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Dr Arth Shah, Resident, Dept ofSurgery, karamsad Medical college Dr Manoj K Ghoda M.D., M.R.C.P. Consultant Gastroenterologist
22 years old male Sudden onset of epigastric pain radiating to back No significant past history No drugs, no alcohol, no heavy meals On examination: In pain Pulse 82/min, B.P.120/80 RR: 16/min, no cyanosis Abdomen: Tenderness +, no guarding, No rigidity, peristalses +
? Acute pancreatitis:Issues:1. Diagnosis2. Defining various terminology3. Assessing severity4. Role of antibiotics5. Role of nutrition6. Role of surgery
Diagnosis Amylase and lipase are the cornerstone lab parameters for the diagnosis. "It is usually not necessary to measure both amylase and lipase (3).
Diagnosis Lipase may be preferable It remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. Lipase is thought to be more sensitive and specific and superior to amylase[3, 4, 5] In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase .
Diagnosis Lipase starts to rise by 4-8 hours, peaks in 24 hours and normalizes by 8- 14 days.
Amylase and Lipase Higher the numerical value more certain is the diagnosis. Although severe pancreatitis could also exist without significant rise in these enzymes. Numerical value of these enzymes have no prognostic value and neither they reflect severity
Diagnosis: Imaging USG is cornerstone CT MR EUS/ ERCP 100 acute pancreatitis….20% severe= 20 20% of severe become infected= 4 Infection usually sets in 2nd week or 3rd week Surgeons would want to delay surgery till about 4 weeks Infected necrosis will always be clinically manifest So why CT scan in first week ????
Issues:Assessing severity at the bedside Clinical features Scoring systems
Clinical features useful inassessing severity Toxic Look Normal look Severe pain Mild pain Persistent tachycardia Normal Pulse rate Breathlessness and Normal Oxygen Cyanosis saturation Sub-normal Adequate urine output temperature Flat and soft and Shock movable abdomen
Acute Necrotizing PancreatitisACG Practice Guidelines
Bedside index of severity in acutepancreatitis (BISAP) scoreThis calculator evaluates the following Clinical Criteria: BUN >25 mg/dL (8.9 mmol/L) Impairment of mental status with a Glasgow coma score <15 SIRS (systemic inflammatory response syndrome) Age >60 years old Pleural effusionEach determinant is given one point The MedCalc 3000 module Bedside index of severity in acute pancreatitis (BISAP) score is available in MedCalc 3000 Complete Edition.SIRS is defined as 2 or more of the following variables; Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F) Heart rate of more than 90 beats per minute Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO 2) of less than 32mm Hg Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10% immature [band] forms)
BISAP Score BISAP Score Observed Mortality0 0.1%1 0.4%2 1.6%3 3.6%4 7.4%5 9.5% Wu et al, Gut 2008
BISAP scores of 3 predict the development of organfailure, persistent organ failure, and necrosis in theprospective cohort of 397 casesA Prospective Evaluation of the Bedside Index for Severity in Acute Pancreatitis Score in Assessing Mortality and Intermediate Markersof Severity in Acute PancreatitisVikesh K Singh, Bechien U Wu, Thomas L Bollen, Kathryn Repas, Rie Maurer, Richard S Johannes, Koenraad J Mortele, Darwin L Conwell and Peter ABanks. Am L Gastroenterol BISAP<3 BISAP>3 OR (95% p CI)Organ 4 23 7.4 <0.0001failurePersistent 2 21 12.7 <0..0001OFNecrosis 12 34 3,8 0.0004
Comparison of BISAP, Ransons, APACHE-II, and CTSI scores inpredicting organ failure, complications, and mortality in acutepancreatitis.Papachristou GI, Muddana V, Yadav D, OConnell M, Sanders MK, Slivka A, Whitcomb DC. Am J Gastroenterol. 2010Feb;105(2):435-41; quiz 442. doi: 10.1038/ajg.2009.622. Epub 2009 Oct 27CONCLUSIONS: BISAP score is an accurate means for risk stratification in patients with AP. Its components are clinically relevant and easy to obtain. The prognostic accuracy of BISAP is similar to those of the other scoring systems.
