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World J. Surg. 21, 136-142, 1997 WORLD Journal of SURGERY < //. © 1997 by the Societe Internationale de Chirurgie Diagnostic Standards for Acute Pancreatitis John H.C. Ranson, B.M., B.Ch., M.A. Department of Surgery, New York University School of Medicine, New York, New York 10016, U.S.A. Abstract. An accurate history and thorough physical examination will often raise clinical suspicion of acute pancreatitis in the differential diagnosis of a patient presenting with acute abdominal pain. An accurate diagnosis is needed to eliminate etiologies of acute abdominal pain and to appropriately direct therapy. Confirmation of the diagnosis is most often made by evaluation of serum amylase and lipase levels. Although hyper- amylasemia is found in the majority of patients with acute pancreatitis, other nonpancreatic acute abdominal conditions may be present with hyperamylasemia. CT scanning provides an accurate confirmation of clinical and laboratory findings and offers excellent anatomic and mor- phologic representation of the pancreas and peripancreatic tissue. The following article, written by the late John H.C. Ranson, presents a discussion of the modalities available for diagnosing acute pancreatitis. —Peter Shamamian, M.D. Acute pancreatitis is a common condition that appears to be increasing in incidence [1, 2], and it is often difficult to diagnose. In a study by Bockus et al., of 94 patients admitted for acute pancreatitis, the initial diagnosis was found to be incorrect in 43% [3]. Pancreatitis was most commonly misdiagnosed as acute cholecystitis (20%), perforated viscus (7%), or intestinal obstruc- tion (5%). In patients with fatal acute pancreatitis the correct diagnosis is not made until the time of autopsy in 41.6% of cases [4].There is, unfortunately, no clinical or laboratory criterion that permits certain diagnosis of acute pancreatitis in all patients. Operative or autopsy findings are available for only a few patients. Radiographic findings on computed tomography (CT) can be diagnostic, but this study may also be normal in patients with mild disease. The diagnostic features of acute pancreatitis are reviewed here. It should be stressed that the initial diagnosis depends primarily on an accurate, well directed history and careful physical exami- nation. Clinical Features The term acute pancreatitis encompasses a wide spectrum of clinical and pathologic findings with varied clinical features. It may closely mimic extrapancreatic conditions that are as different as myocardial infarction and acute gastroenteritis. Correspondence to: Peter Shamamian, M.D., New York University Medical Center, Department of Surgery, 530 First Avenue, Suite 6B, New York, NY 10016, U.S.A. Patient Characteristics Pancreatitis is uncommon in children and increases in frequency with increasing age. The rate per 100,000 population in the United States is 2.7 in those under 15 years old. It is roughly 100-fold greater in those 15 to 44 years old and 200-fold greater in those over 65 years old [1]. The frequency of pancreatitis in men and women is approxi- mately equal. Alcohol-related pancreatitis tends to be more common in men, and biliary pancreatitis is more common in women. The sex ratio, therefore, varies with the dominant etiology. It is reported that the rate of pancreatitis in black Americans is three times greater than in whites. The reasons are unknown [1]. Previous Episodes Previous episodes of similar but milder abdominal pain are reported in about 50% of patients with acute pancreatitis. This entity may represent previous mild pancreatitis or perhaps biliary colic. A previous episode of pancreatitis has been documented in approximately 20% of patients, especially in those with alcohol- associated disease [3]. Symptoms Abdominal pain is the dominant initial symptom in most patients. Characteristically, the pain is most severe in the upper abdomen and often radiates to the back or both flanks. The pain may begin after a heavy meal or during a drinking binge. It initially increases rapidly in intensity, but its onset is less sudden than that due to a perforated viscus. The intensity of pain varies widely but may be severe. Mild pain may be partially relieved by sitting up or by lying curled on the right or left side. The second most prominent symptoms are nausea and vomit- ing, which are almost invariably present. Vomiting may be re- peated but is usually not copious in volume. The vomitus com- prises primarily gastric and duodenal contents and is not feculent. Physical Examination Findings on physical examination are varied in nature and degree. In patients with mild pancreatitis physical examination may be largely unrevealing, whereas with severe disease the patient may