Vol. 67, No. 3
223
Pancreatic Ascites DANIEL MUNA, M.D. Instructor in Surgery SUBHI D. ALI, M.D., Instructor in Surgery ANTHONY JEAN-JACQUES, M.D., Assistant Professor ol Surgery, THOMAS CALHOUN, M.D., Assistant Professor of Surgery, and LEWIS H. KURTZ, M.D., Associate Professor of Surgery and Chief Medical Officer, Howard University Division of Surgery, D. C. General Hospital, Washington, D. C.
T wo cases of pancreatic ascites complicating pancreatic pseudocyst were first reported by Smith' in 1953. Since then, this clinical syndrome is being recognized with increasing frequency. The following two case reports, presenting within a two month period on our surgical service, show this condition to be more common than previously appreciated. A greater awareness of the syndrome, rather than increased incidence, probably accounts for increasing number of reported cases. Accurate diagnoses and differentiation of pancreatic ascites from cirrhotic ascites is critical, since specific and effective surgical therapy is available for the former and not the latter. CASE REPORTS Case No. I. C.F, a black male aged 24, was admitted to D.C. General Hospital on 9/24/72 complaining of epigastric fullness, nausea, vomiting, anorexia, moderate abdominal cramps and gradual weight loss. There were normal bowel habits. He had a previous admission one year earlier for treatment ofacute pancreatitis, complicating his heavy alcoholic history. He used heroin up to 1969, then converted to methadone for treatment of his addiction. Physical examination showed evidence of marked weight loss. The BP was 100/70; pulse 96, respiration 20 and temperature 98.6+F His abdomen was markedly distended with ascitic fluid and was tense. No jaundice or spider angiomas were present. The remainder of his physical examination was unremarkable. An admission CBC, urinalysis, serum electrolytes, BUN cholesterol, alkaline phosphatase were normal. Total bilirubin was 0.4 mg'%o and the total protein 7.8 gm%, albumin 2.4 gm. The SGOT was 120 units (normal less than 180) on admission and rose to 2250 units on 10/5/72. It remained elevated during the preoperative period. Serum calcium was normal. Stool guaiac was negative. UGI series showed moderate widening of the duodenal loop. Esophagascopy was normal.
The patient was treated for acute pancreatitis and placed on diuretics. Abdominal discomfort and ascites persisted. Five weeks after admission, a paracentesis yielded "bloody looking" fluid. The AFB was negative, cytology negative, protein 3.7 gm%o, amylase 18000, RBC 900 and WBC 5. Repeated paracentesis and diuretics failed to control the ascites. A diagnosis of pancreatic ascites secondary to ruptured pseudocyst was made and confirmed by exploratory laparotomy. and operative pancreatogram revealed a point of leakage at a branch of the pancreatic duct which was closed primarily (Fig. 1). A sphincterotomy of the ampulla of Vater was also performed. Six liters of ascitic fluid were evacuated during this procedure. The patient's post-op day. He began to gain weight and showed no signs of recurrence of ascitic fluid. He was doing quite well six months post discharge having returned to his routine activities. Case No. 2. PF, a black female, aged 36, was admitted to D.C. General Hospital on 7/28/72 complaining of abdominal discomfort, nonradiating substernal pain and moderate shortness of breath. She had been discharged three days previously from another hospital where she was admitted on 6/28/72 because of severe abdominal pain, nausea, vomiting and hematemesis. An exploratory laparotomy revealed pancreatitis, cholelithiasis and 900cc of greenish ascitic fluid. A cholecystectomy, operative cholangiogram, and gastrostomy were done. She had a long history of alcoholism. On physical examination 'she was well developed but markedly emaciated and in no acute distress. Her BP was 140/90, pulse 98 and regular, temperature 99+F and respirations 24. Her abdomen was flat on admission but distended progressively during hospitalization. Bowel sounds were normal. There was minimal ascites and the spleen and liver were not enlarged. During four months of evaluation and treatment on the medical service, the patient was anemic with an elevated serum amylase (450-3600 units). The total protein was 5.6 gm% with an albumin of 1.3 gm0/o. Multiple paracenteses revealed a dark greenish fluid with an amylase of 1800-18000 units, protein 2.9, increased RBC and WBC, negative cytology and AFB stain. A G.I. series and selective celiac angiography were unremarkable. Liver biopsy showed mild focal nonspecific pericholangitis. She had lost 30 lbs. since admission in spite of progressive abdominal distension. She was transferred to surgery with a diagnosis of pancreatic ascites from a ruptured pancreatic
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
224
pseudocyst. At laparotomy, ascites, chronic peritonitis, with marked adhesions and a ruptured pancreatic pseudocyst, were found. A cystogastrostomy were performed. Despite intensive post-operative care, the patient's condition continued to deteriorate and she died on the 18th postoperative day DISCUSSION
Although upper abdominal pain and chronic alcoholism are important clues in the diagnosis of pancreatitis, the latter is not often considered when a patient has massive ascites. Instances of abdominal fluid accumulation : ........j. ..Yr~ j .: *~~~~~ 4 ..............., w
~~~~~~~~~~~~~~~~~~~~~~~.... ::~~~~~~~~~~~~
::.:.:........ ...' ..
