Extrapancreatic Necrosis Research Articles

Tu1624 Prognostic Significance of Differentiating Peri-Pancreatic Necrosis From Fluid Collection on Endoscopic Ultrasound in Patients With Presumed Extra-Pancreatic Necrosis Alone

Tu1624 Prognostic Significance of Differentiating Peri-Pancreatic Necrosis From Fluid Collection on Endoscopic Ultrasound in Patients With Presumed Extra-Pancreatic Necrosis Alone

Clinical significance of presence and extent of extrapancreatic necrosis in acute pancreatitis.

Extrapancreatic necrosis (EPN) alone represents a subgroup of pancreatitis with better outcome than patients with pancreatic parenchymal necrosis (PN). However, data on clinical significance of EPN is limited, and significance of the extent of EPN is not known. Two hundred thirteen patients (136 [63.8%] males; mean age: 39.8 ± 13.2 years) with acute pancreatitis were prospectively enrolled and followed up till recovery or death. Contrast-enhanced computed tomography of each patient was retrospectively evaluated for presence of PN and EPN, pleural effusion and ascites. EPN was termed extensive if it extended to paracolic gutters or pelvis. Twenty-one (9.9%) patients had interstitial pancreatitis, seven (3.3%) patients had PN alone, 48 (22.5%) patients had EPN alone, and 137 (64.3%) patients had combined PN and EPN. Patients with EPN alone had significantly higher frequency of organ failure than patients with interstitial pancreatitis. Compared with patients with EPN alone, the patients with combined necrosis had significantly higher frequency of pleural effusion (88.2% vs. 75%), ascites (41% vs. 20.8%), and need for intervention (32.6% vs. 14.6%). Patients with extensive EPN (n = 57) had significantly higher frequency of pleural effusion, ascites, and multi-organ failure than those with limited EPN. EPN alone should be considered as a separate category of acute pancreatitis as it has less severe course than PN but has more severe course than interstitial pancreatitis. Patients with extensive EPN in spite of having increased frequency of ascites, pleural effusion, and multi-organ failure had similar outcome as compared to patients with limited EPN.

Acute Pancreatitis: Extrapancreatic Necrosis Volume as Early Predictor of Severity

To determine the volume of extrapancreatic necrosis that predicts severe acute pancreatitis and to assess the reliability of this threshold in predicting severe acute pancreatitis compared with current scoring systems and C-reactive protein (CRP) levels. This institutional review board-approved, HIPAA-compliant retrospective study included patients with acute pancreatitis who were examined with computed tomography (CT) 2-6 days after disease onset. Extrapancreatic necrosis volume, Balthazar score, and CT severity index (CTSI) were calculated. CRP levels 48 hours after the onset of symptoms were reviewed. Outcome parameters included organ failure, infection, need for surgery or percutaneous intervention, duration of hospitalization, and/or death. Receiver operating characteristic (ROC) curves were constructed to determine the optimal threshold for predicting clinical outcomes. Pairwise comparisons of areas under ROC curves (AUCs) from the different grading systems were performed. Interobserver and intraobserver agreement in the grading of extrapancreatic necrosis was assessed by using κ statistics. In 264 patients, significant relationships were found between extrapancreatic necrosis volume and organ failure, infection, duration of hospitalization, need for intervention, and death (P < .001 for all). The optimal threshold for predicting severe acute pancreatitis was 100 mL. Sensitivity and specificity were 95% (19 of 20) and 83% (142 of 172), respectively, for predicting organ failure (vs 100% [20 of 20] and 46% [79 of 172] for the Balthazar score and 25% [five of 20] and 95% [163 of 172] for the CTSI). The extrapancreatic necrosis AUC was the highest for all systems. Interobserver and intraobserver agreement based on the 100-mL threshold was considered to be excellent. A simple grading system based on an objective criterion such as a threshold of 100 mL of extrapancreatic necrosis provides more reliable information for predicting acute pancreatitis outcomes than do the current scoring systems.

