Chronic Pancreatic Ascites

Vol. 59, No.3

GASTH.OENTEitOI.OGY

Copyright © 1970 by The Williams & Wilkins Co.

Printed in U.S.A.

CASE REPORTS

CHRONIC PANCREATIC ASCITES STEPHEN C. SCHINDLER, M.D., JOHN

w.

SCHAEFEH, M.D., DAVID HULL, M.D.,

AND

WAnD 0. GRIFFEN, Jn., M.D. Departments of Medicine and Surgery, Central Baptist Hospital and the University of Kentucky Medical Center, Lexington, Kentucky ·

The clinical syndrome of chronic pancreatic ascites is defined and previously reported cases are reviewed. Three patients with chronic pancreatic ascites are reported. Typically, these patients were chronic alcoholics who experienced intermittent abdominal pain followed by rapid weight loss and chronic ascites. Diagnosis was confirmed by persistently elevated serum and ascitic fluid amylase. Upon surgical exploration chronic pancreatitis, usually complicated with a pseudocyst, was found. Leakage of pancreatic secretions into the peritoneal cavity was considered to be of major importance in the pathogenesis of the ascites. Partial pancreatic resection or internal drainage of the pseudocyst into the gastrointestinal tract was an effective form of therapy. Chronic pancreatitis as a cause of massive accumulation of intraperitoneal fluid is being recognized with increased frequency. In 1953, Smith reported the first 2 cases of ascites complicating chronic pancreatitis and pancreatic pseudocyst. 1 Since then 29 additional cases have been reported. 2 - l:l The purpose of this paper is to add 3 more cases, review the literature, and define the syndrome.

swelling. Two weeks later he was hospitalized elsewhere and several paracenteses yielded fluid negative for malignant cells. Diuretic therapy was ineffective and despite fluid retention he lost 25 lb of weight. After 4 weeks he was transferred to the Central Baptist Hospital for further evaluation. The patient was cachectic. His blood pressure was 90 over 60, pulse, 80, respiration, 16, and temperature, 98.2 F. There were no signs of chronic liver disease. The abdomen was tensely distended with fluid; no organs or masses were palpable. Soft, pitting edema was present in both lower extremities. A complete blood count, Bromsulphalein retention, prothrombin time, serum glutamic oxaloacetic transaminase, bilirubin, and alkaline phosphatase were normal. The serum albumin was 3.2 g per 100 ml and globulin, 2.4 g per 100 ml. Initial serum amylases were 2,000 and 2,800 Somogyi units. Straw-colored ascitic fluid contained protein, 4 g per 100 ml, white blood cells, 750 per mm" with 60% polymorphonuclear forms, and an amylase content of 30,000 Somogyi units. An oral cholecystogram showed normal function. Upper gastrointestinal tract ·X-rays were intrinsically normal and showed no gastric displacement. At surgery, on the 9th hospital day, a 12-cm

Case Reports Case 1. A 42-year-old Negro man was admitted to the Central Baptist Hospital in Lexington, Kentucky, on January 2, 1968. He had been a "spree" drinker of alcohol for many years, but was in good health until 6 weeks prior to admission. At that time he developed a sudden bout of severe upper abdominal pain which gradually subsided over a period of days. As the pain subsided, he noted abdominal Received January 5, 1970. Accepted March 26, 1970. Address requests for reprints to: Dr. John W. Schaefer, Division of Gastroenterology, University of Kentucky Medical Center, Lexington, Kentucky 40506. 453