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.. .....
FX ...i..~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~. .... . . .. E
Figk.l 1. Operative
weakness,a and anorexia. The serum amylase, the ascitic fluid amylase and protein are usually elevated in patients with pancreatic ascites unlike cirrhotic ascites where the protein content is low and the amylase normal or only minimally elevated. Bockus,3 in 1951, reported that 21% of patients with cirrhosis have elevations of the serum amylase in absence of pancreatic disease. Since pancreatic ascites can masquerade as cirrhotic ascites, a differentiation between the two is important in view of the effectiveness of surgical therapy for the former and not the latter. Typically, the patients are predominantly men in their 3rd to 5th decade of life. Weight loss is rapid and progressive despite fluid accumulation. A common predisposing factor is chronic alcoholism and most patients experience intermittent abdominal pain compatible with attacks of pancreatitis. The ascites is very often massive and refactory to diurectics but occasionally subsides spontaneously. Barua,4 in 1962, suggested that massive pancreatic ascites was the result of chronic peritoneal irritation by pancreatic enzymes. Others suggest that the ascites is due to compression of the portal vein or its tributaries by a pancreatic pseudocyst. MacLaren,s in 1966, hypothesized that obstruction of the retroperitoneal and mesenteric lymphatics was the cause of the ascites. If, however, a pseudocyst is not present, as in some reported cases, a direct pancreatic duct leak must be assumed. Most of the pseudocysts associated with pancreatic ascites seem to be small, probably because they are decompressed into the peritoneal cavity. When a diagnosis of pancreatic ascites seems warranted, laparotomy should be performed. If a pseudocyst is recognized, internal drainage of the cyst should be instituted. If an obvious pseudocyst is not present, operative pancreatography should be performed to identify a pancreatic duct leakage and drainage by a Roux-en-Y loop. In the first case reported above, however, we found it much easier to primarily close the leak and performed a sphincterotomy, since a duodenotomy had already been made for the pancreatogram. If
'' ..
.j,
~........
..
..pneor
revealing a paten
'c'
i. .1~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~...........
M..~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~. .....
.|....:.e.g....~~~~~~~~~~~.
Fig. 1. Operative pancreatogram revealing a patent pancreatic duct with a point of leakage directed cephalad at the junction of the head and body of the pancreas
occur in association with hepatic cirrhosis, intra-abdominal cancer, tuberculous peritonitis, cardiac and renal failure and are usually readily recognizable in patients with pancreatic cancer, in whom ascites is present clinically in 10-20%. Tuberculous and cirrhotic ascites usually have normal amylase, unlike pancreatic ascites, where the amylase is quite high. The lack of correlation between serum and ascitic fluid amylase in some cases as noted by Jensen and Babier suggests two portals of entry into the blood stream: one directly from the blood and the other indirectly from the pancreas via the peritoneal cavity. The outstanding common feature of patients with pancreatic ascites are, heavy alcohol intake, variable degree of intermittent abdominal pain, massive ascites, marked weight loss,
MAY, 1975
(Concluded on page 247)
247
Briefs
Vol. 67, No. 3
opened and closed sites, transported emergency teams and reported to headquarters every hour on general conditions of each site. A few precedents in community affairs were set. One was the concerted effort of more than 400 volunteers who made the program a success. In addition to the Richmond Medical Society and their staffs. The Licensed Practical Nurse's Alumni Association participated as a group and served as registrars and screeners. The Association of Black Social Workers served as registrars and site coordinators. The staff of the Model Neighborhood Policy Board widely publicized the screening program and provided offices for a common post on the days that screening was conducted. The staff of the Churchill MultiService Center distributed more than 10,000 flyers and served as site coordinators. The Red Cross, the Richmond Area Heart Association, the Medical College of Virginia and the Richmond Academy of Medicine solicited volunteers. The Boy Scouts assisted in distributing flyers, and other social and civic clubs participated as registrars and site coordinators. The Richmond Urban League solicited sites, administered the program, compiled statistical data, and did all of the community organization. The Ciba Pharmaceutical Company provided flyers, pamphlets and other printed material. The General Medical Corporation provided 10,000 flyers for distribution and doughnuts and coffee for site workers. Twenty-thousand flyers were distributed and 150 posters were distributed throughout the Churchill Community.
