Major gastrointestinal hemorrhage associated with pancreatic pseudocyst

Major gastrointestinal hemorrhage associated with pancreatic pseudocyst

Major Gastrointestinal Hemorrhage Associated with Pancreatic Pseudocyst James T. Wolstenholme, MD, White River Junction, Vermont Severe upper gas...

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Major Gastrointestinal

Hemorrhage Associated

with

Pancreatic Pseudocyst James T. Wolstenholme,

MD, White River Junction, Vermont

Severe upper gastrointestinal hemorrhage often presents a difficult diagnostic problem and a challenge in the selection of a successful therapeutic approach. Gastrointestinal bleeding is relatively rare secondary to pancreatitis. This fact is often not considered in the differential diagnosis and may delay proper treatment and lead to difficult operative problems for which the surgeon may not be prepared. In an analysis of 1,500 cases of acute gastrointestinal hemorrhage, Palmer [I] observed only one case that originated from the pancreas. Conversely, bleeding is not an uncommon complication of pancreatitis. Kirby, Howard, and Rhoads [2], studying the causes of death in a series of patients dying from pancreatitis at the University of Pennsylvania, found that delayed hemorrhage was the cause of death in 52 per cent. Erb and Grimes [3] reported an unusually high incidence of 38 per cent for gross gastrointestinal hemorrhage complicating the presence of a pseudocyst in seventeen patients with pancreatitis. Others have reported a lower rate of 5 to 10 per cent. Recently the statement was made that operative intervention in patients with pancreatitis and massive bleeding is of little avail because it has been associated with an 80 per cent mortality; therefore, conservative treatment is recommended [4]. I wish to report three cases in which an aggressive surgical approach was used and appeared to be life-saving. From the Surgical Service, Veterans Administration Center, White River Junction, Vermont, and Dartmouth Medical School, Hanover, New Hampshire. Reprint requests should be addressed to Dr Wolstenholme, Veterans Administration Center, White River Junction, Vermont 0500 1. Presented at the Fifty-Fourth Annual Meeting of the New England Surgical Society, Portsmouth, New Hampshire, September 27-29, 1973.

Volume 127, April 1974

Case Reports Case I. Pancreatic pseudocyst with .;pLenic artery hemorrhage: The patient (ET) was a forty year old man who was hospitalized on June 19, 1969, because of epigastric pain of three weeks’ duration. For the five days before. admission the pain had increased greatly in severity. He described the pain as being located in the left upper quadrant, later becoming periumbilical, and being dull with occasional crampy exacerbations. It was accompanied by nonproductive vomiting. The patient had a history of alcoholism for t,he past thirteen years. A diagnosis of peptic uicer had been made ten years previously but there had been no recurrent symptoms since then. Physical examination on admission revealed a pale, cachectic man. Vital signs were normai. There were physical signs of a small pleural effusion on the left side. The abdomen was soft with tenderness to deep palpation in the left upper quadrant and epigastrium. Over this area a loud bruit was heard. No definite masses were palpated, and bowel sounds were absent. The stool was of normal color. On admission the hemoglobin was 8.7 gm per 100 ml, white blood cell count was 23,900 per rnrn:( with a shift to the left, and the erythrocyte sedimentation rate was 123 mm per hour. Electrolyte and blood urea nitrogen levels were within normal limits, butt the serum amylase was 960 Somogyi units. Total bilirubin was 0.9 mg per cent; the direct, 0.3 mg per cent. Alkaline phosphatase was 9.7 King-Armstrong units. The initial chest film showed an infilt,rate at the left base and a small pleural effusion. There was a suggestion of elevation of the left diaphragm. Plain roentgenograms of the abdomen revealed a soft tissue fullness in the left upper quadrant. No pancreatic calcifications were noted. The rugal pattern of the stomach appeared edematous. A Gastrografinm study of the upper gastrointestinal tract showed the stomach to be displaced anteriorly and to the left. He was admitted on the Medical Service and treated with nasogastric suction, intravenous hydration. trans-

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Figure 1. Case II. Operative pancreaticogram filling of the pseudocyst.