454

CASE REPORTS

pseudocyst was found in the tail of a scarred, firm pancreas. The contents of the cyst were leaking through the friable wall. The cyst and the distal pancreas were resected and a Roux-en-Y pancreaticojejunostomy was constructed. The postoperative course was uncomplicated, and the serum amylase level returned to normal. The patient was discharged on the 21st postoperative day and has been followed-up for 2 years. He has regained weight and is in good health, free of ascites or symptoms of pancreatic insufficiency. Case 2. A 37-year-old alcoholic Negro woman was admitted to the University of Kentucky Medical Center on January 19, 1968, with a 1-month history of weakness and 15 lb of weight loss. She also had intense burning paresthesias of the feet and numbness of the legs. For several weeks she had experienced postprandial nausea, vomiting, and upper abdominal pain. She was tremulous, pale, and wasted. Her blood pressure was 110 over 80, pulse, 110, respiration, 20, and temperature, 98 F. There was mild abdominal tenderness in the right upper quadrant, but no palpable organs or masses. Ascites could not be demonstrated. Signs of a peripheral neuropathy were present. Laboratory data included: hematocrit, 33%; white blood cell count, 8400; serum calcium, 3.9 mEq per liter; phosphorus, 1.9 mEq per liter; alkaline phosphatase, 3.8 Bessy-LowreyBrack units; serum glutamic oxaloacetic transaminase, 40 U; serum glutamic pyruvic transaminase, 18 U; bilirubin, 0.2 mg per 100 ml; albumin, 2.2; globulin, 3.1 g per 100 ml. The upper gastrointestinal tract was normal on barium study. During the first 2 weeks of hospitalization, there was general improvement with return of appetite. However, moderately severe episodes of upper abdominal pain recurred and progressive ascites developed. The serum amylase was 1400 Somogyi units and remained elevated on several determinations. A paracentesis yielded 1500 ml of serosanguinous fluid with an amylase concentration of 760 Somogyi units, protein, 2.1 g per 100 ml; 300 white blood cells; 390 red blood cells per mm 3 • Five days later, a second paracentesis produced fluid with similar findings. An exploratory laparotomy was performed on the 27th hospital day, and 2500 cc of serosanguinous fluid was aspirated. The head of the pancreas was enlarged and indurated and a large fluctuant pseudocyst was found in the retrogastric area. Dark fluid was leaking from

Vol. 59, No.3

the cyst. The pseudocyst was drained into the posterior wall of the stomach by a cystogastrostomy. Her postoperative course was complicated by penumonia, pulmonary edema, and fatal cardiac arrest 5 days after surgery. Permission for autopsy was not obtained. Case 3. A 40-year-old Negro woman was admitted to the University of Kentucky Medical Center on January 7, 1969, because of abdominal swelling and weight loss. She had consumed 2 to 4 pints of alcohol daily for at least 10 years. For several months she had experienced severe intermittent epigastric pain, associated with vomiting. During the 6 weeks before admission, following a bout of pain, she noted increasing abdominal distention, weakness, and 20-lb weight loss. She was wasted and chronically ill. The blood pressure was 90 over 70, pulse, 112, respiration, 16, and temperature, 98.6 F. The mucous membranes were pale and jaundice was not present. There were no peripheral signs of chronic liver disease. The abdomen was protuberant with ascites. A firm, nontender liver was balloted 6 em below the right costal margin. Moderate pitting edema was present in the lower extremities. Laboratory studies showed: hematocrit, 26%; hemoglobin, 8.4 g per 100 ml; white blood cell count, 4300 per mm 3 ; reticulocytes, 1.4%; total bilirubin, 0.4 mg per 100 ml; serum glutamic oxaloacetic transaminase, 34 U; serum glutamic pyruvic transaminase, 16 U; alkaline phosphatase, 5.4 Bessy-Lowrey-Brock units. Serial serum amylase determinations ranged from 400 to 690 Somogyi units. The abdomen contained straw-colored fluid with a protein content of 2.0 g per 100 ml and an amylase concentration of 2640 Somogyi units. An oral cholecystogram was normal. Roentgenograms showed extrinsic pressure along the lesser curvature of the stomach with displacement anteriorly and to the left. At the time of exploratory laparotomy on the 30th hospital day, 6000 ml of ascitic fluid were aspirated. The liver was pale, smooth, and enlarged; biopsy subsequently demonstrated fatty metamorphosis. The pancreas was firm and scarred, and contained an excavated mass, the residual of a friable pseudocyst, in the body. At the base of the cavity the proximal and distal portions of the pancreatic duct were identified and cannulated. Hypaque injection outlined the remaining pancreatic ductal system and showed no obstruction or dilation. A cystogastrostomy was performed and the postoperative course was uneventful. At

