Necrosis In Severe Acute Pancreatitis Research Articles

High-Dose Vitamin C Alleviates Pancreatic Necrosis by Inhibiting Platelet Activation Through the CXCL12/CXCR4 Pathway in Severe Acute Pancreatitis.

Platelet activation in the early stage of pancreatitis is the key step developing into pancreatic necrosis. Studies suggested that vitamin C (Vit C) can inhibit platelet activity by targeting CXCL12/CXCR4 pathway. High-dose Vit C were showed to reduce pancreatic necrosis in severe acute pancreatitis (SAP) but the mechanism remains unclear. Here we speculate high-dose Vit C reduce pancreatic necrosis by inhibiting platelet activation through downregulating CXCL12/CXCR4 pathway. The pancreatic microcirculation of rats was observed by intravital microscopy. The platelet activity of SAP rats treated with or without high-dose Vit C was analyzed by platelet function test. Besides, the activity of platelets preincubated with high-dose Vit C or vehicle from SAP patients was also evaluated. Then, the TFA (CXCR4 agonist) and rCXCL12 were used to neutralize the effect of high-dose Vit C in SAP rats treated with high-dose Vit C. Meanwhile, the levels of enzymes and inflammatory cytokines in rat plasma, and rats' pancreatic histopathology and mortality were assessed. Platelets from animals and patients with SAP are more sensitive to agonists and are more easily activated. Administration of high-dose Vit C significantly ameliorated excessive activation of platelets in SAP rats, ultimately increasing the microvessel density and inducing microthrombus and blood stasis; these results were consistent with clinical sample analysis. Moreover, high-dose Vit C significantly inhibited the release of amylase, lipase, TNF-α, and IL-6 in SAP rat plasma, reducing pancreatic damage and the mortality of SAP rats. However, using TFA and rCXCL12 significantly reversed the effect of high-dose Vit C on excessive activation of platelets, aggravating microcirculation impairment and pancreatic damage. The present study suggests that high-dose Vit C can ameliorate pancreatic necrosis by improving microcirculation disorders of SAP. For the first time, the underlying mechanism is related with inhibiting platelet activation through the CXCL12/CXCR4 pathway.

Early Predictors of Infected Pancreatic Necrosis in Severe Acute Pancreatitis: Implications of Neutrophil to Lymphocyte Ratio, Blood Procalcitonin Concentration, and Modified CT Severity Index

Background: Infected pancreatic necrosis (IPN) accounts for 30% mortality in severe acute pancreatitis (SAP). Early prediction of IPN occurrence is critical for prophylactic measures to be taken. This study aimed to evaluate the predicting value for IPN of combined markers at early stages of SAP. Methods: The clinical records of 324 SAP patients admitted within 48 h after disease onset were retrospectively analyzed. As potential predictors, the neutrophil to lymphocyte ratio (NLR), blood procalcitonin (PCT) concentration on the 1st, 4th, and 7th day post admission, as well as modified computerized tomography severity index (MCTSI) on the 5–7th day post admission, were extracted. Correlations between these features with IPN were analyzed using logistic regression, and predictive values were estimated using the receiver operating characteristic curve analyses. Results: NLR, PCT, body mass index, and MCTSI were significantly higher in the IPN group (p < 0.001) compared to the control, among which NLR, PCT, and MCTSI were identified as independent predictors for IPN in logistic regression model. Combination of these parameters yielded significant predicting values with an area under curve of 0.92, sensitivity of 97.2%, and specificity of 77.2% in receiver operating characteristic curve analysis. Conclusion: Combination of NLR, PCT, MCTSI might facilitate the prediction of IPN occurrence in SAP patients.

Endoscopic treatment of infectious necrosis in severe acute pancreatitis

Severe acute pancreatitis (SAP) is one of the most common acute and critical diseases. SAP is often accompanied by necrosis of the pancreas and surrounding tissues.When necrosis is co-infected, it often means high mortality. With the development of endoscopic technology, endoscopic intervention in the treatment of necrotizing pancreatitis has achieved good results, which has the advantages of minimal-invasiveness, effectiveness, and safety, and could significantly improve the prognosis of patients with SAP. This article aims to review the research progress of endoscopic treatment of necrotizing pancreatitis.

