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Background: This study was designed to evaluate the validity of a new rapid urinary trypsinogen-2 test strip (Actim Pancreatitis) for detection of acute pancreatitis in patients with acute abdominal pain., Methods: A total of 525 consecutive patients presenting with abdominal pain at two emergency units was included prospectively and tested with the Actim Pancreatitis test strip. Urine trypsinogen-2 concentrations were also determined by a quantitative method. The diagnosis and assessment of severity of acute pancreatitis was based on raised serum and urinary amylase levels, clinical features and findings on dynamic contrast-enhanced computed tomography., Results: In 45 patients the diagnosis of acute pancreatitis could be established. The Actim Pancreatitis test strip result was positive in 43 of them resulting in a sensitivity of 96 per cent. Thirty-seven false-positive Actim Pancreatitis test strips were obtained in patients with non-pancreatic abdominal pain resulting in a specificity of 92 per cent. Nine patients with severe acute pancreatitis were all detected by the dipstick., Conclusion: A negative Actim Pancreatitis strip result excludes acute pancreatitis with high probability. Positive results indicate the need for further evaluation, i.e. other enzyme measurements and/or radiological examinations. The test is easy and rapid to perform, unequivocal in its interpretation and can be used in healthcare units lacking laboratory facilities.

The pathophysiology of severe acute pancreatitis (AP) resembles other conditions with systemic inflammatory response syndrome (SIRS) such as sepsis predisposing to remote organ failure. Because extracellular phospholipases A2 (PLA2) have been implicated in AP, their serum concentrations were analyzed with respect to SIRS and systemic complications in patients with severe AP. The serum samples were collected daily for 12 days in 57 patients with severe AP. SIRS, early organ complications, local complications, and outcome of AP were recorded. Time-resolved fluoroimmunoassays were used for group I and group II PLA2 measurements. Thirty-nine (68.4%) patients fulfilled the criteria of SIRS within 12 days from admission. Pancreatic necrosis was detected in 43 (75.4%) patients. Infected necrosis was found preoperatively or at operation in five (8.8%) patients. Twenty-six (45.6%) and eight (14.0%) patients had respiratory or renal failure, respectively. Seven (12.3%) patients died of their disease. All patients with systemic complications fulfilled the criteria of SIRS. The increasing number of positive SIRS criteria was associated with increased frequency of systemic complications. Pancreatic necrosis was not significantly associated with SIRS. The serum concentration of group II PLA2 was significantly higher in patients with SIRS (p < 0.05) compared with patients without from day 7 onward. The concentration of group II PLA2 increased (p < 0.01) in patients with SIRS but decreased in patients without. The serum concentration of group II PLA2 did not differ significantly with respect to systemic complications. The concentration of group I PLA2 decreased (p < 0.05) similarly in patients with and without SIRS or systemic complications during follow-up, respectively. Early systemic complications of severe AP are associated with SIRS with increasing frequency as the number of positive SIRS criteria increases. Group II PLA2 but not group I PLA2 may have pathophysiologic importance in severe AP-associated SIRS. Increasing serum concentration of group II PLA2 seems to reflect the ongoing systemic inflammation in severe AP-associated SIRS.

