involve any organ by thrombotic occlusions of the small vessels. Treatment with plasmapheresis is the best therapeutic option at this present moment. Involvement of the pancreas is a well established feature of this disease, which has generally been interpreted as a consequence of pancreatic vascular compromise. However, there are a few cases in the literature in which the clinical signs of TTP developed well after the clinical and laboratory demonstration of acute pancreatitis (AP). Therefore, the possibility of pancreatic inflammation as a triggering factor of TTP may need to be considered. This cause-effect relationship between AP and TTP remains unclear. We report a patient with chronic pancreatitis presenting with two episodes of TTP, triggered by acute relapses of pancreatitis. TTP may, thus, constitute a hematological complication of AP. We discuss the pathophysiological aspects of this association, along with therapeutical options.

Contrasting effects of circulating nitric oxide and nitrergic transmission on exocrine pancreatic secretion in rats.

BACKGROUND: Nitric oxide (NO) blockade by L-nitroarginine methyl ester (L-NAME) inhibits pancreatic secretion in vivo and aggravates caerulein induced pancreatitis. Nitric oxide synthase (NOS) is present in pancreatic islets, endothelium, and nerve fibres. L-NAME blocks all known NOS isoforms. AIM: To investigate the source of NO blocked by L-NAME that inhibits amylase secretion. METHODS: Amylase output was measured in rats in response to caerulein (0.1-50 microg/kg) alone or with indazole. Baseline secretion and the response to supramaximal caerulein were also examined after administration of indazole, L-NAME, haemoglobin, or aminoguanidine under continuous blood pressure measurement. In separate experiments, pancreatic secretion was measured after blockade of afferent nerve fibres by either systemic or local capsaicin. The effect of neural NOS inhibition on caerulein induced pancreatitis was also investigated. RESULTS: L-NAME, haemoglobin, and supramaximal caerulein (10 microg/kg) increased blood pressure, whereas indazole and suboptimal caerulein (0.1 microg/kg) did not. Indazole and capsaicin decreased basal amylase output. L-NAME and haemoglobin reduced basal amylase output to a lesser extent and potentiated the inhibitory response to supramaximal caerulein. In contrast, full neural NOS inhibition by L-NAME partially reversed the expected caerulein induced suppression of amylase output. This effect was reproduced by indazole and capsaicin. Indazole did not alter responses to either optimal (0.25 microg/kg) or suboptimal (0.1 microg/kg) caerulein, nor, in contrast with L-NAME, aggravate the outcome of caerulein induced pancreatitis. CONCLUSIONS: Reduction of circulating NO availability, probably of endothelial origin, is responsible for the decrease in amylase secretion observed in the early response to L-NAME. Nitrergic neurotransmission plays an important role in the control of pancreatic secretion and may induce opposite effects to endothelial NOS activity.

Induction of chronic pancreatic disease by trinitrobenzene sulfonic acid infusion into rat pancreatic ducts.

Despite being a common disease in humans, little is known about the etiopathogenesis of and effective therapeutic approaches to chronic pancreatitis, due mainly to the fact that few simple animal models suitable to study inflammatory and fibrogenetic processes have been described in the pancreas. Trinitrobenzene sulfonic acid (TNBS) induces chronic colitis and cholangitis in the rat. We hypothesized that TNBS instillation into the pancreatic ducts could also result in the development of a chronic pancreatic disease. The biliopancreatic duct of rats was cannulated and tied close to the liver. TNBS [0.4 ml of 2% TNBS in phosphate-buffered saline (PBS)-10% ethanol, pH 8] was infused into the pancreas under a continuous controlled-pressure system. Control rats underwent the same procedure using vehicle only. Pathology assessment of TNBS-treated rats examined at 48 h was consistent with severe acute necrotizing pancreatitis, having a morality rate of 31% and serum amylase activity of 37.4 +/- 8.8 U/ml at 24 h and 13.3 +/- 1.7 U/ml at 48 h (p < 0.01 for both time points compared to PBS/ethanol-treated rats). Groups of 10 rats each were killed at 3, 4, and 6 week after the surgical procedure. Morphological examination revealed changes mimicking features of chronic pancreatitis in humans in 80% (32 of 40) of TNBS-treated rats, consisting in various degrees of periductal and lobular fibrosis, duct stenosis, patchy acute and chronic inflammatory cell infiltrates, and signs of gland atrophy. Animals developing chronic disease had a weight gain rate significantly lower than that of control rats. Serum amylase, fasting glucose, and a glucose tolerance test were not different in diseased or control rats. In conclusion, we were able to induce chronic fibrogenetic inflammatory disease in the pancreas after a single pulse instillation of TNBS into the pancreatic ducts. This might be a useful animal model to study the pathophysiology of inflammatory, fibrogenetic, and reparative processes in pancreatic tissue.

[Acute pancreatitis in cystic fibrosis]. / Pancreatitis aguda en la fibrosis quística.

Cystic fibrosis is the most prevalent hereditary disease in the Caucasian race. It is a multisystemic alteration that affects the quality and quantitative properties of exocrine secretions. The pancreas develops a progressive atrophy causing steatorrhoea and nutritive deficiencies. Acute pancreatitis is an unusual complication. The pancreatic atrophy prevents the inflammatory response. Published series suggest that pancreatitis in 0.5%, including patients without pancreatic insufficiency. We present two cases with cystic fibrosis, with and without pancreatic insufficiency, who developed acute pancreatitis.

[Thrombocytopenia onset in acute episodes of pancreatitis]. / Aparición de trombocitopenia en los episodios agudos de pancreatitis.

BACKGROUND: The objective of this study was to determine the prevalence of thrombocytopenia in acute pancreatitis and its value as a prognostic marker for complications. METHODS: The records of all patients admitted to our institution between January and June 1993 were reviewed. After exclusion of other possible causes of thrombocytopenia, 104 patients were evaluated. The prognostic value of thrombocytopenia was determined by evaluation of the length of hospital stay, radiologic severity, complications, need for ICU care, need for surgery and mortality. RESULTS: The etiology of pancreatitis was as follows: gallstone-induced in 49 patients, alcoholic in 35, idiopathic in 12 and due to other causes in the remaining 8 cases. Thrombocytopenia developed early, within the first 48 hours and was moderate (106 +/- 27 x 10(9)/l). Alcoholic pancreatitis was associated to a higher probability to develop thrombocytopenia (43% vs 36% in gallstone-induced pancreatitis and 4% in idiopathic pancreatitis, p = 0.02). Thrombocytopenic patients had a greater radiologic severity (Balthazar's scores D or E 78% vs 49%, p = 0.04), a higher number of acute complications (28% vs 10%, p = 0.05) and a more frequent need for ICU care (25% vs 7%, p = 0.01). No differences were seen in length of hospital stay, need for surgery and mortality between the two groups of patients. CONCLUSIONS: Thrombocytopenia is frequent in acute pancreatitis, especially in cases of alcoholic origin. Its presence suggests a higher risk to develop complications.