An inexpensive laparoscopic gallbladder retrieval bag.
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Publications and source records attributed to C W Imrie.
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Staging of acute pancreatitis is important for selection of patients for clinical trials, comparison of results between centers, and the early identification of patients who may benefit from therapeutic intervention or transfer to a specialist unit. The APACHE-II score and other multiple-factor scoring systems are widely used for the first two indications, and of these, the APACHE-II score provides the best accuracy at an early stage in the course of the illness. Presently, however, no system provides sufficient predictive power to facilitate clinical decision making. At a time of increasing pressure to involve specialist units at an early stage in the management of these complex patients, a pressing need to identify a system for accurate early staging of acute pancreatitis remains.
For a 30-year period beginning in 1958, the general basis of medical therapy of acute pancreatitis had as its focus the provision of supplementary antiprotease therapy usually given intravenously. This concept was based on the belief that the body's natural antiprotease defense mechanism, which relies heavily on alpha 2-macroglobulin, together with alpha 1-antiprotease (alpha 1-antitrypsin), was inadequate to cope with the vast enzyme release that occurred with the onset of the more severe forms of the disease. This article examines recent studies and emerging theories on the medical therapy of acute pancreatitis.
BACKGROUND: Pain relief after distal pancreatectomy for chronic pancreatitis is reportedly satisfactory in 50-80 per cent of patients. This study attempted to determine clinical and radiological features that might select patients likely to benefit from distal pancreatectomy, and whether splenic preservation influenced the outcome. METHODS: Thirty-eight patients with chronic pancreatitis, who underwent distal pancreatectomy between 1982 and 1998, were reviewed retrospectively. The outcome of surgery was correlated with the aetiology of pancreatitis and radiological appearance on endoscopic retrograde cholangiopancreatography and computed tomography. RESULTS: Good results were achieved in 23 of 36 patients for whom follow-up (median 48 months) was available, including all 11 with obstructive pancreatitis. The spleen was preserved in 22 patients. Twelve patients became diabetic after surgery: three of 20 in whom the spleen was preserved and nine of 16 who underwent splenectomy. CONCLUSION: Non-alcoholic patients with a normal pancreas proximal to a dominant ductal stricture had a consistently good outcome from surgery. Spleen-preserving distal pancreatectomy, although technically demanding, can be performed safely with results equivalent to those of distal pancreatectomy with splenectomy or autotransplantation. Splenic preservation, apart from preventing postsplenectomy sepsis, might also delay the onset of diabetes.
BACKGROUND: Death from acute pancreatitis within the first week after admission is usually a consequence of multiple organ dysfunction. Reports from specialist centres suggest that, with improvements in resuscitation and supportive care, such deaths are becoming uncommon but it is unclear if this is reflected in a decrease in early mortality rate from acute pancreatitis in the general population. METHODS: Data concerning patients discharged with a diagnosis of acute pancreatitis (International Classification of Disease-9 code 577.0) between 1984 and 1995 were obtained from the Information and Statistics Division, National Health Service in Scotland, and analysed on a computer database. RESULTS: The incidence of acute pancreatitis in Scotland continues to increase in both sexes. The in-hospital mortality rate (death from all causes) was 7.5 per cent and showed a slight but significant downward trend over the period of study. Death within 7 days of hospital admission accounted for 53.7 per cent of all deaths and the proportion of early deaths did not decline over the study interval. CONCLUSION: These results suggest that scope remains for considerable improvement in the early management of acute pancreatitis. There is an urgent need to improve the early recognition of severe pancreatitis coupled to a willingness on behalf of clinicians to transfer these patients at an early stage to a centre with high-dependency and intensive care facilities supervised by a multidisciplinary team with expertise in the endoscopic, radiological and surgical management of these patients.
The purpose of this chapter is to examine the possible role of platelet-activating factor (PAF) antagonist therapy as a means of modifying the systemic inflammatory response syndrome (SIRS) and multi-organ dysfunction syndrome (MODS) in the management of patients with severe acute pancreatitis (AP). Supposed specific treatments of AP have not shown clinical benefit, with antiprotease agents such as aprotinin and gabexate mesilate, as well as fresh frozen plasma, being ineffective. In addition, early peritoneal lavage, intravenous glucagon, somatostatin and octreotide have shown no benefit.