Laparoscopic Pancreatic Necrosectomy: Single Port Use

Currently, acute pancreatitis associated with pancreatic necrosis (or extra-pancreatic necrosis) presents with poor outcomes, with mortality reaching up to 20%.1 During the last decade, the management of this dreadful condition has changed through the development of medical resuscitation, computed tomography (CT)-guided or ultrasound (US)-guided drainages.2 Indeed, open surgical necrosectomy is not anymore a first-line treatment, while the percutaneous catheter drainage3 and the endoscopic transluminal drainage (with or without necrosectomy)4 have been demonstrated as safe and effective. Yet, a minimally invasive surgical approach may be required when the noninvasive drainage is inefficient or inaccessible. In this video, we show a reproducible pancreatic necrosectomy using a single port. No funding has been received for this work from any of the following organizations: National Institutes of Health (NIH); Wellcome Trust; Howard Hughes Medical Institute (HHMI); or any others. No competing financial interests exist. Runtime of video: 3 mins 48 secs

Acute necrotizing pancreatitis: Surgical indications and technical procedures.

Necrosis of pancreatic parenchyma or extrapancreatic tissues is present in 10%-20% of patients with acute pancreatitis, defining the necrotizing presentation frequently associated with high morbidity and mortality rates. During the initial phase of acute necrotizing pancreatitis the most important pillars of medical treatment are fluid resuscitation, early enteral nutrition, endoscopic retrograde colangiopancreatography if associated cholangitis and intensive care unit support. When infection of pancreatic or extrapancreatic necrosis occurs, surgical approach constitutes the most accepted therapeutic option. In this context, we have recently assited to changes in time for surgery (delaying the indication if possible to around 4 wk to deal with "walled-off" necrosis) and type of access for necrosectomy: from a classical open approach (with closure over large-bore drains for continued postoperative lavage or semiopen techniques with scheduled relaparotomies), trends have changed to a "step-up" philosophy with initial percutaneous drainage and posterior minimally invasive or endoscopic access to the retroperitoneal cavity for necrosectomy if no improvement has been previously achieved. These approaches are progressively gaining popularity and morbidity and mortality rates have decreased significantly. Therefore, a staged, multidisciplinary, step-up approach with minimally invasive or endoscopic access for necrosectomy is widely accepted nowadays for management of pancreatic necrosis.

Staged multidisciplinary step-up management for necrotizing pancreatitis

Some 15 per cent of all patients with acute pancreatitis develop necrotizing pancreatitis, with potentially significant consequences for both patients and healthcare services. This review summarizes the latest insights into the surgical and medical management of necrotizing pancreatitis. General management strategies for the treatment of complications are discussed in relation to the stage of the disease. Frequent clinical evaluation of the patient's condition remains paramount in the first 24-72 h of the disease. Liberal goal-directed fluid resuscitation and early enteral nutrition should be provided. Urgent endoscopic retrograde cholangiopancreatography is indicated when cholangitis is suspected, but it is unclear whether this is appropriate in patients with predicted severe biliary pancreatitis without cholangitis. Antibiotic prophylaxis does not prevent infection of necrosis and antibiotics are not indicated as part of initial management. Bacteriologically confirmed infections should receive targeted antibiotics. With the more conservative approach to necrotizing pancreatitis currently advocated, fine-needle aspiration culture of pancreatic or extrapancreatic necrosis will less often lead to a change in management and is therefore indicated less frequently. Optimal treatment of infected necrotizing pancreatitis consists of a staged multidisciplinary 'step-up' approach. The initial step is drainage, either percutaneous or transluminal, followed by surgical or endoscopic transluminal debridement only if needed. Debridement is delayed until the acute necrotic collection has become 'walled-off'. Outcome following necrotizing pancreatitis has improved substantially in recent years as a result of a shift from early surgical debridement to a staged, minimally invasive, multidisciplinary, step-up approach.

