Assessment of Severity in Acute Pancreatitis: Use of Prognostic Factors

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1 Qasim O. Al-Qasabi, FRCS(I); Mohammed K. Alam, MS, FRCS(Ed); Mohammed M. Haque, FRCS(Ed), FRCS(Glas); Mohammed I. Sebayel, FRCS(Glas); Saad Al-Faqih, FRCS(Glas); Abdullah Al-Kraida, FRCS(Ed) From the Department of Surgery (Drs. Al-Qasabi, Alam, Haque, Sebayel, Al-Faqih), King Khalid University Hospital, and Department of Surgery (Dr. Al- Kraida), Riyadh Central Hospital, Riyadh, Saudi Arabia. Address reprint requests and correspondence to Dr. Al-Qasabi: Department of Surgery, King Khalid University Hospital, P.O. Box 7805, Riyadh 11472, Saudi Arabia. Accepted for publication 5 November This prospective study evaluates the value of Ranson s prognostic factors in predicting severity of acute pancreatitis. One hundred-fourteen patients with 124 attacks of acute pancreatitis were studied during a 4-year period at Riyadh Central Hospital. The majority of patients were Saudi males, their mean age being 46.5 years. Cholelithiasis was the leading cause of pancreatitis. Ranson s 11 prognostic factors were estimated within 48 hours of admission. Sixty-six percent of the cases were graded as mild pancreatitis with less than 3 Ranson s factors present, whereas 34% were classified as severe pancreatitis with 3 or more of Ranson s factors present. Prognostic factors correctly predicted severity in 66% of patients, but only 36% from the severe group developed severe disease (complications and/or death). Overall mortality was 5.3%. Ranson s prognostic factors help in identifying severe pancreatitis but their accuracy may be improved by the use of modern imaging techniques. QO Al-Qasabi, MK Alam, MI Sebayel, S Al-Faqih, A Al-Kraida, Assessment of Severity in Acute Pancreatitis: Use of Prognostic Factors. 1991; 11(5): Acute pancreatitis is a disease of various etiology, severity, complications and outcome. Most often pancreatitis is mild and resolves promptly without any complication. In 20% of cases, attacks are severe with a protracted course and a mortality rate of 50% [1]. These severe cases of pancreatitis need vigorous treatment in an intensive care facility. Most hospitals with limited intensive care facilities fail to provide such care to every patient with pancreatitis. Moreover, routine adoption of intensive measures would be expensive. Therefore, it is essential to identify at an early stage the few cases that will develop a severe form of the disease, to provide vigorous treatment to them, and to minimize the morbidity and mortality rate. Ranson et al [2], in 1974, identified 11 factors which had a value in predicting the severity of disease. A modification of this system was suggested by Imrie et al [3]. Further modifications have been suggested in an attempt to improve the prognostic value of these scoring systems [4,5]. This prospective study was designed to evaluate Ranson s 11 prognostic factors in our patient population. The aim was to assess their accuracy, which would help in planning the future course of management in our hospital. Clinical Material and Methods This study was carried out on patients admitted to Riyadh Central Hospital during 1986 to 1989 with a diagnosis of acute pancreatitis. The diagnosis of acute pancreatitis was accepted if acute abdominal pain was

