Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage:

Acute pancreatitis Steven Kaplan, Jamie S. Barkin & Arvey I. Rogers To cite this article: Steven Kaplan, Jamie S. Barkin & Arvey I. Rogers (1978) Acute pancreatitis, Postgraduate Medicine, 64:5, 225-236, DOI: 10.1080/00325481.1978.11714984 To link to this article:

Published online: 07 Jul 2016.

Submit your article to this journal

Article views: 1

View related articles

Full Terms & Conditions of access and use can be found at


Acute pancreatitis When the history and findings suggest pancreatitis, the physician must decide what further aspects of the history should be explored and what laboratory and radiographic studies will be helpful in determining the cause.

Steven Kaplan, MD Jamie S. Barkin, MD Arvey I. Rogers, MD

A 32-year-o/d black woman is seen in the emergency room with persistent midepigastric pain of eight hours' duration radiating into the back, associated with nausea, vomiting, and diaphoresis. There is no history ofabdominal pain. Physical examination shows her to be well developed and well nourished. Pulse is I /0 I m in and regular, blood pressure I 22 I 90 mm Hg, respiratory rate 201min, and temperature 100 F. On chest examination. bilateral basilar dry roles are heard. Findings referable to the heart are normal except for tachycardia. The abdomen is mildly distended, and hypoactive bowel sounds are present without rushes or tinkles. 1her~ is diffuse tenderness to palpation, as well as guarding of the left upper quadrant. Rectal examination is unrevealing. The stool contains no occult blood. Laboratory tests yield the following values: hematocrit 43%. WBCs II.500Icu mm with a left shift, and serum amylase 570 Somogyi units I dl (norma/50 to /50). The patient is admitted to the hospital for further examination and observation.

Question: The differential diagnosis of abdominal pain and hyperamylasemia includes which of the following? I. Pancreatitis 2. Mesenteric infarction 3. Ruptured tubal pregnancy 4. Sickle cell crisis 5. Pneumococcal pneumonia Answer: I ,2,3 I. The pancreas is a rich source of amylase, and a variety of pancreatic diseases are associated with hyperamylasemia, such as acute and

,--'-----· I I I I I



One of a group of case reports Incorporating a management seH-test


chronic pancreatitis, pancreatic pseudocyst, carcinoma, and abscess. 2. The brush border of the small intestine contains amylase which is secreted into the bowel lumen; infarction may be associated with mild hyperamylasemia. 1 Mesenteric infarction occurs most commonly in the elderly in association with atherosclerotic cardiac or peripheral vascular disease; however, it may occur in a younger age group secondary to the use of oral contraceptives, hypotensive episodes, cardiac arrhythmias, embolic phenomena associated with valvular heart disease, or hypercoagulable states. The typical history of mesenteric infarction includes nonspecific abdominal pain-either periumbilical or diffuse-associated with nausea, vomiting, or diarrhea which may be bloody. Mild abdominal tenderness may be the only early physical finding; however, peritonitis may evolve. Laboratory data usually reveal leukocytosis with a left shift, an elevated BUN level secondary to volume contraction, and lactic acidosis secondary to bowel necrosis. The patient denies the use of oral contraceptives or a history of rheumatic heart disease. There is no evidence of polycythemia vera, macroglobulinemia, or other hypercoagu/able states. continued



3. The fallopian tubes contain amylase, and a rupture resulting from tubal pregnancy may present as abdominal pain and hyperamylasemia.' A history of recent amenorrhea and breast engorgement should be sought when tubal pregnancy is suspected. The pain is sharp and located in the lower abdomen or pelvis, or it may localize to the side of rupture. Peritonitis may result secondary to bleeding from the ruptured tube into the peritoneal cavity. 4. Sickle cell disease has not been associated with hyperamylasemia. However, the incidence of pigment gallstones is increased in patients with sickle cell disease, and passage of a common~uct stone with resultant pancreatitis may mimic or precipitate a painful sickle cell crisis. 5. Pneumococcal pneumonia has not been associated with hyperamylasemia; however, a basilar pneumonia of any origin may irritate the contiguous diaphragm, causing referred abdominal pain. In addition, a "reflex" ileus may occur in acute chest disease. 1he chest film shows elevation of the left leaf of the diaphragm with basilar atelectasis. No mass or infiltrates are present. Question: The patient is thought to have pancreatitis. Which of the following aspects of the history should be explored further? I. Alcohol abuse 2. Hepatobiliary tract disease 3. Abdominal trauma 4. Intake of drugs Answer: 1,2,3,4