Activated endogenous mediators of inflammation have important roles in the pathogenesis and complications of acute pancreatitis (AP). These mediators include bactericidal/ permeability-increasing protein (BPI) and phospholipase A2 (PLA2). The time course of their activation during human AP is not known. The aim of this study was to evaluate the kinetics of BPI, group I (pancreatic) and group II (synovial type) PLA2 during human AP with temporally defined onset, as being induced by endoscopic retrograde cholangiopancreatography (ERCP). Serum samples of 273 consecutive patients undergoing ERCP were collected before and at 3, 6, and 24 h after ERCP. Twenty-four (8.7%) patients developed ERCP-induced pancreatitis. Seven of them were graded to have a severe disease. Forty randomly selected patients undergoing ERCP without evidence of pancreatitis served as controls. The serum concentrations of BPI and groups I and II PLA2 were measured by specific immunoassays. The mean concentration of BPI increased from 14 to 26 microg/L at 24 h after ERCP in patients with AP. In the control group, BPI values remained unchanged, and the difference was statistically significant (p<0.001). The increase of BPI was seen in 22 of 28 patients with AP at 3 h after the onset of the disease. BPI values were higher in severe post-ERCP pancreatitis than in mild disease (p = 0.07; NS). The serum concentrations of group II PLA2 before ERCP were consistently higher in the control patients than in the patients with pancreatitis, 65.8 and 14.2 microg/L, respectively. High baseline values in the control group were associated with preexisting infectious diseases. Thereafter, the mean concentration decreased in the control group to 44 microg/L and increased in the pancreatitis group up to 27.5 microg/L. The difference was statistically significant (p = 0.007). Increased group II PLA2 values were seen in 10 of 17 patients with mild AP and in five of seven patients with severe disease. There were no significant differences in group I or II PLA2 values in patients with mild or severe AP. The serum concentration of group I PLA2 increased in the patients with post-ERCP pancreatitis from 5.4 to 37.5 microg/L at 24 h. The difference was statistically significant, (p< 0.001) as compared with controls. In conclusion, in acute pancreatitis, the increase of BPI in serum starts at 3 h after the onset of the disease, and the concentration seems to correlate with the severity of the disease. Increased group II PLA2 concentrations also were seen in patients with mild AP. The kinetics of group I PLA2 resembles that of other pancreatic enzymes.

Aims: To evaluate the clinical utility of two new tests for serum trypsinogen 2 and trypsin 2-alpha 1 antitrypsin complex (trypsin 2-AAT) in diagnosing and assessing the severity of acute pancreatitis (AP) induced by endoscopic retrograde cholangiopancreatography (ERCP)., Patients: Three hundred and eight consecutive patients undergoing ERCP at Helsinki University Central Hospital in 1994 and 1995., Methods: Patients were followed prospectively for pancreatitis and clinical outcome. They were tested for serum trypsinogen 2, trypsin 2-AAT, and amylase in samples obtained before and one, six, and 24 hours after ERCP., Results: Pancreatitis developed in 31 patients (10%). Their median serum trypsinogen 2 increased 26-fold to 1401 micrograms/l at six hours after the procedure and trypsin 2-AAT showed an 11-fold increase to 88 micrograms/l at 24 hours. The increase in both markers was stronger in severe than in mild pancreatitis, and in patients without pancreatitis there was no significant increase. Baseline trypsinogen 2 and trypsin 2-AAT concentrations were elevated in 29% and 32% of patients, respectively. The diagnostic accuracy of a threefold elevation over the baseline value was therefore analysed. The sensitivity and specificity of these parameters in the diagnosis of post-ERCP pancreatitis was 93% and 91%, respectively, for serum trypsinogen 2 at six hours after the examination, and 93% and 90%, for trypsin 2-AAT at 24 hours., Conclusions: Serum trypsinogen 2 and trypsin 2-AAT reflect pancreatic injury after ERCP. High concentrations are associated with severe pancreatic damage. The delayed increase in trypsin 2-AAT compared with trypsinogen 2 appears to reflect the pathophysiology of AP. A greater than threefold increase in trypsinogen 2 six hours after ERCP is an accurate indicator of pancreatitis.

Background: Acute pancreatitis can be difficult to diagnose. We developed a rapid dipstick screening test for pancreatitis, based on the immunochromatographic measurement of urinary trypsinogen-2., Methods: We prospectively compared the urinary trypsinogen-2 dipstick test with a quantitative urinary trypsinogen-2 assay, a urinary dipstick test for amylase, and serum and urinary amylase assays in 500 consecutive patients with acute abdominal pain at two emergency departments. Acute pancreatitis was diagnosed according to standardized criteria., Results: The urinary trypsinogen-2 dipstick test was positive in 50 of the 53 patients with acute pancreatitis (sensitivity, 94 percent), including all 7 with severe pancreatitis. Two patients with urinary trypsinogen-2 concentrations below the sensitivity threshold of the test (50 ng per milliliter) and one with a very high concentration had false negative results. The test was also positive in 21 of the 447 patients without pancreatitis (specificity, 95 percent), including 7 with abdominal cancers, 3 with cholangitis, and 2 with chronic pancreatitis. The sensitivity and specificity of the dipstick test were similar to those of the quantitative urinary trypsinogen-2 assay and higher than those of the urinary amylase dipstick test. The serum amylase assay had a sensitivity of 85 percent (with a cutoff value of 300 U per liter for the upper reference limit) and a specificity of 91 percent. The sensitivity and specificity of the urinary amylase assay (cutoff value, 2000 U per liter) were 83 and 88 percent, respectively., Conclusions: In patients with acute abdominal pain seen in the emergency department, a negative dipstick test for urinary trypsinogen-2 rules out acute pancreatitis with a high degree of probability. A positive test usually identifies patients in need of further evaluation.