September 1970

CASE REPORTS

the time of discharge the patient was free of ascites and the serum amylase was 62 Somogyi units. During the 1st postoperative month ascites gradually recurred. Roentgenograms again demonstrated anterior displacement of the stomach. Paracentesis yielded cloudy, yellow fluid containing protein, 3.2 g per 100 ml, and amylase, 136 Somogyi units. Further surgery was contemplated but deferred. The ascites subsided spontaneously over the next month .

Discussion These 3 patients with chronic pancreatic ascites have many comparable clinical features. All were young alcoholics who developed intermittent abdominal pain, weight loss, and ascites. With the onset of ascites the pain subsided or was significantly reduced in severity. Weight loss was rapid and progressive despite the fluid accumulation. Persistent hyperamylasemia was associated with a marked elevation of amylase in the ascitic fluid. In addition the ascitic fluid contained an elevated protein concentration ranging from 2 to 4 g per 100 ml and excessive red and white blood cells. Radiographic evidence of a retrogastric mass was found in only 1 of the 3 patients. However, all were shown at the time of surgery to have chronic pancreatitis with pseudocyst formation. In each, the fluid contents of the cyst were demonstrated to be leaking into the peritoneal cavity. Surgical management consisted of internal drainage of the cyst with cystogastrostomy in 2 patients and distal pancreaticocystectomy with Roux-en-Y jejunal anastomosis in the 3rd. One patient (case 2), died 5 days after cystogastrostomy; the other 2 are alive and well. One of these (case 3) had recurrent ascites in the postoperative period, but this subsided spontaneously. Our cases are similar to the 31 previously reported cases of pancreatic ascites and the pertinent data on all cases are presented in table 1. The frequency of the clinical features characterizing this syndrome are summarized in table 2. Typically the patients, predominantly men, are in the third to fifth decade of life.

455

With rare exception, chronic alcoholism is the common predisposing factor. Most patients experience intermittent abdominal pain which, at least in retrospect, is compatible with attacks of pancreatitis. The significance of the pain is frequently underestimated since with the onset of ascites the episodes of pain tend to subside. Ascites is most often massive, chronic, and refractory to diuretic therapy, but occasionally subsides spontaneously. The profound weight loss and relatively painless ascites may lead to an erroneous diagnosis of intraabdominal malignancy or cirrhosis. If, however, pancreatic ascites is considered, the diagnosis is not difficult to establish. Almost without exception the serum and particularly the ascitic fluid amylase is markedly elevated. The protein content is higher than expected for the ascites of decompensated cirrhosis. The ascitic fluid cell count, both white and red, is elevated and occasionally the lluid is hemorrhagic in appearance. Jaundice is not a significant clinical feature and biochemical evidence of liver dysfunction is mild or absent. Chronic pancreatitis, usually with a pseudocyst, is found at surgery. This high incidence of demonstrable pancreatic pseudocysts frequently with overt leakage of pancreatic secretions into the peritoneal cavity (cases 19, 20, 21, 24, 32, and 33) argues strongly for surgical exploration. In recent years, the treatment of choice has been either caudal resection of the pancreas and cyst or drainage of the pseudocyst into the intestinal tract (table :3). Permanent relief of ascites and return of weight and vigor is the expected result; rarely, recurrent ascites has required further surgery. With other forms of surgical treatment, external drainage of the pseudocyst and sphincterotomy, the results have not been so consistently beneficial. It is of interest that the chronic ascites subsided in 5 of 7 patients having only an abdominal exploration. This could be attributed to the salutary effects of surgical drainage of ascites high in enzyme content, or to fortuitous spontaneous resolution of ascites as observed in a small

