Short learning curve in transition from laparoscopic to robotic-assisted rectal cancer surgery: a prospective study from a Finnish Tertiary Referral Centre.

The narrow pelvis causes special challenges in surgery, and robotic-assisted surgery has been proven beneficial in these circumstances. While robotic surgery has some specific advantages in rectal cancer surgery, there is still limited evidence of the learning curve of the technique involved. The aim here was to study the transition from laparoscopic to robotic-assisted surgery among experienced laparoscopic surgeons. The data for this study were collected from a prospectively compiled register that includes patients operated on by the Da Vinci Xi robot in Tampere University Hospital. Each consecutive rectal cancer patient was included. The information on the surgical and oncological outcomes was analysed. The learning curve was assessed using cumulative sum (CUSUM) analysis. CUSUM already demonstrated an overall positively sloped curve at the beginning of the study, with neither the conversion rate nor morbidity reaching unacceptable thresholds. Conversions (4%) and postoperative complications (Clavien-Dindo III-IV 15%, no intraoperative complications) were rare. One patient died within one month and the death was not procedure-associated. While surgical and oncological outcomes were similar among all surgeons, the console times showed a decreasing trend and were shorter among those with more experience in laparoscopic rectal cancer surgery. Robotic-assisted rectal cancer surgery can be safely adapted by experienced laparoscopic colorectal surgeons.

Computer-generated structured electronic medical records are preferable to conventional medical records for patients with acute abdominal pain - a prospective, double-blinded study.

OBJECTIVES: Structured medical records improve readability and ensure the inclusion of information necessary for correct diagnosis and treatment. This is the first study to assess the quality of computer-generated structured medical records by comparing them to conventional medical records on patients with acute abdominal pain. MATERIALS AND METHODS: A prospective double-blinded study was conducted in a tertiary referral center emergency department between January 2018 and June 2018. Patients were examined by emergency department physicians and by experience and inexperienced researcher. The researchers used a new electronical medical records system, which gathered data during the examination and the system generate structured medical records containing natural language. Conventional medical records dictated by physician and computer-generated medical records were compared by a group of independent clinicians. RESULTS: Ninety-nine patients were included. The overall quality of the computer-generated medical records was better than the quality of conventional human-generated medical records - the structure was similar or better in 99% of cases and the readability was similar or better in 86% of cases, p < 0.001. The quality of medical history, current illness, and findings of physical examinations were likewise better with the computer-generated recording. The results were similar when patients were examined by experienced or inexperienced researcher using the computer-generated recording. DISCUSSION: The quality of computer-generated structured medical records was superior to that of conventional medical records. The quality remained similar regardless of the researcher's level of experience. The system allows automatic risk scoring and easy access for quality control of patient care. We therefore consider that it would be useful in wider practice.

The rate of short-term revisits after diagnosis of non-specific abdominal pain is similar for surgeons and emergency physicians - results from a single tertiary hospital emergency department.

BACKGROUND: Acute abdominal pain can be a diagnostic challenge even for experienced surgeons. Delayed diagnosis can lead to higher morbidity, mortality and increased costs. While readmission rate has been used to evaluate quality of surgical care, studies addressing the issue in emergency departments (ED) are rare. The role of emergency physicians in the care of patients with abdominal pain is increasing in many European countries, including Finland. It is not known whether this has an effect on the number of readmissions. Here we evaluate whether the increasing role of emergency physicians in examining patients presenting with abdominal pain has affected the rate of short-term revisits among patients with non-specific abdominal pain (NSAP). METHODS: We identified consecutive ED patients receiving a diagnosis of NSAP 1.1. 2015-31.12.2016 in the ED of Tampere University Hospital. Those revisiting the ED within 48 h were selected for further analysis. Data were obtained from electronic medical records. We compared the outcomes of those initially examined by surgeons and by emergency physicians. RESULTS: During the study period, 173,630 patients visited our ED, of whom 6.1% (n = 10,609) were discharged with a diagnosis of NSAP. Only 3.0% of patients revisited the ED, 0.7% required hospitalization and 0.06% immediate surgery. The short-term revisit rates among those originally examined by surgeons and by emergency physicians were similar, 2.8 and 3.2% respectively (p = 0.193). CONCLUSIONS: The rate of short-term revisits in patients with NSAP was altogether low. The increasing role of emergency physicians in the care of acute abdominal patients did not affect the revisit rate.

TNF-alpha-dependent regulation of acute pancreatitis severity by Ly-6C(hi) monocytes in mice.