I. Alcohol abuse is the major cations ofany kind. cause of acute pancreatitis in the Question: Which of the following symptoms, signs, or laboratory findUnited States. 1he patient admits to drinking I ings might suggest the diagnosis of pint of liquor daily over the past 15 hemorrhagic pancreatitis? I. Hypovolemia and oliguria years. 2. Methemalbuminemia 2. Choledocholithiasis is the sec3. Decreased serum calcium level ond leading cause of acute pancre4. Ventilation-perfusion pulmonary atitis in the United States and the leading cause in Great Britain. Ob- abnormalities struction of the pancreatic duct by a Answer: I,2,3,4 I. Hemorrhagic pancreatitis is asdistal common~uct stone (common sociated with hypovolemia and olichannel theory) is a presumed mechguria secondary to the exudation of anism. plasma and to bleeding into the retPancreatitis associated with roperitoneal area. Additional fluid stones or pseudocysts is likely to present with an amylase level above loss occurs into distended loops of intestine as well as into the perito1,000 Somogyi units/dl. 1he patient has no history of bili- neal and pleural cavities. Fluid and ary tract disease. A plainfilm of the blood loss may lead to further abdomen shows no calcifications or hemoconcentration, with elevation of stones in the area of the gallbladder, the hematocrit, decreased tissue perbut it should be remembered that fusion, tissue hypoxia, and lactic acionly 15% of gallstones are radi- dosis. These losses may require correction with crystalloid and colloid opaque. 3. Blunt abdominal trauma is an solutions as well as continuous monioften overlooked cause of acute toring of cardiac preload with a cenpancreatitis.' A history of participa- tral venous or Swan-Ganz catheter. tion in contact sports or of abdomiThe ascites and pleural effusion nal injuries from impact of a steering that may occur in edematous wheel may be a clue to the correct di- pancreatitis are due to inflammation agnosis. of the serosal surfaces adjacent to 1he patient has no history of the pancreas. These effusions are ex- . trauma. udates rich in protein and have a 4. Many drugs are associated very high amylase content. In hemwith acute pancreatitis. Among the orrhagic pancreatitis a distinguishmore common are estrogens, ing feature is a hemorrhagic corticosteroids, isoniazid, indo- exudative ascites. In either edemamethacin, thiazides, azathioprine, tous or hemorrhagic pancreatitis, tetracycline, ethacrynic acid, and the ascites usually regresses with ressalicylazosulfapyridine.' olution of the acute stage. The patient denies the use ofmedi2. The hallmark of hemorrhagic


pancreatitis is hemorrhagic necrosis of the pancreas with bleeding into the retroperitoneal area. Extravasation into subcutaneous tissue may then create ecchymoses in the flanks (Grey Turner's sign) or periumbilical area (Cullen's sign) which ~re usually noted three to five days after the acute event. Reabsorption of these collections of extravascular blood causes methemalbuminemia, which may be detected in hemorrhagic pancreatitis but is not diagnostic. 3. The serum calcium level indicates the severity of pancreatitis. Hypocalcemia in acute pancreatitis may result from the precipitation of calcium salts in the necrotic pancreatic bed or from hormonal abnormalities (ie, the blunted response of parathyroid hormone release to a hypocalcemic stimulus), or both.2 This state requires the prompt intravenous administration of calcium to prevent hypocalcemic tetany, seizures, or disturbances in cardiac rhythm. Magnesium supplementation· may be necessary therapy for the alcoholic patient with magnesium depletion. 4. In severe pancreatitis, adult respiratory distress syndrome may occur secondary to damage to the pulmonary capillary membrane, with exudation of fluid causing noncardiac pulmonary edema. 3 This syndrome may be due to the effects of circulating toxins released by the necrotic pancreas. Mild pancreatitis may be associated with dyspnea and hypoxia due to atelectasis caused by

diaphragm splinting. 1he patient is given intravenous fluids with electrolyte replacement and nothing by mouth. No ascites is detected. Hematocrit value and serum calcium level remain stable. No acid-base disturbance or other markers of hemorrhagic pancreatitis are noted. Question: Which of the following laboratory measurements confirm the diagnosis of pancreatitis? 1. Serum lipase 2. Liver function studies 3. Two-hour urinary amylase 4. Amylase-creatinine clearance ratio (urine) 5. Serum calcium 6. Serum lipids