Background and Aims: In acute pancreatitis, contrast-enhanced CT is widely accepted to give reliable information in the early assessment of severity. This study critically evaluates the clinical data, outcome, and CE-CT findings in patients with incorrect radiological estimation of the severity of the condition., Material and Methods: All patients suspected of having severe pancreatitis underwent contrast-enhanced CT. Clinical data and CE-CT findings of 341 patients were re-examined., Results and Conclusions: In 28 patients (8.2%) the radiological diagnosis was inconsistent with the clinical findings. The most common reason--in 20 of the 28 patients (71.4%)--for failure to estimate the severity of pancreatitis was partial necrosis of the gland. In severe cases the partial necrosis was overlooked in nine patients (32.1%). In mild cases clinical significance of partial necrosis--overestimated as representative for the whole gland and technical failure both explained the incorrect interpretation in six (21.4%) patients; and in five patients (17.9%) intermediate patchy enhancement was incorrectly regarded as low. The misleading estimation remained inexplicable in only two (7.1%) patients. These results emphasize adequate assessment of CE-CT and inclusion of all areas of the pancreas in the estimation of enhancement.

Objective: To estimate the usefulness of serum concentrations of the complex of trypsin 2 and alpha 1 antitrypsin in diagnosing and assessing the severity of acute pancreatitis in comparison with serum C reactive protein, amylase, and trypsinogen 2 concentrations (reference markers)., Design: Markers were measured in consecutive patients admitted with acute abdominal pain that was either due to pancreatitis or to other disease unrelated to the pancreas (controls)., Setting: Department of surgery of a teaching hospital in Helsinki., Subjects: 110 patients with acute pancreatitis and 66 with acute abdominal diseases of extrapancreatic origin. On the basis of the clinical course, acute pancreatitis was classified as mild (82 patients) or severe (28 patients)., Main Outcome Measures: Clinical diagnosis of acute pancreatitis and severity of the disease., Results: At admission all patients with acute pancreatitis had clearly raised concentrations of trypsin 2-alpha 1 antitrypsin complex (32 micrograms/l), whereas only three of the controls had such values. Of the markers studied, trypsin 2-alpha 1 antitrypsin complex had the largest area under the receiver operating curve, both in differentiating acute pancreatitis from extrapancreatic disease and in differentiating mild from severe disease., Conclusions: Of the markers studied, trypsin 2-alpha 1 antitrypsin complex was the most accurate in differentiating between acute pancreatitis and extrapancreatic disease and in predicting a severe course for acute pancreatitis.

A total of 161 primary contrast-enhanced computed tomography (CT) scans of patients with acute necrotizing pancreatitis taken between 1982 and 1994 were analysed retrospectively. The aim was to assess the prognostic significance of the extent and anatomical site of pancreatic tissue necrosis in the first contrast-enhanced CT scan. The scans were obtained a mean of 2.9 days after the onset of symptoms. The pancreatic head was affected in 107 patients, the body in 119 and the tail in 138. Pancreatic tissue necrosis, when divided into four groups according to anatomical site, correlated with overall clinical outcome. The anatomical site of necrosis was clearly better than its crude extent in predicting the risk of complications. For patients with necrosis in the head of the pancreas, the outcome was as severe as when the entire pancreas was affected. In contrast, for patients with necrosis only in the distal part of the pancreas, the outcome was favourable with few complications. The exact site of pancreatic tissue necrosis should be known when early contrast-enhanced CT is used in prognostic scoring.

