CASE REPORT
P a n c r e a t i c Ascites A Case Report and Review of the Literature Jose N. Munoz, MD, and Shyamal Bose, MD
M a s s i v e ascites in a c h r o n i c a l c o h o l i c p a t i e n t is u s u a l l y a t t r i b u t e d to h e p a t i c c i r r h o s i s (1) b u t the
association
chronic
between
pancreatitis,
massive although
ascites
and
extremely
r a r e (2, 3), is b e i n g r e c o g n i z e d w i t h i n c r e a s i n g f r e q u e n c y (4). L e a k a g e o f p a n c r e a t i c s e c r e t i o n s into t h e p e r i t o n e a l c a v i t y is c o n s i d e r e d t h e m a j o r etiologic f a c t o r in t h e p a t h o g e n e s i s o f ascites (5, 6). D i a g n o s i s is b a s e d o n d e m o n s t r a t i o n o f e l e v a t e d a m o u n t s of p a n c r e a t i c a m y l a s e a n d l i p a s e in b o t h s e r u m a n d ascitic fluid (6). Establishment
of
the
diagnosis
and
differ-
e n t i a t i o n f r o m liver c i r r h o s i s , i n t r a a b d o m i n a l m a l i g n a h c y , o r t u b e r c u l o u s p e r i t o n i t i s is i m p o r t a n t b e c a u s e s u r g i c a l i n t e r v e n t i o n m a y o f t e n be t h e u l t i m a t e c u r a t i v e p r o c e d u r e (7). A case o f p a n c r e a t i c ascites is r e p o r t e d a n d t h e l i t e r a t u r e is r e v i e w e d .
CASE REPORT A 42-year-old black male chronic alcoholic was admitted to Mt. Sinai Hospital of Chicago for the sixth time on December 11, 1972, with the chief complaint of abdominal pain. The diagnoses on the previous admissions, all within the past 2 years, were acute pancreatitisl The family history was negative. He had been a heavy alcoholic for 15 years. The abdominal pain with which he presented started 3-4 weeks prior to admission and was characterized as mild, dull, and starting at the epigastric and periumbiiical regions with radiation to the back. The patient reported anorexia and a 30-1b weight loss in the past 14 weeks, accompanied by progressive abdominal dlstention. He denied fever, chills, From the Mount Sinai Hospital Medical Center, Chicago, Illinois. Address for reprint requests: Dr. Shyamal Bose, Mount Sinai Hospital Medical Center, California Avenue at 15 Street, Chicago, illinois 60608.
1178
light-colored stools, and dark-colored urine but he had had hematemesis and melena a year ago, during which time a duodenal ulcer was suspected on the upper-gastrointestinal series. Physical examination revealed a markedly cachectic male in acute distress. There was no jaundice or spider angiomata. The abdomen was markedly distended with ascitic fluid and there was guarding over the epigastrium and left upper quadrant. Bowel sounds were normoactive and no organs or masses were palpable. The rest of the physical examination was negative. The values for complete blood count, urinalysis, serum electrolytes, urea, sugar, bilirubin, calcium, and phosphorus were normal. Serum carotene and stool fat values were normal. SGOT was 33 and alkaline phosphatase was 278 MIU/dl (normal is up to 220). Serum albumin was 2.9 g/ dl and globulins were 4.5 g/dl. Initial serum amylase was 542 units/dl (normal is 30-150) and lipase was 4.9 units/dl (normal is up to 1). Subsequent pancreatic enzyme values in the serum, ascitic fluid, and urine are given in Table 1. Cox'rected BSP retention test and protime were normal. Plain films of the abdomen showed ascites without pancreatic calcification. The UGIS on this admission revealed an impression on the medifil border of the duodenal sweep suggestive of pancreatitis, in contrast to the UGIS done on a previous admission 6 months ago, which showed definite evidence of pancreatitis. The patient was ti'eated with intravenous fluids, nasogastric suction, analgesics, antacids, and vitamins for 7 weeks due to persistence of the abdominal pain and the serum amylase elevation. Abdominal paracentesis yielded a cloudy, yellowish-brown fluid with an amylase content of 1,765 units/dl and a protein content of 4.3 g/100 ml. No malignant cells or acid-fast bacilli were seen. Repeated paracentesis, diuretic therapy, and suctionsaline treatment were done in an attempt to control the ascites. Ascitic fluid amylase during the next 7 weeks ranged from 1,765 to 2,780 units/dl and the protein content ranged from 4.3 to 5.2 g/t00 ml. The serum amylase values during the same period ranged from 542 to 450 units/dl. A technetium colloid scan revealed borderline hepatomegaiy and a normal-size spleen. Superior mesenteric and celiac arteriograms revealed some widening of the gastrodundenal artery. No mass lesions were seen.