Fatty Acid Ethyl Esters Are Less Toxic Than Their Parent Fatty Acids Generated during Acute Pancreatitis

Although ethanol causes acute pancreatitis (AP) and lipolytic fatty acid (FA) generation worsens AP, the contribution of ethanol metabolites of FAs, ie, FA ethyl esters (FAEEs), to AP outcomes is unclear. Previously, pancreata of dying alcoholics and pancreatic necrosis in severe AP, respectively, showed high FAEEs and FAs, with oleic acid (OA) and its ethyl esters being the most abundant. We thus compared the toxicities of FAEEs and their parent FAs in severe AP. Pancreatic acini and peripheral blood mononuclear cells were exposed to FAs or FAEEs in vitro. The triglyceride of OA (i.e., glyceryl tri-oleate) or OAEE was injected into the pancreatic ducts of rats, and local and systemic severities were studied. Unsaturated FAs at equimolar concentrations to FAEEs induced a larger increase in cytosolic calcium, mitochondrial depolarization, and necro-apoptotic cell death. Glyceryl tri-oleate but not OAEE resulted in 70% mortality with increased serum OA, a severe inflammatory response, worse pancreatic necrosis, and multisystem organ failure. Our data show that FAs are more likely to worsen AP than FAEEs. Our observations correlate well with the high pancreatic FAEE concentrations in alcoholics without pancreatitis and high FA concentrations in pancreatic necrosis. Thus, conversion of FAs to FAEE may ameliorate AP in alcoholics.

Aspirin Protects against Acinar Cells Necrosis in Severe Acute Pancreatitis in Mice.

Aspirin has a clear anti-inflammatory effect and is used as an anti-inflammatory agent for both acute and long-term inflammation. Previous study has indicated that aspirin alleviated acute pancreatitis induced by caerulein in rat. However, the role of aspirin on severe acute pancreatitis (SAP) and the necrosis of pancreatic acinar cell are not yet clear. The aim of this study was to determine the effects of aspirin treatment on a SAP model induced by caerulein combined with Lipopolysaccharide. We found that aspirin reduced serum amylase and lipase levels, decreased the MPO activity, and alleviated the histopathological manifestations of pancreas and pancreatitis-associated lung injury. Proinflammatory cytokines were decreased and the expression of NF-κB p65 in acinar cell nuclei was suppressed after aspirin treatment. Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased. Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue. In conclusion, our data showed that aspirin could protect pancreatic acinar cell against necrosis and reduce the severity of SAP. Clinically, aspirin may potentially be a therapeutic intervention for SAP.

Efficacy of recombinant human soluble thrombomodulin in preventing walled-off necrosis in severe acute pancreatitis patients.

To investigate the efficacy of recombinant human soluble thrombomodulin (rTM) in preventing the development of walled-off necrosis (WON) in severe acute pancreatitis (SAP) patients. We retrospectively analyzed 54 SAP patients divided into two groups: SAP patients treated by rTM (rTM group, 24 patients) and not treated by rTM (control group, 30 patients). rTM was administered to patients with disseminated intravascular coagulation (DIC). Initially, on the admission day, we recorded patient severity and pancreatic necrosis/ischemia positive or negative. Then we investigated development of WON using 4 weeks later CT/MRI. Finally we compared the proportions of patients developing WON in the rTM group and the control group. On the admission day, the condition of patients treated by rTM was significantly worse than patients in the control group; rTM group vs. 71.8±13.9 vs. 59.8±15.3 years for age, 10.7±3.5 vs. 8.0±4.4 for Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and 3.3±1.8 vs. 2.2±1.8 for sequential organ failure assessment (SOFA) score (p<0.05). We found no significant differences on the admission day in rate of pancreatic necrosis/ischemia between patients treated by rTM and controls (58.3% vs. 63.3%, p=0.71). Nevertheless, the proportion of patients developing WON was significantly lower among those administered rTM than in those not administered rTM {29.2% (7/24 patients) vs. 56.7% (17/30 patients), p<0.05}. Treatment of SAP patients treated by rTM may prevent progression from pancreatic necrosis/ischemia to WON.