35M

47 M 37 F 26M 25 F

27M 307

46M 200-496 S units

30 F

46M 300-1,800 S units

28 F

19M 5,042-7,000 S units

4

5 6 7 8

9

10

11

12

13

14

Schmidt and Whitehead, 19623

Barua et al., 1962'

Burrows and Poll, 19665

MacLaren et al. , 19666

Cameron et al., 1967'

Jensen and Babior, 19678

Parish et a!., 19689

Ascitic fluid

1,850-2,280 S units

855-1,800 mg per 100 ml

u

-

-

20,000-39,000 S units

6,000-29,750 S units

100-3,600 S units

3,860-5,170 mg per 100 ml

-

640U

2,024 W units' 1,024 W units 512 W units 4,096 W units

-

64 W units 64-252 W units 128-256 W units

-

-

450 S units" 6,850 S units

Amylase

Laboratory data

-

-

54 M

3

Gambill et a!., 1960'

Serum amylase

30 F Normal 44 M 1,500 S units

Age and sex

1 2

No.

Case

Protein

Pseudocyst Pseud ocyst Pseudocyst

Pseudocyst · Pseudocyst Pseudocyst

4.0 2.8

-

Pseudocyst

Pseudocyst

6.2

5.7

CJl

~ c.,

~

Recurrence Recovered Exploration only Distal pancreaticocystectomy External tube drainage Cystogastrostomy

Recovered

Died

None

~

::tl

0

~

~

t>l

52V:!

O"l

.;.o

Recovered Distal pancreaticocystectomy

.... Ol

Recurrence

Recovered

Recovered Cystogastrostomy

External tube drainage

Recovered Died Recovered Exploration only Peritonescopy Peritonescopy Exploration only

Pseudocyst Pseudocyst Pseudocyst Pseudocyst

2.9 3.4

-

Recovered Cystogastrostomy

Pseudocyst

3.2

-

Recovered

Recovered Recurrence Recovered

Exploration only External drainage Exploration only Exploration only

Chronic pancreatitis Pseudocyst Pseudocyst

Course

Chronic pancreatitis

b

Surgical procedure

-

-

g/lOOml

Diagnosis

Abdominal exploration

1. Laboratory values, surgical procedures, and course of patients "th chronic vancreatic ascite ~·

Smith, 1953'

Authors

TABLE

1969

51 M

21

37 F 1,400 S units 40 F 400-690 S units

33 34

32M 1,000 mg per 100 ml 26M 595 mg per 100 ml 4F 120 mg per 100 ml

29 30 31

42 M 2,000-2,800 S units

44 M 544 mg per 100 ml 37 F 340 mg per 100 ml

27 28

32

38M 1,060 mg per 100 ml 57 F 1,970 mg per 100 ml

29M 785 mg per 100 ml

29M Normal

57 M 225 S units

-

25 26

24

23

22

42 M 1,020 S units

20

a

u

768 S units 2,640 S units

30,000 S units

8,000 mg per 100 ml 2,875 mg per 100 ml 630 mg per 100 ml

360 mg per 100 ml 510 mg per 100 ml

16,800 mg per 100 ml 4,035 mg per 100 ml

8,250 mg per 100 ml

343

370 S units

-

15,000 S units

15,000 S units

600-800 S units

29 F

20,000 S units 160,000 S units 70,000 S units 20,000 S units

500 S units 1,600 S units 608 S units 200 S units

19

F M M F

41 45 41 42

15 16 17 18

Somogyi units, normal value 60 to 180 U. ' -, indicates information not included in case reports. 'Wohlgemuth units, normal value 0 to 32 U.

