Hemorrhoidal Artery Ligation Operations-Recto-Anal Repair (HALO-RAR) Procedure for Recurrent Haemorrhoids: Excellent Patient Satisfaction.

Background Haemorrhoid is the most common anal canal disease. Treatments may vary from non-invasive to invasive depending on the symptoms. Haemorrhoidectomy has been widely used. However, it has some drawbacks like severe postoperative pain, longer time to return to daily activities and complications such as anal stenosis. To overcome these, various new treatment methods have been introduced. Doppler-guided hemorrhoidal artery ligation operations (HALO) are becoming popular among surgeons. HALO has been reported to have a lower recurrence rate of less than 10% and higher patient satisfaction of approximately 90% with minimal postoperative pain. It achieves very good postoperative outcomes in the treatment of early haemorrhoids where per rectal bleeding and/or perianal discomfort are main symptoms. Nevertheless, it has a limitation in the treatment of prolapsing haemorrhoids. To tackle this, simultaneous recto-anal repair (RAR) has been recently introduced. HALO, in combination with RAR, has been reported to achieve good postoperative outcomes and excellent patient satisfaction. This is a two-stage open operation. The stages are:  - Doppler-guided HALO and  - RAR (recto-anal repair) Methods We are presenting a single-centre one-year experience of Doppler-guided haemorrhoidal artery ligation operation and recto-anal repair (DG-HALO and RAR) conducted on haemorrhoidal patients to evaluate the outcomes and effectiveness of the procedure. Retrospective data were collected for the patients who underwent HALO over one year period from June 2018 to August 2019. A total of 10 patients were treated with the HALO-RAR procedure. Results The male to female ratio was 7:3, median age was 47.98 (28.38 - 61.7) years, median body mass index (BMI) was 30.23 (23.8 - 39.1). Eight patients were American Society of Anesthesiologists (ASA) Grade II, one patient was ASA I and one was ASA III. Time from initial consultation to the HALO procedure was 9.90 (3.5 - 19.8) months. All patients complained of preoperative bleeding and six of them complained of pain or discomfort. Nine patients underwent previous bandings in the clinic and one patient declined banding. The average time of the procedure was 57 mins. The average number of ligations was 10 (0-21). In one case, the proctoscope did not pair with the speaker. The average number of plications was three (2-4). Postoperatively, nine patients had no immediate complications; one patient had acute urinary retention. Seven patients were discharged on the same day. One patient had to stay overnight for monitoring prior to restarting apixaban, one patient for his learning difficulties and one patient had an unplanned overnight stay due to acute urinary retention requiring catheterization. Eight patients had their first follow-up; improvement of symptoms was found in 100% patients on the first follow-up. Conclusion HALO-RAR should be considered as a treatment option for recurrent symptoms after banding for haemorrhoids. The study showed good overall results with no immediate surgical complications. Excellent patient satisfaction was found even in long-term follow-up.

Pathways of care for patients with suspected cancer of the pancreas: a tiered questionnaire-based survey of medical personnel across a single United kingdom Calman-Hine cancer network.

OBJECTIVE: This study examines clinical management pathways for patients with suspected pancreatic cancer within a single United Kingdom Calman-Hine NHS cancer network with particular focus on referral patterns and the primary care-hospital specialist interface. METHODS: A questionnaire-based study appraising responses from three key groups (general practitioners, gastrointestinal physicians and gastrointestinal surgeons) practising within a cancer network. The questionnaire addressed caseload, referral pathways, multidisciplinary care teams and involvement of specialists. PARTICIPANTS: The study population comprised 448 general practitioners, 14 gastroenterologists and 23 gastrointestinal surgeons. RESULTS: The mean number of new patients with suspected pancreatic cancer seen per general practitioner per annum was 0.4 (range: 0-1). Fifty-three percent of general practitioners refer to gastrointestinal physicians and 47% to gastrointestinal surgeons. In hospital, a relatively large number of physicians and surgeons see a small number of new patients each per annum. The involvement of multidisciplinary teams and referral of patients with non-resectable disease for chemotherapy is limited. Fourteen (60.9% out of 23 general surgeons) refer all patients to pancreatic specialists, 4 (17.4%) selectively refer and 5 (21.7%) never refer. CONCLUSION: The findings suggest divergence in standards of care from those advocated in governmental cancer strategic plans. In particular, not all patients with suspected pancreatic cancer see specialists, many hospital specialists see small numbers of cases and multidisciplinary care is limited.