American College of Gastroenterology Guideline: Management of Acute Pancreatitis

This guideline presents recommendations for the management of patients with acute pancreatitis (AP). During the past decade, there have been new understandings and developments in the diagnosis, etiology, and early and late management of the disease. As the diagnosis of AP is most often established by clinical symptoms and laboratory testing, contrast-enhanced computed tomography (CECT) and/or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically. Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed. Patients with organ failure and/or the systemic inflammatory response syndrome (SIRS) should be admitted to an intensive care unit or intermediary care setting whenever possible. Aggressive hydration should be provided to all patients, unless cardiovascular and/or renal comorbidites preclude it. Early aggressive intravenous hydration is most beneficial within the first 12-24 h, and may have little benefit beyond. Patients with AP and concurrent acute cholangitis should undergo endoscopic retrograde cholangiopancreatography (ERCP) within 24 h of admission. Pancreatic duct stents and/or postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients. Routine use of prophylactic antibiotics in patients with severe AP and/or sterile necrosis is not recommended. In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis may be useful in delaying intervention, thus decreasing morbidity and mortality. In mild AP, oral feedings can be started immediately if there is no nausea and vomiting. In severe AP, enteral nutrition is recommended to prevent infectious complications, whereas parenteral nutrition should be avoided. Asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts do not warrant intervention regardless of size, location, and/or extension. In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed, preferably for 4 weeks, to allow the development of a wall around the necrosis.

Predictors of Surgery in Patients With Severe Acute Pancreatitis Managed by the Step-Up Approach

Initial management of severe acute pancreatitis (SAP) is conservative. As a step-up approach, percutaneous catheter drainage (PCD) with saline irrigation is reported to be effective. Factors leading to surgery are unclear. In this ongoing prospective study, 70 consecutive patients with SAP were recruited. As a step-up approach, all patients initially received medical management and later underwent PCD and surgery as per the indication. Of the 70 consecutive patients with SAP, 14 were managed medically, 29 managed with PCD alone, whereas 27 required surgery after initial PCD. Sepsis reversal was achieved with PCD alone in 62.5%. The curative efficacy of PCD alone was in 27 patients (48%). Overall mortality in the whole group was 24%. On univariate analysis, factors significantly affecting surgical intervention included initial acute physiology and chronic health evaluation (APACHE) II score, APACHE II score at first intervention, sepsis reversal by PCD within a week, number of organs failed, organ failure within a week of the onset of disease, number of bacteria isolated per patient, renal failure, respiratory failure, Escherichia coli, computerized tomography severity index score at admission, parenteral nutrition requirement before or after radiological intervention, maximum extent of necrosis of more than 50% of the pancreas, and extrapancreatic necrosis. On multivariate analysis, renal failure (P = -0.03), APACHE II score at first intervention (P = -0.006), and the number of bacteria isolated per patient (P = -0.01) remained independent predictors of surgery. An APACHE II score of more than 7.5 at first intervention (PCD) had the ability to predict surgery with a sensitivity of 88.9% and a specificity of 69%. PCD reversed sepsis in 62% and avoided surgery in 48% of the patients. Reversal of sepsis within a week of PCD, APACHE II score at first intervention (PCD), and organ failure within a week of the onset of disease could predict the need for surgery in the early course of disease.

Extrapancreatic necrosis without pancreatic parenchymal necrosis: a separate entity in necrotising pancreatitis?

ObjectiveIn the revised Atlanta classification of acute pancreatitis, the term necrotising pancreatitis also refers to patients with only extrapancreatic fat necrosis without pancreatic parenchymal necrosis (EXPN), as determined on contrast-enhanced...

An Assessment of the Severity of Interstitial Pancreatitis

There is limited information on the incidence of and factors associated with severe disease among patients with interstitial pancreatitis (IP). We evaluated a large cohort of patients with IP and compared data with those from patients with extrapancreatic necrosis (EXPN). We evaluated 149 consecutive patients with IP admitted over a 2.5-year period. Transferred patients were excluded. We collected data on age, Charlson comorbidity score (CCI), measures of severity on admission or within 24 hours (Acute Physiology and Chronic Health Evaluation II, bedside index for severity of acute pancreatitis scores), persistent (>48 h) systemic inflammatory response syndrome, persistent organ failure, need for intensive care unit, length of hospital stay (in days), and mortality. We also analyzed levels of severity among those with IP and EXPN. Statistical analysis was performed using SAS version 9.1 (Cary, NC). Among the patients with IP, the median CCI score was 1, the median Acute Physiology and Chronic Health Evaluation II score was 7, and the median bedside index for severity of acute pancreatitis score was 1. In addition, the median length of hospital stay was only 4 days; only 1% had persistent organ failure and only 1% to 2% required intervention. The mortality rate of IP was 3%; it was associated significantly with comorbidity (the median CCI scores of nonsurvivors and survivors was 4 and 1, respectively, P = .003). Patients with EXPN had greater levels of disease severity, compared with patients with IP. IP is severe in only 1% to 3% of patients; mortality of IP is associated strongly with comorbidity. EXPN is more frequently severe than IP; EXPN must be distinguished from IP in clinical studies.