Answer: 1,3,4,6 I. An elevated serum amylase level is a nonspecific finding. In contrast, serum lipase level is elevated only with pancreatitis. The serum lipase level is found to be 9 Tietz-Somogyi units/ 100 m/ (normal 0 to 1.2). 2. Liver function tests will not confirm the diagnosis of pancreatitis, but abnormalities of liver function may have the same etiology as or may be a complication of acute pancreatitis, or both. Abnormal values may be seen with alcoholic pancreatitis and hepatotoxicity, drug-induced pancreatitis and hepatotoxicity (ie, from isoniazid), and acute pancreatitis secondary to choledocholithiasis. Acute pancreatitis may cause bile duct narrowing with cholestasis. Results of liver function tests are continued


Steven Kaplan Or Kaplan (pictured) is chief, gastrointestinal endoscopy unit, Mount Sinai Medical Center, Miami Beach. Or Bar kin is assistant professor of medicine, division of gastroenterology, University of Miami School of Medicine, and staff physician, Veterans Administration Hospital, Miami. Dr Rogers is professor of medicine, division of gastroenterology, University of Miami School of Medicine, and chief, division of gastroenterology, VA Hospital, Miami.



collection. Impaired renal function may result in mild elevation of serum amylase level (two or three times normal), while urine amylase concentration remains normal. 4. One of the most specific tests for diagnosis of acute pancreatitis is determination of the amylasecreatinine clearance ratio (A:C ratio), because renal clearance of amylase tends to be much greater than that of creatinine in acute pancreatitis.4-6 The ratio is determined by the measurement of a random urine specimen for amylase (Ua) and creatinine (Ucr) and the simultaneous determination of serum amylase (Sa) and creatinine (Scr>· The ratio is calculated using the following formula:


voltS. Ucr X vol/Scr

Figure 1. Ileus oftransverse colon (colon cutoff sign), a nonspecific finding in acute pancre-

atitis. Figures I, 3, and 4 courtesy Albert Weinfeld, M D. associate professor of radiology. University of Miami School of Medicine.

normal. 3. Serum amylase is filtered by the renal glomerulus and reabsorbed in the proximal renal tubule, so that only a fraction is found in urine. However, during acute pancreatitis a transient defect in proximal tubular reabsorptive capacity develops which allows a greater proportion of flltered amylase to be excreted in a timed urine






mination in the absence of renal insufficiency, or by a very low A:C ratio, which reflects this lack of flltration. In acute pancreatitis, an increase in pancreatic release of amylase is associated with an increase in renal excretion of amylase. The result is an A:C ratio usually above 5.5o/o. which allows pancreatitis to be distinguished from the other causes of hyperamylasemia. Measurement of the patient's spot urine and blood specimens yields the following values: urinary amylose 4,560 Somogyi units I dl, urinary creatinine 10 mgI dl. serum amylose 570 Somogyi units I dl, and serum creatinine 0.8 mg I dl. Using the formula for A:C ratio,

4,560 X 0.8 10 X 570

100 =

100 =A: C ratio

Because this formula takes into account the limitations of the glomerular filtering mechanism, the A:C ratio will be normal in renal failure despite the presence of hyperamylasemia. Macroamylasemia is an asymptomatic state of hyperamylasemia in which amylase is complexed to IgG (and lgA) into macromolecules which exceed the "pore size" of the glomerulus and, therefore, are not flltered.1.s This laboratory curiosity can be diagnosed by a normal finding on two-hour urinary amylase deter-


