Massive Lower Gastrointestinal From Intestinal Varices Samuel E. Wilson, MD; Richard T. Stone, MD; John P.

Christie, MD; Edward Passaro, Jr,

\s=b\ Lower gastrointestinal bleeding from intestinal varices cannot readily be detected at operation; hence, preoperative identification is important. Our experience with six patients having sudden, massive bleeding per rectum from intestinal varices suggests a group of common findings. These patients had cirrhosis, no blood in the stomach or duodenum, characteristic mucosal imprints on barium enema, or direct visualization of varices on sigmoidoscopy or colonoscopy. Only two had demonstrable esophageal varices. The diagnosis was confirmed and the site of the varices localized on the venous phase of selective mesenteric angiography in five patients. Varices were located in the duodenojejunum in two, in the cecum and ascending colon in two, and in the rectum and sigmoid colon in two patients. Three patients were treated nonoperatively with transfusion and intraarterial infusion of vasopressin into the superior mesenteric artery; one died. One patient with cecal varices had a right hemicolectomy that controlled the bleeding, but progressive hepatic failure resulted in postoperative death. The remaining two patients had successful decompression of left colonic varices by portasystemic shunt.

(Arch Surg 114:1158-1161, 1979)

lower gastrointestinal (GI) bleeding from varices is rare but often lethal. Unsus¬ pected extraesophageal varices are virtually impossible to find at operation; hence, successful management is contin¬ gent on preoperative identification. Our experience with six patients with massive lower GI tract bleeding from intestinal varices suggests a group of common findings. This report defines the characteristic clinical pattern that suggests the diagnosis, and recommends appropriate diag¬ nostic procedures and a method of surgical management.

Massive intestinal

publication May 3, 1979. Surgical Service, Veterans Administration Wadsworth Medical Angeles (Drs Wilson, Stone, and Passaro); the Department of Surgery, University of California at Los Angeles School of Medicine (Drs Accepted

for

From the Center, Los

Wilson and Passaro); and the South Miami Medical Center, Miami (Dr

Christie). Reprint requests

to Surgical Service (691/112K), Veterans Administration Wadsworth Medical Center, Los Angeles, CA 90073 (Dr Wilson).

Bleeding

MD

REPORT OF CASES

During the three years 1976 through 1978, a total of 309 patients with esophageal varices were treated at a university and Veterans Administration hospital. Five patients (1.6%) had bleeding from extraesophageal varices. An additional patient (No. 5) was seen in a community hospital. The six cases are summarized in Table 1. Case 1.—A 73-year-old woman was hospitalized for melena and intermittent, bright-red rectal bleeding of one year's duration. Upper GI tract x-ray film series, barium enema, proctosigmoidoscopy, and bone marrow biopsy all gave normal findings. A liver biopsy specimen showed postnecrotic cirrhosis. There were hepatosplenomegaly and pitting edema of the lower extremities. Laboratory data included a hematocrit value of 33 vol%. The chest roentgenogram showed moderate congestive heart failure. Shortly after admission, the patient started to pass large amounts of burgundy-colored blood. Emergency superior mesenteric arteriogram showed tortuous varices in the jejunum. The inferior vena cava and hepatic pressures were 5 mm Hg, and the hepatic wedge pressure was 20 mm Hg. After transfusion of 1,000 mL of whole blood, bleeding stopped spontaneously. The patient's cardiac fail¬ ure responded well to diuretics and digoxin. Although guaiacpositive stools and melena have again been noted, massive bleed¬ ing has not recurred after one year. Case 2.—A 64-year-old man had melena that progressed to massive, dark-red rectal bleeding. He was a chronic alcoholic, had hepatosplenomegaly and ascites, but no jaundice. The serum albumin level was 2.8 mg/dL; total bilirubin level, 1.0 mg/dL; hematocrit, 26 vol%; and platelets, 72,000/cu mm. A liver biopsy specimen obtained during a previous admission had shown severe Laènnec's cirrhosis. Endoscopy showed only "gastric tube erosion" and nonbleeding gastroesophageal varices. On the fifth hospital day, he began passing large quantities of maroon-colored blood per rectum. Endoscopy to the fourth portion of the duodenum now showed multiple duodenal and jejunal varices that were actively bleeding. Gastroesophageal varices again were not bleeding. A superior mesenteric arteriogram confirmed the duodenojejunal varices. The patient underwent emergency end-to-side portacaval shunt, resulting in a decrease in portal venous pressure from 38 to 22 cm of saline. The postoperative course was unremarkable, and he has had no further bleeding at 18 months. Case 3.—A 48-year-old woman had a 12-hour history of bright-