Admission Visfatin Levels Predict Pancreatic and Peripancreatic Necrosis in Acute Pancreatitis and Correlate With Clinical Severity

Adipocytes of peripancreatic and intrapancreatic adipose tissue secret adipocytokines such as leptin, adiponectin, and resistin. For resistin, a role as an early predictor of peripancreatic necrosis and clinical severity in acute pancreatitis has been reported. It was the aim of this study to investigate whether the adipocytokine visfatin is able to serve as an early marker predicting peripancreatic necrosis and clinical severity. A total of 50 patients (20 females and 30 males) with acute pancreatitis were included in this noninterventional, prospective, and monocentric cohort study on diagnostic accuracy. Clinical severity was classified by the Ranson score and APACHE-II (Acute Physiology and Chronic Health Evaluation II) score. Pancreatic and peripancreatic necrosis were quantified by the computed tomography-based Balthazar score, the Schroeder score, and the pancreatic necrosis score. Visfatin was measured at admission and daily for 10 days by enzyme-linked immunosorbent assay (ELISA). Visfatin values were significantly and positively correlated with clinical severity (APACHE-II score and Ranson score) and with clinical end points such as death and need for interventions. Admission visfatin levels were significantly elevated in patients with higher pancreatic and extrapancreatic necrosis scores. It was shown by receiver operator characteristics that admission visfatin concentration provides a positive predictive value of 93.3% in predicting the extent of peripancreatic necrosis (area under the curve (AUC): 0.89, P<0.001, sensitivity: 93.3%, specificity: 81.8%, likelihood ratio: 5.1, post-test probability: 93%) by using a cutoff value of 1.8 ng/ml. Admission visfatin concentration serves as an early predictive marker of peripancreatic necrosis and clinical severity in acute pancreatitis. Visfatin may have potential for clinical use as a new and diagnostic serum marker.

Admission Resistin Levels Predict Peripancreatic Necrosis and Clinical Severity in Acute Pancreatitis

Peripancreatic necrosis determines clinical severity in acute pancreatitis. Early markers predicting peripancreatic necrosis and clinical severity are lacking. Because adipocytes of peripancreatic adipose tissue secret highly active adipocytokines, the aim of the study was to investigate whether adipocytokines are able to serve as early markers predicting peripancreatic necrosis and clinical severity. A total of 50 patients (20 women, 30 men) with acute pancreatitis were included in this noninterventional, prospective, and monocentric cohort study on diagnostic accuracy. Clinical severity was classified by the Ranson score and the APACHE (Acute Physiology And Chronic Health Evaluation) II score. Pancreatic and peripancreatic necrosis were quantified by using the computed tomography-based Balthazar score, the Schroeder score, and the pancreatic necrosis score. Adiponectin, leptin, and resistin were measured at admission and daily for at least 10 days by enzyme-linked immunosorbent assay. In contrast to admission C-reactive protein values, admission resistin values were significantly correlated with clinical severity and even with clinical end points such as death and need for interventions. Admission resistin levels were significantly elevated in patients with higher pancreatic and extrapancreatic necrosis scores. It was shown by receiver-operator characteristics that admission resistin concentration provides a positive predictive value of 89% in predicting the extent of peripancreatic necrosis (area under the curve, 0.8; P=0.002; sensitivity, 80%; specificity, 70%) by using a cutoff value of 11.9 ng/ml. Admission resistin concentration serves as an early predictive marker of peripancreatic necrosis and clinical severity in acute pancreatitis. Resistin may have potential for clinical use as a new and diagnostic serum marker.