Yatak başı akut pankreatit şiddet indeksinin Türk toplumunda değerlendirilmesi

Background and Aims: Identification of patients at risk for severe disease early in the course of acute pancreatitis is essential to optimize management and to improve outcomes. We aimed to assess the Bedside Index for Severity in Acute Pancreatitis score as a predictor of disease severity in acute pancreatitis in a Turkish population. Materials and Methods: We analyzed retrospectively acute pancreatitis patients between January 1999 and December 2006. Bedside Index for Severity in Acute Pancreatitis, Ranson and Computed Tomography Severity Index scores were calculated. Clinical data, laboratory results, pancreatic necrosis, organ failure, and mortality were registered. Accuracy of the scoring system for predicting severity was measured by the area under the receiver operating characteristic curve. Results:Of the 111 patients, 63 (56.8%) were female. The median age was 59.1 years. Of all patients, 23 (20.7%) had severe acute pancreatitis and 57.7% had biliary pancreatitis. Of patients with severe acute pancreatitis, 15 (65.2%) developed organ failure, 7 (30.4%) developed pancreatic necrosis, and 2 (8.6%) died. Bedside Index for Severity in Acute Pancreatitis generated similar area under the receiver operating characteristic curve values to those of the Ranson score in predicting severe acute pancreatitis. The area under the receiver operating characteristic curve for the Bedside Index for Severity in Acute Pancreatitis score to detect pancreatic necrosis was 0.60 (0.38-0.80) and for the Ranson score was 0.70 (0.48-0.87), with no significant differences. To predict pancreatic necrosis, a Bedside Index for Severity in Acute Pancreatitis score >2 had a sensitivity, specificity, and positive and negative predictive values of 57%, 69%, 44%, and 79%, respectively. The Bedside Index for Severity in Acute Pancreatitis score was not as good as Ranson and Computed Tomography Severity Index scores for predicting organ failure. Conclusions:The Bedside Index for Severity in Acute Pancreatitis score was a useful method in a Turkish population for predicting the severity of acute pancreatitis, with the advantage of being simple and based on parameters obtained on the first day of hospitalization. The Bedside Index for Severity in Acute Pancreatitis score is valuable in predicting pancreatic necrosis in severe acute pancreatitis in Turkish patients

Laparotomy versus retroperitoneal laparoscopy in debridement and drainage of retroperitoneal infected necrosis in severe acute pancreatitis

The aim of this study was to compare laparotomy and retroperitoneal laparoscopy in debridement and drainage of retroperitoneal infected necrosis of severe acute pancreatitis (SAP), and to evaluate the curative efficacy and the timing of retroperitoneal laparoscopic debridement drainage (RLDD) for SAP patients. We performed a retrospective analysis of 50 SAP cases, including 18 patients in the RLDD group and 32 patients in the laparotomy group. Observed indices included gender, age, CT severity index, Ranson score, APACHE II score, preoperative course, length of stay, operation time, mortality, postoperative complications, drainage tube indwelling time, and change of body temperature and peripheral white blood cell (PWBC) count between the time before the operation and at 48 h after surgery. Between the RLDD group and the laparotomy group, there was a significant difference in operation time (130 ± 15 vs. 148 ± 25 h; P = 0.007), length of stay [40.8 (6-121) vs. 55.9 (28-133) days; P = 0.053], and preoperative course [14.7 (5-31) vs. 18.3 (6-31) days; P = 0.05], but no significant difference in average drainage tube indwelling time [44.4 (2-182) vs. 49.8 (2-175) days; P = 0.663]. More improvement in body temperature and PWBC count was observed in the patients of the RLDD group. There was one death (1/18) in the RLDD group and four (4/32) in the laparotomy group. Fourteen cases (14/32) in the laparotomy group had postoperative complications, including pancreatic fistula (n = 11), intestinal fistula (n = 2), retroperitoneal hemorrhage (n = 2), infection of incision (n = 9), and 5 cases (5/18) in the RLDD group, including pancreatic fistula (n = 4) and retroperitoneal hemorrhage (n = 1). RLDD, as minimally invasive surgery, is technically feasible, safe, and effective in the treatment of retroperitoneal infected necrosis in SAP patients, in contrast to the laparotomy technique, and can be performed in the early phase of SAP to prevent the deterioration of the disease.