Digestive Diseases, Vol, 20, No. 12 (December 1975)
PANCREATIC ASCITES Table 1. Enzyme and Protein Values in a Patient with Pancreatic Asr Serum
Amylase Lipase Protein
Ascitic fluid
Urine
12112
1128
213 (Postop)
12/12
1/28
12/12
1/28
542 4.9 7.4
450 1.8 7.5
220 1.6 7.8
1768 40 4.3
2780 51 5.2
428Q ---
8240 ---
Exploratory laparotomy was performed on January 31, 1973, because of persistent ascites and a downhill clinical course. Three liters of yellowish-brown fluid was aspirated. The liver was smooth and slightly enlarged without obvious evidence of cirrhosis. The spleen, gallbladder, common bile duct, and the rest of the gastrointestinal tract v4ere normal. The peritoneum showed areas of adhesions and fat necrosis. Several enlarged mesenteric lymph nodes were seen. Biopsies of the liver, peritoneum, and mesenteric lymph nodes were obtained. The region of the head of the pancreas was occupied by a firm and lumpy mass, which was adherent to the posterior surface of the gastric antrum with marked inflammatory reaction. The body and tail of the pancreas were edematous, inflamed, and surrounded with patchy areas of fat necrosis. No pseudocyst was discernible on gross inspection. Exploratory needle aspiration of the mass in the pancreatic head and attempts at a transduodenal pancreatic biopsy and an operative pancreatogram were unsuccessful. Further attempts were not made because of the marked necrosis and edema of the pancreas. Histologic examination of the respective specimens revealed acute and chronic capsular and subcapsular inflammation of the liver, mesenteric fat necrosis, lymphoid hyperplasia, and fibroplastie peritonitis. The postoperative course was uneventful and the serum amylase value fell on the 3rd postoperative day. The patient was discharged on February 14, 1973, and since then has had no recurrence of ascites. On a 2-year follow-up, the patient had no evidence of progressive pancreatic disease or deficiency.
DISCUSSION
Massive ascites, although a rare complication of chronic pancreatitis, is increasingly being recognized and differentiated from alcoholic cirrhosis with ascites. T h e case reported here is s i m i l a r to m o s t of t h o s e d e s c r i b e d s i n c e 1953 (8), to the 3 cases reported by H a r t l e y et Digestive Diseases, Vol. 20, No. 12 (December 1975)
al in 1967 (9), to the 34 cases reviewed and reported by Schindler et al in 1970 (2, 4-6, 8, 1 0 17), and to the cases reported by Pacifico et al in 1971 (2, 4, 5, 7, 8, 10-14, 18, 19), b y Akers et al in 1972 (20), by B a r a k a t et al in 1972 (21), by Smith et al in 1973 (22), by D o n o w i t z et al in 1974(23), and by K a l w i n s k y et al in 1974 (24). T h e patient is usually a y o u n g male between the ages of 30 and 50, the average age being 37, with the youngest patient reported aged 4 m o n t h s (9) and the oldest case reported aged 57 (16). In adults , a history of chronic alcoholism is usually present (78% of the patients reviewed by Smith e t a l ) (22) and the patient usually experiences repeated episodes of abd o m i n a l pain, compatible with attacks of p a n creatitis, which tend to subside with the onset of ascites (2, 3, 6, 8, 10, 12), whereas in children the most c o m m o n etiologic factor is t r a u m a (9). Very rarely, biliary or pancreatic duct malform a t i o n (20) or a n intraductal stone m a y be the causative factor. (See T a b l e 2.) T h e OUtstanding clinical features are the massive, chronic, painless, and rapidly progressive ascites, often refractory to diuretics, and the profound weight loss with m a r k e d wasting of the muscles of the shoulder girdle and extremities (7), all of which this patient had. Additional features reported include subcutaneous fat necrosis a p p e a r i n g as erythema n o d o s u m like skin lesions, systolic hypertension, and thrombophlebitis (23). T h e diagnosis of pancreatic ascites, once considered, is not hard to establish with the d e m o n 1179
MUNOZ & BOSE
stration of the triad of elevated serum amylase levels, elevated ascitic fluid amylase levels, ranging from 328 Somogyi units to 160,000 Somogyi units in the reported cases (6, 8, 1316, 22-24); and an elevated ascitic fluid protein value ranging from 2.0 to 6.2 g/100 ml, with an average value of 3.5 g/100 ml (6). Large numbers of red and white blood cells, predominantly polymorphonuclears, are us.ually present and occasionally the fluid may appear hemorrhagic. Serum amylase values are usually much lower than the ascitic fluid content; this may be due to rapid urinary amylase excretion (25) and to the fact that intraperitoneal amylase does not traverse the capillary bed as readily as the pancreatic portal of entry (26). Radiographic studies may suggest the presence of a pancreatic mass. Pancreatic calcifications, if present, may suggest that the pancreas is the source of the ascites but this is not a frequent finding (27). The clinical picture of pancreatic ascites, as in our patient, has to be differentiated from cirrhosis, tuberculous peritonitis, and intraabdominal malignancy. Although a history of alcoholism is usually present, jaundice is not a significant finding, there are no signs of chronic liver disease, and liver function tests are minimally abnormal except for the serum albumin test. When pancreatic ascites and cirrhosis can be logically assumed to coexist--and, in fact, one-third of patients with cirrhosis have chronic pancreatitis at autopsy(28)--the significant. elevation of amylase and lipase and the higher protein content of the fluid in pancreatic ascites easily differentiates it from the transudate of cirrhosis. Thus, it has been suggested that a routine amylase test should be performed on all patients with ascites because an ascitic fluid amylase value of over 60Somogyi units is highly indicative of primary pancreatic disease (29). Tuberculous peritonitis should be ruled out by peritoneal fluid cultures and intraabdominal malignancy should be ruled out by appropriate tests. Adjunct studies include radiographic studies of the chest, which may show pleural effusion (30), and of the gastrointestinal tract, 1180