Acute PancreatitisIssue:Definitions of various disease determinants
Classification of acute pancreatitis--2012:Revision of the Atlanta classification anddefinitions by international consensus.Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, Tsiotos GG, Vege SS; AcutePancreatitis Classification Working Group.Gut. 2013 Jan;62(1):102-11. doi: 10.1136/gutjnl-2012-302779. Epub 2012 Oct 25
Determinants of revised Atlantaclassification Local Pancreatic or peripancreatic fluid collection Sterile Infected Necrosis Sterile Infected Pseudocyst and walled-off necrosis (sterile or infected). Organ failure
Revised Atlanta...... Acute pancreatitis identified two phases of the disease: early and late. Severity is classified as mild, moderate or severe. Mild: the most common form, has no organ failure, local or systemic complications and usually resolves in the first week. Moderate: Presence of transient organ failure, local complications or exacerbation of co-morbid disease. Severe: Persistent organ failure >48 h. Local complications are peripancreatic fluid collections, pancreatic and peripancreatic necrosis (sterile or infected),
Objections to revised Atlantaclassification Mere presence of fluid or necrosis do not determine the outcome It is the infection that determines the outcome A number of studies have demonstrated that infectious (peri)pancreatic complications (IPCs), rather than the presence of necrosis per se, are a key determinant of the high morbidity and mortality in patients with acute pancreatitis. (Büchler MW, Gloor B, Müller CA et al. Acute necrotizing pancreatitis: treatment strategy according to the status of infection. Ann Surg 2000;232:619–626. | Article | PubMed | ISI | ChemPort |Lytras D, Manes K, Triantopoulou C et al. Persistent early organ failure: defining the high-risk group of patients with severe acute pancreatitis? Pancreas 2008;36:249–254. | Article | PubMed) ,Le Mée J, Paye F, Sauvanet A et al. Incidence and reversibility of organ failure in the course of sterile or infected necrotizing pancreatitis. Arch Surg 2001;136:1386–1390. | Article | PubMed Mere organ failure does not determine the outcome It is the rapidity, the severity, reversibility and number of organs affected that determines the outcome (5,6,7,8,9)
Determinant-based classificationof acute pancreatitis severity: aninternational multidisciplinaryconsultation.Dellinger EP, Forsmark CE, Layer P, Lévy P, Maraví-Poma E, Petrov MS, Shimosegawa T, SiriwardenaAK, Uomo G, Whitcomb DC, Windsor JA; Pancreatitis Across Nations Clinical Research and EducationAlliance (PANCREA). Ann Surg. 2012 Dec;256(6):875-80. doi: 10.1097/SLA.0b013e318256f778
The presence of one determinant can modify the effect of another such that the presence of both infected (peri)pancreatic necrosis and persistent organ failure have a greater effect on severity than either determinant alone. The derivation of a classification based on the above principles results in 4 categories of severity- mild, moderate, severe, and critical.
Acute Pancreatitis: ManagementIssue Fluid replacement Vigorous hydration to optimize outcomes has been increasingly recognized. The ACG guidelines stress, “Patients with evidence of significant third-space losses require aggressive fluid resuscitation.” Many patients sequester substantial amounts of fluid into the retroperitoneal space, producing very high fluid requirements. Intravascular volume depletion may lead to tachycardia, hypotension, renal failure, hemoconcentration, and generalized circulatory collapse. More than 6 L of fluid sequestration within the first 48 hours is considered a marker of increased severity, according to the Ranson criteria
Acute Pancreatitis:Issues: Antibiotics Time frame: Severe pancreatitis can be observed in 15–20 % of all cases. The first two weeks after onset of symptoms are characterized by the systemic inflammatory response syndrome (SIRS). Pancreatic necrosis develops within the first 4 days after the onset of symptoms to its full extent, Infection of pancreatic necrosis develops most frequently in the 2nd and 3rd week
Acute pancreatitis andantibiotics: Cochrane ReviewObjectives: To determine the efficacy and safety of prophylactic antibiotics in acute pancreatitis complicated by CT proven pancreatic necrosis.
Main results: Seven evaluable studies randomised 404 patients. No statistically significant effect on reduction of mortality with therapy: 8.4% versus controls 14.4%, and infected pancreatic necrosis rates: 19.7% versus controls 24.4%. Non‐pancreatic infection rates and the incidence of overall infections were not significantly reduced with antibiotics: 23.7% versus 36%; 37.5% versus 51.9% respectively. Operative treatment and fungal infections were not significantly different. Insufficient data were provided concerning antibiotic resistance.
With beta‐lactam antibiotic prophylaxis there was less mortality (9.4% treatment, 15% controls), and less infected pancreatic necrosis (16.8% treatment group, 24.2% controls) but this was not statistically significant. The incidence of non‐pancreatic infections was non‐significantly different (21% versus 32.5%), as was the incidence of overall infections (34.4% versus 52.8%), and operative treatment rates.
No significant differences were seen with quinolone plus imidazole in any of the end points measured. Imipenem on its own showed no difference in the incidence of mortality, but there was a significant reduction in the rate of pancreatic infection (p=0.02; RR 0.34, 95% CI 0.13 to 0.84)
Authors conclusions: No benefit of antibiotics in preventing infection of pancreatic necrosis or mortality was found, except for when imipenem (a beta‐lactam) was considered on its own, where a significantly decrease in pancreatic infection was found. None of the studies included in this review were adequately powered. Further better designed studies are needed if the use of antibiotic prophylaxis is to be recommended
Acute PancreatitisIssue:Other pathogenesis inhibiting drugs To date, inhibition of any known pathogenetic step (that is, octreotide, gabexate mesilate, lexipafant) has not effectively reduced mortality or increased long term survival in severe acute pancreatitis.8,28–30
Background facts.. Nutritional management during acute pancreatitis has • the purpose to avoid a negative influence on the outcome and to preserve the morphofunctional integrity of the gut, • preventing bacterial translocation. • Preventing SIRS• When the course of the disease is longer and the severity is higher, an early artificial nutritional support is advisable.• Caloric needs thought to be useful are 25-30 kcal/kg/d;• 40-60% of nutrient mixture should consist of carbohydrates and 20-30% of lipids. Proteins should be approximately 1.0-1.5 g/kg/d McClave SA, Chang WK, Dhaliwal R, Heyland DK. Nutrition support in acute pancreatitis: a systematic review of the literature. JPEN J Parenter Enteral Nutr. 2006 Mar-Apr;30(2):143-56.