Percutaneous drainage of infected necrosis in severe acute pancreatitis

Percutaneous drainage of infected necrosis in severe acute pancreatitis

Effects of Pantoprazole in experimental acute pancreatitis

Aims Oxidative stress with free radicals plays a crucial role in acute pancreatitis (AP). Pantoprazole (PPZ), widely used as a proton pump inhibitor, possesses reactivity towards hydroxyl radicals. The aim of the study was to examine the effect of PPZ on the course of experimental AP. Main methods Mild AP was induced in rats by caerulein (n = 12). Severe AP was induced by infusion of glycodeoxycholic acid (10 mM) into the pancreatic duct combined with caerulein (n = 12). Both AP models were randomized to PPZ treatment (20 mg/kg at baseline and after 12 h) or placebo. Control animals received Ringer solution (n = 6) without AP induction. After 24 h severity of AP was examined by histology, enzyme levels, edema and inflammatory markers (myeloperoxidase, protein profiling). Furthermore, CD62P and CD31 for leukocyte and platelet activation were investigated. Key findings Histology showed that PPZ treatment reduced tissue infiltration of inflammatory cells and acinar cell necrosis in severe AP. After PPZ treatment CD62P expression in mild AP and CD31 expression in severe pancreatitis decreased, indicating an inhibition of platelet activation. In mild and severe AP, PPZ significantly decreased amylase, LDH, edema and myeloperoxidase activity. Protein profile of pancreatic juice and serum revealed different spectra and less pancreatic juice proteins in PPZ treated groups indicating less acinar cell leakage. Significance PPZ possesses anti-inflammatory in vivo properties and attenuates the course of AP. This is mediated via a reduced expression of inflammatory and adhesive proteins with a consecutive decrease in platelet and leukocyte activation as key steps in the pathogenesis of AP.

Rapid hemodilution is associated with increased sepsis and mortality among patients with severe acute pancreatitis

Background Hemoconcentration may be an important factor that determines the progression of severe acute pancreatitis (SAP). In addition, it has been proposed that biomarkers may be useful in predicting subsequent necrosis in SAP. However, it is still uncertain whether hemodilution in a short term can improve outcome. We aimed to investigate the effect of rapid hemodilution on the outcome of patients with SAP. Methods One hundred and fifteen patients were admitted prospectively according to the criteria within 24 hours of SAP onset. Patients were randomly assigned to either rapid hemodilution (hematocrit (HCT) &lt;35%, n=56) or slow hemodilution (HCT ≥35%, n=59) within 48 hours of onset. Balthazar CT scores were calculated on admission, day 7, and day 14, after onset of the disease. Time interval for sepsis presented, incidence of sepsis within 28 days and in-hospital survival rate were determined. Results The amount of fluid used in rapid hemodilution was significantly more than that used in slow hemodilution (P &lt;0.05) on the admission day, the first day, and the second day. There were significant differences between the rapid and slow hemodilution group in terms of hematocrit, oxygenation index, pH values, APACHE II scores and organ dysfunction at different time during the first week. There were significant differences in the time interval to sepsis in rapid hemodilution ((7.4±1.9) days) compared with the slow hemodilution group ((10.2±2.3) days), and the incidence of sepsis (78.6%) was higher in the rapid group compared to the slow (57.6%) in the first 28 days. The survival rate of the slow hemodilution group (84.7%) was better than the rapid hemodilution (66.1%. P &lt;0.05). Conclusions Rapid hemodilution can increase the incidence of sepsis within 28 days and in-hospital mortality. Hematocrit should be maintained between 30%-40% in the acute response stage.

Prevention, detection, and management of infected necrosis in severe acute pancreatitis

The management of infected peripancreatic or pancreatic necrosis in patients with severe pancreatitis has changed considerably in recent years. This review discusses the recent literature on prevention, detection, and management of infected necrosis. Though antibiotics, probiotics, and enteral nutrition have been tried to prevent infected necrosis, only enteral nutrition has consistently proven to be effective. Antibiotics and probiotics have not shown a consistent beneficial effect on outcome. Enteral nutrition reduced infectious complications and mortality in severe pancreatitis, compared with parenteral nutrition. The detection of infection of pancreatic necrosis is important for clinical decision making. Fine-needle aspiration may be used to confirm suspected infection, but if its results will not change clinical decisions, it should be omitted, as it may even introduce infection. Minimally invasive surgical, radiologic, or endoscopic intervention is increasingly being applied. In the absence of level 1 evidence, local expertise dictates which type of intervention is applied.