Table 2. Etiology of Pancreatic Disease in 55 Cases of Pancreatic Ascites Pediatric cases ( N )
Adult
cases (N) Cause
Male
Female
Male
Female
Alcohol
29
12
--
--
Trauma
1
1
--
3
Pancreatic
duct
duplication
--
--
1
1
Stenosis of sphincter
of
Oddi Carcinoma
1
--
--
--
1
--
--
--
Unknown
1
1
1
2
which may suggest the presence of a pancreatic mass. The value of the more recent adjunct procedures, such as celiac and superior mesenteric angiography and ultrasonography to delineate pseudocysts (31) and retrograde cholangiopancreatography preoperatively to determine the site of ductal rupture, needs further evaluation. Many mechanisms of the etiology of ascites have been postulated for example, chronic peritoneal irritation and blocked abdominal lymphatics, suggested by Gambill et al (10) and by Schmidt and Whitehead (5), and peritoneal exudation secondary to chronic irritation by pancreatic enzymes, suggested by Barua et al (2). Cirrhosis and portal hypertension with or without portal vein compression do not seem to be important factors. Disruption of the pancreatic duct system in chronic pancreatitis or by abdominal trauma (18) seems to be the primary etiologic event, followed usually by pseudocyst formation to contain the leak. Escape of the enzyme-rich exocrine secretions with resultant chemical peritonitis and protein exudation may then occur as a result of leakage from a pseudocyst, an internal pancreatic fistula (4, 7), or a direct pancreatic perforation into the retroperitoneal space. An operative pancreatogram reveals the site of communication by showing Digestive Diseases, Vol. 20, No, 12 ( D e c e m b e r 197~;)
PANCREATIC ASCITES
Table 3. Pathological Findings in 55 Cases of Pancreatic Ascites Pancreatic pathology Pancreatic pseudocyst Chronic pancreatitis Documented duct disruption No documented duct disruption Inflammatory mass with pancreatic duct duplication Acute hemorrhagic pancreatitis Subacute pancreatitis with small cyst Unknown or unstated Total
Cases (N) 32 12 7 of 12 5 of 12 2 1 1 7 55
the passage of contrast material. Of 55 cases reported in the literature (1-34), a pseudocyst was found in 32 cases; 12 patients had chronic pancreatitis only and 7 of these 12 had demonstrable duct disruption. In some cases, however, obvious escape of pancreatic secretions could not be demonstrated; these could well represent spontaneous resealing of the ductal leakage as inflammation subsided with time and with abstinence from alcohol. (See Table 3.) The treatment of choice for pancreatic ascites needs to be clarified_ Since spontaneous resolution does occur in a significant number of cases, for example, Patient 8 in the series of Cameron et al (4) and Patients 3 and 5 in the series of Donowitz et al (23), a conservative medical regimen of prolonged suction-saline treatment, diuretic therapy, salt restriction, and oral or parenteral hyperalimentation should be tried, usually for an 8-week period. When clinical deterioration occurs, as in our patient, or when the patient does not respond to the medical regimen, requires repeated paracentesis, and develops rapid fluid accumulation and excessive weight loss, surgical intervention is then clearly indicated because it enables not only confirmation of the diagnosis but also the repair of a ruptured pancreatic duct; the excision or internal drainage of a pseudoeyst (4, 6) by cystogastrosDigestive Diseases, Vol. 20, No. 12 (December 1975)
tomy or Roux-en-Y cystojejunostomy (current evidence suggesting a defunctionalized Rouxen-Y jejunostomy as the technique of choice) (22); and sphincterotomy if there is fibrosis of the sphincter of Oddi (32). Operative panereatograms, if possible, should be obtained when ductal perforation is suspected or if no obvious pseudocyst is present (33). If the pancreatic duct leak cannot be identified, a Duval or Puestow duct drainage should be performed. Pancreatic irradiation has also been tried when surgery was inadvisable or impossible (34). Preoperatively, celiac and superior mesenteric arteriograms and ultrasonography may help delineate small pseudocysts and/or differentiate true pseudocysts from inflammatory peripancreatic masses. Permanent relief of the ascites and improvement in health usually follow surgery, except after external drainage, which has not been consistently beneficial. In 5 of 7 patients (as in our patient), ascites did not recur after peritoneoscopy or laparotomy, presumably because the irritant pancreatic secretions were removed from the peritoneal cavity. More rarely, duct leakage may spontaneously seal off as the pancreatitis subsides and ascites may resolve without drainage. Abstinence from alcohol and good nutrition influence the prognosis of the disease.