Nutrition in Acute pancreatitisEnteral versus parenteral nutrition for acutepancreatitis. Cochrane Review.Cochrane Database Syst Rev. 2010 Jan 20;(1):CD002837. doi: 10.1002/14651858.CD002837.pub2.Al-Omran M, Albalawi ZH, Tashkandi MF, Al-Ansary LA.Intern Med. 2012;51(6):523-30. Epub 2012 Mar 15.Meta-analysis: total parenteral nutrition versus total enteral nutrition in predicted severe acute pancreatitis.Yi F, Ge L, Zhao J, Lei Y, Zhou F, Chen Z, Zhu Y, Xia B Objectives: To compare the effect of TPN versus EN on mortality, morbidity and length of hospital stay in patients with acute pancreatitis.
Main results: Eight trials with a total of 348 participants were included. Comparing EN to TPN for acute pancreatitis, the relative risk (RR) for death was 0.50 (95% CI 0.28 to 0.91), for multiple organ failure (MOF) was 0.55 (95% CI 0.37 to 0.81), for systemic infection was 0.39 (95% CI 0.23 to 0.65), for operative interventions was 0.44 (95% CI 0.29 to 0.67), for local septic complications was 0.74 (95% CI 0.40 to 1.35), and for other local complications was 0.70 (95% CI 0.43 to 1.13).
Mean length of hospital stay was reduced by 2.37 days in EN vs TPN groups (95% CI ‐7.18 to 2.44). Furthermore, a subgroup analysis for EN vs TPN in patients with severe acute pancreatitis showed a RR for death of 0.18 (95% CI 0.06 to 0.58) and a RR for MOF of 0.46 (95% CI 0.16 to 1.29).
Authors conclusions: In patients with acute pancreatitis, enteral nutrition significantly reduced mortality, multiple organ failure, systemic infections, and the need for operative interventions compared to those who received TPN. In addition, there was a trend towards a reduction in length of hospital stay. These data suggest that EN should be considered the standard of care for patients with acute pancreatitis requiring nutritional support.
Nutrition Support in Acute Pancreatitis: A SystematicReview of the LiteratureStephen A. McClave, Wei-Kuo Chang, Rupinder Dhaliwal, Daren K. Heyland,JPEN J Parenter Enteral Nutr MARCH-APRIL 2006 vol. 30 no. 2 143-156 doi: 10.1177/0148607106030002143 Patients with acute severe pancreatitis should begin EN early because such therapy modulates the stress response, promotes more rapid resolution of the disease process, and results in better outcome. In this sense, EN is the preferred route and has eclipsed PN as the new “gold standard” of nutrition therapy. When PN is used, it should be initiated after 5 days. Individual variability allows for a wide range of tolerance to EN, even in severe pancreatitis
Nutrition in AP: NG or NJ?Nasogastric tube feeding in predicted severe acute pancreatitis. A systematic review of the literature to determine safety andtolerance.Petrov MS, Correia MI, Windsor JA. JOP. 2008 Jul 10;9(4):440-8. CONTEXT: Nasogastric tube feeding is safe and well tolerated in most critically ill patients. However, its safety and tolerance in the setting of severe acute pancreatitis is debatable. OBJECTIVE: to review all available studies on nasogastric feeding in patients with severe acute pancreatitis to determine the safety and tolerance of this approach. A further aim was to perform a meta- analysis of the available randomized controlled trials regarding nasogastric versus nasojejunal feeding.
RESULTS: A total of four studies on nasogastric tube feeding in 92 patients with predicted severe acute pancreatitis were identified. Documented infected pancreatic necrosis developed in 11 patients (16.9%) and multiple organ failure in 10 (15.4%) out of 65 patients with available data. Overall, there were 15 deaths (16.3%). An exacerbation of pain after initiation of feeding occurred in 3 (4.3%) out of 69 patients with available data. Full tolerance was achieved in 73 (79.3%) patients who did not require temporary reduction, stoppage or withdrawal of nasogastric feeding.
CONCLUSION: Nasogastric feeding appears safe and well tolerated in patients with predicted severe acute pancreatitis. An adequately powered randomized trial on nasogastric versus nasojejunal feeding is required to support this approach as routine clinical management.