The roles of monocytes/macrophages and their mechanisms of action in the regulation of pancreatitis are poorly understood. To address these issues, we have employed genetically altered mouse strains that either express the human diphtheria toxin receptor (DTR) coupled to the CD11b promoter or have global deletion of TNF-α. Targeted, conditional depletion of monocytes/macrophages was achieved by administration of diphtheria toxin (DT) to CD11b-DTR mice. We show that in the absence of DT administration, pancreatitis is associated with an increase in pancreatic content of Ly-6C(hi) monocytes/macrophages but that this response is prevented by prior administration of DT to CD11b-DTR mice. DT administration also reduces pancreatic edema and acinar cell injury/necrosis in two dissimilar experimental models of acute pancreatitis (a secretagogue-induced model and a model elicited by retrograde pancreatic duct infusion of sodium taurocholate). In the secretagogue-elicited model, the DT-induced decrease in pancreatitis severity is reversed by adoptive transfer of purified Ly-6C(hi) monocytes harvested from non-DT-treated CD11b-DTR mice or by the transfer of purified Ly-6C(hi) monocytes harvested from TNF-α(+/+) donor mice, but it is not reversed by the transfer of Ly-6C(hi) monocytes harvested from TNF-α(-/-) donors. Our studies indicate that the Ly-6C(hi) monocyte subset regulates the severity of pancreatitis by promoting pancreatic edema and acinar cell injury/necrosis and that this phenomenon is dependent upon the expression of TNF-α by those cells. They suggest that therapies targeting Ly-6C(hi) monocytes and/or TNF-α expression by Ly-6C(hi) monocytes might prove beneficial in the prevention or treatment of acute pancreatitis.

Experimental acute biliary pancreatitis induced by retrograde infusion of bile acids into the mouse pancreatic duct.

Mechanistic studies of acute pancreatitis require animal models because clinical material is generally not available during the early phases of the disease. Here we describe a protocol to induce biliary pancreatitis by retrogradely infusing bile acids into the pancreatic duct of anesthetized mice. The resulting model replicates events believed to be responsible for the onset of clinical biliary (i.e., gallstone) pancreatitis and creates highly reproducible pancreatitis with a severity that depends on the concentration of infused bile acid. Pancreatitis reaches its maximal level of severity within 24 h of induction, and it resolves over the subsequent week. This protocol enables the investigator to use genetically modified strains of mice, and it requires only relatively simple and easily learned techniques of small animal surgery. With practice and gentle technique, the surgery (from induction of anesthesia to completion of the infusion) can be completed within 25 min per animal.

Biliary acute pancreatitis in mice is mediated by the G-protein-coupled cell surface bile acid receptor Gpbar1.

BACKGROUND & AIMS: The mechanisms by which reflux of bile acids into the pancreas induces pancreatitis are unknown. We reasoned that key events responsible for this phenomenon might be mediated by Gpbar1, a recently identified and widely expressed G-protein-coupled, cell surface bile acid receptor. METHODS: Acute pancreatitis was induced in wild-type and Gpbar1(-/-) mice by either retrograde ductal infusion of taurolithocholic acid-3-sulfate (TLCS) or supramaximal secretagogue stimulation with caerulein. In vitro experiments were performed in which acini obtained from wild-type and Gpbar1(-/-) mice were exposed to either submicellar concentrations of TLCS (200-500 microM) or a supramaximally stimulating concentration of caerulein (10 nM). RESULTS: Gpbar1 is expressed at the apical pole of acinar cells and its genetic deletion is associated with reduced hyperamylasemia, edema, inflammation, and acinar cell injury in TLCS-induced, but not caerulein-induced, pancreatitis. In vitro, genetic deletion of Gpbar1 is associated with markedly reduced generation of pathological calcium transients, intracellular activation of digestive zymogens, and cell injury when these responses are induced by exposure to TLCS, but not when they are induced by exposure to caerulein. CONCLUSIONS: Gpbar1 may play a critical role in the evolution of bile-acid-induced pancreatitis by coupling exposure to bile acids with generation of pathological intracellular calcium transients, intra-acinar cell zymogen activation, and acinar cell injury. Acute biliary pancreatitis may be a "receptor-mediated" disease and interventions that interfere with Gpbar1 function might prove beneficial in the treatment and/or prevention of biliary acute pancreatitis.

Protease-activated receptor-2 exerts contrasting model-specific effects on acute experimental pancreatitis.