Ranson: Pancreatitis: Diagnostic Standards 137 Table 1. Routine laboratory findings in 100 patients with acute pancreatitis versus those in 100 patients with other acute abdominal emergencies. Acute pancreatitis Other Laboratory test (%) (%) Serum amylase (Somogyi units/dl) > 500 59 1 200-500 36 4 < 200 5 95 Hematocrit (%) >45 31 23 <45 69 77 White blood cell count (cells/mm3) > 12,000 41 53 < 12,000 59 47 Blood glucose (mg/dl) > 300 7 0 200-300 9 7 Diabetics excluded: < 200 84 93 Serum calcium (mg/dl) >9 76 67 8-9 15 31 <8 9 2 Serum LDH (IU/L) > 225 48 24 < 225 52 76 Serum GOT (Sigma-Frankel units/dl) > 100 37 8 < 100 63 92 be hypotensive and comatose. Characteristically, the patient is restless with a rapid pulse and respiratory rate. Cyanosis may be present in severe cases. The abdomen is usually moderately distended and may exhibit a characteristic fullness of the epigas- trium. Tenderness is usually most marked over the upper abdo- men but may be generalized. Moderate muscle spasm is usual, but true rigidity is infrequent [5-8]. Grey Turner's sign or a gray- green discoloration of the flank is present in about 1% of patients. It is impossible to know how frequently the diagnosis of nonlethal acute pancreatitis is missed, as no diagnosis is made in most such cases. However, with fatal acute pancreatitis, the diagnosis is missed in 30% to 40% of patients until the time of autopsy [9, 10]. The diagnosis may be particularly difficult in two circumstances. The first is following surgery in the upper abdo- men, when abdominal pain and vomiting may be attributed to the recent surgery, and the possibility of concomitant pancreatitis is overlooked. The second circumstance occurs in patients who do not have significant abdominal pain. They may present with cardiopulmonary collapse, confusion, or hypothermia. In most such cases the diagnosis can be made if it is considered. Accord- ingly, when unexplained collapse occurs in the postoperative or other settings, biochemical and imaging studies for possible pancreatitis should be considered. Laboratory Findings Routine laboratory findings in 100 patients with acute pancreatitis are shown in Table 1. They are compared with those in 100 patients with acute cholecystitis, perforated ulcer, intestinal ob- struction, and appendicitis. The initial serum amylase was ele- vated in 95% of patients with acute pancreatitis and in 5% of those with other acute abdominal conditions. Two of the five patients with acute pancreatitis and reported normal serum amylase levels had lipemic serum. In the presence of hyperlipidemia, serum amylase activity may be inhibited [11]. Elevated serum amylase levels may be demonstrated by dilution of serum in this setting. Hyperglycemia or glycosuria may be associated with acute pancreatitis. Marked elevations of serum glucose levels are more common with pancreatitis than with other abdominal conditions. Hypocalcemia is also a well recognized feature of acute pancre- atitis but may occur in patients with perforated peptic ulcer as well [12]. If gastroduodenal perforation can be excluded, an initial serum calcium level below 8 mg/dl supportsa diagnosis of acute pancreatitis. Elevation of serum glutamic oxaloacetic transami- nase (SGOT) and lactic dehydrogenase (LDH) are more common in patients with pancreatitis than in those with other acute intraabdominal conditions but usually are not helpful for diagnos- ing pancreatitis. Laboratory Diagnosis Serum Amylase Elman et al. in 1929 demonstrated the value of serum amylase measurements in patients with acute pancreatitis, and it remains the most widely used diagnostic test of acute pancreatitis [13]. The reported sensitivity is difficult to estimate because an elevated amylase level is frequently used as a diagnostic criterion [14-17]. In a collective review of 5781 patients with acute abdominal conditions, Stefanini et al. reported that 20% had elevated serum amylase levels [18]. Moreover, 75% of patients with hyper- amylasemia had acute pancreatitis and 25% had other conditions. Of the latter, only 53% had illnesses that might be confused with pancreatitis. The nonpancreatic intraabdominal diseases most commonly associated with elevated amylase levels are perforated peptic ulcer, biliary disease, intestinal obstruction, and mesenteric infarction. Urinary Amylase Elevated amylase levels occur in the urine of patients with pancreatitis, a reflection of glomerular filtration of increased serum amylase concentrations combined with decreased tubular reabsorption during pancreatitis. Urinary amylase levels may remain elevated longer than serum levels. Furthermore, elevated serum amylase levels secondary to macroamylasemia may be detected by decreased urinary amylase levels. Urinary amylase measurements have little