Nasogastric or nasointestinal feeding in severeacute pancreatitis.Piciucchi M, Merola E, Marignani M, Signoretti M, Valente R, Cocomello L, Baccini F, Panzuto F, Capurso G, Delle Fave G.World J Gastroenterol. 2010 Aug 7;16(29):3692-6. AIM: To assess the rate of spontaneous tube migration and to compare the effects of naso-gastric and naso-intestinal (NI) (beyond the ligament of Treitz) feeding in severe acute pancreatitis (SAP). CONCLUSION: Spontaneous distal tube migration is successful in 40% of SAP patients, with higher CT severity index predicting intragastric retention; In such cases EN by NG tubes seems to provide a pragmatic alternative opportunity with similar outcomes
Nutritional strategies in severe acutepancreatitis: A systematic review of theevidence.Ahmad Al Samaraee, Iain J.D. McCallum, Peter E. Coyne, Keith SeymourThe Surgeon; Volume 8, Issue 2 , Pages 105-110, April 2010 Evidence supports naso–jejunal enteral nutrition (NJ-EN) over parenteral nutrition (PN) reducing infectious morbidity and showing a trend towards reduced organ failure although there is no detectable difference in mortality. NJ-EN is safe when started immediately (level 3 evidence). NJ-EN is often impractical and naso-gastric (NG) feeding seems to be equivalent in terms of safety and outcomes whilst being more practical (level 2 evidence). Regarding feed supplementation, probiotic feed supplementation is not beneficial (level 1 evidence) the and may cause harm with excess mortality (level 2 evidence). No evidence exists to confirm benefit of the addition of prokinetics in severe acute pancreatitis (SAP) although their use is proven in other critically ill patients. Level 2 evidence does not currently support the use of combination immuno- nutrition though further work on individual agents may provide differing results. Level 2 evidence does not support intravenous supplementation of anti-oxidants and has demonstrated that these too may cause harm
Timing of NG feedingEarly nasogastric tube feeding versus nil per os inmild to moderate acute pancreatitis: Arandomized controlled trial.Petrov MS, McIlroy K, Grayson L, Phillips AR, Windsor JA. Clin Nutr. 2012 Dec 31. pii: S0261-5614(12)00284-1. doi:10.1016/j.clnu.2012.12.011BACKGROUND & AIMS: Nasojejunal tube feeding is a standard of care in patients with predicted severe acute pancreatitis (AP) and several recent trials suggested that nasogastric tube feeding (NGT) is as safe and efficient as nasojejunal tube feeding in these patients. The aim was to investigate whether NGT presents any benefit to patients with mild to moderate AP.
Early NGT feeding in acutepancreatitis...contdMETHODS: The study design was a randomized controlled trial. The patients in the intervention group received NGT within 24 h of hospital admission. The patients in the control group were on nil per os (NPO). The severity of acute pancreatitis was determined according to the new international multidisciplinary classification.CONCLUSIONS: NGT commenced within 24 h of hospital admission is well tolerated in patients with mild to moderate acute pancreatitis. Further, when compared with NPO, it significantly reduces the intensity and duration of abdominal pain, need for opiates, and risk of oral food intolerance, but not overall hospital stay
Acute PancreatitisIssues: Intervention in form of ERCP
Timing and need for ERCPObjectives: To systematically review evidence from randomized controlled trials (RCTs) assessing the clinical effectiveness and safety of the early routine ERCP strategy compared to the early conservative management with or without selective use of ERCP strategy, based on all important, clinically relevant and standardized outcomes including mortality, local and systemic complications as defined by the Atlanta Classification (Bradley 1993) and by authors of the primary study, and ERCP‐related complications in unselected patients with acute gallstone pancreatitis
Selection criteria: RCTs comparing the early routine ERCP strategy versus the early conservative management with or without selective use of ERCP strategy in patients with suspected acute gallstone pancreatitis. Included studies in which the population with acute gallstone pancreatitis was a subgroup within a larger group of patients. Only included studies involving only a selected subgroup of patients with acute gallstone pancreatitis (actual severe pancreatitis) in subgroup analyses.
Main results: Five RCTs comprising 644 participants were included in the main analyses. Two additional RCTs, comprising only patients with actual severe acute gallstone pancreatitis, were included only in subgroup analyses. In unselected patients with acute gallstone pancreatitis, there were no statistically significant differences between the two strategies in mortality (RR 0.74, 95% CI 0.18 to 3.03), local and systemic complications as defined by the Atlanta Classification (RR 0.86, 95% CI 0.52 to 1.43; and RR 0.59, 95% CI 0.31 to 1.11 respectively) and by authors of the primary study (RR 0.80, 95% CI 0.51 to 1.26; and RR 0.76, 95% CI 0.53 to 1.09 respectively).
Among trials that included patients with cholangitis, the early routine ERCP strategy significantly reduced mortality (RR 0.20, 95% CI 0.06 to 0.68), local and systemic complications as defined by the Atlanta Classification (RR 0.45, 95% CI 0.20 to 0.99; and RR 0.37, 95% CI 0.18 to 0.78 respectively) and by authors of the primary study (RR 0.50, 95% CI 0.29 to 0.87; and RR 0.41, 95% CI 0.21 to 0.82 respectively).
Among trials that included patients with biliary obstruction, the early routine ERCP strategy was associated with a significant reduction in local complications as defined by authors of the primary study (RR 0.54, 95% CI 0.32 to 0.91), and a non‐significant trend towards reduction of local and systemic complications as defined by the Atlanta Classification (RR 0.53, 95% CI 0.26 to 1.07; and RR 0.56, 95% CI 0.30 to 1.02 respectively) and systemic complications as defined by authors of the primary study (RR 0.59, 95% CI 0.35 to 1.01). ERCP complications were infrequent
Authors conclusions: In patients with acute gallstone pancreatitis, there is no evidence that early routine ERCP significantly affects mortality, and local or systemic complications of pancreatitis, regardless of predicted severity. Our results, however, provide support for current recommendations that early ERCP should be considered in patients with co‐existing cholangitis or biliary obstruction
Emergency ERCP in AP In persistent and severe biliary pancreatitis, when an obstructing gallstone lodged at the ampulla of Vater
Acute PancreatitisIssue:Surgery/Removal of sterile or infected necrosis
Any role of early Surgery? Except in the unusual situation of fulminating acute pancreatitis with organ failure and a rapidly progressive downhill course soon after admission to the hospital, most patients should not undergo operation during the first week of their illness. When clinical deterioration is rapid and surgery is undertaken during the first week, these patients have a high mortality rate. The outcome is better when surgery is postponed at least until the second week or later, when the margins of the pancreatic necrosis have become better defined, and the acute inflammation has subsided somewhat.