showing

fusions, and antibiotics. On the second hospital day, because of a temperature elevation to 101.8’F, an increase in the white blood cell count, and more acute signs in the abdomen, a peritoneal tap of both lower abdominal quadrants was performed. Serum amylase determination of the cloudy fluid obtained was 326 Somogyi units. Smear of this fluid was noncontributory. The patient’s condition improved slowly with the medical regimen despite intermittently bloody nasogastric drainage. On the fifth hospital day he suddenly vomited approximately 1,500 cc of bright red blood and showed signs of shock. After resuscitation, laparotomy was performed and revealed that the stomach was filled with clots. These were evacuated by gastrotomy. The posterior wall of the stomach was indented by a cystic mass. Adherent to the gastric mucosa overlying this indentation was a small blood clot, and when this was wiped away, massive arterial bleeding took place that threatened exsanguination. An incision was quickly made through the posterior wall of the stomach into a 10 cm pancreatic pseudocyst. Arterial hemorrhage was originating deep within the cystic cavity. Bleeding was controlled temporarily by pressure on either side of the cyst wall, and after the cystic cavity was suctioned, the splenic artery could be seen coursing in the base of the cyst with a 2 to 3 mm erosion. Control of the bleeding was accomplished by figure-of-eight suture-ligatures on either side of the arterial opening. Cystogastrostomy was performed. His postoperative course was uneventful, and he has since been well.

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Case II. Pancreatic pseudocyst with gastroduodenal artery hemorrhage: Three weeks previous to admission the patient (RKW), a fifty-five year old man, began to experience dull epigastric pain that occasionally radiated through to the back. Prior to admission he vomited a large quantity of blood and passed several tarry stools. He was admitted to a nearby hospital, given transfusions, and subsequently transferred on February 5,197O to White River Junction Veterans Administration Hospital. There was a long history of heavy alcoholic intake. On examination the patient was thin, blood pressure was 110/80 mm Hg, pulse was 78 per minute, and he was in no acute distress. Examination of the abdomen revealed scars of previous surgery. No organs or masses were palpable, but there was moderate tenderness to deep palpation in the midepigastrium. Bowel sounds were hyperactive. The stool was Hemateste-positive. On admission hemoglobin was 9.3 gm per 100 ml; white blood cell count was 8,650 per mm3 with a normal differential, and the erythrocyte sedimentation rate was 37 mm per hour. Electrolyte and blood urea nitrogen levels were within normal limits. A nasogastric tube was passed, and no blood was present in the drainage. Sigmoidoscopy and gastroscopy as well as a barium enema gave negative results. An upper gastrointestinal series showed norma! results of subtotal gastrectomy. There was no calcification in the region of the pancreas. A long intestinal tube was passed in an attempt to localize the bleeding, but the results were inconclusive. Because of the patient’s continued loss of blood despite transfusions, laparotomy was performed and an indurated pancreas with a 4 cm mass in the head was found. This mass was biopsied and reported as showing chronic pancreatitis. Gastrotomy did not reveal any source of bleeding. No marginal ulcer was visualized. Choledochotomy together with choledochography was performed, which showed the common duct to be bowed in a smooth fashion by an extrinsic mass in the head of the pancreas. Pancreatography performed by means of a duodenotomy showed filling of a 3 to 4 cm pseudocyst in the head. (Figure 1.) At operation, transduodenal sphincterotomy was performed together with T tube drainage of the common duct and subdiaphragmatic vagotomy. The patient did well until the twentieth postoperative day when he had a grossly bloody bowel movement. A repeated upper gastrointestinal series showed no change from that performed on admission. A T tube choledochogram revealed compression of the common duct with apparent increase in the size of the pancreatic mass noted previously. He continued to recuperate slowly until the seventh postoperative week when he suddenly vomited a large amount of blood, had several bloody bowel movements, and went into shock. Because of persistent blood loss, laparotomy was undertaken. The mass in the head of the pancreas was again noted; however, no site of bleeding was obvious. Gastrotomy was again performed, and

The

American

Journalof Surgery

Gastrointestinal

only after careful search was it noted that a small amount of fresh blood was emanating from the afferent limb of the gastrojejunostomy. Duodenotomy revealed blood coming from the ampulla of Vater. Because of the solid feel of the mass in the head of the pancreas, the mass was interpreted to represent most likely a bleeding tumor and resection was undertaken. After the head of the pancreas had been mobilized, it became apparent that the mass was cystic and intimately adherent to the gastroduodenal artery. The mass was opened and proved to be a thick-walled pancreatic pseudocyst filled with fresh blood and actively bleeding from the site of adherence to the gastroduodenal artery. The gastroduodenal artery was ligated, and the head of the pancreas containing the cyst and the duodenum were resected. The pathology report showed acute and chronic pancreatitis and wall consistent with pancreatic pseudocyst. The patient had a slow uncomplicated recovery and has since continued to do well.