other advantage over serum measure- ments. The normal urinary clearance of serum amylase is about 3 ml/min. Because the creatinine clearance is usually 100 ml/min, the ratio of amylase clearance to creatinine clearance (ACCR) is approximately 2% to 4%. In patients with pancreatitis this ratio is increased and may exceed 10%. Although an increased ACCR was thought to be helpful for the diagnosis, it has been shown to have little value because of its low specificity [19-23]. Isoamylase Measurements Amylase activity in the serum derives not only from the pancreas but from the salivary glands and to a lesser extent other tissues as 138 World J. Surg. Vol. 21, No. 2, February 1997 Table 2. Incidence of radiographic signs suggesting acute pancreatitis on initial chest and abdominal radiographs in 73 patients with acute pancreatitis. Radiographic sign Incidence (%) Segmental small bowel ileus 41 Colonic dilation 22 Obscure psoas margin 19 Increased epigastric soft tissue density 19 Increased gastrocolic separation 15 Gastric greater curvature distortion 14 Duodenal ileus 11 Pleural effusion 4 Pancreatic calcification 3 One or more of the above signs 79 well, including the fallopian tube, lung, and liver. These amylases have differing physicochemical properties. Normal serum amylase has three isoamylase peaks with isoelectric points of 7.0, 6.4, and 6.0. Pancreatic isoamylase has an isoelectric point of 7.0 and can be isolated from other isoamylases. Although not available on a routine basis, pancreatic isoenzyme measurements are more specific than total amylase levels and may persist after the onset of disease [14, 24-29]. Lipase Serum lipase originates for the most part from the pancreas. Reports indicate that it is more specific and more sensitive than amylase levels for detecting acute pancreatitis [17, 21, 30]. The serum lipase level has not been widely used, perhaps because the available assays were not suitable for widespread rapid use. The availability of simple methods to measure lipase levels may lead to wider use of this diagnostic parameter [31, 32]. Other Tests Serum immunoreactive trypsin, chymotrypsin, elastase, phospho- lipase A2 , a2 macroglobulin levels, methemalbumen, carboxypep- tidases, and carboxyl ester hydrolase levels have been reported to be of possible value for the diagnosis of pancreatitis. At this time, their superiority to measurements of amylase and lipase levels is unproved [15, 17, 21, 30, 33-37]. Radiology Plain radiographs of the chest and abdomen are a standard part of the evaluation of patients with acute abdominal findings. These findings are often examined only for the possible presence of free air, an intestinal gas pattern indicating intestinal obstruction, or calcification in the biliary or urinary tracts. Most patients with acute pancreatitis have one or more of the radiographic findings listed in Table 2 [38]. The incidence of the various findings is also shown. The diagnostic value of the signs varies considerably, with demonstration of an enlarged pancreatic head by a gas-filled duodenum being the most specific (Fig. 1). Ultrasonographic evaluation of the pancreas may show in- creased size and decreased echodensity as well as possible fluid collections [39]. Computed tomography (CT) is more costly and involves radiation exposure but clearly provides superior imaging of the pancreas and peripancreatic retroperitoneum [40]. CT findings reported for acute pancreatitis include diffuse or segmen- Fig. 1. Plain abdominal radiograph demonstrating duodenal ileus in a patient with acute pancreatitis. From Ranson, J.H.C.: Acute pancreatitis. In Current Problems in Surgery, Vol. 16, No. 11, St. Louis, Mosby-Year Book Inc., 1979. Fig. 2. CT image of acute pancreatitis demonstrating pancreatic enlarge- ment and fluid in the left anterior pararenal space. tal enlargement of the pancreas, irregularity of the pancreatic contour with obliteration of the peripancreatic fat planes, heter- ogeneous appearance and areas of decreased density within the pancreas, and variable ill-defined fluid collections. Fluid accumu- lation may occur within the pancreas or outside the gland in the lesser sac and in the pararenal spaces (Fig. 2) [41]. CT findings supporting a diagnosis of pancreatitis are present in 85.5% of our patients [42]. The frequency of CT findings depends on the severity of the pancreatitis being studied. Normal CT findings Ranson: Pancreatitis: Diagnostic Standards 139 Table 3. Etiologic factors of acute pancreatitis. Metabolic Alcohol abuse Hyperlipoproteinemia Hypercalcemia Drugs Genetic Scorpion venom Mechanical Cholelithiasis Postoperative (gastric, biliary) Pancreas divisum Posttraumatic Retrograde pancreatography Pancreatic duct obstruction: pancreatic tumor, Ascaris infestation