Acute PancreatitisIssue: Surgery:Background facts More than 80% of deaths amongst patients with acute pancreatitis are caused by infected necrosis Aggressive surgical treatment required in such cases Patients with infected necrosis require emergent surgery.
Common Organisms Enteric Gram Negative organisms like E.coli Gram positive organisms Anaerobes Fungal Infection is a late event usually following prolonged antibiotic therapy Daziel D J. Doolas A. “Pancreatic abscess and pancreatic necrosis: current concepts and controversies.” Problems in General Surgery, vol 7 (3) pp 415-27. 1990
Diagnosis of infected necrosis Most reliably by CT or ultrasound-guided fine needle aspiration (FNA) with Gram staining and culture of the aspirate. The material should be sent for bacterial and fungal culture. Some patients with infection have only a low grade fever and a WBC <15,000. Thus, threshold must be low. In a minority of patients, gas bubbles are evident on the CT study in the area of the pancreas. If this is found, FNA is unnecessary.
Surgical indications in acutepancreatitis.Haas B, Nathens AB. Curr Opin Crit Care. 2010 Apr;16(2):153-8. doi: 10.1097/MCC.0b013e328336ae88.) Infected pancreatic necrosis remains the primary indication for surgery in patients with acute pancreatitis. Up to a quarter of patients with acute pancreatitis develop early bacteremia and pneumonia, and assessment of patients for surgery should include a thorough search for nonpancreatic sources of infection. Retroperitoneal, percutaneous and endoscopic approaches to pancreatic debridement can be used with success in appropriately selected critically ill patients. All minimally invasive approaches to necrosectomy are evolving, and there is currently insufficient evidence to advocate one approach over another. Management of patients with acute pancreatitis at high-volume centers appears to be associated with a survival benefit.
Role of open necrosectomy in the currentmanagement of Acute NecrotizingPancreatitis: A Review ArticleK. Vasiliadis, C. Papavasiliou, A.Al Nimer, N. Lamprou, C. Makridis. ISRN Surg. 2013;2013:579435. doi: 10.1155/2013/579435.Epub 2013 Jan 28Contraindications for open necrosectomy [14, 17]. Pancreatic and/or peripancreatic necrosis without evidence of infection or clinical deterioration Early operation (within 1 week from onset of acute pancreatitis)
Role of Open... (Vasiliadis contd) Indications and timing for open necrosectomy [14, 17]. The operation should be undertaken as late as possible, when necroses have been ceased, viable and nonviable tissues are well demarcated, and infected necrotic tissues are “walled off”. Pancreatic and/or peripancreatic necrosis complicated by documented infection (guided FNA culture or extraluminal retroperitoneal gas) Sterile necrosis: (a) Progressive clinical deterioration despite maximal medical treatment (b) “Fulminant acute pancreatitis” Massive hemorrhage or hollow viscus perforation
Surgery in Acute Pancreatitis: Indicationsother than Infected Necrosis.1. When the patients condition deteriorates, often with the failure of one or more organ systems even in sterile necrosis2. To drain a pancreatic abscess, if percutaneous drainage does not produce the desired result.
Timing of cholecystectomy after mildbiliary pancreatitis: a systematic review. van Baal MC, Besselink MG, Bakker OJ, van Santvoort HC, Schaapherder AF, Nieuwenhuijs VB,Gooszen HG, van Ramshorst B, Boerma D; Dutch Pancreatitis Study Group. Ann Surg. 2012 May;255(5):860-6. doi: 10.1097/SLA.0b013e3182507646. Interval cholecystectomy (40 days) after mild biliary pancreatitis is associated with a high risk of readmission for recurrent biliary events, especially recurrent biliary pancreatitis. Cholecystectomy during index admission for mild biliary pancreatitis appears safe, but selection bias could not be excluded.
Timing of cholecystectomy after mild biliary pancreatitis.Bakker OJ, van Santvoort HC, Hagenaars JC, Besselink MG, Bollen TL, Gooszen HG, Schaapherder AF;Dutch Pancreatitis Study Group. Br J Surg. 2011 Oct;98(10):1446-54. doi: 10.1002/bjs.7587. Epub 2011 Jun 27 Between 2004 and 2007, patients with acute pancreatitis were registered prospectively in 15 Dutch hospitals. Patients with mild biliary pancreatitis were candidates for cholecystectomy. Recurrent biliary events requiring admission before and after cholecystectomy, and after endoscopic sphincterotomy (ES), were evaluated. CONCLUSION: A delay in cholecystectomy after mild biliary pancreatitis carries a substantial risk of recurrent biliary events. ES reduces the risk of recurrent pancreatitis but not of other biliary events .