s :hindler,

1969'"

c 1meron et a!.,

1969 12

w, ~gner and Tolins,

1969 11

L zaro eta!. ,

1969 10

R, 'sen berg et a!.,

Pseudocyst Pseudocyst Pseudocyst

4.0 2.1 2.0

-

--

Pseudocyst Chronic pancreatitis, duct disrupted Chronic pancreatitis Chronic pancreatitis, duct disrupted

Pseudocyst

Pseudocyst

Chronic pancreatitis

Pseudocyst Pseudocyst Pseudocyst Pseudocyst Pseudocyst

-

Pseudocyst

-

Pseudocyst

-

Pseudocyst

3.0 4.4 2.2

5.0 2.9

4.3 3.9

3.5

3.0

3.1

-

-

3.8

3.1 3.6 3.0 3.5

'

Died Recovered

Recovered

Recovered Recovered Persistent ascites

None None None Partial pancreaticocystectomy Cystogastrostomy Cystogastrostomy

Recovered Recovered

Died Recovered

Recovered

Puestow drainage Exploration only

Partial pancreaticocystectomy Cystogastrostomy Roux-en-Y drainage

Recovered

Recurrence spontaneous recovery

Sphincterotomy

Cystogastrostomy

Recurrence Recovered Recurrence Recurrence Recovered Recurrence Recovered Recurrence Recovered Recurrence Recovered

External drainage None Cystogastrostomy Exploration only Cystogastrostomy Exploration only External drainage External drainage Cystoduodenostomy Exploration only External drainage

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CASE REPORTS

458

Vol. 59, No. 3

2. Characteristic features of the 34 reported patients with chronic pancreatic ascites

TABLE

Hcco rd cd observat ions

Average

Range

Clinical features

Incidence

Age .. . . .. . . Sex Male . .. . .. . . ... . . . . . Female . .. . .. . ... . Alcoholism .. Abdominal pain .. · · · · ·· · . . .. . . . . . . Weight Joss . . . . . . . . ...... . . .. . . Ascites Demonstrable pseudocyst •

•

•

•

•

0

•

•

•

•

•

•

•

•

•

•

•

•

0

•

4- 57 yr

37 yr

10-50 lb

27 lb

•

•

•

•

•

•

•

0

•

•

•

•

•

•

•

0

•

•

2-6.2 g per 100 ml

TABLE 3. Response to surgical therapy of the 34 reported patients with chronic pancreatic ascites

No. of ope ra-

tions

Internal drainage of 12 pseudocyst . Resection of pseudocyst . 4 External drainage of 7 pseudocyst . Sphincterotomy . 1 Abdominal explorat ion only . 10 No Surgery ... . . 7

RecurRecov-

21/34 13/34 28/33 17/ 22 17/ 17 34/34 24/30

62 38 85 77 100 100 80

28/30 30/30

93 100

22/26

85

•

Elevated serum amylase . . . . . . . . . . . . Elevated ascitic fluid amylase Ascitic fluid protein Ascitic fluid protein > 2.5 g per 100 ml

Surgical procedure

Percentage

renee or

ery

persis-

9

1

Died

Un· kn own

tence

2

4 3

4 1

5 4

4 1

1 2

number of unoperated patients. In either instance one could postulate the reestablishment of effective internal drainage through the pancreatic ductal system as the inflammatory process subsides. In view of these "spontaneous" remissions it seems prudent to defer surgery, at least when pseudocyst formation is not clearly documented, until the patient's course clearly indicates that nonoperative management is ineffective. The ultimate prognosis may depend largely on the degree of continuing alcoholism and, in turn, on the frequency and severity of recurrent pancreatitis. The etiology of the ascites in chronic pancreatitis is incompletely understood.