Pancreatic ductal bleeding Duodenal obstruction Vascular Postoperative (cardiopulmonary bypass) Periarteritis nodosa Atheroembolism Infection Mumps Coxsackie B Cytomegalovirus Cryptococcus have been reported in 24% to 67% of patients [40, 43, 441. The clinical course of patients with normal findings on CT is usually benign. Preliminary experiences with magnetic resonance imaging have not identified major advantages compared to contrast-enhanced CT [45]. In the absence of CT scanning, a water-soluble contrast study of the upper gastrointestinal tract can help exclude perforation or obstruction of the stomach or small intestine. The differential diagnosis of acute pancreatitis from obstructive cholangitis or gangrenous cholecystitis associated with elevated amylase levels maybe particularly difficult. In this situation, ultrasonography may demonstrate gallbladder stones but does not provide sufficiently precise anatomic information. Biliary scanning is not reliable, as cystic duct obstruction may be demonstrated during acute pan- creatitis even in the absence of biliary lithiasis. Direct imaging of the biliary tree by percutaneous transhepatic cholangiography or endoscopic retrograde cholangiography may be required to ex- clude cystic duct or common bile duct obstruction [46]. Diagnostic Paracentesis Paracentesis and examination of the peritoneal exudate or of the return following lavage of the peritoneal cavity has been used in the diagnosisof acute abdominal findings [47, 48]. The gross appearance, amylase content, and white blood cell count of the peritoneal fluid in patients with acute pancreatitis vary widely and overlap with those in patients with other causes of peritonitis. Paracentesis does not therefore usually provide strong positive evidence of pancreatitis. Its main usefulness is when it demon- strates findings such as bile or dietary fiber, indicating life- threatening extrapancreatic disease. Diagnostic Laparotomy Although a reasonably certain diagnosis of acute pancreatitis can be reached in most patients on the basis of clinical, radiographic, and laboratory findings, there are patients in whom diagnostic celiotomy is required to exclude life-threatening extrapancreatic disease. In this regard, it should be stressed that strong positive evidence of acute pancreatitis does not exclude the possibility of concomitant extrapancreatic abnormalities in the occasional pa- tient. If diagnostic celiotomy is undertaken, exploration must be complete and establish the diagnosis beyond question. The pan- creas should be inspected and the extent of inflammation, asso- ciated fluid collections, pancreatic and peripancreatic necrosis, and hemorrhage noted. The presence of gallstones should be evaluated, although palpation of the gallbladder in this setting fails to detect stones in about 20% of patients who harbor cholelithiasis. Any further choice of surgical procedure should be determined by specific therapeutic goals. Etiologic Diagnosis The more common identified causes of acute pancreatitis are listed in Table 3. About 60% to 80% of these patients either harbor gallstones or have a history of alcohol abuse. In many instances the etiology can be determined by an accurate history. Others, such as those with hyperlipoproteinemia, require bio- chemical evaluation, which may have to await subsidence of the acute episode. In most etiologic groups, management of the acute episode is not greatly altered by knowledge of the etiology. In patients with gallstone-associated pancreatitis, early management may include endoscopic retrograde cholangiography. Attempts have therefore been made to identify this etiologic subgroup. It has been found that the patient's age, serum amylase, alkaline phosphatase, glutamyl transpeptidase, and transaminase levels were significantly higher in patients with gallstone pancreatitis [49-51]. Several scoring systems have been reported. Blarney et al. identified five factors: alkaline phosphatase >_ 300 IU/L, age >_ 50 years, alanine aminotransferase ? 100 IU/L, female sex, and amylase ? 4000 IU/L. The incidence of gallstones rose from 5% if none of these findings was present to 100% when all five were present [50]. Early ultrasonography has been reported to have a lower sensitivity than biochemical findings in detecting gallstone disease. However, a combination of ultrasonography and bio- chemical measures has an overall accuracy of 93.2% [49]. Prognostic Assessment The clinical spectrum of acute pancreatitis ranges from mild, self-limiting symptoms to a fulminant, rapidly lethal disease. Early objective identification of the risk of major complications or death is essential for appropriate management of individual patients and for assessment of the efficacy of treatment. Clinical Criteria A