lOO: 6.4~


1his ratio is consistent with acute pancreatitis. 5. Elevated calcium levels do not confirm the presence of acute pancreatitis, but hypercalcemia from any cause may be a predisposing factor. Conversely, serum calcium level may be low with severe pancreatitis. 6. Hyperlipoproteinemia may be the cause or result of pancreatitis. Types I and V may cause pancreatitis with onset often in early adulthood. Hyperchylomicronemia occurs in both types. Type IV hyperlipoproteinemia with elevated triglyceride and cholesterol levels may result from acute pancreatitis and regress with resolu-


tion of the acute event. It is important to remember that profound hyperlipidemia may inhibit serum amylase activity. Thus, measurement by routine laboratory methods may not detect an elevated level. 7 Serial dilutions of the serum allow accurate determination of serum amylase level. The serum of this patient is not /ipemic. Question: An appropriate therapeutic regimen would include which of the following? I. Regular diet 2. Nothing by mouth; intravenous fluid administration 3. Nasogastric intubation with suction and administration of intravenous fluid 4. Antibiotic coverage 5. Administration of anticholinergics Answer: 2,3(maybe) I. The pancreas must be kept at rest to allow resolution of the inflammatory process. Oral feeding has several stimulatory effects on the pancreas. Protein ingestion and distention of the stomach stimulate acid production. Upon entering the duodenum, acid releases secretin, which in turn stimulates pancreatic production of water and bicarbonate. Chyme stimulates the duodenum to produce pancreozymin, which stimulates pancreatic enzyme production. Feeding may therefore perpetuate the symptoms and prolong the course of pancreatitis. 2. Patients must be parenterally hydrated and given nothing by

mouth. Careful attention to fluid and electrolyte balance is required to avoid the metabolic derangements resulting from volume sequestration, with occasional lactic acidosis or superimposed renal failure. Fluid and electrolyte balance is best maintained when central venous pressure is monitored so that adjustments can be made as necessary. 3. Indications for the use of nasogastric intubation with suction include nausea and vomiting not responsive to parenteral antiemetics, ileus (evidenced by absence of bowel sounds and air- and fluid-filled loops of bowel), and abdominal distention.s 4. Antibiotic use should be limited to situations where sepsis is suspected clinically, such as choledocholithiasis with cholangitis and pancreatitis, or where the patient's deteriorating condition leads to suspicion of pancreatic abscess or an infected pseudocyst. In addition to antibiotic coverage, surgical intervention is often required to treat these complications. 5. The efficacy of anticholinergics in reducing pancreatic secretion remains in doubt. Their use may be accompanied by gastric or urinary retention, tachycardia, or prolongation of intestinal ileus, which may increase the morbidity and prolong hospitalization. Question: Which of the following radiographic studies could be of diagnostic value? I. Chest and plain abdominal


Fipre 2. Extraintestinal air bubbles in area of pancreas, a finding compatible with pancreatic

abscess. Courtesy Robert Feltman. MD. chiefofradio/ogy, Cedars of Lebanon Hospital, Miami.

films 2. Upper gastrointestinal series 3. Oral cholecystogram 4. Intravenous cholangiogram Answer: 1,2.3,4(maybe) I. Although the chest film may be normal in acute pancreatitis, it may show a reflex pleural effusion (usually on the left) as well as elevation of the left leaf of the diaphragm, possibly with the presence of basilar ateleccontinued



Figure 3. Large mass depressing ligament of Treitz to right :1nd down (lower arrow). Stomach is displaoed and indented (top arrows).

tasis secondary to splinting. The abdominal roentgenogram may show several indirect signs, including: the so-called sentinel loop, a localized ileus of a loop of small bowel in the left upper quadrant; the colon cutoff sign, a segmental colonic ileus with absence of gas distal to the splenic flexure (figure l); calcifications in the bed of the pancreas; calculi in the biliary or renal system; absence of psoas shadows; and the soap-bubble sign, a localized collection of extraintestinal