Characteristics and Outcomes of Patients Undergoing Debridement of Pancreatic Necrosis

BackgroundPancreatic necrosis is associated with high morbidity and mortality. The Atlanta Classification underwent proposed revisions in 2007 to better categorize acute pancreatitis. MethodsFrom 1999 to 2008, patients with pancreatic necrosis treated with surgical debridement were analyzed. Computed tomography (CT) images were independently reviewed to classify of pancreatic collections according to the revised Atlanta classification. ResultsSeventy-three patients were categorized as infected extrapancreatic necrosis (40%), sterile extrapancreatic necrosis (29%), infected pancreatic necrosis (15%), sterile pancreatic necrosis (11%), or post-necrotic collection (5%). Mortality was 14%, and morbidity was 55%. Debridement with external drainage or open packing was associated with higher mortality than cystgastrostomy (p = 0.03). Atlanta Classification was not associated with operative procedure or mortality. Degree of chronic disease, demonstrated by albumin level, and infection were associated with longer stay (p < 0.05). ConclusionType of necrosis by the revised Atlanta Classification was not associated with outcomes or type of operation. Debridement by cystgastrostomy was associated with lower mortality rates than external drainage or open packing. Length of stay was increased in patients with evidence of chronic disease, infection, and postoperative complications. Necrotizing pancreatitis continues to be associated with significant morbidity and mortality and should undergo aggressive treatment at tertiary care centers.

Clinical study on a novel modified computed tomography severity index for predicting the severity of acute pancreatitis

Objective To introduce a novel modified CT severity index based on the assessment of extrapancreatic inflammation and pancreatic necrosis on CT index (EPIPN) and to evaluate its effect in predicting the severity and prognosis of acute pancreatitis. Methods Seventy-seven consecutive patients diagnosed as acute pancreatitis (AP) from August 2006 to December 2007 were retrospectively analyzed. The clinical data included age, sex, cause, the C-reactive protein(CRP) level with in 72 hours of onset of symptom, Ranson signs, the APACHE I1 score, the disappearing time of the abdominal pain, the presence of organ failure, the length of hospital stay, etc. All patients underwent contrast-enhanced multisection CT scan after admission of 48-72 hours. The CT severity index (CTSI) and EPIPN scores were obtained. The severity of pancreatitis for each patient was then categorized as severe if CTSI≥7 or EPIPN>5. The diagnostic value of EPIPN in predicting the severe acute pancreatitis (SAP) was compared with that of CTSI using ROC curve. The correlation of EPIPN or CTSI with clinical coutcome was conducted. Results Of 77 patients, 34 were males and 43 were females with mean age of 51.79 years (age range 22-92 years). The causes of AP were gallstones (63 cases), hyperlipemia (6 cases), alcohol (1 case) and idiopathic (7 cases). Organ system failure was present in 14 (18.2%) of the 77 patients. The area under the ROC curve of CTSI in predicting the SAP was 0.72 (95% CI: 0.59-0.88) with sensitivity of 80.4% and specificity of 55% when CTSI≥7, and that in EPIPN was 0.82 (95% CI: 0.73-0.91) with sensitivity of 91.3% and specificity of 63% when EPIPN >5. EPIPN was well correlated with hospital stay, APACHE Ⅱ score and CRP levels. Conclusions The EPIPN allows accurate estimation of disease severity and prognosis in AP patients. The diagnostic effect of EPIPN for predicting SAP is superior to CTSI. The EPIPN index is-both convenient and practical, and has clinical value. Key words: Pancreatitis,acute necrotizing; Severity of disease index; Prognosis