Case III. Pancreatic pseudocyst with splenic artery erosion, demonstrated by angiography: This was the fifteenth admission of the patient, a forty-seven year old man (CB), to White River Junction Veterans Administration Hospital. His chief complaint on admission was severe abdominal pain, nausea, and vomiting of twentyfour hours’ duration. The history revealed prolonged heavy alcoholic intake and multiple admissions for alcoholism, pancreatitis, fractures, and Laennec’s cirrhosis. Physical examination on admission indicated that the patient was in acute distress. Blood pressure was 112/80 mm Hg, pulse 80 per minute, respirations 16, and temperature 99’F. There was diffuse abdominal tenderness, most marked on the left; the liver and spleen were both palpable. Bowel sounds were hypoactive. The stool was positive for occult blood. On admission hemoglobin was 10.2 gm per 100 ml and white blood cell count was 5,300 per mm3 with no shift. The electrolytes were within the normal range. Serum amylase was 720 Somogyi units. Alkaline phosphatase level was slightly elevated as was the serum glutamic oxalacetic transaminase. Total serum bilirubin was 3.9 mg per cent (direct, 2.7 mg per cent). A plain x-ray film of the abdomen showed no gross distention of the small bowel. Pancreatic calcifications were present. An upper gastrointestinal series suggested the presence of an epigastric mass, consistent with a pancreatic pseudocyst and causing a definite widening of the retrogastric diameter. The patient was transferred to the Surgical Service for elective drainage of the pseudocyst. On February 13, 1972 the patient suddenly vomited blood but did not require transfusions. A repeated upper gastrointestinal series showed no change in cornparison with the recent examination that demonstrated the pseudocyst. On February 23 the patient again vomited a large amount of blood, and despite transfusions, vital signs

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were poorly maintained. Emergency laparotomy was performed. The stomach was distended with clotted blood, and after gastrotomy pulsatile bleeding could be seen coming from a small eroded area of the midportion of the posterior wall of the stomach at the site of an indentation consistent with the presence of a retrogastric pulsating mass. The bleeding area was effectively controlled with several silk figure-of-eight sutures. Because of surrounding inflammatory reaction, no approach could be made to definitely delineate whether this mass was a true aortic aneurysm or a pseudoaneurysm involving a pancreatic cyst, and it was thought that further diagnostic studies were indicated. No further surgery was performed at this time. The gastrotomy and abdomen were closed. Early in the postoperative course a celiac axis angiogram was taken which demonstrated the filling of the pseudocyst by the splenic artery. (Figure 2.) Reoperation was carried out with the ligation of the splenic artery from within the cyst. Cystogastrostomy was performed. The patient had a slow postoperative recovery with several draining sinus tracts. He has been hospitalized on two occasions since his operation, once for pneumonia and once for jaundice secondary to cirrhosis. Comments Bleeding often process;

acute

with

the outcome

ally fatal pancreatic control

in the

associated

phase

of pancreatitis

a necrotizing,

is

suppurative

in many of these cases is usu-

[2]. Conversely, bleeding caused by a pseudocyst often lends itself to surgical

and

and operative

therefore

requires

intervention

prompt

diagnosis

[5,15].

Figure 2. Case Ill. Celiac ax& angiogram detinstrating communication between splenic artery and pancreatic pseudocyst (arrows).

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In t.he process of enlarging, a pseudocyst incorporates adjacent vessels into its wall. Some of these vessels, especially veins, become thromhosed; arteries appear to continue to maintain their patency as they are exposed to the digestive activity of t.he contents of the pseudocyst. If a main artery is eroded by the digestive process, the pseudocyst is converted into a pseudoaneurysm

WI. The wall of the cyst is now subjected to the arterial pressure. With continued pressure-erosion, the pseudocyst may perforate into an adjacent segment of the gastrointestinal tract, resulting in hemorrhage [5]. Occasionally the pseudocyst, now a pseudoaneurysm, may decompress itself through the pancreatic ductal system and ampulla of Vater [7,R]. Rarely, such a pseudocyst will rupture directly into the peritoneal cavity, resulting in a hemoperitoneum [9, IO]. In the patient with gastrointestinal bleeding and pancreatitis or in the patient who has had a pseudocyst surgically decompressed, the need to distinguish the cause of this bleeding is imperative but may be exceedingly difficult. The palpation of an upper abdominal mass may help in establishing the presence of a pseudocyst. If the mass shows a rapid increase or decrease in size, bleeding into or from the cyst should be suspected. The presence of a bruit or pulsations in the upper part of the abdomen would support the vascular nature of the lesion. It then becomes necessary to differentiate such a mass from a true aneurysm of t,he aorta or one of its visceral branches.

