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INTRODUCTION: The incidence of colorectal cancer (CRC) increases with age. The aim of this study was to investigate the impact of age and age-related factors on post-operative mortality and survival following CRC resections. METHODS: A prospectively collected database of 459 CRC resections was analysed. RESULTS: The mean age of the patients was 70 years (range: 25-95 years) and 54% were male. The relative proportion of female patients increased with age so that for patients aged over 77 more women were treated than men. The probability of undergoing an emergency resection (25%) did not change with age. In older patients the proportion of rectal cancers resected decreased and the proportion of hemicolectomies and Hartmann's operations performed increased. The 30-day mortality rate was 4% after elective and 11% after emergency resections. Most deaths were caused by medical complications, reflecting increased co-morbidity in the elderly. Post-operative mortality was 1% in patients under the age of 59. This increased by 3 percentage points every 10 years after elective resections and by 8 percentage points every 10 years after emergency resections. CRC-specific survival was independent of age whereas overall survival decreased so the likelihood of dying from CRC decreased with age: at age 50 half the deaths were from CRC, at age 70 a third and at age 80 a quarter. CONCLUSIONS: CRC stage and the probability of presenting as an emergency did not change with age but older patients were more likely to be female and have colon cancer. Post-operative mortality progressively increased with age. Most deaths were caused by medical complications, reflecting increased co-morbidity. Older patients were less likely to die from CRC.

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BACKGROUND: Predicted patient life expectancy, based on a patient's medical history, is an important component of medical decision making. This study therefore aimed to determine the consistency, accuracy and precision with which doctors, nurses and medical students predict life expectancy (LE). METHODS: 20 doctors, 20 nurses and 20 medical students (4th and 5th year) independently examined 70 hypothetical patient case scenarios containing age, sex and comorbidity; this included 13 duplicate scenarios. Accuracy and consistency of prediction was assessed by comparison with statistical LE estimates generated using evidence-based actuarial and life insurance industry methods in collaboration with a team of professional actuaries. RESULTS: Doctors, nurses and medical students underestimated LE by a mean (95% confidence interval) of -1.46 (-0.31 to -2.61), -1.79 (-0.52 to -3.06) and -2.24 (-1.16 to -3.32) years with an equivalent root mean squared error (RMSE) of 4.74, 5.49 and 5.08 years respectively. LE predictions were equal to actuarial LE in less than 10% of cases and accurate to within 25% of actuarial LE in less than 45% of cases. Intra-observer reliability was 91%, 85% and 87% for doctors, nurses and medical students respectively. Inter-observer reliability was 66%, 57% and 57% for the three groups. CONCLUSION: Doctors, nurses and medical students were inconsistent, inaccurate and imprecise in their prediction of LE with a tendency toward underestimation. This may lead to patients being managed inappropriately. There is a need for improved training and objective outcome prediction models.

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BACKGROUND: Cystic duct leak is an infrequent but potentially serious complication of laparoscopic cholecystectomy. The aims of this audit were to assess the efficacy of locking absorbable clips for closing the cystic duct and to compare the results with those for simple clips used previously. METHODS: The records for all laparoscopic cholecystectomies performed in one hospital over a 5-year period were reviewed. The results were compared using Fisher's exact test. RESULTS: Of 518 laparoscopic cholecystectomies attempted, 24 were excluded. There was no difference in age or sex ratio between the two groups. Cystic duct leaks were identified either on endoscopic retrograde choloangio pancreatography or at laparotomy. No cystic duct leak occurred in any of the 344 locking clip cases, as compared with 3 leaks in the 146 (2%) simple clip cases (p < 0.03). CONCLUSION: Locking clips are a safe and effective method for cystic duct closure. They are associated with a reduced cystic duct leak rate, as compared with that for simple clips.