We examined the clinical utility of urine trypsinogen-2 as a marker of acute pancreatitis (AP). Fifty-nine patients with AP, 42 with acute abdominal diseases of extrapancreatic origin, and 63 without evidence of acute abdominal disease were studied. Urine trypsinogen-2 was determined by a time-resolved immunofluorometric assay. As reference methods we used serum trypsinogen-2, urine amylase, and serum amylase. The diagnostic accuracy of the markers was evaluated by receiver-operating characteristic (ROC) analysis. At admission, urine trypsinogen-2 differentiated patients with AP from controls with high accuracy. The area under the ROC curve (AUC) was 0.978, which was equal to that of serum trypsinogen-2 (0.998) and serum amylase (0.969) and significantly larger than that of urine amylase. For differentiation between severe and mild AP, urine trypsinogen-2 (0.730) was equal to serum trypsinogen-2 (0.721), and clearly better than amylase in serum and urine. These results suggest that determination of urine trypsinogen-2 is a useful test to detect AP and to evaluate disease severity.

Background: A simple, rapid test is specific and sensitive enough to distinguish, in patients with clinically suspected acute pancreatitis, those whose abdominal pain is indeed of pancreatic origin has proved elusive., Methods: In two consecutive series of surgical patients in a teaching hospital, whose acute abdominal pain turned out to be due to acute pancreatitis (n-57) or extrapancreatic in origin (n=40), we studied urinary trypsinogen-2 in two ways. A test strip, incorporating monoclonal antibodies to two epitopes on trypsinogen-2, recorded a blue line when concentrations exceeded 50 microgram/L; we also measured trypsinogen-2 concentrations in the laboratory., Findings: In the patients with acute pancreatitis the test strip was positive in 52 and negative in five, whereas in the 40 extrapancreatic controls there were four false positives. In a further set of 57 orthopaedic controls, one urine was strip-test positive. Concentrations of urinary trypsinogen-2 and the test-strip results were in good agreement and in only three of the 154 patients were the two approaches discrepant, at the 50 microgram/L cut-off., Interpretation: These findings, in patients whose acute abdominal pain was known to be pancreatic in origin or not, are encouraging but need to be confirmed in a consecutive series of patients in whom the diagnosis of pancreatitis is in doubt.

Despite improvements in surgical treatment and intensive care, mortality from severe acute pancreatitis remains high. We have carried out a randomised study of 60 consecutive patients with alcohol-induced necrotising pancreatitis to find out whether early antibiotic treatment can improve outcome. 30 patients were assigned cefuroxime (4.5 g/day intravenously) from admission. In the second group, no antibiotic treatment was given until clinical or microbiologically verified infection or after a secondary rise in C-reactive protein. The inclusion criteria were C-reactive protein concentration above 120 mg/L within 48 h of admission and low enhancement (< 30 Hounsfield units) on contrast-enhanced computed tomography. There were more infectious complications in the non-antibiotic than in the antibiotic group (mean per patient 1.8 vs 1.0, p = 0.01). The most common cause of sepsis was Staphylococcus epidermidis; positive cultures were obtained from pancreatic necrosis or the central venous line in 14 of 18 patients with suspected but blood-culture-negative sepsis. Mortality was higher in the non-antibiotic group (seven vs one in the antibiotic group; p = 0.03). Four of the eight patients who died had cultures from pancreatic necrosis positive for Staph epidermidis. We conclude that cefuroxime given early in necrotising pancreatitis is beneficial and may reduce mortality, probably by decreasing the frequency of sepsis.