114. In order not to obscure the opacification of the major vessels by barium retained in the intestinal tract, angiography of the celiac axis and superior mesenteric artery should be undertaken early. By demonstrating a pseudocyst-aneurysm [12], such a study would confirm the diagnosis and, in addition, might identify the leaking vessel. A more precise surgical approach would be possible that might include the isolation and control of the bleeding vessel prior to opening the pseudocyst. Gastroscopy may not be very rewarding but could help to exclude other causes of gastrointestinal hemorrhage. Barium x-ray studies may be performed if the condition of the patient permits. A scan of the spleen has been employed in two instances to localize a pseudocyst in the tail of the pancreas and suggest erosion into the splenic hilus [13].

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In the surgical approach consideration should be to isolation of the major feeding vessel. Extracystic dissection may prove, to he t8echnicaliy difficult because of surrounding inflammation secondary to pancreatitis but it ha’; been recommended [14]. In two of the cases reported herein, intracystic control of the bleeding by sut,ure-ligature was accomplished after adequate exposure had been obtained by opening the pseudocyst.. Care must be taken not to injure underlying structures, such as the common duct or aorta, by the hemostatic suture-ligatures. lntraluminal intubation of the bleeding artery with a Fogarty catheter may he feasible to achieve temporarily control of the bleeding and plan a more definitive approach. Tamponading the cyst while the aorta is freed at the diaphragm for cross-clamping is feasible. A novel method in the treat,ment of an unruptured pseudocyst-aneurysm was utilized by Greenstein, DeMaio, and Nabseth [ lEi] who wired the cystic cavity to induce thrombosis with a successful result.

given

Summary

Although the pancreas is not a frequent source of major gastrointestinal hemorrhage, bleeding in patients with pancreatitis is not an uncommon complication. In patients with bleeding who are known to have pancreatitis or a pseudocyst, this organ must be considered a possible site of hemorrhage. It is recommended that celiac axis and superior mesenteric artery angiography he performed prior to barium contrast studies. If bleeding is originating from a pancreatic aggressive surgical intervention pseudocyst, should be undertaken. Three cases are described in which prompt operation was successful. Intracystic suture-ligation of the bleeding vessel together with cystogastrostomy was performed in two cases. One case of bleeding from a pseudocyst in the head of the pancreas and involving the gastroduodenal artery was treated by excision of the cyst and head of the pancreas. Aclznowledgment: I wish to thank Dr Walter B. Crandell for his help and suggestions in the preparation of this manuscript and Mrs Evelyn Putney for secretarial assistance.

The American Journal of Surgery

Gastrointestinal

References

’ Palmer t. Upper Gastrointestinal Hemorrhage. Springfield, Ill, 2

3. 4. 5. 6. 7.

8. 9. 10. 11.

12.

13.

14. 15.

Thomas, 1970. Kirby CK. Howard JM, Rhoads JE: Death due to delayed hemorrhage in acute pancreatitis. Surg Gynecol Obstet 100: 458, 1955. Erb WH. Grimes EL: Pseudocyst of the pancreas. Am J Surg 100: 30, 1960. Trapnell JE: Management of complications of acute pancreatitis. Ann R CollSurg Eng149: 361, 1971. Cogbill CL: Hemorrhage in pancreatic pseudocysts. Ann Surg 167: 112, 1968. Bardenheier JA, Quintero 0, Barner H: False aneurysm in a pancreatic pseudocyst. Ann Surg 172: 53, 1970. Dalton WE, Lee HM, Williams GM, Hume D: Pancreatic pseudocyst causing hemobilia and massive gastrointestinal hemorrhage. Am J Surg 120: 106. 1970. Glass I?. Newstedt JR: Hemobilia: an unusual complication of chronic pancreatitis. Missouri Med61: 853, 1964. Dardik I. Dardik H: Patterns of hemorrhage into pancreatic pseudocysts. Am J Surg 115: 774, 1968. Case Records of Massachusetts General Hospital (case 35202). NewfnglJMed240: 815, 1949. lnglis FG. McKee NH: Unusual cause of upper gastrointestinal bleeding: rupture of splenic artery aneurysm into stomach with survival. Can J Surg 15: 276, 1972. Kadell B, Riley JM: Major arterial involvement by pancreatic pseudocyst. Am J Roentgen01 Radium Ther Nucl Med 99: 632, 1967. Warshaw AL, Chesney T, Evans GW, McCarthy HF: Intrasplenic dissection by pancreatic pseudocyst. N fngl J Med 287: 72, 1972. Buchnam CA: Arterial hemorrhage in pseudocyst of pancreas. Arch Surg 92: 405, 1966. Greenstein A, DeMaio EF, Nabseth DC: Arterial hemorrhage associated with pancreatic pseudocysts. Surgery 69: 56, 1971