The diagnosis of chronic pancreatitis in the UK largely rests on the combination of the clinical presentation which usually features pain which is often provoked by food and/or alcohol. There is usually a 30 to 40-min delay between the stimulus and the pain and, after exclusion of other causes of pain, an ERCP is performed. A minority of patients will have pancreatic function tests carried out while increasingly the diagnosis is being made by MR scanning. The control of pain is often the most important aspect of management to the patient. In those with large ducts due to compression of focal areas of the duct system surgical by-pass therapy is indicated. There is a bigger problem in patients with small ducts and chronic pancreatitis in whom extensive resection may be inappropriate. Our experience with minimally invasive thoracoscopic splanchnicectomy has been encouraging over the last three years. Having previously tried both percutaneous coeliac ganglion block and surgical excision of this nerve tissue, it is a great deal easier to carry out this procedure which usually takes only 15-20 min per side. Patients are usually only admitted for 48 h and the immediate beneficial effect usually results in opiate analgesia being discontinued with considerable improvement in the quality of life. While there is a slight drop-off in benefit between 6 and 12 months post-operatively, the clinical effectiveness of this approach is to be commended and the author's experience will be presented to support this view.
Primary sclerosing cholangitis as the cause of acute pancreatitis is a rare phenomenon with only one previous case having been found by ourselves in the English literature. Over a period of 2 yr, two patients with acute pancreatitis secondary to primary sclerosing cholangitis were seen in this unit. The first patient is currently being treated with ursodeoxycholic acid and repeat endoscopic sphincterotomies, whereas the second required liver transplantation.
Metastatic carcinoma to the pancreas is uncommon. Pancreatic metastasis from a renal cell carcinoma is exceptional, but may occur many years after the initial diagnosis and treatment of the primary tumor. Presentation of our patient mimicked a head of the pancreas carcinoma so well that it was only after the resectional phase of a Whipple operation that the diagnosis of metastatic renal carcinoma was made 18 years after left nephrectomy. The patient is alive and well 18 months after surgery, having gained weight.
Clinical assessment of acute pancreatitis by experts is as accurate as any of the individual approaches which have been recommended. What is important in a hospital setting is for one or more of these systems to be applied in individual hospitals so that forewarning is given, especially to the less experienced clinicians, of the patient who is likely to run into difficulties and requires high dependency or intensive care. One practical approach which can be personally recommended is to employ the Glasgow scoring system plus C-reactive protein levels and also to take into account body mass index. Any patient with three positive Glasgow factors, or CRP > 150 mg/l or BMI > 30 kg/m2 has severe acute pancreatitis. More refined systems may ultimately be developed but we are still some way from a single substance in blood or urine being easily and cheaply measured and representing an accurate prognostic indicator of severe acute pancreatitis. Part of the journey has been completed but there is still considerable potential to make the rest of the journey an improvement for both clinicians and patients.
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BACKGROUND: Many patients with severe acute pancreatitis develop organ system failure during the first few days of illness, and this accounts for the majority of early deaths. No specific therapy is available and treatment remains supportive. METHODS: In a randomized controlled trial conducted in 11 hospitals in the West of Scotland, 50 patients with predicted severe acute pancreatitis were selected from 188 screened over a 14-month period. Patients received placebo or lexipafant, a potent platelet-activating factor antagonist, by continuous intravenous infusion at a dose of 100 mg/day for up to 7 days. Early systemic complications were assessed by the measurement of organ failure scores. RESULTS: There was a significantly greater fall in organ failure score in the treatment group during the 7 days of study (mean and median changes in organ failure score were 0.17 and 0 in the placebo group versus -1.42 and -1 in the treatment group; P = 0.003, Wilcoxon rank sum test), associated with trends towards a reduction in mortality and a reduced incidence of systemic complications. CONCLUSION: These results suggest that lexipafant may be a useful adjunct to full supportive care in the early management of patients with severe acute pancreatitis.