Twenty-one patients with acute fulminant alcoholic pancreatitis were randomly allocated to either pancreatic resection group (11 patients) or nonoperative peritoneal lavage group (10 patients). Only patients under 50 years were included in the study to minimize the role of other severe disease. These patients represented the most severe cases of acute pancreatitis at our Department, constituting only 2% of all patients with acute pancreatitis during this period. The diagnosis was based on clinical symptoms and on signs indicating severely impaired systemic organ functions. All patients underwent contrast-enhanced computed tomography (CT), which showed contrast enhancement below 30 Hounsfield units. In the operated cases, the diagnosis of necrotizing pancreatitis was verified histologically. All patients with conservative treatment had dark brown fluid at peritoneal puncture. There was a difference (nonsignificant) in mortality (3/11 and 1/10, respectively), complication rate, or in the need of reoperations between the groups. Nonoperative peritoneal lavage was followed with shorter treatment at the intensive care unit (16.2 versus 25.9 days, respectively). The hospital stay also was significantly shorter in the nonoperative group (44.3 versus 56.1 days). The results indicate that intensive conservative treatment is justified as an initial therapy even in the most severe cases of acute pancreatitis.

The pancreatic blood flow and contrast enhancement in computed tomography (CT) were studied in 10 piglets weighing 17-25 kg with experimental pancreatitis. Each animal served as its own control. CT and blood flow measurements were made both before induction of pancreatitis and 5-6 h after the onset of the disease. Cardiac output was measured by thermodilution, and was kept constant throughout the study by infusion of dextran and saline. Although the pancreatic blood flow remained constant in this experiment, CT showed a significant decrease in contrast enhancement.

Thirty-five patients with acute fulminant (hemorrhagic) pancreatitis, verified at laparotomy, were allocated to either pancreatic resection (18 patients) or peritoneal lavation (17 patients) therapy groups. Pancreatic resection was carried out by removing the distal pancreas well cephalad to the portal vein. For peritoneal lavation, two inlet silicone catheters were inserted at laparotomy around the pancreas and an outlet catheter was inserted in the lower abdomen, and the peritoneal cavity was thereafter lavated (1000 ml/hr) with a standard peritoneal dialysis fluid for 7 to 12 days (or until death if met earlier). In other respects, the postoperative care was similar, including intravenous fluids with total parenteral nutrition until oral intake of food was resumed, prophylactic antibiotics (tobramycin and clindamycin) and stress ulcer prophylaxis (cimetidine and antacids). In the resection group, four of the 18 patients (22.2%) died, while in the lavation group eight of the 17 patients (47.1%) died. The most common cause of death was septic complications with multiple organ failure, but one patient in each group died accidentally of airway complications. There was no difference in the incidence of septic complications (sepsis and/or intra-abdominal abscesses), but the incidence and severity of pulmonary and renal complications were greater in the lavation group. However, these complications accumulated to patients who ultimately died. Also, the need for reoperation was greater in the lavation group (20 reoperations/10 patients versus 12 reoperation/eight patients). Yet, the length of overall hospital stay was equal in the two groups. Six of the 14 survivors in the resection group developed diabetes, whereas none of the nine survivors in the lavation group got this complication. The results suggest that pancreatic resection is superior to peritoneal lavation in the management of acute fulminant (hemorrhagic) pancreatitis, decreasing mortality and affording smoother postoperative course. However, these benefits are gained at the expense of higher incidence of postoperative diabetes.

58 patients with alcohol-induced acute pancreatitis were studied by contrast enhanced computed tomography (CT). The patients were divided into groups both on the basis of the clinical course and the prognostic signs. The contrast enhancement curves were then plotted for these patients. All patients with uncomplicated pancreatitis had increased or normal contrast enhancement, whereas all those with fulminant pancreatitis had decreased contrast enhancement of the pancreas. The patients with three, or more prognostic signs had lower enhancement values than those with fewer prognostic signs, but the prognostic signs did not correlate as well with the clinical course as did the contrast enhancement.

The present study reports 18 patients operated on for chronic pancreatitis complicated by bleeding in the upper gastrointestinal tract, the peritoneal cavity or the retroperitoneal space. Damage to the splenic artery by a pancreatic pseudocyst was the most common reason for the bleeding (10 patients, 56%) and the most common site was the duodenum (10 patients, 56%). Eleven patients were treated by transcystic multiple suture ligations combined with external drainage of the pseudocyst, and seven by pancreatic resection or total pancreatectomy. Hospital mortality was 33% (6 patients); two patients had undergone transcystic suture ligation, and four pancreatic resection. Five patients needed a reoperation because of further bleeding, four of them having been treated initially by transcystic suture ligation. Our results suggest that haemostasis by suture ligation is a method to be recommended if the patient's condition has been exacerbated by severe haemorrhage.