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BACKGROUND: The left subcostal closed approach utilizing the Veress needle has been the preferred method at one surgical practice for the past 5 years. The aims of this study were to determine whether this was a safe method for creating a pneumoperitoneum and its success rate. METHODS: The medical records for all laparoscopic procedures performed at one practice from 1996 through 2001 were reviewed. RESULTS: A total of 352 laparoscopic cases were reviewed. The median age of the patients was 55 years (range, 14-72), with a sex ratio of 1 male to 3.5 females. The left subcostal closed approach was not attempted in 8 patients (2%) due to left subcostal surgical scars. The left subcostal approach was successful in 342 of 344 attempts (99%). In 2 patients the method failed because the Veress needle hole could not be placed in the peritoneal cavity. An omental hematoma in one patient was the only complication. CONCLUSION: The left subcostal closed approach is a safe and effective method for creating a pneumoperitoneum.

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John Hunter studied comparative anatomy of the pancreas but was unaware of pancreatic infection which is now the leading cause of mortality in pancreatitis. This was investigated using a feline model of pancreatitis. Pathogens spread to the healthy and inflamed gland from many sources including colon, gallbladder, or a septic focus and by various routes including the circulation, reflux into the pancreatic duct or by transmural migration from the colon. Colonisation risk was proportional to necrosis and inflammation, confirming clinical observations. These studies showed that pathogens frequently colonised the pancreas, but infection developed only in animals with pancreatitis. In cats with pancreatitis, phagocytic function was reduced by 28%. This was probably owing to phagocytic capacity being overwhelmed by protease-antiprotease complexes because, in humans, granulocyte and lymphocyte function was normal. These experiments suggested that it would be difficult to prevent pancreatic colonisation, but indicated some types of therapy may have potential. These were investigated using this animal model of pancreatic infection. Treatment with either cefotaxime or levamisole (an immunostimulant) were effective. However, the anti-inflammatory drug dopamine, which reduced inflammation, did not eradicate all pathogens.

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Circulating lymphocyte numbers and activation together with granulocyte function were measured in 20 patients in the early stages of an attack of acute pancreatitis and in 20 healthy controls. Circulating lymphocytes, T lymphocytes, and CD4 and CD8 T lymphocyte subsets were decreased in both mild pancreatitis (67-80 per cent of controls) and severe pancreatitis (22-40 per cent of controls). CD4:CD8 ratios were unchanged and median (interquartile range) interleukin 2 receptor expression was increased from less than 1 per cent in controls to 14(6) per cent in severe pancreatitis, suggesting lymphocyte activation. Median granulocyte chemiluminescence was increased to 293 per cent of controls in severe pancreatitis and random motility was reduced to 77 per cent of controls, indicating increased metabolic activity. Complement-mediated antibody-independent opsonization and chemotaxis toward endotoxin were normal. Immune function is not reduced early in acute pancreatitis. Granulocyte hyperactivity may be important in the development of multiple organ failure.

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Mean anaesthetic, surgical and turnover times were used to predict finishing times for elective general surgical operating lists. A predicted early finish was correct in 70 per cent, a predicted on-time finish in 19 per cent, and a predicted late finish in 56 per cent. Overall, predictions of an early or late finish had a low sensitivity (62 per cent and 65 per cent) and high false positive rate (30 per cent and 44 per cent). Over-runs, caused by too many cases, and early finishes, owing to insufficient cases were reliably predicted. It is suggested that mean procedure times can be used to identify under or over utilisation caused by under or over-booking but indiscriminate use will not improve list utilisation.

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We reviewed our experience with open cholecystectomy since laparoscopic cholecystectomy became the treatment of choice for symptomatic gallstones. Over a 3 year period 35 open (6%) and 578 laparoscopic cholecystectomies (94%) were performed. Fourteen trainee surgeons performed only 16 open cholecystectomies and assisted at 19. The proportion of open cholecystectomies declined through the study period. Ten emergency cholecystectomies were performed for empyema, gallbladder perforation, severe acute cholecystitis, liver abscess, and cholangitis. In 12 patients, laparoscopic surgery was converted to an open procedure because of severe inflammation, empyema, dense adhesions, carcinoma of the gallbladder, cholecystoduodenal fistula, and perforated small bowel. Ten patients underwent open cholecystectomy and bile duct exploration after failure to clear duct stones endoscopically, and three patients had Mirizzi's syndrome. Open cholecystectomy is infrequently performed giving trainee surgeons little experience. However, such cases are occasionally inevitable and laparoscopic surgeons need to have the appropriate skills.