number of early clinical findings have been reported to have prognostic value. They include age, Grey Turner's sign, and the severity of abdominal findings on physical examination. In most instances these clinical findings cannot be objectively quantified. In patients with acute pancreatitis, recurrent episodes are common unless the etiologic findings can be identified and corrected. In general, the virulence of each new recurrent attack tends to diminish. In our experience the mortality of the first 140 World J. Surg. Vol. 21, No. 2, February 1997 Table 4. Measurements reported to be of early prognostic value in acute pancreatitis. Measurement Reference Hemodynamic tests 52 Hematocrit 53 White blood cell count 5 Coagulation factors 54 Complement activation 55 C-reactive protein 56 Serum amylase 57 Serum phospholipase A 2 58 Serum elastase 56 Serum calcium 59 Blood glucose 60 Renal function 60 Respiratory insufficiency 60 Acidosis 60 Liver function 60 Serum methemalbumin 60 Serum ribonuclease 61 Serum cyclic adenosine 3'5'-monophosphate 62 a,-Protease inhibitor 63 az Macroglobulin 64 Trypsinogen activation peptides 65 episodes was 9.6%. It fell to 5.3% during the second episode and was 1.1% for subsequent episodes. Table 4 lists some of the measurements reported to be of early prognostic value [5, 52-65]. In many instances, clinical evaluation involves only small numbers of patients. In others the measure- ment has been correlated with "necrotizing" pancreatitis, rather than with the overall clinical course. A distinction must be drawn between diagnostic tests and prognostic measurements. Thus serum pancreatic ribonuclease determination is a measurement that, if levels rise during the course of acute pancreatitis, has been reported to indicate pan- creatic necrosis. It is a diagnostic, rather than a prognostic, measurement, as early levels do not discriminate severity of disease or probability of complications in the future. Correlations have also been reported between a t -protease inhibitor, a2-macroproteins, complement factors C3 and C4, and C-reactive protein and necrotizing pancreatitis. Most of these measures are diagnostic, rather than prognostic. Most intriguing, from a morphologic standpoint, has been the use of contrast-enhanced CT. Radiographic enhancement of the pancreas following contrast injection has been interpreted as evidence of tissue viability. Failure of enhancement has been interpreted as evidence of tissue necrosis. Estimations of pancre- atic necrosis using contrast-enhanced CT have been reported to correlate well with operative estimates of the extent of pancreatic necrosis [66]. The timing of these studies relative to the onset of symptoms of pancreatitis, however, is not always reported. The prognostic (in contrast to diagnostic) value of this study in terms of necrosis is uncertain. Furthermore, identification of the pres- ence of necrosis is of value only if it is shown to be associated with specific complications or overall morbidity. In our studies, approx- imately 70% of patients who had nonenhancement on early contrast-enhanced CT went on to develop infection of devitalized pancreatic and peripancreatic tissue. Approximately 30% of pa- tients, however, escaped this complication. In our experience, the risk of pancreatic infection in patients with early normal pancre- Table 5. Early objective prognostic signs that correlate with the risk of major complications or death from acute pancreatitis. At admission or diagnosis Age > 55 years White blood cell count > 16,000/µl Blood glucose level > 200 mg/dl Serum lactic dehydrogenase concentration > 350 IU/L Serum glutamic oxaloacetic transaminase > 250 Sigma-Frankel units/dl During initial 48 hours Hematocrit decrease of > 10% Blood urea nitrogen increase of > 5 mg/dl Serum calcium level < 8 mg/dl Arterial P02 < 60 mmHg (8 kPa) Base deficit > 4 mEq/L Estimated fluid sequestration > 6000 ml atic enhancement was only 8.5%. Therefore although nonen- hancement is a finding of ominous prognostic significance in terms of infection, its overall sensitivity and specificity are limited. A study of the prognostic value of CT findings, not based on enhancement following contrast administration, was reported in 1985. Early CT findings were grouped into five categories: (1) normal; (2) peripancreatic enlargement alone; (3) inflammation confined to the peripancreatic area; (4) one peripancreatic fluid collection; and (5) two or more fluid collections. The frequencies of these findings in our population of patients were 14.5%, 22.9%, 20.5%,14.5%, and 27.7%, respectively. There was a weak relation between the grade of CT finding and overall morbidity, but it was of little clinical value. CT findings, however, did provide a valuable guide to the risk of late