Cholecystectomy in Gall StonePancreatitis In mild gallstone-associated acute pancreatitis, cholecystectomy should be performed as soon as the patient has recovered and ideally during the same hospital admission. In severe gallstone-associated acute pancreatitis, cholecystectomy should be delayed until there is sufficient resolution of the inflammatory response and clinical recovery.
Summary: Surgery in AcutePancreatitisBüchler MW, Gloor B, Müller CA et al. Acute necrotizing pancreatitis: treatment strategy according to the status of infection. Ann Surg2000;232:619–626. | Article | PubMed | ISI | ChemPort |Lytras D, Manes K, Triantopoulou C et al. Persistent early organ failure: defining the high-risk group of patients with severe acutepancreatitis? Pancreas 2008;36:249–254. | Article | PubMedLe Mée J, Paye F, Sauvanet A et al. Incidence and reversibility of organ failure in the course of sterile or infected necrotizingpancreatitis. Arch Surg 2001;136:1386–1390. | Article | PubMed
Summary Mild acute pancreatitis is not an indication for pancreatic surgery. Infected pancreatic necrosis in patients with clinical signs and symptoms of sepsis is an indication for intervention including surgery and radiological drainage.
Summary Patients with sterile pancreatic necrosis should be managed conservatively and only undergo intervention in selected cases. Minimally invasive approach to necrosectomy is expected to play a significant role in a selected group of patients Surgical and other forms of interventional management should favor an organ-preserving approach, which involves debridement or necrosectomy combined with a postoperative management concept that maximizes postoperative evacuation of retroperitoneal debris and exudate. Cholecystectomy should be performed to avoid recurrence of gallstone-associated acute pancreatitis. ES is alternative to cholecystectomy but there is a theoretical risk of introducing infection into sterile pancreatic necrosis.
ThanksDr Arth Shah Dr Manoj K GhodaAcute Pancreatitis Revisited
SAP SAP is defined by the Atlanta classification as an AP with local and/or systemic complications[Bradley EL 3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch Surg. 1993;128:586–590.] . Some patients develop pancreatitis-associated organ failure during the early phase of the SAP [Stanten R, Frey CF. Comprehensive management of acute necrotizing pancreatitis and pancreatic abscess. Arch Surg. 1990;125:1269–1274; discussion 1274-1275.].
Severe Acute PancreatitisClinical features and DiagnosisandIts Interpretation
Diagnosis of Severity“C” reactive Protein: Together with both amylase and lipase, often provides a precise picture of the clinical situation (Del Prete M et al.) C-reactive protein (cut-off of 150 mg/L) is a useful indicator of necrosis with a sensitivity and specificity of 80% It is required to be measured more than 48 h after the onset of symptoms [Dervenis C, Johnson CD, Bassi C, Bradley E, Imrie CW, McMahon MJ, Modlin I. Diagnosis, objective assessment of severity, and management of acute pancreatitis. Santorini consensus conference. Int J Pancreatol. 1999;25:195–210. ].
Diagnosis of Severity Urinary trypsinogen activation peptide (TAP), Serum and urinary trypsinogen [Hirano T, Manabe T. A possible mechanism for gallstone pancreatitis: repeated short-term pancreaticobiliary duct obstruction with exocrine stimulation in rats. Proc Soc Exp Biol Med. 1993;202:246–252., Lempinen M, Stenman UH, Finne P, Puolakkainen P, Haapiainen R, Kemppainen E. Trypsinogen-2 and trypsinogen activation peptide (TAP) in urine of patients with acute pancreatitis. J Surg Res. 2003;111:267–273. ] , But these are less widely available.
Diagnosis of Severity Urinary trypsinogen-2 is comparable diagnostic accuracy, and provides greater (99%) negative predictive value. The novel serum markers procalcitonin and interleukin 6 allow earlier prediction (12 to 24 hours after admission) of severity. [Papachristou GI, Papachristou DJ, Avula H, Slivka A, Whitcomb DC. Obesity increases the severity of acute pancreatitis: performance of APACHE-O score and correlation with the inflammatory response. Pancreatology. 2006;6:279–285.], Serum interleukins-6 and -8 and polymorphonuclear elastase at 24 h after admission. [Rau BM. Predicting severity of acute pancreatitis. Curr Gastroenterol Rep. 2007;9:107–115. ].
Other tests 61-80 % of patients show leukocytosis with shift to the left. 54-82 % lymphopenia is noted. Anemia S. Bil, Urea, SGOT,LDH, Sugar, Calcium, and ABG abnormal Daily urine examination is helpful. In urine the proteinuria, a microhematuria, and casts may be seen.