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In experimental obstructive chronic pancreatitis the normal hyperaemic response to secretory stimulation is lost, suggesting abnormal vascular regulation. Vascular regulatory mechanisms were investigated by observing the effect of increments in portal pressure on pancreatic blood flow in normal cats and cats with chronic pancreatitis. Normal cats maintained pancreatic blood flow until portal pressure was > 15 mm Hg, after which it decreased. Total vascular resistance decreased until the portal pressure was 15 mm Hg and increased thereafter. These observations suggested that metabolic regulatory mechanisms prevailed while portal pressure was in the physiological range but myogenic mechanisms became dominant during portal hypertension. In chronic pancreatitis the basal pancreatic blood flow was reduced and was inversely proportional to portal pressure. Total vascular resistance increased as portal pressure increased. In chronic pancreatitis myogenic regulatory responses prevailed at all levels of portal pressure. In conclusion, intrinsic regulation of pancreatic blood flow was abnormal in cats with chronic pancreatitis. The loss of the predominance of metabolic regulation over the normal range of portal pressure may partly explain the reduction of pancreatic blood flow in response to secretory stimulation.

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The routes of spread of pathogens into the pancreas in acute pancreatitis were investigated. Four experiments were performed: (1) cats with and without acute pancreatitis were given 10(7) Escherichia coli (E coli) intravenously, (2) in cats with acute pancreatitis 10(8) E coli was placed in the colon. In half of them the colon was then enclosed in an impermeable bag to prevent transmural spread. (3) E coli (10(4)) was placed in the pancreatic duct in cats with and without acute pancreatitis. (4) In cats with acute pancreatitis 10(5) E coli was placed in the gall bladder. In half of them the common bile duct was ligated to prevent biliary-pancreatic reflux. After 24 hours, intravenous E coli infected the pancreas in six of nine cats with acute pancreatitis and three of 10 controls. After 72 hours E coli spread to the pancreas from the colon in six of nine cats with acute pancreatitis. This was prevented by enclosing the colon in an impermeable bag (p = 0.02). In five of six cats with acute pancreatitis and five of six controls E coli placed in the pancreatic duct colonised the pancreas within 24 hours. Pancreatic colonisation from the gall bladder occurred in five of six cats with a patent common bile duct and in three of six with an obstructed common bile duct. In conclusion, in cats E coli can spread to the pancreas by the blood stream, transmurally from the colon, and by reflux into the pancreatic duct.

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The source(s) of pancreatic pathogens is uncertain, although the colon is usually implicated. We studied whether pathogens may spread from different sites in a feline model of the disease. Acute pancreatitis was induced using a standard technique and a distinctive clinical strain of Escherichia coli as the marker bacterium. E. coli were placed in the colon, gall bladder, main pancreatic duct, or obstructed renal pelvis of control cats (no pancreatitis) and acute pancreatitis cats. Pancreases were colonized from each source, whether or not pancreatitis was present. The pancreatic colonization rate was greater in acute pancreatitis only when E. coli had been placed in the colon. In conclusion, E. coli may spread to the pancreas from different sources. The high rate of pancreatic colonization in both control and inflamed glands suggested that, clinically, bacteria may spread to the pancreas more frequently than is currently thought.

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An investigation examined the efficacy of antibiotics in a novel feline model of pancreatic infection in acute pancreatitis. Acute pancreatitis was induced in cats using an established technique. In control animals (no pancreatitis) and cats with pancreatitis, Escherichia coli (10(4) in 0.1 ml) was placed in the pancreatic duct. Reoperation was performed after 24 h in six controls and six cats with pancreatitis. E. coli was cultured from the pancreas in five control animals and five cats with pancreatitis. Reoperation was performed after 1 week in ten controls, in 11 cats with pancreatitis and in nine with pancreatitis that were treated with cefotaxime (50 mg/kg intramuscularly three times daily) started 12 h after the induction of pancreatitis and administration of E. coli. Pancreatic infection developed in eight cats with pancreatitis compared with none of the cefotaxime-treated animals and none of the controls (P < 0.05). Cefotaxime reached bactericidal levels in pancreatic tissue and juice. In conclusion, ductal administration of E. coli caused pancreatic infection only in cats with acute pancreatitis. Early administration of an appropriate antibiotic was effective in treating pancreatic infection in acute pancreatitis.