2 associated with a serum amylase level greater than 1000IU/L (normal up to 200 IU/L). Ranson s 11 prognostic factors were estimated within 48 hours of admission. Fluid sequestration was estimated by subtracting the volumes of nasogastric and urinary drainage from the volumes of intravenous fluids administered [2]. All the data were recorded on prescribed pro forma. Cases of pancreatitis were classified as a mild attack when less than three of Ranson s factors were present. Cases with three or more factors were classified as severe. The progress of each group was closely monitored. Complications and mortality in each group were recorded and their final outcome compared. Ultrasonography was performed on the majority of the patients to establish the etiology of pancreatitis. Computed tomographic (CT) scan and endoscopic retrograde cholangiopancreatogram (ERCP) were selectively performed to establish the etiology, identify complications and monitor their progress. Results One hundred-fourteen patients were admitted during the study period with 124 attacks of acute pancreatitis. The majority were Saudis (54%). Males (53%) outnumbered females (47%). Patient age ranged from 7 to 100 years, the mean age being 46.5 years. Seventy-five patients (66%) were under 55 years of age. Cholelithiasis was the leading cause (54%) of pancreatitis, followed by idiopathic pancreatitis (24.5%). Alcohol was responsible for pancreatitis in 7% of the patients. Other less common causes of pancreatitis are presented in Table 1. Epigastric pain (91%) and vomiting (74%) were the two most common presenting symptoms (Table 2). Significant clinical signs on admission and their frequencies are also presented in Table 2. Age (> 55 years) and elevated LDH (> 350 IU/L) were the most frequent factors. The relative incidence of each factor is presented in Table 3. Seventy-five patients (82 attacks) were graded as having mild pancreatitis (less than three factors present). Thirty-nine patients (42 attacks) were classed as having severe attacks (three or more factors present) of pancreatitis. Table 4 presents the mean value of each factor compared with the mild and the severe group. Nine factors showed significant difference between mild and severe attacks of pancreatitis. Of 124 attacks (114 patients) of acute pancreatitis, 66% had severity correctly predicted by prognostic factors. Of twenty-two patients, 12 (16%) from the mild group and 10 (26%) from the severe group developed complications (Table 5). Two patients (2.7%) from the mild group and 4 patients (10.3%) from the severe group died, denoting an overall mortality of 5.3% (Table 6). Table 7 compares our mortality with other studies. Four patients were directly admitted to the intensive care unit due to their advanced age or hypoxia. Twenty-four patients from both groups were subsequently transferred to the intensive care unit for respiratory support and intensive monitoring. Table 1. Analysis of etiological factors. Etiology Number Percentage Gallstones 62 54% Idiopathic 28 24% Alcohol 8 7% Post-ERCP 7 6% Drugs 6 5% Blunt trauma (RTA) 1 1 % Burn injury 1 1% Hyperparathyroidism 1 1% Hyperlipidemia 1 1% Total % ERCP = endoscopic retrograde cholangiopancreatogram; RTA = road traffic accident.

3 Table 2. Clinical features of acute pancreatitis in 114 patients. Number Percentage Symptoms Epigastric pain Vomiting (more than 3 times) Right hypochondrial pain Left hypochondrial pain Signs Tachycardia Dehydration Fever Jaundice Hypotension 9 8 Table 3. Relative incidence of each prognostic factor. Ranson s prognostic criteria Number of patients Percentage LDH (> 350IU/L) Age > 55 yrs SGOT(> 250 SF units %) WBC (> 16,000/cmm) FBS (> 200 mg % or 11.2 mmol/l) Serum calcium (8 mg/%) Blood urea nitrogen (> 5 mg % rise) Base deficit (> 4 meq/l) P0 2 < 60 mm Hg Diminution of hematocrit (10% or more) 10 9 Fluid loss (6 liters or more) - - LDH = lactic dehydrogenase; SGOT = serum glutamic oxaloacetic transaminase; WBC = white blood cells; FBS = fasting blood sugar.