SUMMARY A case of pancreatic ascites is reported and compared with 55 previously reported cases. A 42-year-old black male chronic alcoholic presenting with abdominal pain was found at operation to have chronic pancreatitis with no pseudocyst formation or overt duct disruption, in contrast to the majority of cases reported. The diagnosis and differentiation from cirrhosis of the liver were based on the operative findings, elevated serum amylase level, ascitic fluid amylase value, and protein content. Surgical exploration alone has proven beneficial--the patient has done well in the past 2 years with no recurrence of the ascites and continued weight 1181
MUNOZ & BOSE
gain. T h e clinical course was compatible with pancreatitis although the radiographic and angiographic studies were not diagnostic. It is suggested that the clinical entity of pancreatic ascites occurs more often than reported and a workup for it should be done even in the face of unconvincing radiographic and angiographic evidence.
REFERENCES
1. Patek A J: Portal cirrhosis (Laennec's cirrhosis). Diseases of the Liver, 2nd Ed. L Schiff (ed). Philadelphia, JB Lippincott Company, 1963, pp 2. Barua RL, Villa F, Steigmann F: Massive ascites due to pancreatitis. Am J Dig Dis 7:900906, 1962 3. Cameron JL, Anderson RR, Zuidema GD: Pancreatic ascites. Surg Gynecol Obstet 125:328-332, 1967 4. Cameron JL, Brawley RK, Bender HW, Zuidema GD: The treatment of pancreatic ascites. Ann Surg 170:668-676, 1969 5. Schmidt EH, Whitehead RP: Recurrent ascites as an unusual complication of chronic pancreatitis. J A M A 180:533, 1962 6. Schindler SC, Schaefer JW, Hull D, Griffin J r WO: Chronic pancreatic aseites. Gastroenterology 59:453-459, 1970 7. Paeifico AD, Russell J r EM, Diethelm AG: Pancreatic ascites associated with an internal pancreatic fistula: Case report and review of the literature. Am Surg 37:331-334, 1971 8. Smith EB: Hemorrhagic ascites and hemothorax associated with benign pancreatic disease. Arch Surg (Chicago) 67:52-56, 1953 9. Hartley RC: Pancreatitis under the age of 5 years: A report of three cases. J Pediatr Surg 2:419-423, 1967 10. Gambill EE, Waiters W, Scanlon PW: Chronic relapsing pancreatitis and extensive subacute peritonitis and chronic, recurrent massive "chylous ascites". Am J Med 28:668-670, 1960 11. Burrows L, Poll MD: Unusual problems in surgery. J Mt. Sinai Hosp NY 33:396.-403, 1966 12. MacLaren IF, Howard JM, Jordan GL: Ascites associated with pseudocyst of the pancreas. 1182
Arch Surg (Chicago) 93:301-303, 1966 13. Jensen NM, Babior BM: Ascites due to chronic pancreatitis. J A M A 201:488-489, 1967 14. Parrish RA, Humphries AL, Moretz WA: Massive pancreatic ascites. Arch Surg (Chicago) 96:887-891, 1968 15. Rosenberg IK, Kahn JA, Walt AJ: Surgical experience with pancreatic pseudoeysts. An J Surg 117:11-17, 1969 16. Lazaro E J, Das PB, Abraham PV: Pancreatic ascites. Am J Gasteroenterol 51:287-292, 1969 17. Wagner RB, Tolins SH: Pancreatic ascites. J Mt. Sinai Hosp NY 36:216-219, 1969 18. Hardy JD, Bowlin JW: Some complications of pancreatic disease: Illustrative cases with notes in management. Ann Surg 145:848, 1957 19. Elmslie RG: Complications of acute non-traumatic panereatitis. Med J Aust 2:895, 1968 20. Akers DR, Favara BC, Franciosi RA, Nelson JM: Duplication of the alimentary tract: Report of three unusual cases associated with bile and pancreatic ducts. Surgery 71:817-823, 1972 21. Barakat M, Raj GK, Hirsh T: Pancreatic ascites: Rupture of pancreatic duct in a patient with chronic pancreatitis. South Med J 65:1377-1379, 1972 22. Smith III RB, Warren WD, Rivard J r AA, Amerson JR: Pancreatic ascites: Diagnosis and management with particular reference to surgical techniques. Ann Surg 177:538-546, 1973 23. Donowitz M, Kerstein MD, Spiro HM: Pancreatic ascites. Medicine 53:183-195, 1974 24. Kalwinsky D, Frittelli G, Oski FA: Pancreatitis presenting as unexplained ascites. Am J Dis Child 28:734-736, 1974 25. Mulhausen RD, Brown C, Onstad G: Renal clearance of amylase during panereatitis. Metab Clin Exp 18:669, 1969 26. Keith LM, Zollinger RM, McCleery RS: Peritoneal fluid amylase as an aid in the diagnosis of acute pancreatitis. Arch Surg 61:930, 1950 27. Tucker PC, Webster PD: Traumatic pseudocysts of the pancreas. Arch Intern Med 129:583586, 1972 28. Twiss JR, Oppenheim E: Liver, Pancreas and Biliary Tract. PhiladelPhia, Lea and Febiger, 1955, p 498 29. Ende N: Amylase activity in body fluids. Cancer 14:1109-1114, 1961 30. Kaiser MH, Roth JLA, Bockus HL: Relapsing Digestive Diseases, VoL 20, No, 12 (December 1975)
PANCREATIC ASCITES
pancreatitis with pseudocyst of the pancreas and enzyme containing pleural effusion. Gastroenterology 28:842-850, 1955 31. Ferruci Jr JT, Eaton JB: Radiology of the pancreas. N Engl J Med 288:506-510, 1973 32. Mallet-Guy P: The place of sphincterotomy in the treatment of diseases of the pancreas. J R