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In patients with symptomatic gallstones the management of choledocholithiasis has been controversial since the introduction of laparoscopic cholecystectomy. A prospective study was made of 300 consecutive patients with symptomatic gallstones managed by laparoscopic cholecystectomy and preoperative endoscopic retrograde cholangiography (ERC) over 2 years. Fourteen patients were excluded either because urgent surgery was required or because they were unfit for laparoscopic cholecystectomy. ERC was performed on 96 patients (34 per cent) who were at risk of choledocholithiasis. The presence of bile duct calculi was confirmed in 59 patients (21 per cent of the total, 61 per cent of those undergoing ERC); stones were removed endoscopically in 53 cases (90 per cent of attempts). The remaining six patients underwent open cholecystectomy and bile duct exploration. Laparoscopic cholecystectomy was attempted in 280 patients (98 per cent); it was necessary to convert to open operation in only three (1 per cent). There were no deaths, no retained stones and no bile duct injuries, and only three patients (1 per cent) developed a significant postoperative complication. Symptomatic gallstones can be managed by preoperative ERC and laparoscopic cholecystectomy with minimal morbidity and mortality.

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Acute oedematous pancreatitis and acute haemorrhagic pancreatitis were studied using the low pressure duct perfusion models of alcoholic pancreatitis in cats. After creating either form over 24 hours, each pancreas was histologically graded and assigned an inflammatory score (0-16; absent-severe). Urinary trypsinogen activation peptide concentrations were also used as a measure of severity. Using the model of acute haemorrhagic pancreatitis, it was previously shown that low dose dopamine (5 micrograms/kg.m) reduced the inflammatory score at 24 hours and that this effect was mediated by a reduction in pancreatic microvascular permeability acting via dopaminergic and beta adrenergic receptors. Further studies were conducted and are reported here. In experiment 1 different doses of dopamine in established alcoholic acute haemorrhagic pancreatitis were studied. In group 1 control cats (no dopamine), the inflammatory score was 10.5 (interquartile range (IQR)4). In groups 2, 3, and 4, haemorrhagic pancreatitis was induced. Twelve hours later dopamine was infused for six hours, in the doses of 2 micrograms/kg.min, 5 micrograms/kg.min, and 50 micrograms/kg.min respectively. The inflammatory score in group 2 was 7 (IQR 0.5, p < 0.05 v group 1), in group 3 it was 7 (IQR 2, p < 0.05 v group 1), and in group 4 it was 7 (IQR 4, p < 0.05 v group 1). This was matched by significantly lower levels of urinary tripsinogen activation peptide at 24 hours. In experiment 2 (group 5) we tried to reduce microvascular permeability further by combining dopamine with antihistamines, but there was no improvement in the inflammatory score. As oedematous pancreatitis is the commoner and milder form of acute pancreatitis in clinical practice, in experiment 3 we looked at the effect of dopamine in this model. In group 6 control cats (no treatment), the inflammatory score was 7 (IQR 3, p < 0.05 v group 1). In group 7 cats given dopamine (5 micrograms/kg.min for six hours) from 12 hours after the onset of actue oedematous pancreatitis, the inflammatory score was reduced to 4(IQR 2, p < 0.05 v group 6). This was matched by a significant reduction in the 24 hour urinary tripsin activation peptide concentration.