Toward an Update of the Atlanta Classification on Acute Pancreatitis

The 1992 Atlanta classification is a clinically based classification system that defines the severity and complications of acute pancreatitis. The purpose of this review was to assess whether the terms abandoned by the Atlanta classification are really discarded in the literature. The second objective was to review what new terms have appeared in the literature since the Atlanta symposium. We followed a Medline search strategy in review and guideline articles after the publication of the Atlanta classification. This search included the abandoned terms: "phlegmon," "infected pseudocyst," "hemorrhagic pancreatitis," and "persistent pancreatitis." A total of 239 publications were reviewed, including 10 guideline articles and 42 reviews. The abandoned terms "hemorrhagic pancreatitis" and "persistent pancreatitis" are hardly encountered, in contrast, both "infected pseudocyst" and "phlegmon" are frequently used, and several authors question their abandonment. New terminology in acute pancreatitis consists of "organized pancreatic necrosis," "necroma," "extrapancreatic necrosis," and "central gland necrosis." This review demonstrates that the Atlanta classification is still not universally accepted. Several abandoned terms are frequently used, and new terms have emerged that describe manifestations in acute pancreatitis that were not specifically addressed during the Atlanta symposium.

Potential of adipocytokines in predicting peripancreatic necrosis and severity in acute pancreatitis: Pilot study

Severe acute pancreatitis is characterized by lipase-induced peripancreatic fat cell necrosis. Because adipocytes secret several highly active molecules, the aim of the present study was to investigate the hypothesis that adipocytokines could serve as potential markers predicting peripancreatic necrosis and severity in acute pancreatitis. A total of 23 patients (11 females, 12 males) with acute pancreatitis were included and a computed tomography (CT) examination was available in 20 patients. Balthazar score, Schröder score, pancreatic necrosis score, Ranson score and APACHE II score were calculated, correlated with biochemical parameters and analyzed using receiver-operator characteristics (ROC) analysis. Adipocytokine serum levels were measured daily by enzyme-linked immunosorbent assay (ELISA) over 10 days after admission. Resistin and leptin were significantly elevated in patients with severe pancreatitis and were correlated with a radiological scoring system for extrapancreatic necrosis. Whereas resistin correlated positively with clinical scoring systems, time until discharge and the need for interventions, leptin was correlated positively with C-reactive protein (CRP) levels. Resistin levels measured on the day of admittance had a positive predictive value of 93.3% (cut-off: >6.95 ng/mL) in predicting a Schröder score >3. Resistin, and to a lesser extent leptin, but not adiponectin levels are novel potential markers for extrapancreatic necrosis and severity of acute pancreatitis and should therefore be tested in larger cohorts of patients.

TOWARDS AN UPDATE OF THE ATLANTA CLASSIFICATION ON ACUTE PANCREATITIS

Objectives: The 1992 Atlanta symposium abandoned several terms that were used at that time to define the severity and complications of acute pancreatitis. The purpose of this review was to assess whether these terms are really discarded in the literature. The second objective was to review new terms that have appeared in the literature since the Atlanta symposium. Methods: A Medline search was conducted to identify reviews and guidelines on acute pancreatitis and its complications, published since the Atlanta classification: "review OR guidelines AND acute pancreatitis". For identification of articles regarding the abandoned terms a search strategy was followed that included the following terms: 'phlegmon'; 'infected pseudocyst'; 'hemorrhagic pancreatitis'; and 'persistent pancreatitis'. We also searched the Medline database for new terms introduced after the publication of the Atlanta classification. Results: A total of 239 studies were reviewed, including 10 guideline articles and 42 reviews. 'Hemorrhagic pancreatitis' and 'persistent acute pancreatitis' were hardly encountered in the literature since the Atlanta classification. In contrast, both 'infected pseudocyst' and 'phlegmon' were frequently used and several authors criticized the fact that these terms were abandoned by the Atlanta symposium. New terms that were frequently found in the literature were 'organized pancreatic necrosis,' 'necroma', 'extrapancreatic necrosis' and 'central gland necrosis'. Conclusion: Several terms abandoned by the Atlanta symposium are still used frequently in the literature. Moreover, new terms have been introduced. This implies that the Atlanta definitions are not universally accepted and revision of the Atlanta classification may be required.

Necrosectomy and postoperative local lavage in necrotizing pancreatitis.