Digestive Diseases, Vol. 20, No. 12 (December 1975)
Coil Surg Edinburgh 12:318-325, 1967 33. Keddie N, Nordi GL: Pancreatography: A safe and effective technique. Am J Surg 110:863865,'1965 34. Kavin H, Sobel SD, Dembo AJ: Pancreatic ascites treated by irradiation of the pancreas. Br Med J 2:503-504, 1971
1183
P a n c r e a t i c Ascites A Case Report and Review of the Literature Jose N. Munoz, MD, and Shyamal Bose, MD
M a s s i v e ascites in a c h r o n i c a l c o h o l i c p a t i e n t is u s u a l l y a t t r i b u t e d to h e p a t i c c i r r h o s i s (1) b u t the
association
chronic
between
pancreatitis,
massive although
ascites
and
extremely
r a r e (2, 3), is b e i n g r e c o g n i z e d w i t h i n c r e a s i n g f r e q u e n c y (4). L e a k a g e o f p a n c r e a t i c s e c r e t i o n s into t h e p e r i t o n e a l c a v i t y is c o n s i d e r e d t h e m a j o r etiologic f a c t o r in t h e p a t h o g e n e s i s o f ascites (5, 6). D i a g n o s i s is b a s e d o n d e m o n s t r a t i o n o f e l e v a t e d a m o u n t s of p a n c r e a t i c a m y l a s e a n d l i p a s e in b o t h s e r u m a n d ascitic fluid (6). Establishment
of
the
diagnosis
and
differ-
e n t i a t i o n f r o m liver c i r r h o s i s , i n t r a a b d o m i n a l m a l i g n a h c y , o r t u b e r c u l o u s p e r i t o n i t i s is i m p o r t a n t b e c a u s e s u r g i c a l i n t e r v e n t i o n m a y o f t e n be t h e u l t i m a t e c u r a t i v e p r o c e d u r e (7). A case o f p a n c r e a t i c ascites is r e p o r t e d a n d t h e l i t e r a t u r e is r e v i e w e d .
CASE REPORT A 42-year-old black male chronic alcoholic was admitted to Mt. Sinai Hospital of Chicago for the sixth time on December 11, 1972, with the chief complaint of abdominal pain. The diagnoses on the previous admissions, all within the past 2 years, were acute pancreatitisl The family history was negative. He had been a heavy alcoholic for 15 years. The abdominal pain with which he presented started 3-4 weeks prior to admission and was characterized as mild, dull, and starting at the epigastric and periumbiiical regions with radiation to the back. The patient reported anorexia and a 30-1b weight loss in the past 14 weeks, accompanied by progressive abdominal dlstention. He denied fever, chills, From the Mount Sinai Hospital Medical Center, Chicago, Illinois. Address for reprint requests: Dr. Shyamal Bose, Mount Sinai Hospital Medical Center, California Avenue at 15 Street, Chicago, illinois 60608.
1178
light-colored stools, and dark-colored urine but he had had hematemesis and melena a year ago, during which time a duodenal ulcer was suspected on the upper-gastrointestinal series. Physical examination revealed a markedly cachectic male in acute distress. There was no jaundice or spider angiomata. The abdomen was markedly distended with ascitic fluid and there was guarding over the epigastrium and left upper quadrant. Bowel sounds were normoactive and no organs or masses were palpable. The rest of the physical examination was negative. The values for complete blood count, urinalysis, serum electrolytes, urea, sugar, bilirubin, calcium, and phosphorus were normal. Serum carotene and stool fat values were normal. SGOT was 33 and alkaline phosphatase was 278 MIU/dl (normal is up to 220). Serum albumin was 2.9 g/ dl and globulins were 4.5 g/dl. Initial serum amylase was 542 units/dl (normal is 30-150) and lipase was 4.9 units/dl (normal is up to 1). Subsequent pancreatic enzyme values in the serum, ascitic fluid, and urine are given in Table 1. Cox'rected BSP retention test and protime were normal. Plain films of the abdomen showed ascites without pancreatic calcification. The UGIS on this admission revealed an impression on the medifil border of the duodenal sweep suggestive of pancreatitis, in contrast to the UGIS done on a previous admission 6 months ago, which showed definite evidence of pancreatitis. The patient was ti'eated with intravenous fluids, nasogastric suction, analgesics, antacids, and vitamins for 7 weeks due to persistence of the abdominal pain and the serum amylase elevation. Abdominal paracentesis yielded a cloudy, yellowish-brown fluid with an amylase content of 1,765 units/dl and a protein content of 4.3 g/100 ml. No malignant cells or acid-fast bacilli were seen. Repeated paracentesis, diuretic therapy, and suctionsaline treatment were done in an attempt to control the ascites. Ascitic fluid amylase during the next 7 weeks ranged from 1,765 to 2,780 units/dl and the protein content ranged from 4.3 to 5.2 g/t00 ml. The serum amylase values during the same period ranged from 542 to 450 units/dl. A technetium colloid scan revealed borderline hepatomegaiy and a normal-size spleen. Superior mesenteric and celiac arteriograms revealed some widening of the gastrodundenal artery. No mass lesions were seen.