pancreatic sepsis. In patients with CT grades A or B, the incidence of abscess was zero. In those with grades C or D, it was 11.8% and 16.7%, respectively; and in those with grade E it was 60.9%. Multiple Prognostic Criteria In 1974 we developed the 11 early objective prognostic criteria listed in Table 5 [67]. These signs were developed from a statistical analysis of the relation between early measurements and overall morbidity and mortality of acute pancreatitis. The relation between the number of signs present and morbidity in a group of 450 patients is shown in Fig. 3. More complex statistical methods or examination of specific etiologic groups may improve accuracy. Several modifications of these multiple criteria have been proposed. Overall accuracy of differing modifications are roughly comparable. All suffer from lack of simplicity and a 48-hour delay in final assessment. The APACHE II (acute physiology and chronic health evalua- tion) illness grading system has been applied to prognostic assessment of pancreatitis [68, 69]. Reports indicate that the accuracy of this system is comparable to that of specific multiple prognostic criteria. It is more complex but has the advantage that it may be applied at times other than at diagnosis. Conclusions In most patients acute pancreatitis can be diagnosed on the basis of careful clinical evaluation combined with biochemical and radiographic studies. When positive findings are present, CT examination may provide valuable confirmation in selected cases. Ranson: Pancreatitis: Diagnostic Standards 141 Fig. 3. Incidence of death and complications that required at least 7 days of intensive care related to the number of positive prognostic signs. From Ranson, J.H.C.: Acute pancreatitis. In Current Problems in Surgery, Vol. 16, No. 11, St. Louis, Mosby-Year Book Inc., 1979. Biochemical measurements and ultrasonography may be helpful for early identification of those patients who harbor gallstones. We continue to use the prognostic criteria listed in Table 5 to identify patients with a high risk of life-threatening complications. Early contrast-enhanced CT provides additional morphologic information in severely ill patients and those with an atypical clinical course. Resume La pancreatitc aigue est une maladie relativement frequente dont l'incidence est en hausse. Son diagnostic est difficile. Dans une etude presentee par Bockus a partir de 94 admissions pour pancreatite aigue, le diagnostic etait inexact chez 43 % des cas. La pancreatite a ete prise le plus souvent pour une cholecystitc aigue (20%), une perforation de viscere creux (7%) ou une occlusion intestinale (5%). Chez le patient ayant une pancreatite aigue fatale, le diagnostic correct n'a pas ete fait avant 1'autopsie dans 41.6% des cas. Il n'existe aucun critere clinique ou biologique qui permette le diagnostic certain de pancreatite aigue a tous les coups. Les donnees operatoires ou autopsiques ne sont dis- ponibles que chez un faible pourcentage des patients. Les donnees de la tomodensitometrie sont parfois diagnostiques, mais cet examen peut titre normal chez le patient ayant une forme mineure de la maladie. Les criteres diagnostiques de la pancreatite aigue sont passes en revue. I1 faut souligner que le diagnostic initial depend principalement d'un interrogatoire precis ainsi que d'un examen physique soigneux. Resumen La pancreatitis aguda es una entidad comun, con frecuencia de dificil diagnostico, cuya incidencia es creciente. En un estudio realizado por Bockus en 94 pacientes hospitalizados por pancre- atitis aguda, el diagn6sti co inicial resulto incorrecto en 43% de los casos. Comunmente se confundio la pancreatitis aguda con colecistitis aguda (20%), viscera perforada (7%) u obstruccion intestinal (5%). En los casos de pancreatitis aguda letal, el diagnostico correcto solo es establecido en el momento de la autopsia, lo cual ocurre en 41.6% de los casos. Desafortunada- mente no existen criterios clinicos o de laboratorio que permitan un diagnostico certero de pancreatitis aguda en la totalidad de los pacientes. Los hallazgos operatorios o de necropsia estan dis- ponibles solo en una pequeiia minoria de los casos. Los hallazgos radiologicos en tomografia computadorizada pueden ser diagnos- ticos de la entidad, pero el estudio puede aparecer normal en los pacientes con enfermedad leve. Es por ello que en el presente articulo se revisan las caracteristicas diagnosticas. Debe hacerse enfasis en que el diagnostico inicial depende, primordialmente, de una Bien orientada historia clinica y de un meticuloso examen fisico. References 1. Go, V.L.W.: Etiology of pancreatitis in the United States. In Acute Pancreatitis: Diagnosis and Therapy, E.L. Bradley, editor. 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