talk show interviews, coverage in the local newspaper, and radio personalities conducting remote broadcasting served to increase the enthusiasm and participation of the city and the target area. Educational materials were selected and developed for the black community; keeping in mind the degree of literacy of the majority of the adult population within the community. Ciba's CHEC Program materials were also used. Blood pressures were taken from a total of 39 East End sites. Screening was conducted from 15 sites on Friday, May 24, 15 sites on Saturday, May 25, and from 19 sites on Sunday, May 26. The Friday sites were open from 4:00 to 9:00 p.m. The Saturday sites were open from 9:00 a.m. to 4:00 p.m., and the Sunday sites were open from 10:00 a.m. to 3:00 p.m. All screening sites on Sunday, May 26, were from churches, except for the site at Chimboraze Park. East End ministers had declared the Sunday of May 26, High Blood Pressure Sunday. Screening on Friday and Saturday was conducted from schools, shopping plazas, recreational centers, and drug stores within housing developments. Screening at shopping centers was conducted in office trailers on their parking lots. A mobile van from St. Mary's Hospital (custom built medical office on wheels), roved the community concentrating its coverage on barber shops, beauty salons, pool halls and out-laying areas that did not have a screening site. The mobile van's route of travel was known in advance. The van was equipped with a telephone, which made it easy to locate in an emergency to send an additional team to it or send it to a screening site to help until a team could be sent. Each screening site had one or more physicians present. In addition, the physicians of the Richmond Medical Society closed their offices and brought their staffs into the field for the entire program. The large number of screening sites necessitated the need for field coordinators. The social workers of the community took charge of this function. In teams of two, each group was responsible for three screening sites. Their responsiblities were to insure that data was collected properly, each site received equipment and materials,
RESULTS After 13 hours of screening on the three days, 4,480 persons were screened, of whom 1,849 or 38% had elevated pressures; 405 or 22% (N = 1,849) completed follow-up, of which 293 or 72% (N = 349) were hypertensive and 227 were placed under treatment. Unfortunately, it was discovered too late that at many sites the data cards were given to the screenees. After collaboration with the volunteers it was estimated that 8 to 10 thousand persons had been screened. The project was conducted under the auspices of the Virginia Regional Medical Program, Inc. .
(Muna et al., from page 224)
the pancreatic duct leakage cannot be identified, a ductal drainage procedure, such as the Duval or Puestow procedures, should be done to allow the leak to seal. SUMMARY
Two cases of pancreatic ascites secondary to ruptured pseudocyst presenting within a two month period in a major city hospital are reported. The clinical syndrome is being recognized with increasing frequency. A distinction between pancreatic ascites and cirrhotic ascites should be made since surgical treatment is favorable for the former. Elevated serum and
ascitic fluid amylases and protein are diagnostic of pancreatic ascites. LITERATURE CITED
1. SMITH, E. B. Hemorrhagic Ascites and Hemothorax Associated with Benign Pancreatic Disease. Arch. Surg., 67:52-56, 1953. 2. JENSEN, N. M. and B. M. BABIER. Ascites Due to Chronic Pancreatitis. J.A.M.A., 201:488-489, 1967 3. BOCKUS, H. Gastroenterology, Vol. 3 Saunders, Philadelphia and London, 1964, pp. 840. 4. BARUA, R. L. and F VILLA and F STEIGMANN. Massive Ascites Due to Pancreatitis. Amer. J. Digest. Dis., 7:900, 1962. 5. MACLAREN, I. F and J. M. HOWARD, and G. L. JORDAN. Ascites Associated with a Pseudocyst of Pancreas. Arch. Surg., 93:301-303, 1966.