Digestive Diseases, Vol, 20, No. 12 (December 1975)
PANCREATIC ASCITES Table 1. Enzyme and Protein Values in a Patient with Pancreatic Asr Serum
Amylase Lipase Protein
Ascitic fluid
Urine
12112
1128
213 (Postop)
12/12
1/28
12/12
1/28
542 4.9 7.4
450 1.8 7.5
220 1.6 7.8
1768 40 4.3
2780 51 5.2
428Q ---
8240 ---
Exploratory laparotomy was performed on January 31, 1973, because of persistent ascites and a downhill clinical course. Three liters of yellowish-brown fluid was aspirated. The liver was smooth and slightly enlarged without obvious evidence of cirrhosis. The spleen, gallbladder, common bile duct, and the rest of the gastrointestinal tract v4ere normal. The peritoneum showed areas of adhesions and fat necrosis. Several enlarged mesenteric lymph nodes were seen. Biopsies of the liver, peritoneum, and mesenteric lymph nodes were obtained. The region of the head of the pancreas was occupied by a firm and lumpy mass, which was adherent to the posterior surface of the gastric antrum with marked inflammatory reaction. The body and tail of the pancreas were edematous, inflamed, and surrounded with patchy areas of fat necrosis. No pseudocyst was discernible on gross inspection. Exploratory needle aspiration of the mass in the pancreatic head and attempts at a transduodenal pancreatic biopsy and an operative pancreatogram were unsuccessful. Further attempts were not made because of the marked necrosis and edema of the pancreas. Histologic examination of the respective specimens revealed acute and chronic capsular and subcapsular inflammation of the liver, mesenteric fat necrosis, lymphoid hyperplasia, and fibroplastie peritonitis. The postoperative course was uneventful and the serum amylase value fell on the 3rd postoperative day. The patient was discharged on February 14, 1973, and since then has had no recurrence of ascites. On a 2-year follow-up, the patient had no evidence of progressive pancreatic disease or deficiency.
DISCUSSION
Massive ascites, although a rare complication of chronic pancreatitis, is increasingly being recognized and differentiated from alcoholic cirrhosis with ascites. T h e case reported here is s i m i l a r to m o s t of t h o s e d e s c r i b e d s i n c e 1953 (8), to the 3 cases reported by H a r t l e y et Digestive Diseases, Vol. 20, No. 12 (December 1975)
al in 1967 (9), to the 34 cases reviewed and reported by Schindler et al in 1970 (2, 4-6, 8, 1 0 17), and to the cases reported by Pacifico et al in 1971 (2, 4, 5, 7, 8, 10-14, 18, 19), b y Akers et al in 1972 (20), by B a r a k a t et al in 1972 (21), by Smith et al in 1973 (22), by D o n o w i t z et al in 1974(23), and by K a l w i n s k y et al in 1974 (24). T h e patient is usually a y o u n g male between the ages of 30 and 50, the average age being 37, with the youngest patient reported aged 4 m o n t h s (9) and the oldest case reported aged 57 (16). In adults , a history of chronic alcoholism is usually present (78% of the patients reviewed by Smith e t a l ) (22) and the patient usually experiences repeated episodes of abd o m i n a l pain, compatible with attacks of p a n creatitis, which tend to subside with the onset of ascites (2, 3, 6, 8, 10, 12), whereas in children the most c o m m o n etiologic factor is t r a u m a (9). Very rarely, biliary or pancreatic duct malform a t i o n (20) or a n intraductal stone m a y be the causative factor. (See T a b l e 2.) T h e OUtstanding clinical features are the massive, chronic, painless, and rapidly progressive ascites, often refractory to diuretics, and the profound weight loss with m a r k e d wasting of the muscles of the shoulder girdle and extremities (7), all of which this patient had. Additional features reported include subcutaneous fat necrosis a p p e a r i n g as erythema n o d o s u m like skin lesions, systolic hypertension, and thrombophlebitis (23). T h e diagnosis of pancreatic ascites, once considered, is not hard to establish with the d e m o n 1179
MUNOZ & BOSE
stration of the triad of elevated serum amylase levels, elevated ascitic fluid amylase levels, ranging from 328 Somogyi units to 160,000 Somogyi units in the reported cases (6, 8, 1316, 22-24); and an elevated ascitic fluid protein value ranging from 2.0 to 6.2 g/100 ml, with an average value of 3.5 g/100 ml (6). Large numbers of red and white blood cells, predominantly polymorphonuclears, are us.ually present and occasionally the fluid may appear hemorrhagic. Serum amylase values are usually much lower than the ascitic fluid content; this may be due to rapid urinary amylase excretion (25) and to the fact that intraperitoneal amylase does not traverse the capillary bed as readily as the pancreatic portal of entry (26). Radiographic studies may suggest the presence of a pancreatic mass. Pancreatic calcifications, if present, may suggest that the pancreas is the source of the ascites but this is not a frequent finding (27). The clinical picture of pancreatic ascites, as in our patient, has to be differentiated from cirrhosis, tuberculous peritonitis, and intraabdominal malignancy. Although a history of alcoholism is usually present, jaundice is not a significant finding, there are no signs of chronic liver disease, and liver function tests are minimally abnormal except for the serum albumin test. When pancreatic ascites and cirrhosis can be logically assumed to coexist--and, in fact, one-third of patients with cirrhosis have chronic pancreatitis at autopsy(28)--the significant. elevation of amylase and lipase and the higher protein content of the fluid in pancreatic ascites easily differentiates it from the transudate of cirrhosis. Thus, it has been suggested that a routine amylase test should be performed on all patients with ascites because an ascitic fluid amylase value of over 60Somogyi units is highly indicative of primary pancreatic disease (29). Tuberculous peritonitis should be ruled out by peritoneal fluid cultures and intraabdominal malignancy should be ruled out by appropriate tests. Adjunct studies include radiographic studies of the chest, which may show pleural effusion (30), and of the gastrointestinal tract, 1180