air bubbles in the pancreatic area (figure 2), which is strong evidence for pancreatic abscess. 2. Enlargement of the pancreas by inflammation, pseudocyst, or a mass may be reflected in an upper gastrointestinal series by enlargement or widening of the duodenal loop, downward displacement of the ligament of Treitz (normal location at level of duodenal bulb), anterolateral displacement of the stomach, and downward displacement of the transverse colon (figure 3). An upper gastrointestinal series reveals edematous folds and spiculation of the barium along the entire duodenal sweep (figure 4). 3. An oral cholecystogram should be obtained in all patients with acute pancreatitis, because cholelithiasis is a curable cause. Failure to visualize the gallbladder in the presence of acute pancreatitis does not indicate gallbladder disease but requires repeat examination in one month.9 Nonvisualization at that time would indicate gallbladder disease, assuming normal hepatic function. 4. An intravenous cholangiogram is indicated if choledocholithiasis is suspected clinically. It is valuable only if clear visualization of the extrahepatic ducts is obtained. Nonvisualization of a normal biliary tree may occur in the presence of acute pancreatitis, and delayed films or repeat examination in one week may be needed.9 An oral cholecystogram performed prior to the upper gastrointestinal series shows opacification of

a normal gallbladder. The patient continues to improve clinically. with amylase level returning to baseline, and is discharged without medication ten days after admission. Six months later she returns to the emergency room with acute pain in the left upper quadrant associated with nausea and diaphoresis. She admits to continued alcohol consumption. On examination she is lying with her knees drawn to her chest and appears to be in moderate distress. Pulse is 120/min and regular, blood pressure 130/90 mm Hg, respiration 20/min. and temperature 101 F. Pertinent physical findings are abdominal distention with hypoactive bowel sounds without rushes or tinkles; no fluid wave is detected. The epigastrium is tender to palpation, and a rounded fullness extends from the epigastrium to the left upper quadrant. Laboratory tests give the following values: hematocrit 42%. WBCs 12,500/cu mm with a left shift. and serum amylase 650 Somogyi unitsfdl. A plain abdominal film discloses an ileus pattern without extraluminal gas. The presumptive diagnosis is recurrent pancreatitis, and therapy is instituted. The patient becomes afebri/e on the second hospital day, and abdominal pain decreases over a week's time. However, palpation of the abdomen continues to elicit epigastric tenderness with a suggestion of fullness in the left upper quadrant. Laboratory data show a


persistent elevation of serum amylase and A:C ratio. Question: At this time which of the following studies would be appropriate? I. Upper gastrointestinal series 2. Pancreatic sonography 3. Endoscopic retrograde pancreatography 4. Gallium scan Answer: 1,2 I. See previous question, answer 2. An upper gastrointestinal series discloses a widened duodenal loop with inferior displacement of the ligament of Treitz. The stomach and upper jejunum are displaced anteriorly and laterally. A hazy density in the midabdomen suggests pseudocyst formation. No pancreatic calcifications are seen. 2. Pseudocyst formation following acute pancreatitis can result in persistent abdominal pain and hyperamylasemia. Ultrasound scanning can detect abdominal masses of ~ cm or more and can determine whether they are solid or cystic. It cannot, however, differentiate a solid tumor with central necrosis from a cystic mass filled with amorphous debris, such as a pancreatic phlegmon. A pancreatic sonogram reveals a 6x8-cm cystic structure in the body of the pancreas (figure 5) 3. Endoscopic retrograde pancreatography should not be attempted in the presence of acute pancreatitis or of a pseudocyst. The injection of contrast material into the pancreatic

duct may cause a recrudescence of pancreatitis, and fllling of a pseudocyst with nonsterile contrast material may result in infection and abscess formation.1o 4. Gallium scanning is useful only if a pancreatic abscess is suspected. Gallium is localized to areas of infection or to lymphoma, hepatoma, and uncommonly a few other solid carcinomas but not to uncomplicated pancreatic pseudocysts. · Question: Which course of treatment would be more appropriate at this time? I. Immediate surgical drainage of the pseudocyst 2. Hyperalimentation for four to six weeks and repeat sonography

Answer: 2 I. Acute pseudocysts are thinwalled collections of exudate and debris in the pancreatic bed. Unless sepsis suggests infection and abscess formation, the status of the pseudocyst over four to six weeks should be checked with sonography. Acute pseudocysts may resolve over this period or may ripen into mature, fibrotic, thick-walled lesions which after six weeks should be surgically drained because of possible complications. 2. Hyperalimentation is indicated for nutritional support as well as possibly to rest the pancreas and allow for repair. An argument favoring total parenteral hyperalimentation is that oral feeding of a protein and carbohydrate hydrolysate may cause significant pancreatic stimulation. The advantage of oral hyperalimentation is that there