223
Pancreatic Ascites DANIEL MUNA, M.D. Instructor in Surgery SUBHI D. ALI, M.D., Instructor in Surgery ANTHONY JEAN-JACQUES, M.D., Assistant Professor ol Surgery, THOMAS CALHOUN, M.D., Assistant Professor of Surgery, and LEWIS H. KURTZ, M.D., Associate Professor of Surgery and Chief Medical Officer, Howard University Division of Surgery, D. C. General Hospital, Washington, D. C.
T wo cases of pancreatic ascites complicating pancreatic pseudocyst were first reported by Smith' in 1953. Since then, this clinical syndrome is being recognized with increasing frequency. The following two case reports, presenting within a two month period on our surgical service, show this condition to be more common than previously appreciated. A greater awareness of the syndrome, rather than increased incidence, probably accounts for increasing number of reported cases. Accurate diagnoses and differentiation of pancreatic ascites from cirrhotic ascites is critical, since specific and effective surgical therapy is available for the former and not the latter. CASE REPORTS Case No. I. C.F, a black male aged 24, was admitted to D.C. General Hospital on 9/24/72 complaining of epigastric fullness, nausea, vomiting, anorexia, moderate abdominal cramps and gradual weight loss. There were normal bowel habits. He had a previous admission one year earlier for treatment ofacute pancreatitis, complicating his heavy alcoholic history. He used heroin up to 1969, then converted to methadone for treatment of his addiction. Physical examination showed evidence of marked weight loss. The BP was 100/70; pulse 96, respiration 20 and temperature 98.6+F His abdomen was markedly distended with ascitic fluid and was tense. No jaundice or spider angiomas were present. The remainder of his physical examination was unremarkable. An admission CBC, urinalysis, serum electrolytes, BUN cholesterol, alkaline phosphatase were normal. Total bilirubin was 0.4 mg'%o and the total protein 7.8 gm%, albumin 2.4 gm. The SGOT was 120 units (normal less than 180) on admission and rose to 2250 units on 10/5/72. It remained elevated during the preoperative period. Serum calcium was normal. Stool guaiac was negative. UGI series showed moderate widening of the duodenal loop. Esophagascopy was normal.
The patient was treated for acute pancreatitis and placed on diuretics. Abdominal discomfort and ascites persisted. Five weeks after admission, a paracentesis yielded "bloody looking" fluid. The AFB was negative, cytology negative, protein 3.7 gm%o, amylase 18000, RBC 900 and WBC 5. Repeated paracentesis and diuretics failed to control the ascites. A diagnosis of pancreatic ascites secondary to ruptured pseudocyst was made and confirmed by exploratory laparotomy. and operative pancreatogram revealed a point of leakage at a branch of the pancreatic duct which was closed primarily (Fig. 1). A sphincterotomy of the ampulla of Vater was also performed. Six liters of ascitic fluid were evacuated during this procedure. The patient's post-op day. He began to gain weight and showed no signs of recurrence of ascitic fluid. He was doing quite well six months post discharge having returned to his routine activities. Case No. 2. PF, a black female, aged 36, was admitted to D.C. General Hospital on 7/28/72 complaining of abdominal discomfort, nonradiating substernal pain and moderate shortness of breath. She had been discharged three days previously from another hospital where she was admitted on 6/28/72 because of severe abdominal pain, nausea, vomiting and hematemesis. An exploratory laparotomy revealed pancreatitis, cholelithiasis and 900cc of greenish ascitic fluid. A cholecystectomy, operative cholangiogram, and gastrostomy were done. She had a long history of alcoholism. On physical examination 'she was well developed but markedly emaciated and in no acute distress. Her BP was 140/90, pulse 98 and regular, temperature 99+F and respirations 24. Her abdomen was flat on admission but distended progressively during hospitalization. Bowel sounds were normal. There was minimal ascites and the spleen and liver were not enlarged. During four months of evaluation and treatment on the medical service, the patient was anemic with an elevated serum amylase (450-3600 units). The total protein was 5.6 gm% with an albumin of 1.3 gm0/o. Multiple paracenteses revealed a dark greenish fluid with an amylase of 1800-18000 units, protein 2.9, increased RBC and WBC, negative cytology and AFB stain. A G.I. series and selective celiac angiography were unremarkable. Liver biopsy showed mild focal nonspecific pericholangitis. She had lost 30 lbs. since admission in spite of progressive abdominal distension. She was transferred to surgery with a diagnosis of pancreatic ascites from a ruptured pancreatic
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
224
pseudocyst. At laparotomy, ascites, chronic peritonitis, with marked adhesions and a ruptured pancreatic pseudocyst, were found. A cystogastrostomy were performed. Despite intensive post-operative care, the patient's condition continued to deteriorate and she died on the 18th postoperative day DISCUSSION
Although upper abdominal pain and chronic alcoholism are important clues in the diagnosis of pancreatitis, the latter is not often considered when a patient has massive ascites. Instances of abdominal fluid accumulation : ........j. ..Yr~ j .: *~~~~~ 4 ..............., w
~~~~~~~~~~~~~~~~~~~~~~~.... ::~~~~~~~~~~~~
::.:.:........ ...' ..