Table 2. Etiology of Pancreatic Disease in 55 Cases of Pancreatic Ascites Pediatric cases ( N )
Adult
cases (N) Cause
Male
Female
Male
Female
Alcohol
29
12
--
--
Trauma
1
1
--
3
Pancreatic
duct
duplication
--
--
1
1
Stenosis of sphincter
of
Oddi Carcinoma
1
--
--
--
1
--
--
--
Unknown
1
1
1
2
which may suggest the presence of a pancreatic mass. The value of the more recent adjunct procedures, such as celiac and superior mesenteric angiography and ultrasonography to delineate pseudocysts (31) and retrograde cholangiopancreatography preoperatively to determine the site of ductal rupture, needs further evaluation. Many mechanisms of the etiology of ascites have been postulated for example, chronic peritoneal irritation and blocked abdominal lymphatics, suggested by Gambill et al (10) and by Schmidt and Whitehead (5), and peritoneal exudation secondary to chronic irritation by pancreatic enzymes, suggested by Barua et al (2). Cirrhosis and portal hypertension with or without portal vein compression do not seem to be important factors. Disruption of the pancreatic duct system in chronic pancreatitis or by abdominal trauma (18) seems to be the primary etiologic event, followed usually by pseudocyst formation to contain the leak. Escape of the enzyme-rich exocrine secretions with resultant chemical peritonitis and protein exudation may then occur as a result of leakage from a pseudocyst, an internal pancreatic fistula (4, 7), or a direct pancreatic perforation into the retroperitoneal space. An operative pancreatogram reveals the site of communication by showing Digestive Diseases, Vol. 20, No, 12 ( D e c e m b e r 197~;)
PANCREATIC ASCITES
Table 3. Pathological Findings in 55 Cases of Pancreatic Ascites Pancreatic pathology Pancreatic pseudocyst Chronic pancreatitis Documented duct disruption No documented duct disruption Inflammatory mass with pancreatic duct duplication Acute hemorrhagic pancreatitis Subacute pancreatitis with small cyst Unknown or unstated Total
Cases (N) 32 12 7 of 12 5 of 12 2 1 1 7 55
the passage of contrast material. Of 55 cases reported in the literature (1-34), a pseudocyst was found in 32 cases; 12 patients had chronic pancreatitis only and 7 of these 12 had demonstrable duct disruption. In some cases, however, obvious escape of pancreatic secretions could not be demonstrated; these could well represent spontaneous resealing of the ductal leakage as inflammation subsided with time and with abstinence from alcohol. (See Table 3.) The treatment of choice for pancreatic ascites needs to be clarified_ Since spontaneous resolution does occur in a significant number of cases, for example, Patient 8 in the series of Cameron et al (4) and Patients 3 and 5 in the series of Donowitz et al (23), a conservative medical regimen of prolonged suction-saline treatment, diuretic therapy, salt restriction, and oral or parenteral hyperalimentation should be tried, usually for an 8-week period. When clinical deterioration occurs, as in our patient, or when the patient does not respond to the medical regimen, requires repeated paracentesis, and develops rapid fluid accumulation and excessive weight loss, surgical intervention is then clearly indicated because it enables not only confirmation of the diagnosis but also the repair of a ruptured pancreatic duct; the excision or internal drainage of a pseudoeyst (4, 6) by cystogastrosDigestive Diseases, Vol. 20, No. 12 (December 1975)
tomy or Roux-en-Y cystojejunostomy (current evidence suggesting a defunctionalized Rouxen-Y jejunostomy as the technique of choice) (22); and sphincterotomy if there is fibrosis of the sphincter of Oddi (32). Operative panereatograms, if possible, should be obtained when ductal perforation is suspected or if no obvious pseudocyst is present (33). If the pancreatic duct leak cannot be identified, a Duval or Puestow duct drainage should be performed. Pancreatic irradiation has also been tried when surgery was inadvisable or impossible (34). Preoperatively, celiac and superior mesenteric arteriograms and ultrasonography may help delineate small pseudocysts and/or differentiate true pseudocysts from inflammatory peripancreatic masses. Permanent relief of the ascites and improvement in health usually follow surgery, except after external drainage, which has not been consistently beneficial. In 5 of 7 patients (as in our patient), ascites did not recur after peritoneoscopy or laparotomy, presumably because the irritant pancreatic secretions were removed from the peritoneal cavity. More rarely, duct leakage may spontaneously seal off as the pancreatitis subsides and ascites may resolve without drainage. Abstinence from alcohol and good nutrition influence the prognosis of the disease.