Tumour necrosis factor (TNF) alpha, interleukin (IL) 1 beta, IL-6 and IL-8 are thought to play a central role in the pathophysiology of sepsis but their role in acute pancreatitis is unknown. In the present study, monocytes were isolated from the peripheral blood of 26 patients with moderate or severe acute pancreatitis without biliary sepsis. Secretion of these cytokines in vitro was measured at intervals during the first week of illness. Sixteen patients developed systemic complications. Peak TNF-alpha secretion was significantly higher in patients who developed systemic complications (median (interquartile range (i.q.r.)) 18.5 (5.5-28.5) ng/ml) than in those with an uncomplicated course (3.7 (2.3-6.4) ng/ml, P < 0.01). Similarly, peak IL-6 and peak IL-8 secretion were significantly higher in the complicated group (IL-6: complicated median (i.q.r.) 48.9 (12.1-71.0) ng/ml, uncomplicated 16.3 (14.2-37.9) ng/ml, P < 0.05; IL-8: complicated 748 (643-901) ng/ml, uncomplicated 608 (496-749) ng/ml), P < 0.05). No significant difference in peak IL-1 beta secretion was observed between the two groups. Systemic complications of acute pancreatitis are associated with a significant increase in monocyte secretion of TNF-alpha, IL-6 and IL-8 suggesting that, as in sepsis, these cytokines play a central role in the pathophysiology of the disease.
The pathophysiology of systemic organ failure in acute pancreatitis has been the subject of debate for many years but there is growing evidence that increase production of pro-inflammatory cytokines plays an important role. from this work and from the results of studies in experimental pancreatitis there exists a rationale for the use of PAF antagonists in the treatment of acute pancreatitis. Two pilot studies have now demonstrated a beneficial effect of the PAF antagonist Lexipafant on acute pancreatitis which may lead to an important advance in the treatment of these patients. A multicentre trial aiming to recruit 300 patients with severe acute pancreatitis is now underway in the UK, the results of which will be awaited with interest.
Severe, acute pancreatitis is commonly associated with a systemic illness which may result in multiple organ failure. There is evidence that an aberrant immune response, involving increased secretion of proinflammatory cytokines from activated monocytes and mononuclear phagocytes, is responsible for another systemic illness--septic shock. Previous studies have investigated whether there is a correlation between plasma cytokine levels and severity of pancreatitis. However, these results may not reflect mononuclear phagocyte activation. In this paper, monocytes (collected from patients with severe pancreatitis) were cultured in vitro and secreted cytokine levels measured after 24 hours by ELISA. Secretion of tumour necrosis factor alpha, interleukin-6 and interleukin-8 was higher in cells taken from patients who later developed systemic complications. There was no difference in the secretion of interleukin-1 beta. The mechanism by which mononuclear phagocytes are activated in acute pancreatitis, and the role of genetic predisposition, are discussed.
It has been suggested that the severity of an attack of acute pancreatitis is related to the presence of intraglandular trypsinogen activation and that disease severity is also reflected by the degree of the acute-phase protein response. In this study we examine the relationships among amylase release, the degree of trypsinogen and prophospholipase A2 activation [as measured by urinary trypsinogen activation peptide (TAP) and prophospholipase A2 activation peptide (PLAP) concentrations], and the serum concentrations of the acute phase-protein C-reactive protein (CRP) and the principal mediator of the acute-phase protein response, interleukin-6 (IL-6). Twenty-four patients (14 mild and 10 severe attacks) were studied. Peak serum amylase concentrations were seen within 12 h and peak urinary TAP/creatinine (Cr) and PLAP/Cr ratios between 12 and 24 h after the onset of symptoms, preceding those of IL-6 and CRP. The integrated TAP/Cr and PLAP/Cr responses were significantly greater in those with severe disease [95% confidence internal (CI) = 106-259.6 pmol/mmol/h, p < 0.0008; and 95.1% CI = 462.2-3887 pmol/mmol/h, p < 0.003, respectively]. The integrated amylase response was not significantly greater in those with severe disease (95.6% CI = -415 to 832 IU/L/h, p < 0.14). There was a strong correlation among the integrated IL-6, TAP/Cr (r = 0.63, p < 0.01), and PLAP/Cr (r = 0.64, p < 0.01) responses but a poor correlation with the integrated amylase response (r = 0.19, NS).(ABSTRACT TRUNCATED AT 250 WORDS)