Figure 4. Swelling of head ot pancreas, edema of mucosal folds, and indentation of duodenal loop (left arrows) with depression ofligament of Treitz (right arrow), fmdings indicative of acute pancreatitis.

is no need for a large-bore central venous catheter for long periods and, therefore, no risk of sepsis. Good controlled studies have not been performed to compare these alternatives. However, in view of the comparative risks, an initial trial with oral hyperalimentation seems appropriate. Oral hyperalimentation is attempted but is tolerated poorly because of continued postprandial pain. Total paremeral hyperalimentation for six weeks results in continued



resolution of all abdominal pain. Findings on repeat sonography are unchanged. Question: The complications of pancreatic pseudocysts include which of the following? I. Gastrointestinal or intraperitoneal bleeding 2. Infection 3. Ascites Answer: 1,2,3 I. Pancreatic pseudocysts may erode into surrounding structures, including any hollow viscus or vascular structure. This may result in intraluminal or intraperitoneal bleeding. 2. A pseudocyst may become infected spontaneously, after endoscopic retrograde pancreatography, or following erosion into a hollow viscus (eg, the colon) with significant bacterial colonization. 3. Pseudocysts may rupture or leak, allowing fluid with a high amylase content either to accumulate in the peritoneal cavity, eventuating in chronic pancreatic exudative ascites, or to leak through fistula tracts into the mediastinum or pleural spaces. Elective cyst decompression with routine cystogastrostomy is performed. 1he postoperative course is uncomplicated, and the patient is discharged from the hospital without medication. Address reprint requests to Jamie S. Barkin, MD, Division of Gastroenterology, PO Box 520875, Biscayne Annex, Miami, FL 33152. Series coordinator for hypothetical cases referable to gastroenterology: Dr Rogers.


Figure 5. Pancreatic sonogram showing large pancreatic pseudocyst (Pc), edema of body of pancreas (P), and liver (H).

Courtesy Stuart Goulieb, MD, assistant professorofradiology, UniversityofMiDmiSchool of Medicine.

References I. Salt WB 11, Schenker S: Amylase-Its clinical significance: A review of the literature. Medicine (Baltimore) 55:269-289, 1976 2. Robertson GM Jr, Moore EW, Switz DM, et al: Inadequate parathyroid response in acute pancreatitis. N Engl J Med 294:512-516, 1976 3. Interiano B, Stuard ID, Hyde RW: Acute respiratory distress syndrome in pancreatitis. Ann Intern Med 77:923-926, 1972 4. Johnson SG, Ellis C, Spring B, et al: Mechanism of elevated renal clearance of amylase: Clearance of creatinine in acute pancreatitis. (Abstr) Clin Res 24:433A, 1976 5. Warshaw AL, Fuller AF Jr: Specificity of increased renal clearance of amylase in diagnosis of acute pancreatitis. N Engl J Med 292:325-328, 1975 6. Dreiling DA, Leichtling JJ, Janowitz





HD: The amylase-creatinine clearance ratio: Diagnostic parameter of physiologic phenomenon? Am J Gastroenterol 61:290-296, 1974 Lesser PB, Warshaw AL: Diagnosis of pancreatitis masked by hyperlipemia. Ann Intern Med 82:795-798, 1975 Levant JA, Secrist DM; Resin H, et al: Nasopstric suction in the treatment of alcoholic pancreatitis: A controlled study. JAMA 229:51-52, 1974 Kaden VG, Howard JM, Doubleday LC: Cholecystographic studies during and immediately following acute pancreatitis. Surgery 38:1082, 1955 Bilbao MK, Dotter CT, Lee TG, et al: Complications of endoscopic retrograde cholangiopancreatography (ECRP): A study of 10,000 cases. Gastroenterology 70:314-320, 1976


Acute pancreatitis.

Postgraduate Medicine ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: Acute pancreatitis Steven K...
4MB Sizes 0 Downloads 0 Views