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Chronic pancreatitis is characterized by persistent and severe pain, which can be relieved by decompression of the main pancreatic duct (MPD). Both ductal and interstitial pressures have been shown to be increased in chronic pancreatitis in patients. A study was carried out of pancreatic interstitial pressure and pancreatic blood flow in normal cats and those in which chronic obstructive pancreatitis had been induced 5 weeks earlier to determine the effect of decompression of the MPD. In the normal pancreas, median(interquartile range (i.q.r.)) basal interstitial pressure was 0.05(1.2) mmHg and median(i.q.r.) basal pancreatic blood flow 58.3(24.3) ml per min per 100 g. Secretory stimulation did not change the interstitial pressure significantly, but was associated with a 40 per cent increase in median(i.q.r.) blood flow to 81.8(45.8) ml per min per 100 g. In contrast, in chronic obstructive pancreatitis, the median(i.q.r.) basal interstitial pressure was 2.0(1.5) mmHg, which was significantly higher than in the normal gland, and median(i.q.r.) pancreatic blood flow was 38.3(9.8) ml per min per 100 g, significantly lower than in the normal pancreas. Furthermore, secretory stimulation was associated with a significant increase in median(i.q.r.) interstitial pressure to 3.3(1.6) mmHg and a simultaneous decrease in median(i.q.r.) blood flow to 31.5(13.7) ml per min per 100 g. After decompression of the MPD in cats with chronic obstructive pancreatitis, the median(i.q.r.) basal interstitial pressure was 2.0(1.4) mmHg and on secretory stimulation 1.8(1.5) mmHg. Decompression thus prevented the increase in interstitial pressure seen in the animals with obstruction. In contrast, ductal decompression improved the median(i.q.r.) basal pancreatic blood flow to 45.9(38.4) ml per min per 100 g and, furthermore, this increased significantly on secretory stimulation to a median(i.q.r.) of 81.4(47.8) ml per min per 100 g. Decompression thus restored the normal pattern of secretory hyperaemia. Within the confines of this model, these observations demonstrate that chronic obstructive pancreatitis exhibits a compartment syndrome that is relieved by duct drainage.

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The distribution and concentration of calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), and gastrin-releasing peptide (GRP) immunoreactivities in the pancreas of cats with experimentally induced chronic pancreatitis and of age- and sex-matched controls were investigated. By narrowing the main pancreatic duct between the head and the body to approximately 25% of its normal diameter, we induced within 5 weeks chronic pancreatitis restricted to the body and tail. In control animals, peptide immunoreactive nerves were distributed to the islets, acini, and ducts; the latter were predominantly innervated by fibers immunoreactive for NPY, VIP, or CGRP. The vasculature received an abundant supply of NPY-, CGRP-, and, to a lesser extent, SP-containing axons. Within intrapancreatic ganglia, peptide immunoreactivities were identified in fibers and ganglion cells, with the exception of CGRP and SP immunostaining, which could be visualized only in fibers. In animals with chronic pancreatitis, the innervation pattern of each peptidergic system was comparable to that described in controls. However, there was a remarkable increase in the density and staining intensity of VIP and NPY immunoreactive fibers in the exocrine parenchyma and fibrous septa of the body and tail, where chronic pancreatitis developed. Fibers immunoreactive for CGRP and SP also were moderately denser than in controls, whereas those containing GRP immunoreactivity did not show any detectable changes. In addition, a marked increase of the immunostaining for VIP and, to a much lesser extent, for NPY and GRP, was observed in neurites supplying the head of the pancreas, which appeared devoid of histologically detectable pathological alterations. Radioimmunoassay analysis confirmed the immunohistochemical observations. The increased density of distinct peptidergic nerves in the pancreas with induced chronic pancreatitis might be the result of compensatory phenomena in response to the inflammatory process.

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One method of making optimal use of prophylactic antibiotics is for interested parties to agree on guidelines. A postal survey was undertaken to determine the prevalence of this practice within UK hospitals and details of any guidelines used. Eighty-one of the 160 respondents (51%) stated that guidelines were available or in preparation. Prophylaxis was recommended by 100% of respondents for colorectal surgery and prosthetic joint replacement and by 96% for gastro-oesophageal surgery, procedures where it has been proven to be of benefit. Prophylaxis was recommended for the following procedures for which its efficacy remains controversial: cholecystectomy (100%); peripheral vascular grafting (93%); hysterectomy (95%) and noncardiac thoracic surgery (63%). Although 35 combinations of 22 different antimicrobials were recommended, 63% included a cephalosporin; the greatest variety of antibiotics recommended was for peripheral vascular grafting. In 88% of policies it was advocated that prophylaxis be started preoperatively and in 79% that it be continued for less than 24 h. When surgery involved the implantation of a prosthesis the duration of prophylaxis tended to be prolonged. Policies for the prescribing of antimicrobial prophylaxis in surgery are available in many hospitals and for the most part conform with established principles.

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