3.5 g per 100 ml

Cirrhosis and portal hypertension with or without portal vein compression do not seem to be important. Blockage of abdominal cavity lymphatics by an inflammatory reaction has been proposed. However, a recent report by Dreiling and Rudick 14 of dramatic improvement in chronic pancreatic ascites following thoracic duct drainage suggests that lymphatic blockade at the peritoneal surface is not a major factor. The 3 patients that we report lend strong support to the contention that escape of pancreatic enzyme into the peritoneal cavity is an important and perhaps the major factor in the pathogenesis of ascites in this syndrome. Overt leakage of pancreatic secretions has been observed from ductal disruption in an inflammatory mass (case 26), from a collapsed or disintegrated pseudocyst (case 34), and through the friable wall of an intact cyst (cases 19, 20, 21, 24, 32, and 33). Less apparent leakage has been demonstrated by injection of contrast material into the main pancreatic duct (case 28). In some, however, obvious escape of pancreatic secretions could not be demonstrated (case 23). Whatever the degree of leakage, establishment of free drainage of pancreatic secretions into the gastrointestinal tract by internal drainage of the pseudocyst or Roux-en-Y anastomosis to a partially resected pancreas usually led to disappear-

CASE REPORTS

September 1970

ance of ascites. The occasional spontaneous resolution of ascites may well be explained by sealing of subtle ductal leakage as pancreatic inflammation subsides. This condition is more common than previously appreciated. Greater awareness of the syndrome rather than increased incidence probably accounts for the increasing number of reported cases. Accurate diagnosis is critical since specific and effective surgical therapy is available. In this regard the diagnostic reliability of a markedly elevated ascitic fluid amylase is emphasized and its routine determination in all cases of chronic ascites is justified. REFERENCES I. Sm it h EB : Hemorrhagic asc ites and hemothorax associated with benign pancreatic disease. Arch S urg (Chicago) 67:52-56, 1953 2. Gambill EE, Walters W, Sca nlon PW: Chron ic relapsing pancreatitis with exte n s ive subacute peritonitis and chronic, recurrent massive "chylous" ascites. Amer J Med 28:668- 670, 1960 3. Sch midt E H, Whitehead RP: Recurrent ascites as a n unusua l complication of c hron ic pancreatitis. JA M A 180:135- 137, 1962

459

4. Barua RL, Villa F, Steigmann F: M assive ascites due to pancreatitis. Amer ,J Dig Dis 7:!J00- 90G, 1962 5. Burrows L, Poll MD: Unusual problems in sur· gery. J Mount S inai Hosp NY :l :l::l9G - ~O:l, J!JGG 6. MacLaren IF, Howard .JM, ,Jordan GL: Ascites assoc iated with a pseudocyst of the pa ncreas. Arch Surg (C hicago) 9:J::Jo 1- :lO:l, !9GG 7. Cameron JL, Anderson RP, Zuidema GD: Pancreatic asc ites. Surg Gynec Obstet 12!i::l28-:J:l2, 1967 8 . ,J ensen NM, Babior BM: Ascites du e to chronic pancreatitis. ,J A M A 201:488-489, 1%7 9. Parrish RA, Humphries AL, Moretz WA: Mass ive pancreatic ascites. Arch Surg (C hicago) !JG : 887- 891, 1968 10. Rosenberg IK, Kahn .JA, W a lt A.J: Surgical experience with pancreatic pseudocysts. Amer ,J Surg 117:11-17, 1969 11. Lazaro EJ, Das PB, Abraham PV: Pancreatic asc ites. Amer ,J Gastroen t 51:287-292, 1!)fi9 12. Wagner RB , Tolins SH: Pancreatic ascites. ,J Mount Sinai Hosp NY :JG:2JG-219, 19fi!l 13. Cameron JL, Brawley RK, Bender HW, et al: The t reatment of pancreatic ascites. Amer Smg 170 :668-676, 19G9 14. Dre iling DA, Rudick .1: Massive in traclahle ascites in pancreatitis: pathogen es is and t reatment (abstr). Gastroen te rology !iG: 1lfi:l, l!lfi!l