4 Table 4. Table presenting mean value of prognostic factor in mild and severe pancreatitis. Factors Mean ± SD P value Mild Severe One-tailed Remarks Age ± ± HS (7-80) (22-100) WBC ± ± S (3.7-35) ( ) Hematocrit ± ± NS ( ) ( ) Urea ± ± S (10-184) (13-100) LDH ± ± s ( ) ( ) SGOT ± ± s (15-912) (10-673).. PO ± ± HS (48-152) ( ) CA ± ± HS ( ) ( ) Base deficit 2.39 ± ± S ( ) ( ) FBS ± ± HS (55-373) (84-441) Fluid sequestration ± ± NS ( ) ( ) HS = highly significant; S = significant; NS = not significant. For other abbreviations, see Table 3. Table 5. Complications of acute pancreatitis. Local complications Mild No. (%) Severe No. (%) Pseudocyst 2(12.6) 4(3.5) Hemorrhagic necrotizing pancreatitis pancreatitis 0 4(3.5 ) Pancreatic phlegmon 0 3(2.6) Ileus 1 ( 0.9) 2(1.8) Pancreatic abscess 0 2(1.8) Duodenal obstruction 1 ( 0.9) 1(0.9) Systemic complications Metabolic Diabetes mellitus 4( 3.5) 7 (6.09) Respiratory Pleural effusion 0 3(2.63) Adult respiratory distress 1 (0.87) 2(1.75) Renal Acute renal failure 1 (0.87) 2(1.75) Gastrointestinal Upper GI bleeding 0 2(1.75) Peritonitis 0 1 (0.87) GI = gastrointestinal

5 Table 6. Analysis of fatal cases (mortality 5.3%). Number Patients Ranson of N Age Sex factors Type of complications Certified cause of death o 1 50 F 3 Pancreatic abscess; pseudocyst; upper GI bleeding; hepatic failure; acute Cardiac arrest Persistent renal failure high fever; chest 2 90 F 7 infection; pleural effusion Septicemia; bronchopneumonia; 3 45 Μ 1 High fever (septicemic) cardiac arrest 4 15 F 4 Pleural effusion; acute respiratory distress syndrome; intraperitoneal Acute renal failure; septicemia Respiratory failure hemorrhage; respiratory acidosis 5 65 Μ 1 Pseudopancreatic cyst; cardiorespiratory and Acute renal failure; 6 56 Μ 4 GI = gastrointestinal. hepatorenal failure Intraperitoneal hemorrhage; chest infection; oliguria Discussion encephalopathy; cardiorespiratory arrest Cardiac arrest In the year 1889, Reginald Fitzgerald [6], a Harvard pathologist, established acute pancreatitis as a definite pathological entity. Elman [6], a surgical resident at the Barnes Hospital in St. Louis, Missouri, discovered serum amylase in 1927, and Michael Somoygi a biochemist at the Jewish Hospital in Missouri established the unit of measurement of amylase and correlated it to the diagnosis of acute pancreatitis. The majority of acute pancreatitis cases are mild, self-limiting, and respond to only supportive medical therapy such as fluid replacement, nasogastric suction and analgesics. A small proportion (5 to 20%) [1,7] of patients who develop the severe form of disease may require more intensive and invasive methods of management to minimize morbidity and mortality. Various methods have been used to identify severe attacks of the disease. Clinical methods can identify only about one third of patients with acute pancreatitis who will develop serious complications [8]. Cyanosis, shock, fever, Grey-Turner sign (bluish discoloration of the flank), tetany and an abdominal mass are serious signs, but they are often absent in patients who have serious complications [9,10]. Williamson [11] and his associates have used a combination of 4 factors: hypotension, blood pressure < 100 mm Hg; hypocalcemia, < 2 mmol/l; hypoxemia, PaO2 < 8 KPa; and toxic broth, volume > 10 ml, or dark return fluid on abdominal paracentesis. Presence of any factors constitutes a severe attack. Williamson [11] has claimed diagnostic accuracy of 84% in distinguishing severe pancreatitis from mild pancreatitis. Table 7. Comparison of mortality in various studies. Overall mortality Ranson 1979 (80 cases) 4.4% Imrie 1984 (405 cases) 10.6% Present study (114 cases) 5.26% Since the description by Ranson et al [2] of the 11 prognostic factors, several studies have been carried out to modify and improve the accuracy of these scoring systems [3-5]. Other studies have attempted to evaluate the value of a single factor such as plasma fibrinogen level [7], total compliment activity [12], hypocalcemia [9] and serum methemalbumin [13] estimation to identify severe pancreatitis. Subsequent studies have failed to confirm the value of some of these factors in predicting severity [7,14]. Ranson s [2,15] studies were mainly performed on patients with alcoholic pancreatitis. As a majority of our patients present with biliary pancreatitis, we decided to evaluate this prognosticsystem on our patients. Fourteen patients (19%) from the 75 patients with less than three prognostic factors developed severe pancreatitis (complication and/or death) whereas 14 patients (36%) of 39patients with three or more prognostic factors developed a severe form of the disease (complications and/or death). Although prognostic factors correctly predicted the severity of disease in 66% of the attacks of pancreatitis, their accuracy among the severe group was only 36%.