Calpain I inhibitor ameliorates the indices of disease severity in a murine model of cerulein-induced acute pancreatitis.

OBJECTIVE: Nuclear factor-kappaB (NF-kappaB) is a transcription factor which plays a pivotal role in the induction of genes involved in the response to injury and inflammation. Calpain I inhibitor is a potent antioxidant which is an effective inhibitor of NF-kappaB. This study examined whether the postulate that calpain I inhibitor attenuates experimental acute pancreatitis. DESIGN AND SETTING: In a murine model we measured NF-kappaB activation, expression of intercellular adhesion molecule (ICAM) 1, nitrotyrosine, inducible nitric oxide synthase (iNOS), nuclear enzyme poly(ADP-ribose) synthetase (PARS), myeloperoxidase, malondialdehyde, amylase and lipase and determined histological evidence of lung and pancreas injury in four groups: control (saline only), cerulein, calpain I inhibitor plus cerulein and calpain I inhibitor plus saline. MEASUREMENTS AND RESULTS: Intraperitoneal injection of cerulein in mice resulted in severe, acute pancreatitis characterised by oedema, neutrophil infiltration, tissue haemorrhage and necrosis and elevated serum levels of amylase and lipase. Infiltration of pancreatic and lung tissue with neutrophils (measured as increase in myeloperoxidase activity) was associated with enhanced lipid peroxidation (increased tissue levels of malondialdehyde). Immunohistochemical examination demonstrated a marked increase in immunoreactivity for nitrotyrosine, iNOS and PARS in the pancreas and lung of cerulein-treated mice. In contrast, pre-treatment with calpain I inhibitor markedly reduced: the degree of pancreas and lung injury; upregulation/expression of ICAM-1; staining for iNOS, nitrotyrosine and PARS; and lipid peroxidation. Additionally, calpain I inhibitor treatment significantly prevented the activation of NF-kappaB as suggested by the inhibition of IkappaB-alpha; degradation in the pancreas tissues after cerulein administration. CONCLUSIONS: Taken together, our results clearly demonstrate that prevention of the activation of NF-kappaB by calpain I inhibitor ameliorates experimental murine acute pancreatitis.

Pyrrolidine dithiocarbamate reduces the severity of cerulein-induced murine acute pancreatitis.

The nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays a pivotal role in the induction of genes involved in the response to injury and inflammation. Dithiocarbamates are antioxidants that are potent inhibitors of NF-kappaB. This study tested the hypothesis that pyrrolidine dithiocarbamate (PDTC) attenuates experimental acute pancreatitis. Intraperitoneal injection of cerulein in mice resulted in severe, acute pancreatitis characterized by edema, neutrophil infiltration, tissue hemorrhage and necrosis, and elevated serum levels of amylase and lipase. Infiltration of pancreatic and lung tissue with neutrophils (measured as increase in myeloperoxidase activity) was associated with enhanced lipid peroxidation (increased tissue levels of malondialdehyde). Immunohistochemical examination demonstrated a marked increase in immunoreactivity for nitrotyrosine and intracellular adhesion molecule-1 in the pancreas and lung of cerulein-treated mice. In contrast, the degree of 1) pancreas and lung injury, 2) upregulation/expression of intracellular adhesion molecule-1, 3) staining for nitrotyrosine, and 4) lipid peroxidation was markedly reduced by pretreatment with PDTC. This study demonstrates that prevention of the activation of NF-kappaB by PDTC ameliorates the tissue injury associated with experimental murine acute pancreatitis and provides an important insight into the molecular biology of acute pancreatitis.

Differential nitric oxide synthase expression during hepatic ischemia-reperfusion.