Necrosectomy with postoperative continuous local lavage was performed in a prospective study involving 95 patients with necrotizing pancreatitis. In the same period 567 patients with oedematous-interstitial pancreatitis were treated non-operatively with a hospital mortality rate of 0.7 per cent. In patients with necrotizing pancreatitis the median Ranson criteria score was 4.5 points; operation was required at a median of 7 days after the onset of symptoms because of non-response to conservative treatment. In all, 59 per cent of the patients (56 out of 95) developed extended intrapancreatic parenchymal necrosis, 70 per cent had ascites, and 66 per cent had intra- and extrapancreatic necrosis; 42 per cent of the patients had bacterial infection of the necrotic tissue. For lavage a median of 8 l/24 h of fluid were instilled postoperatively for 25 days (median). The lavage fluid showed high levels of immunoreactive trypsin, phospholipase A2, and endotoxin in the early postoperative period. Hospital mortality rate was 8.4 per cent. Necrosectomy and continuous postoperative lavage can achieve high survival rates in patients with necrotizing pancreatitis. Postoperative local lavage allows the continuous non-operative evacuation of biologically active compounds and devitalized tissue, and avoids damage to remaining vital exocrine and endocrine pancreatic tissue.

Natural course of acute pancreatitis.

Acute pancreatitis comprises, in terms of clinical, pathologic, biochemical, and bacteriologic data, four entities. Interstitial edematous pancreatitis and necrotizing pancreatitis are the most frequent clinical manifestations; pancreatic pseudocyst and pancreatic abscess are late complications after necrotizing pancreatitis, developing after 3 to 5 weeks. Determinants of the natural course of acute pancreatitis are pancreatic parenchymal necrosis, extrapancreatic retroperitoneal fatty tissue necrosis, biologically active compounds in pancreatic ascites, and infection of necrosis. Early in the course of acute pancreatitis multiple organ failure is the consequence of various inflammatory mediators that are released from the inflammatory process and from activated leukocytes attracted by pancreatic injury. During the late course, starting the second week, local and systemic septic complications are dominant. Around 80% of deaths in acute pancreatitis are caused by septic complications. The infection of pancreatic necrosis occurs in 8% to 12% of acute pancreatitis and in 30% to 40% of patients with necrotizing pancreatitis. Bacteriologic analysis of intraoperative smears and aspirates reveals predominantly gram-negative germs deriving from the intestine, most frequently Escherichia coli. It has been confirmed that after necrotizing pancreatitis a considerable large group of patients suffer long-lasting exocrine and endocrine insufficiency.

Similar morphological and intracellular biochemical changes in alcoholic acute pancreatitis and ischemic acute pancreatitis in rats.

Pancreatic hyperstimulation with simultaneous duct obstruction does not cause the typical features of acute pancreatitis, therefore the role of an additional challenge, such as either ethanol intoxication or short-term ischemia, was studied. Alcoholic pancreatitis was induced in 28 rats by acute ethanol intoxication (0.25 LD50) and an obstruction/hyperstimulation mechanism (clip of the biliopancreatic duct for 20 min and intravenous stimulation with 5 U of cholecystokinin and secretin each). Ischemic pancreatitis was performed by obstruction/hyperstimulation and subsequent pancreatic ischemia by clamping the supplying arteries for 40 min. The macro- and microscopic alterations were evaluated and graded by a scoring system. Additionally, the pancreas was removed in 50% of the animals and the pancreatic acini were prepared. From those acini the intracellular enzymes trypsinogen, kallikreinogen, amylase, lipase, glucuronidase, and acidic phosphatases were determined. While obstruction/hyperstimulation, 40 min of ischemia, or ethanol alone did not induce acute pancreatitis, a combination of obstruction/hyperstimulation with either ethanol or ischemia resulted in acute pancreatitis in 68 and 60% of treated rats, respectively. Similarly, both models were characterized by extrapancreatic fat necrosis and acinar necrosis at the periphery of the lobules. Almost all intracellular enzymes were elevated in both pancreatitis models compared to sham-operated controls. Both alcohol and ischemia were insults that sensitize the pancreas to develop acute pancreatitis after obstruction/hyperstimulation. Since the observed morphologic and enzymatic alterations in both models are very similar, alcohol and ischemia might have some common pathways by which they make the pancreas vulnerable to enzymatic attacks.