Sequential organ failure assessment score (SOFA) .1SOFA: Sequential organ failure assessment, World J Gastroenterol. 2009 June 28; 15(24): 2945–2959. Published online 2009 June 28. doi: 10.3748/wjg.15.2945. Organ system Score involved 1 2 3 4 5 Dopamine > 5 Dopamine < 0.1 μg/kg per min or μg/kg per min or > adrenaline Dopamine or 15 μg/kg per min or (epinephrine) < 0.1 Cardiovascular No hypotension MAP < 70 mmHg dobutamine (any adrenaline > 0.1 μg/kg per min or dose) μg/kg per min or noradrenaline noradrenaline > 0.1 (norepinephrine) < μg/kg per min 0.1 μg/kg per min Respiratory PaO2/FiO2 > 400 400-300 300-200 200-1001 ≤ 1001 (mmHg) Renal creatinine < 100 100-200 200-350 350-500 > 500 (μmol/L) Neurological glasgow coma 15 14-13 12-10 9-7 ≤6 score Haematological platelet count (× > 150 150-100 100-50 20-50 ≤ 20 109/L) Hepatic bilirubin < 20 20-60 60-120 120-240 > 240 (μmol/L)
Since the mortality in the presence of pancreatic necrosis increases from 1% to 10%-23%, the importance of early detection of pancreatic necrosis is not to be overlooked [Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology. 2002;223:603–613. ]. Contrast-enhanced CT has been considered the “gold standard” for the diagnosis of pancreatic necrosis [Ranson JH, Balthazar E, Caccavale R, Cooper M. Computed tomography and the prediction of pancreatic abscess in acute pancreatitis. Ann Surg. 1985;201:656–665. Simchuk EJ, Traverso LW, Nukui Y, Kozarek RA. Computed tomography severity index is a predictor of outcomes for severe pancreatitis. Am J Surg. 2000;179:352–355. ].
Therefore, immediate assessment should include clinical evaluation particularly of any cardiovascular, respiratory and renal compromise, BMI, chest X-ray and different acute diseases scores. The presence of any single and/or multiple organ failure has been increasingly recognized as an important variable for predicting mortality from AP. The most common organ dysfunction scores used for critically ill patients are the Multiple Organ Dysfunction Score (MODS) and the Sequential Organ Failure Assessment (SOFA)[Vincent JL, de Mendonça A, Cantraine F, Moreno R, Takala J, Suter PM, Sprung CL, Colardyn F, Blecher S. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Working group on "sepsis-related problems" of the European Society of Intensive Care Medicine. Crit Care Med. 1998;26:1793– 800. Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung CL, Sibbald WJ. Multiple organ dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med. 1995;23:1638–1652.] (Tables 3 and 4).
Although these scoring systems can help the physician in a first assessment of the patient, the most important distinction in terms of prediction of severity is the presence of severe manifestations of the disease such as evidence of SIRS and presence of organ failure.
Mofidi, in a recent retrospective study of 259 patients admitted with AP, showed that the mortality rate was significantly higher in patients who developed or had persistent SIRS at 48 h after admission (25.4%) than in patients who had transient SIRS (8%) or no SIRS in the first 48 h (0.7%)[ Mofidi R, Duff MD, Wigmore SJ, Madhavan KK, Garden OJ, Parks RW. Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis. Br J Surg. 2006;93:738–744. .
Acute pancreatitis graded with CT and CT severity index table Grade CT finding Points Necrosis Severity index Percentage Additional points A Normal pancreas 0 0 0 0 B Pancreatic enlargement 1 0 0 1 C Pancreatic inflammation and/or peripancreatic fat 2 < 30 2 4 D Single peripancreatic fluid collection 3 30-50 4 7 E Two or more fluid collections and/or retroperitoneal air 4 > 50 6 10 World J Gastroenterol. 2009 June 28; 15(24): 2945–2959. Published online 2009 June 28. doi: 10.3748/wjg.15.2945.
Although CT is useful in detecting pancreatic necrosis, it is not able to detect a super-infection of necrosis in the later stage of the disease unless gas bubbles are seen within the necrotic area[Uhl W, Roggo A, Kirschstein T, Anghelacopoulos SE, Gloor B, Müller CA, Malfertheiner P, Büchler MW. Influence of contrast-enhanced computed tomography on course and outcome in patients with acute pancreatitis. Pancreas. 2002;24:191–197. ]. Patients with persisting organ failure, or in whom new organ failure develops, and in those with persisting pain and signs of sepsis, will require evaluation by dynamic contrast enhanced CT. CT evidence of necrosis correlates well with the risk of other local and systemic complications. Since pancreatic necrosis commonly remains stable in appearance, a follow-up CT scan at 3 to 4 wk is not normally considered[Vitellas KM, Paulson EK, Enns RA, Keogan MT, Pappas TN. Pancreatitis complicated by gland necrosis: evolution of findings on contrast- enhanced CT. J Comput Assist Tomogr. 1999;23:898–905. ].
Ranson’s CriteriaAt 48 hours Calcium < 8.0 mg/dL) Hematocrit fall > 10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L
APACHE II score Hemorrhagic peritoneal fluid Obesity Indicators of organ failure Hypotension (SBP <90 mm HG) or tachycardia > 130 beat/min PO2 <60 mmHg Oliguria (<50 mL/h) or increasing BUN and creatinine Calcium <8.0 mg/dL or Albumin <3.2.g/dL)
APACHE II score Apache score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT) Interpretation If the score ≥ 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely, Or Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality
DiagnosisAbdominal ultrasound: Very popular and useful High positive predictive value >95% Moderate to high negative predictive value, 85=90%
DiagnosisComputerized tomography (CT) scan. Positive predictive value, negative predictive value, sensitivity and specificity as good as USG More useful for peripancreatic lesion and Necrosis.