BACKGROUND: In recent years the important role of nitric oxide in hepatic ischemia-reperfusion injury has been increasingly recognised. The prevailing consensus is that reperfusion injury may be partly the result of decreased production of nitric oxide from endothelial nitric oxide synthase and excessive production of nitric oxide from the inducible isoform. We therefore undertook this study to characterize the expression of different nitric oxide synthase isoforms during hepatic reperfusion. METHODS: Male Wistar rats (n = 6) were subjected to 45 minutes of partial hepatic ischemia (left lateral and median lobes) followed by 6 hours of reperfusion. Control animals (n = 6) were subjected to sham laparotomy. The expression of endothelial and inducible nitric oxide synthase was examined using immunohistochemistry and Western blotting. Liver sections were also stained with nitrotyrosine antibody, a specific marker of protein damage induced by peroxynitrite (a highly reactive free radical formed from nitric oxide). RESULTS: Liver sections from all the control animals showed normal expression of the endothelial isoform and no expression of inducible nitric oxide synthase. Livers from all the animals subjected to hepatic ischemia showed decreased expression of endothelial nitric oxide synthase, and all but one animal from this group showed expression of the inducible isoform both in inflammatory cells and in hepatocytes. Western blotting confirmed these findings. Staining with the antinitrotyrosine antibody was also confined to five liver sections from animals subjected to hepatic ischemia. CONCLUSIONS: During the reperfusion period after hepatic ischemia, endothelial nitric oxide synthase is downregulated while inducible nitric oxide synthase is expressed in both hepatocytes and inflammatory cells. The presence of nitrotyrosine in livers subjected to hepatic ischemia-reperfusion suggests that the expression of inducible nitric oxide synthase plays an important role in mediating reperfusion injury in this model.

Differential expression of pulmonary nitric oxide synthase isoforms after intestinal ischemia-reperfusion.

BACKGROUND/AIMS: Nitric oxide has been implicated in both attenuating and aggravating ischemia-reperfusion injury in most organs. This study aimed to investigate the role of nitric oxide produced by the two principal isoforms of nitric oxide synthase in the lung during post-ischemic reperfusion of the intestine. METHODOLOGY: Rats were randomized into four groups of 6 animals: Group A: laparotomy and superior mesenteric artery dissection without occlusion and maintenance for 2 h (control group at 2 h). Group B: laparatomy and superior mesenteric artery occlusion for 30 min and reperfusion of the intestine for 2 h (ischemia-reperfusion group at 2 h). Group C: control animals at 6 h. Group D: ischemia-reperfusion animals at 6 h. Arterial blood pressure was monitored throughout the procedure. Animals were euthanazed at the end of the experiment, and lungs were harvested for histological assessment of injury and for immunohistochemical examination of nitric oxide synthase isoforms and nitrotyrosine. RESULTS: In all animals subjected to intestinal ischemia a period of systemic hypotension occurred immediately upon reperfusion. Histological evidence of lung injury was limited to those animals subjected to an intestinal reperfusion insult. Compared to control animals, pulmonary endothelial nitric oxide synthase expression was diminished at 2 h (p = 0.002), while expression of inducible nitric oxide synthase (p = 0.002) and nitrotyrosine (p = 0.02) was increased at 6 h. CONCLUSIONS: Following intestinal ischemia-reperfusion, early pulmonary damage is associated with decreased endothelial nitric oxide synthase expression in the lung. Expression of inducible nitric oxide synthase occurs during the later stages of reperfusion; this leads to overproduction of nitric oxide with consequent nitrosylation of protein tyrosine residues and thus aggravated pulmonary injury.

Adenosine preconditioning attenuates hepatic reperfusion injury in the rat by preventing the down-regulation of endothelial nitric oxide synthase.

BACKGROUND: Previous work has suggested that in the liver, adenosine preconditioning is mediated by nitric oxide. Whether the endothelial isoform of nitric oxide synthase plays a part in this mechanism has however not yet been investigated. METHODS: Wistar rats were used (6 in each group)--Groups: (1) sham, (2) ischemia-reperfusion, (3) adenosine + ischemia-reperfusion, (4) endothelial isoform inhibitor + adenosine + ischemia-reperfusion. RESULTS: Using immunohistochemistry, this study has revealed a decrease in the expression of endothelial nitric oxide synthase following hepatic ischemia-reperfusion. This was prevented by adenosine pre-treatment. When an inhibitor of endothelial nitric oxide synthase was administered prior to adenosine pre-treatment, pre-conditioning did not occur despite normal expression of endothelial nitric oxide synthase. CONCLUSIONS: These findings suggest that adenosine attenuates hepatic injury by preventing the downregulation of endothelial nitric oxide synthase that occurs during ischemia-reperfusion.