Perfusion CT to Predict the Development of Necrosis in Severe Acute Pancreatitis: More Studies Are Needed

Perfusion CT to Predict the Development of Necrosis in Severe Acute Pancreatitis: More Studies Are Needed

Acute pancreatitis

To review advances over the last year in the prevention, diagnosis and management of acute pancreatitis. Obesity is an independent risk factor for severity in acute pancreatitis, and heavy alcohol consumption for the development of necrosis in severe acute pancreatitis. Biochemical markers have been further tested, including carbohydrate-deficient transferrin for the diagnosis of alcohol-induced acute pancreatitis, urinary trypsinogen-2 as a diagnostic marker for acute pancreatitis, and interleukin-6 and procalcitonin as markers of disease severity. A new, simple stratification system, the 'panc 3 score', has been described. There are conflicting data on the use of antibiotic prophylaxis in acute necrotizing pancreatitis, and on the chemoprevention of postendoscopic retrograde cholangiopancreatography pancreatitis. Enteral feeding is established as standard practice early in the management of acute pancreatitis of all aetiologies; probiotics and other compounds may also play a role. Over the last year, there have been further innovations in the risk stratification and management of acute pancreatitis. Unresolved issues include chemoprevention of endoscopic retrograde cholangiopancreatography-induced acute pancreatitis, the indications for antibiotic prophylaxis in severe acute pancreatitis and nutritional supplementation with probiotics and synbiotics.

Antimicrobial activity of a multispecies probiotic (Ecologic 641) against pathogens isolated from infected pancreatic necrosis

Although probiotic prophylaxis has been suggested to prevent small bowel bacterial overgrowth, bacterial translocation and infection of pancreatic necrosis in severe acute pancreatitis, limited data are available on their antimicrobial activity. Using the well-diffusion method, we studied the antimicrobial properties of a multispecies probiotic product (Ecologic 641) against a collection of pathogens cultured from infected pancreatic necrosis. All individual probiotic strains included in the multispecies preparation were able to inhibit the growth of the pathogens to some extent. However, the combination of the individual strains (i.e. the multispecies preparation) was able to inhibit all pathogenic isolates. Probiotic-free supernatants adjusted to pH 7 were not able to inhibit pathogen growth. Ecologic 641 is capable of inhibiting growth of a wide variety of pathogens isolated from infected pancreatic necrosis. The antimicrobial properties are to a large extent explained by the production of organic acids. Ecologic 641 is currently being used in a Dutch nationwide double-blind, placebo-controlled, randomized multicentre trial in patients with predicted severe acute pancreatitis.

Value of routine clinical tests in predicting the development of infected pancreatic necrosis in severe acute pancreatitis

Objective. Fine-needle aspiration (FNA) is the procedure of choice for accurate diagnosis of infected necrosis. However, invasive procedures increase the risk of secondary pancreatic infection and the timing of FNA is still a matter for debate. Our objective was to assess the value of routine clinical tests to determine the minimal risk for infected necrosis, thereby optimizing timing and selection of patients for image-guided FNA. Material and methods. This prospective, non-randomized study comprised 90 patients with acute necrotizing pancreatitis. The data of 52 patients were used for discriminant function analysis to determine the differences between patients with infected necrosis and those with sterile necrosis. Cut-off points for variables were established using receiver operating characteristic (ROC) curve analysis and logistic regression was performed to determine the risk of infected necrosis. The clinical relevance of the defined diagnostic system was prospectively tested in a further 38 consecutive patients with acute necrotizing pancreatitis (ANP). Results. Discriminant function analysis showed that C-reactive protein (CRP) and white blood cell (WBC) values were significant discriminators between patients with sterile necrosis and those with infected necrosis. Cut-off values of 81 mg/l for CRP and 13×109/l for WBC were established. The predicted risk for infected necrosis is approx. 1.4% if both tests are below the defined cut-off values. Consequently, we found FNA unnecessary in this subset of patients, unless otherwise indicated, as this invasive procedure per se carries a certain risk of bacterial contamination. Conclusions. Routine clinical tests are helpful in diagnosing the development of infected necrosis. Based on the application of classification functions, the timing and selection of patients for image-guided FNA can be optimized.

Direct retroperitoneal approach to necrosis in severe acute pancreatitis.