DiagnosisEndoscopic ultrasound (EUS): Excellent Mode Comparable or superior to both CT and USG Additional advantage of accurately visualizing Lower CBD. Useful for outlining the treatment
DiagnosisMRCP / MRI Comparable to CT Use of Gadolinium may increase sensitivity and specificity No “contrast” related renal problems Additional advantage of visualizing Biliary tree
DiagnosisERCP: ERCP is usually used only in the presence of gallstones. The benefits of ERCP with sphincterotomy (ES) has been studied in 3 randomized trials[Neoptolemos JP, Carr-Locke DL, London NJ, Bailey IA, James D, Fossard DP. Controlled trial of urgent endoscopic retrograde cholangiopancreatography and endoscopic sphincterotomy versus conservative treatment for acute pancreatitis due to gallstones. Lancet. 1988;2:979–983] and 2 meta- analyses[Petrov MS, van Santvoort HC, Besselink MG, van der Heijden GJ, van Erpecum KJ, Gooszen HG. Early endoscopic retrograde cholangiopancreatography versus conservative management in acute biliary pancreatitis without cholangitis: a meta-analysis of randomized trials. Ann Surg. 2008;247:250–257.]. Patients with predicted mild acute biliary pancreatitis (ABP) in the absence of cholangitis have not shown benefits from an early ERCP. The decision on management of patients with predicted severe ABP is still debatable. The most recent United Kingdom guidelines recommend that urgent therapeutic ERCP should be performed within 72 h of admission in all patients with predicted severe ABP, whether or not cholangitis is present[UK guidelines for the management of acute pancreatitis. Gut. 2005;54 Suppl 3:iii1–iii9.]. However, a recent meta-analysis by Petrov et al[Petrov MS, van Santvoort HC, Besselink MG, van der Heijden GJ, van Erpecum KJ, Gooszen HG. Early endoscopic retrograde cholangiopancreatography versus conservative management in acute biliary pancreatitis without cholangitis: a meta-analysis of randomized trials. Ann Surg. 2008;247:250–257. ] demonstrated that early ERCP with or without ES had no beneficial effect in patients with predicted mild or severe ABP without cholangitis. The conclusion of this study was partially supported by the 2007 guidelines of the American Gastroenterology Association which stated that early ERCP in patient with severe ABP without signs of acute cholangitis is still not uniformly accepted in the literature[Forsmark CE, Baillie J. AGA Institute technical review on acute pancreatitis. Gastroenterology. 2007;132:2022–2044. ].
Diagnosis of Various Forms ofdisease The acute interstitial pancreatitis is characterized by rapidity, a relative short duration of disease. Clinical features usually disappear during 3-7, and acute pathological changes by 10-14 days. In most mild cases at an early stage, few of abnormal signs of disease are observed. Pain and vomiting are and quickly pass under the influence of conservative treatment, The systemic involvement is minimal and metabolic abnormalities are very few.
Acute necrotizing pancreatitis Clinical implications of necrosis last for more than 3 4 weeks, and pathological changes may last from 1- 5 months. Anemia, moderate to severe abdominal pain and repeated vomiting are usually present. The patient may go in to shock. Vigorous resuscitative measures are mandatory in these cases.
Aseptic reactive process involve not only a gland and a retroperitoneal fat, but also surrounding organs. The most important objective sign is palpated in region glands the infiltrate arising for 5-7th day and later from the beginning of an attack. This conglomerate is not very painful, has no accurate borders and becomes more expressed at a premise under a back of the patient of a pillow or the platen. The condition of the patient more often moderately severe, becomes perceptible the appetite depression, moderately expressed pallor of integuments, is frequent - a paresis GASTROINTESTINAL TRACT. Temperature, as a rule, afebrile, the leukocytosis with neutrophilic alteration is moderately expressed. Indicators of an ESR, the S-jet protein, a fibrinogen are raised.
Clinical Classifications Depending on a phase of development of pathological process it is possible to delineate 4 forms of an acute pancreatitis: acute interstitial, corresponding to an edema phase acute necrotic, expressing a phase of formation of a necrosis infiltrative-necrotizing it is purulent-necrotizing, corresponding to a phase of fusion and a sequestration of the necrotic locuses.
Pancreas, liver, and kidney functions (including levels of pancreatic enzymes amylase and lipase) Signs of infections Blood cell counts indicating signs of anemia Pregnancy test Blood sugar, electrolyte levels (an imbalance suggests dehydration) and calcium level Results of the blood tests may be inconclusive if the pancreas is still making digestive enzymes and insulin. Diagnostic imaging tests are usually needed to look for complications of pancreatitis, including gallstones. Diagnostic imaging tests may include the following: X-ray films may be ordered to look for complications of pancreatitis as well as for other causes of discomfort.
Chinese herbal medicine in AP Authors conclusions: Some Chinese medicinal herbs may work in acute pancreatitis. However, because the trials were of low quality, the evidence is too weak to recommend any single herb. Rigorously designed, randomized, double‐blind, placebo‐controll ed trials are required.