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.. .....
FX ...i..~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~. .... . . .. E
Figk.l 1. Operative
weakness,a and anorexia. The serum amylase, the ascitic fluid amylase and protein are usually elevated in patients with pancreatic ascites unlike cirrhotic ascites where the protein content is low and the amylase normal or only minimally elevated. Bockus,3 in 1951, reported that 21% of patients with cirrhosis have elevations of the serum amylase in absence of pancreatic disease. Since pancreatic ascites can masquerade as cirrhotic ascites, a differentiation between the two is important in view of the effectiveness of surgical therapy for the former and not the latter. Typically, the patients are predominantly men in their 3rd to 5th decade of life. Weight loss is rapid and progressive despite fluid accumulation. A common predisposing factor is chronic alcoholism and most patients experience intermittent abdominal pain compatible with attacks of pancreatitis. The ascites is very often massive and refactory to diurectics but occasionally subsides spontaneously. Barua,4 in 1962, suggested that massive pancreatic ascites was the result of chronic peritoneal irritation by pancreatic enzymes. Others suggest that the ascites is due to compression of the portal vein or its tributaries by a pancreatic pseudocyst. MacLaren,s in 1966, hypothesized that obstruction of the retroperitoneal and mesenteric lymphatics was the cause of the ascites. If, however, a pseudocyst is not present, as in some reported cases, a direct pancreatic duct leak must be assumed. Most of the pseudocysts associated with pancreatic ascites seem to be small, probably because they are decompressed into the peritoneal cavity. When a diagnosis of pancreatic ascites seems warranted, laparotomy should be performed. If a pseudocyst is recognized, internal drainage of the cyst should be instituted. If an obvious pseudocyst is not present, operative pancreatography should be performed to identify a pancreatic duct leakage and drainage by a Roux-en-Y loop. In the first case reported above, however, we found it much easier to primarily close the leak and performed a sphincterotomy, since a duodenotomy had already been made for the pancreatogram. If
'' ..
.j,
~........
..
..pneor
revealing a paten
'c'
i. .1~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~...........
M..~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~. .....
.|....:.e.g....~~~~~~~~~~~.
Fig. 1. Operative pancreatogram revealing a patent pancreatic duct with a point of leakage directed cephalad at the junction of the head and body of the pancreas
occur in association with hepatic cirrhosis, intra-abdominal cancer, tuberculous peritonitis, cardiac and renal failure and are usually readily recognizable in patients with pancreatic cancer, in whom ascites is present clinically in 10-20%. Tuberculous and cirrhotic ascites usually have normal amylase, unlike pancreatic ascites, where the amylase is quite high. The lack of correlation between serum and ascitic fluid amylase in some cases as noted by Jensen and Babier suggests two portals of entry into the blood stream: one directly from the blood and the other indirectly from the pancreas via the peritoneal cavity. The outstanding common feature of patients with pancreatic ascites are, heavy alcohol intake, variable degree of intermittent abdominal pain, massive ascites, marked weight loss,
MAY, 1975
(Concluded on page 247)
247
Briefs
Vol. 67, No. 3
opened and closed sites, transported emergency teams and reported to headquarters every hour on general conditions of each site. A few precedents in community affairs were set. One was the concerted effort of more than 400 volunteers who made the program a success. In addition to the Richmond Medical Society and their staffs. The Licensed Practical Nurse's Alumni Association participated as a group and served as registrars and screeners. The Association of Black Social Workers served as registrars and site coordinators. The staff of the Model Neighborhood Policy Board widely publicized the screening program and provided offices for a common post on the days that screening was conducted. The staff of the Churchill MultiService Center distributed more than 10,000 flyers and served as site coordinators. The Red Cross, the Richmond Area Heart Association, the Medical College of Virginia and the Richmond Academy of Medicine solicited volunteers. The Boy Scouts assisted in distributing flyers, and other social and civic clubs participated as registrars and site coordinators. The Richmond Urban League solicited sites, administered the program, compiled statistical data, and did all of the community organization. The Ciba Pharmaceutical Company provided flyers, pamphlets and other printed material. The General Medical Corporation provided 10,000 flyers for distribution and doughnuts and coffee for site workers. Twenty-thousand flyers were distributed and 150 posters were distributed throughout the Churchill Community.