Protease-activated receptor-2 (PAR2) is a 7-transmembrane G-protein-coupled tethered ligand receptor that is expressed by pancreatic acinar and ductal cells. It can be physiologically activated by trypsin. Previously reported studies (Namkung, W., Han, W., Luo, X., Muallem, S., Cho, K. H., Kim, K. H., and Lee, M. G. (2004) Gastroenterology 126, 1844-1859; Sharma, A., Tao, X., Gopal, A., Ligon, B., Andrade-Gordon, P., Steer, M. L., and Perides, G. (2005) Am. J. Physiol. 288, G388-G395) have shown that PAR2 activation exerts a protective effect on the experimental model of pancreatitis induced by supramaximal secretagogue (caerulein) stimulation. We now show that PAR2 exerts a worsening effect on a different model of experimental pancreatitis, i.e. one induced by retrograde pancreatic ductal infusion of bile salts. In vitro studies using freshly prepared pancreatic acini show that genetic deletion of PAR2 reduces bile salt-induced pathological calcium transients, acinar cell injury, and activation of c-Jun N-terminal kinase, whereas genetic deletion of PAR2 has the opposite or no effect on these pancreatitis-related events when they are elicited, in vitro, by caerulein stimulation. Studies employing a combination of trypsin inhibition and activation of PAR2 with the activating peptide SLIGRL show that all these differences indeed depend on the activation of PAR2. These studies are the first to report that a single perturbation can have model-specific and opposite effects on pancreatitis, and they underscore the importance of performing mechanistic pancreatitis studies using two dissimilar models of the disease to detect idiosyncratic, model-specific events. We suggest PAR2 activation exerts a worsening effect on the severity of clinical pancreatitis and that interventions interfering with PAR2 activation may be of benefit in the treatment of patients with severe pancreatitis.

A mouse model of acute biliary pancreatitis induced by retrograde pancreatic duct infusion of Na-taurocholate.

OBJECTIVE: Most mechanistic studies of pancreatitis in mice employ the secretagogue-induced model. The currently reported studies were designed to develop an alternative, and possibly more clinically relevant, mouse model of pancreatitis. DESIGN: Na-taurocholate (10-50 microl, 1-5%) in saline, or saline alone, was retrogradely infused into the mouse pancreatic duct. The animals were killed 6-24 hours later and the severity of pancreatitis in the pancreatic head and tail was examined by quantitating hyperamylasemia, pancreatic edema, acinar cell necrosis, and pancreatic inflammation. In addition, intrapancreatic activation of trypsinogen, generation of IL-6, intrapulmonary sequestration of neutrophils, and alterations in lung compliance were evaluated. The effects of Na-taurocholate on in-vitro acinar cell calcium transients, viability, and trypsinogen activation were examined. RESULTS: Little or no evidence of pancreatitis was observed in mice infused with saline alone or in the tail of pancreata removed from animals infused with Na-taurocholate. In the head of the pancreas, evidence of pancreatitis was observed 12-24 hours after infusion of 20-50 microl 2-5% Na-taurocholate and the earliest morphological changes involved terminal duct and acinar cells. Intrapancreatic trypsin activity was transiently elevated within 5 minutes of Na-taurocholate infusion and pancreatic IL-6 levels were elevated 24 hours later. Under in-vitro conditions, Na-taurocholate triggered pathological acinar cell calcium transients, cell death, and calcium-dependent trypsinogen activation. CONCLUSION: This clinically relevant model of acute biliary pancreatitis yields reproducible results and its severity can be easily manipulated. It is ideally suited for use in mechanistic studies employing genetically modified mouse strains.

A novel biodegradable biliary stent in the normal duct hepaticojejunal anastomosis: an 18-month follow-up in a large animal model.

Creating a well-functioning hepaticojejunostomy (HJ) anastomosis with nondilated bile ducts remains a challenge. Our aim was to study the use in a large animal model of a novel, braided polylactide barium sulfate biodegradable biliary stent (BDBS) without external connection and with no need for later removal. Fifty swine were randomly operated on for Roux-Y HJ with or without BDBS in the anastomosis, and followed up (dynamic biligraphy, x-ray, serum determinations, anastomosis inner diameter, and histology) for 1.5, 3, 6, 12, and 18 months. During the follow-up, one nonstented animal died because of anastomotic leakage. In x-ray BDBS was seen in place until 1.5 months in all of the stented animals. In the nonstented animals HJ anastomosis inner diameter was decreased at 18 months [6.3 (5.0-7.0) mm vs 7.4 (7.0-9.0) mm, p = 0.05] and liver clearance reduced at 12 and 18 months compared to stented animals. Serum liver values and liver and bile duct histology did not differ between the groups. We conclude that this novel BDBS is easy to insert into the HJ anastomosis with nondilated ducts. It is nontoxic, dissolves safely, and may be associated with a larger and better draining anastomosis at 18-month follow-up. These results encourage us to proceed to clinical studies.