The records of 30 consecutive patients treated by pancreatic resection for acute hemorrhagic or necrotizing pancreatitis from 1974 to 1978 were reviewed. Formal subtotal or near to total resection of the pancreas was undertaken whenever vigorous nonoperative therapeutic measures did not bring rapid improvement of the condition of the patient. The rationale was that removal of the diseased pancreatic tissue would prohibit the progress of inflammation and abolish the development of complications directly associated to the inflammatory process itself. There was no intraoperative mortality, but 11 patients died after the operation. Of the 19 survivors, eight had an uncomplicated postoperative course, whereas 11 patients recovered only after severe complications, usually requiring multiple reoperations. Among the most important complications were intra-abdominal sepsis, septicemia, upper gastrointestinal tract bleeding, respiratory insufficiency, renal insufficiency and perforations of the gastrointestinal tract. After a follow-up period of one to five years, five patients have remained completely free of symptoms. In 12 patients, diabetes has developed, and four patients had recurrent mild attacks of pancreatitis. All but two patients have resumed their previous work or other activities of living.

Enterobacterial common antigen is a highly immunogenic component of the Gram negative bacterial cell wall that is common to all enteric bacteria. In the present study, the humoral antibody response against enteric bacteria was investigated by measuring antibodies to enterobacterial common antigen in paired serum samples in 38 patients with acute pancreatitis and in 31 healthy subjects. In mild pancreatitis (11 patients), no changes in anti-enterobacterial common antigen titres were observed as compared with healthy controls. Nine of the 10 patients had a significant increase (greater than or equal to 8 times) in anti-enterobacterial common antigen titres during the disease. Similarly, in patients with fulminant (haemorrhagic) pancreatitis who survived, a significant increase in anti-enterobacterial common antigen titres occurred during the course of the disease (in nine of the 11 patients). Paradoxically, only one of the six patients with fulminant pancreatitis with fatal outcome showed a significant increase in his anti-enterobacterial common antigen titre. The results suggest that Gram negative bacterial components escape into the systemic circulation in acute pancreatitis. This may have pathophysiologic significance in this disease.

Twenty-three patients with acute fulminant pancreatitis were studied. The diagnosis was confirmed at laparotomy in every case. Blood samples for the assay of phospholipase A2 were collected for 14 days, and the pulmonary status of the patients was followed by monitoring the blood gases and the inspired oxygen fraction and studying a derived variable, the alveolar to arterial oxygen tension difference--the arterial oxygen tension ratio (A--aDo2/PaO2). The serum phospholipase A2 activities correlated with the changes in pulmonary function and with the outcome of the disease. Eight patients succumbed and they showed higher phospholipase A2 activities and A--aDo2/PaO2 ratios than the five patients who survived after major complications and the ten patients who survived without major complications. The results suggest that in acute fulminant pancreatitis serum phospholipase A2 activity correlates with the severity of the pulmonary changes. Furthermore, it seems to reflect the prognosis.

Computed tomography (CT) has proven reliable in the early detection of acute haemorrhagic pancreatitis. In the present study the extrapancreatic changes at CT were studied in 60 patients with acute pancreatitis. The CT findings were correlated to the early "prognostic signs" by Ranson and the clinical course of the disease. All the patients with minor extrapancreatic changes recovered without complications. When moderate to severe extrapancreatic changes were seen the incidence of haemorrhagic pancreatitis and the risk of development of pseudocyst or abscess was high. In these patients a dynamic contrast enhanced CT should be done in order to select the patients with haemorrhagic pancreatitis.