Discussion Donald C. Nabseth (Boston, Mass): Several years ago we reported a small series of cases of hemorrhagic pancreatic pseudocysts. Our series was similar to that of Dr Wolstenholme except that two patients had hemorrhagic cysts that did not communicate with the gastrointestinal tract. This indicates that the cystic contents have a digestive quality capable of eroding into major blood vessels without direct activation of pancreatic enzymes by intestinal content. Any patient suspected of having a pancreatic pseudocyst and in whom sudden enlargement of the mass, an arterial bruit, or gastrointestinal bleeding develops should have angiography for confirmation of the diagnosis and precise identification of the responsible blood all hemorrhagic pseudocysts vessel. Furthermore, should be regarded as possible false aneurysms and should carry a sense of surgical urgency. We agree with the author that transcystic suture-ligation of the eroded artery together with internal drainage of the cyst is usually the procedure of choice. However, this was impossible in one of our patients because of the poor condition of the patient and the inaccessible location of the cyst posterior to the head of the pancreas in close proximity to the hepatic arteries. (Slide) It was elected to use the ancient technic of wir-

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Hemorrhage

and Pancreak.

Pseudocyst

ing which resulted in complete obllterarlc3rl of the p$eudocyst-aneurysm and recovery of the patient. An angiogram at six months shows the wired cyst in close proximity to the right and left hepatic, arteries. Obviously, this is not a procedure to be widely rec,)mmended. but it, seemed to be a good solution to this palien t’s pro hlem. Gerald 0. Strauch (Stamford, Corm): I would like to support the thrust of Dr Wolstenholme’s report wit,h the report of a patient we recently treated. An alcoholic woman entered our hospital with a third episode of massive gastrointestinal hemorrhage. Mesenteric angiography at another hospital had failed to establish the cause of bleeding. Celiac angiograms at Stamford Hospital revealed hemorrhage from the dorsal pancreatic artery into a large intrapnncreatic pseudocyst. At operation the pseudocyst was found to communicate with a markedly dilated duct of Wirsung. The mechanism of gastrointestinal hemorrhage was demonstrated to be entrance of blood from the pseudocyst into the duodenum by way of the duct of Wirsung. Splenectomy was performed and the splenic artery was dissected to the dorsal pancreatic artery, which was ligated at its origin. The intrapancreatic cyst was drained by a cystoduodenostomy created by incisional enlargement of the orifice of the duct of Wirsung, unroofing of the cyst, and anastomosis of the cyst wall to the duodenal mucosa. Drainage of the common bile duct and complementary Stamm gastrostomy were also carried out. The patient recovered after a complicated early postoperative course. Unfortunately, this episode provided only a hrief interruption in the alcohol consumption. Claude Welch (Boston, Mass): I support Dr Wolstenholme’s conclusion about the necessity for intervention in many of these cases and the results that may be expected after rather difficult procedures. I have three cases that I would like to mention. One of them, the easiest to manage, occurred in a patient who had lower rather than upper gastrointestinal bleeding. I failed to find the lesion at the first laparotomy which was a very extensive procedure. Doctor Hedberg had to re-explore the patient a few weeks later because of recurrent hemorrhage. He found a bleeding artery from the distal pancreas that was pouring blood directly into the splenic flexure. The patient was cured immediately by resection of this area. In another case, as soon as we opened the abdomen, there was severe hemorrhage. Then, with a finger deep in the dike, we completed the difficult exposure and finally identified the source of bleeding as the left renal artery. We repaired it in continuity with arterial sutures. In a third case repeated episodes of hemorrhage occurred after cystogastrostomy from a large rent in the superior mesenteric vein. The defect was closed and the patient recovered. These patients should not be thought of as lost. They may be saved by a difficult operation as Dr Wolstenholme has proved.

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