SUMMARY A case of pancreatic ascites is reported and compared with 55 previously reported cases. A 42-year-old black male chronic alcoholic presenting with abdominal pain was found at operation to have chronic pancreatitis with no pseudocyst formation or overt duct disruption, in contrast to the majority of cases reported. The diagnosis and differentiation from cirrhosis of the liver were based on the operative findings, elevated serum amylase level, ascitic fluid amylase value, and protein content. Surgical exploration alone has proven beneficial--the patient has done well in the past 2 years with no recurrence of the ascites and continued weight 1181
MUNOZ & BOSE
gain. T h e clinical course was compatible with pancreatitis although the radiographic and angiographic studies were not diagnostic. It is suggested that the clinical entity of pancreatic ascites occurs more often than reported and a workup for it should be done even in the face of unconvincing radiographic and angiographic evidence.
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Arch Surg (Chicago) 93:301-303, 1966 13. Jensen NM, Babior BM: Ascites due to chronic pancreatitis. J A M A 201:488-489, 1967 14. Parrish RA, Humphries AL, Moretz WA: Massive pancreatic ascites. Arch Surg (Chicago) 96:887-891, 1968 15. Rosenberg IK, Kahn JA, Walt AJ: Surgical experience with pancreatic pseudoeysts. An J Surg 117:11-17, 1969 16. Lazaro E J, Das PB, Abraham PV: Pancreatic ascites. Am J Gasteroenterol 51:287-292, 1969 17. Wagner RB, Tolins SH: Pancreatic ascites. J Mt. Sinai Hosp NY 36:216-219, 1969 18. Hardy JD, Bowlin JW: Some complications of pancreatic disease: Illustrative cases with notes in management. Ann Surg 145:848, 1957 19. Elmslie RG: Complications of acute non-traumatic panereatitis. Med J Aust 2:895, 1968 20. Akers DR, Favara BC, Franciosi RA, Nelson JM: Duplication of the alimentary tract: Report of three unusual cases associated with bile and pancreatic ducts. Surgery 71:817-823, 1972 21. Barakat M, Raj GK, Hirsh T: Pancreatic ascites: Rupture of pancreatic duct in a patient with chronic pancreatitis. South Med J 65:1377-1379, 1972 22. Smith III RB, Warren WD, Rivard J r AA, Amerson JR: Pancreatic ascites: Diagnosis and management with particular reference to surgical techniques. Ann Surg 177:538-546, 1973 23. Donowitz M, Kerstein MD, Spiro HM: Pancreatic ascites. Medicine 53:183-195, 1974 24. Kalwinsky D, Frittelli G, Oski FA: Pancreatitis presenting as unexplained ascites. Am J Dis Child 28:734-736, 1974 25. Mulhausen RD, Brown C, Onstad G: Renal clearance of amylase during panereatitis. Metab Clin Exp 18:669, 1969 26. Keith LM, Zollinger RM, McCleery RS: Peritoneal fluid amylase as an aid in the diagnosis of acute pancreatitis. Arch Surg 61:930, 1950 27. Tucker PC, Webster PD: Traumatic pseudocysts of the pancreas. Arch Intern Med 129:583586, 1972 28. Twiss JR, Oppenheim E: Liver, Pancreas and Biliary Tract. PhiladelPhia, Lea and Febiger, 1955, p 498 29. Ende N: Amylase activity in body fluids. Cancer 14:1109-1114, 1961 30. Kaiser MH, Roth JLA, Bockus HL: Relapsing Digestive Diseases, VoL 20, No, 12 (December 1975)
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pancreatitis with pseudocyst of the pancreas and enzyme containing pleural effusion. Gastroenterology 28:842-850, 1955 31. Ferruci Jr JT, Eaton JB: Radiology of the pancreas. N Engl J Med 288:506-510, 1973 32. Mallet-Guy P: The place of sphincterotomy in the treatment of diseases of the pancreas. J R
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Coil Surg Edinburgh 12:318-325, 1967 33. Keddie N, Nordi GL: Pancreatography: A safe and effective technique. Am J Surg 110:863865,'1965 34. Kavin H, Sobel SD, Dembo AJ: Pancreatic ascites treated by irradiation of the pancreas. Br Med J 2:503-504, 1971
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