talk show interviews, coverage in the local newspaper, and radio personalities conducting remote broadcasting served to increase the enthusiasm and participation of the city and the target area. Educational materials were selected and developed for the black community; keeping in mind the degree of literacy of the majority of the adult population within the community. Ciba's CHEC Program materials were also used. Blood pressures were taken from a total of 39 East End sites. Screening was conducted from 15 sites on Friday, May 24, 15 sites on Saturday, May 25, and from 19 sites on Sunday, May 26. The Friday sites were open from 4:00 to 9:00 p.m. The Saturday sites were open from 9:00 a.m. to 4:00 p.m., and the Sunday sites were open from 10:00 a.m. to 3:00 p.m. All screening sites on Sunday, May 26, were from churches, except for the site at Chimboraze Park. East End ministers had declared the Sunday of May 26, High Blood Pressure Sunday. Screening on Friday and Saturday was conducted from schools, shopping plazas, recreational centers, and drug stores within housing developments. Screening at shopping centers was conducted in office trailers on their parking lots. A mobile van from St. Mary's Hospital (custom built medical office on wheels), roved the community concentrating its coverage on barber shops, beauty salons, pool halls and out-laying areas that did not have a screening site. The mobile van's route of travel was known in advance. The van was equipped with a telephone, which made it easy to locate in an emergency to send an additional team to it or send it to a screening site to help until a team could be sent. Each screening site had one or more physicians present. In addition, the physicians of the Richmond Medical Society closed their offices and brought their staffs into the field for the entire program. The large number of screening sites necessitated the need for field coordinators. The social workers of the community took charge of this function. In teams of two, each group was responsible for three screening sites. Their responsiblities were to insure that data was collected properly, each site received equipment and materials,
RESULTS After 13 hours of screening on the three days, 4,480 persons were screened, of whom 1,849 or 38% had elevated pressures; 405 or 22% (N = 1,849) completed follow-up, of which 293 or 72% (N = 349) were hypertensive and 227 were placed under treatment. Unfortunately, it was discovered too late that at many sites the data cards were given to the screenees. After collaboration with the volunteers it was estimated that 8 to 10 thousand persons had been screened. The project was conducted under the auspices of the Virginia Regional Medical Program, Inc. .
(Muna et al., from page 224)
the pancreatic duct leakage cannot be identified, a ductal drainage procedure, such as the Duval or Puestow procedures, should be done to allow the leak to seal. SUMMARY
Two cases of pancreatic ascites secondary to ruptured pseudocyst presenting within a two month period in a major city hospital are reported. The clinical syndrome is being recognized with increasing frequency. A distinction between pancreatic ascites and cirrhotic ascites should be made since surgical treatment is favorable for the former. Elevated serum and
ascitic fluid amylases and protein are diagnostic of pancreatic ascites. LITERATURE CITED
1. SMITH, E. B. Hemorrhagic Ascites and Hemothorax Associated with Benign Pancreatic Disease. Arch. Surg., 67:52-56, 1953. 2. JENSEN, N. M. and B. M. BABIER. Ascites Due to Chronic Pancreatitis. J.A.M.A., 201:488-489, 1967 3. BOCKUS, H. Gastroenterology, Vol. 3 Saunders, Philadelphia and London, 1964, pp. 840. 4. BARUA, R. L. and F VILLA and F STEIGMANN. Massive Ascites Due to Pancreatitis. Amer. J. Digest. Dis., 7:900, 1962. 5. MACLAREN, I. F and J. M. HOWARD, and G. L. JORDAN. Ascites Associated with a Pseudocyst of Pancreas. Arch. Surg., 93:301-303, 1966.