From 1981 to 1987, 40 patients with severe acute pancreatitis were operated on using a direct retroperitoneal approach, 22 primarily and 18 after a first operation performed through another incision. The severity of the disease was assessed by Ranson's bioclinical and computed tomography scan scoring systems. The retroperitoneal approach consisted of a left lateral incision, just anterior to the 12th rib, allowing direct access to the pancreas and a complete manual exploration of the gland and peripancreatic spaces. All patients but one were operated on for infected necrosis. The overall mortality rate was 33 per cent but was lower in the patients operated on primarily through a direct retroperitoneal approach (18.2 per cent). Twenty patients (50 per cent) developed a local complication (haemorrhage, colon fistula and/or necrosis). The direct retroperitoneal approach permits the removal of necrosis and several reoperations without the risk of large wound dehiscence and does not preclude the extension of the incision to a subcostal incision when necessary.

Management of pancreatic necrosis in severe acute pancreatitis

Management of pancreatic necrosis in severe acute pancreatitis

Prophylactic antibiotics alter the bacteriology of infected necrosis in severe acute pancreatitis.

Use of appropriate prophylactic antibiotics has been shown to decrease infectious complications and mortality rate in patients with severe acute pancreatitis, but its influence on the bacteriology of secondary pancreatic infection is poorly defined. Operative cultures from 61 consecutive patients with pancreatic necrosis treated during routine prophylactic antibiotic use (1993-2001) were compared with 34 consecutive patients with necrosis treated before routine antibiotic use (1977-1992). The two groups of patients were similar in demographics, etiology of pancreatitis, and severity of illness. All patients in the antibiotic group received prophylactic antibiotics compared with only 38% (13 of 34) in the control group. Routine broad-spectrum prophylactic antibiotics altered the bacteriology of secondary pancreatic infection in severe acute pancreatitis from predominantly gram-negative coliforms (56% versus 26%, p = 0.005) to predominately gram-positive organisms (23% versus 52%, p = 0.009) without a significant increase in either the rate of beta-lactam resistance or fungal infections. The overall hospital stay in patients treated with prophylactic antibiotics was significantly reduced (61 +/- 24 days versus 41 +/- 28 days, p = 0.002), and there was a trend toward a decline in mortality rate in the antibiotic treatment group. Routine broad-spectrum prophylactic antibiotic use has altered the bacteriology of secondary pancreatic infection in severe acute pancreatitis from predominantly gram-negative coliforms to predominantly gram-positive organisms without altering the rate of beta-lactam resistance or fungal superinfection.

Can Fluid Resuscitation Prevent Pancreatic Necrosis in Severe Acute Pancreatitis?

Background/Aims: In previous studies, we have demonstrated that hemoconcentration was an early marker for necrotizing pancreatitis.The aim of the present study was to determine whether fluid resuscitation could prevent pancreatic necrosis among patients with hemoconcentration at the time of admission. Methods: Data was pooled from the prior two studies of all patients with necrotizing pancreatitis and interstitial pancreatitis with a hematocrit of ≧44 on admission. Hematocrit values in necrotizing pancreatitis and interstitial pancreatitis were compared at admission and at 24 h. Statistical analyses were performed using the Wilcoxon rank-sum test. Results: A total of 39 patients satisfied our inclusion criteria, 28 with necrotizing pancreatitis and 11 with interstitial pancreatitis. Patients with necrotizing pancreatitis presented earlier than patients with interstitial pancreatitis (median 18 vs. 38 h, respectively) (p = 0.005). There was no significant difference between the intergroup median hematocrits on admission and at 24 h. All patients with hematocrits that failed to decrease at 24 h developed necrotizing pancreatitis (12/28 with necrotizing pancreatitis vs. 0/11 with interstitial pancreatitis) (p = 0.009). There was no significant difference at 24 h in rehydration among the three groups: 4.0 liters among the 12 patients with necrotizing pancreatitis whose hematocrits increased and 4.5 liters among the 16 whose hematocrits decreased at 24 h, and 4.1 liters among the 11 patients with interstitial pancreatitis (p = 0.81). Conclusion: Patients who presented early were more likely to have necrotizing pancreatitis than interstitial pancreatitis. While fluid resuscitation was not shown to prevent pancreatic necrosis, all patients with inadequate fluid resuscitation as evidenced by persistence of hemoconcentration at 24 h developed necrotizing pancreatitis.