6 Ranson et al [15] achieved an accuracy of 63% among the severe group. This difference could be due to difference in patient population. Biliary disease was the predominant cause of pancreatitis in our patients, whereas Ranson s patients were mainly cases of alcoholic pancreatitis. A low overall mortality of 5.3% may have been due to early identification and intensive care treatment of the severe pancreatitis group. Recently the role of CT scan in evaluation of severity of pancreatitis has been studied. The main objection this study raises against Ranson s prognostic system is that it.only assesses the systemic effect while it fails to give any information about the extent of pancreatic disease. CT scan, on the other hand, provides an image of the entire pancreas and peripancreatic area and helps to accurately assess the extent of disease [16]. In this study, CT scan was used selectively, therefore no comparison with Ranson s prognostic factors could be made. The usefulness of ultrasonography in assessing the severity of pancreatic disease is limited as associated paralytic ileus hinders thorough ultrasonographic examination of the gland [17]. However, it has high accuracy in detecting gallstones, a leading cause of pancreatitis in this study. In conclusion we have found that: (1) gallstones are the leading cause (54%) of pancreatitis in the Riyadh region, (2) use of Ranson s prognostic factors correctly predicted the severity of the disease in 66% of patients but its accuracy was only 36% among the severe group, (3) prognostic factors in combination with clinical assessment and CT scan will increase the accuracy of true identification of severe cases. References 1. Leese T, Shaw D. Comparison of three Glasgow multifactor prognostic scoring systems in acute pancreatitis. BrJSurg 1988;75: Ranson JHC, Rickfind KM, Rose DF, et al. Prognostic signs and the role of operative management in acute pancreatitis. Surg Gynaecol Obstet 1974;139: Imrie CW, Benjamin IS, Fergusan JC, et al. A single centre double blind trial of trasylol therapy in primary acute pancreatitis. Br J Surg 1978;65: Osborne DH, Imrie CW, Carter DC. Biliary surgery in the same admission for gallstone associated acute pancreatitis. Br J Surg 1981 ;68: Blarney SL, Imrie CW, O Neill J, et al. Prognostic factors in acute pancreatitis. Gut 1984;25: Busnardo AC, Didio LJA, Tidrick RT, Thomford NR. History of pancreas. Am J Surg 1983;146: Berry AR, Taylor TV, Davies GC. Diagnostic tests and prognostic indicators in acute pancreatitis. J R Coll Surg Edinb 1982;27: Corfield AP, Cooper MJ, Wilhamson RCN, et al. Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices. Lancet 1985 ;2: Trapnell JE. Natural history and prognosis of acute pancreatitis. Ann R Coll Surg Engl 1966;38: Jacobs ML, Dagget WM, Civetta JM, et al. Acute pancreatitis: analysis of factors influencing survival. Ann Surg 1977;185: Williamson RCN. Early assessment of severity in acute pancreatitis. Gut 1984;25: Galloway DJ, Murray WR, Foulis AK, et al. Endotoxaemia and compliment activation in acute pancreatitis. Br J Surg 1981;68: Lankisch PG, Koop H, Otto J, Oberdieck V. Evaluation of methaemalbumin in acute pancreatitis. Scand J Gastroenterology 1978;13: McMahon MJ, Playforth MJ, Pickford IR. A comparative study of methods for the prediction of severity of attacks of acute pancreatitis. Br J Surg 1980;167: Ranson JHC, Rickfind KM, Turner JW. Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. Surg Gynaecol Obstet 1976;143: Nordesgaard AG, Wilson SE, Williams RA. Early computerized tomography as a predictor of outcome in acute pancreatitis. Am J Surg 1986;152: Moosa AR. Diagnostic tests and procedures in acute pancreatitis. N Engl J Med 1984;311: Jacobs ML, Daggett WM, Civetta JM, et al. Acute pancreatitis: analysis of factors influencing survival. Ann Surg 1977;185(1):43-51.