The main problem in the diagnosis of acute pancreatitis is the early detection of the fulminant forms. So far, there is no single laboratory test that affords an unequivocal measure of the severity of the disease. We have studied the serum phospholipase A2 concentrations of 66 consecutive patients with acute or chronic relapsing pancreatitis. Fifty-two patients had a mild spontaneously healing form of the disease, whereas eight patients developed a pseudocyst or an abscess. Six patients had operatively established haemorrhagic pancreatitis. The serum phospholipase A2 concentrations were significantly higher in the patients with haemorrhagic pancreatitis than in those with a spontaneously healing disease. Moreover, in the patients with a milder form of the disease the serum phospholipase A2 concentrations correlated with prognostic signs suggested by others. The results suggest that the assaying of serum phospholipase A2 might be a valuable tool in the diagnosis and follow-up study of patients with acute pancreatitis.

The cause of hemodynamic changes occurring during acute pancreatitis remains obscure. Using a pig model of acute hemorrhagic pancreatitis and the reference sample method with 113Tin and 46 Scandium labelled microspheres, blood flow to organs was determined before and five hours after the induction of pancreatitis. Blood pressure, pulse rate and cardiac output were measured hourly. There were two treatment groups. The first group received dextran 70 (5.7 milliliters per kilogram per hour) and saline solution (7.5 milliliters per kilogram per hour) in sufficient amounts to maintain cardiac output at the initial (prepancreatic) level. The second group received saline solution (26 milliliters per kilogram per hour) only and during the experiment the cardiac output was allowed to decrease to approximately one-half of the initial level. In the dextran 70 group, blood flow in various organs stayed at the initial level or was slightly increased. However, in the saline solution group there was a marked and significant decrease in the blood flow in all organs except the antral mucosa, gallbladder and adrenal glands. The changes in the pancreatic fraction of the cardiac output during the experiment were similar to those of other organs in respective treatment groups. In conclusion, adequate infusion of dextran maintains cardiac output and organ microcirculation at the initial level during the early phase of acute hemorrhagic pancreatitis. It is suggested that the hemodynamic changes which develop during acute pancreatitis are mainly secondary to the ensuing hypovolemia and not direct consequences of the pancreatic inflammatory process.

Twenty-eight consecutive patients with a first attack of acute alcohol-induced pancreatitis were examined by computed tomography (CT). After a survey scan of the abdomen a rapid contrast bolus (400 mg I/kg) was given intravenously, and the contrast enhancement of the pancreatic parenchyma was measured from a consecutive series of pancreatic scans. Nine patients with a fulminant course of the disease were operated on, and haemorrhagic necrotizing pancreatitis was found in eight. In all of these the contrast enhancement was decreased or absent. Patients recovering by conservative treatment showed normal or increased enhancement. The contrast enhancement seems to constitute a useful criterion for the early differentiation of acute fulminant pancreatitis from less severe forms of the disease.

Preoperative symptoms, diagnoses, and postoperative outcomes in 102 consecutive patients with pancreatic pseudocysts were analyzed. Upper epigastric pain, loss of weight, obstructive jaundice, and sudden arterial bleeding from the pseudocyst were the most common preoperative symptoms. Ultrasonography, computed tomography, and endoscopic retrograde cholangiopancreatography were the most useful diagnostic tools in the evaluation of the presence, size, location, and possible pancreatic ductal communications of the pseudocyst. In a single thick-walled pseudocyst, the best long-term results were achieved by internal drainage. Pancreatic resection is justified if the patient already has diabetes or multiple pseudocysts or if the pseudocyst is not amenable to internal drainage. The most fatal preoperative complication was a sudden arterial bleeding from a pseudocyst. In treating this complication, hemostasis with transcystic arterial ligation and external drainage of the pseudocyst gave the best results.

Twenty-eight consecutive patients with a first attack of alcohol-induced pancreatitis were studied using contrast-enhanced CT. The findings on CT were then related to the course of the disease. The patients with acute hemorrhagic-necrotizing pancreatitis showed significantly lower enhancement values of the pancreatic parenchyma than those with milder forms of the disease. The next 20 patients with severe pancreatitis were scanned using a slightly modified procedure. The enhancement values were calculated and plotted on the graphs for the 2 former groups. Two categories of pancreatic enhancement were found: "low enhancement" and "high enhancement." In all 10 patients with "low-enhancement" values surgery revealed hemorrhagic-necrotizing pancreatitis. In the 10 patients with "high-enhancement" values conservative treatment was continued, and the clinical course was nonfulminant in all of them.