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red rectal bleeding. She had a ten-year history of alcoholism characterized by intermittent jaundice and confusion. Spider angiomata, palmar erythema, and hepatosplenomegaly were all present on physical examination. Red blood was present on rectal examination. Serum bilirubin level was 2.0 mg/dL; albumin level, 3.0 mg/dL; hematocrit, 35 vol%; and prothrombin time, 21 s (control, 14 s). On sigmoidoscopy, the colon was filled with blood proximal to 25 cm from the anus. There were no esophageal varices or other lesions on gastroscopy. Angiography showed massive right colonie varices, but no definite bleeding point was noted. The superior mesenteric, splenic, and portal veins were patent. No gastroesophageal varices were seen. Infusion with vasopressin (Pitressin) via the superior mesenteric artery tran¬ siently slowed the bleeding, but hepatic coma ensued and the patient died. Autopsy confirmed active Laënnec's cirrhosis as the cause of the portal hypertension. Massively dilated, tortuous, right colic varices with saccules up to 2 cm in diameter were the source of lower GI tract bleeding (Fig 1). Case 4.—A 59-year-old man was admitted with a three-day history of hematochezia. The patient was an alcoholic with known cirrhosis; an episode of bleeding esophageal varices had been treated two years previously. On physical examination, mild ascites, jaundice, and hepatomegaly were noted. Prothrombin time was 16.5 s (control, 12 s); albumin level, 2.1 mg/dL; and bilirubin level, 3.5 mg/dL. A prior liver biopsy specimen had shown severe Laënnec's cirrhosis. Barium enema suggested varices of the cecum (Fig 2). On upper GI tract endoscopy, the esophageal varices were not bleeding. Sigmoidoscopy was limited because of bright red blood originating above the 25-cm level. Visceral angiography showed varices of the cecum and ascending colon. The superior mesenteric artery catheter was left in place for intra-arterial vasopressin infusion. The superior mesenteric, splenic, and portal veins were patent. Bleeding continued and the patient required operation to prevent exsanguination. Although a right hemicolectomy controlled bleeding, progressive liver failure and hepatorenal syndrome developed, and the patient died on the tenth postopera¬ tive day. Case 5.-A 63-year-old woman with known postnecrotic cirrhosis had anemia and hematochezia. There was no blood in the esopha¬ gus or stomach. Bleeding ceased spontaneously after transfusion of 1,000 mL of blood. Sigmoidoscopy gave normal findings, but barium enema disclosed a 1-cm "polypoid mass" in the sigmoid colon. Colonoscopy showed extensive submucosal varices begin¬ ning at the splenic flexure and involving the descending and sigmoid colons. The polypoid mass in the sigmoid was, in fact, a projecting varix. No further treatment was instituted. Although the patient continues to have guaiac-positive stools and anemia,

major bleeding has not resumed at two years. Case 6.-A 62-year-old man, a chronic alcoholic for more than 20 years, complained of passing large amounts of bright-red rectal blood for two days. Physical examination disclosed minimal ascites and mild icterus. There was no blood on gastric aspiration. Hematocrit value was 19 vol%; prothrombin time, 17 s (control, 12 s); albumin level, 2.6 mg/dL; and bilirubin level, 2.9 mg/dL. Sigmoidoscopy showed nonbleeding internal hemorrhoids, with red blood filling the rectal ampulla. A large submucosal venous sinusoid was seen at 10 cm, clearly above the internal hemorrhoids. Angiogram showed a dilated inferior mesenteric vein and varices of the left colon (Fig 3). Colonoscopy confirmed varices of the sigmoid and descending colon. Bleeding continued and, at opera¬ tion, massively dilated varices of the inferior mesenteric vein were present in the sigmoid mesocolon. Portal venous pressure was 36 cm of saline initially, decreasing to 21 cm of saline after decom¬ pression by a side-to-side central splenorenal shunt (Fig 4). The patient has remained asymptomatic for one year. COMMENT

patients, the source of massive gastrointestinal bleeding is either pancolonic diveror angiodysplasia of the cecum and ascending colon. By reporting our experience with these six patients in In

than 80% of

lower ticula

whom the lower GI tract bleeding was due to varices, we wish to emphasize the diversity of lesions causing hemato¬ chezia, and, consequently, the necessity for accurate preoperative identification. Bleeding due to portal hypertension most commonly occurs from gastroesophageal varices. Clinical reports, however, indicate that bleeding varices may occur in any' ' area of the GI tract, including the stomach,' duodenum,-

jejunum,' cecum,s" descending colon," rectosigmoid,171" and the total colon." Even ileostomy stomas in the cirrhotic patient may develop a caput medusae of varices at the mucocutaneous junction due to the enlargement of portasplenic venous anastomotic vessels."214 In our patients, the intestinal varices were located in the duode¬ num and jejunum (two), the cecum and ascending colon (two), and the descending and sigmoid colon (two). The overall incidence of symptomatic extraesophageal varices is unknown but can be approximated. Colonie varices were noted as a source of bleeding in two patients among 2,912 consecutive adult autopsies for an incidence of

Table 1.—Clinical Data: Lower Gastrointestinal

Bleeding

From Intestinal Varices

Diagnostic

Yes

Cause of Portal Hypertension Postnecrotic cirrhosis Laënnec's cirrhosis

No

Laënnec's cirrhosis

SMA

Cecum

Yes

Laënnec's cirrhosis

SMA arteriogram, barium enema

Right colectomy

Rectosigmoid

No

Postnecrotic cirrhosis

Colonoscopy,

Medical

Died 10 days after opera¬ tion Alive at 2 yr

Rectosigmoid

No

Splenorenal

Alive at 1 yr

Patient/

Esophageal

Age, yr/Sex

Site

1/73/F 2/64/M

Jejunoileal Duodenojejunal

3/48/F

Right

4/59/M

5/63/F

6/62/M

more

colon

Varices No

Test

arteriogram Endoscopy, SMA arteriogram

SMA4

arteriogram

barium Laënnec's cirrhosis

Treatment

Outcome

Medical Portacaval shunt Medical

Alive at 1 yr Alive at 18 mo

Died at 5

days

enema

Colonoscopy, SMA arteriogram

'Superior mesenteric artery.

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shunt

0.07%/' This incidence is probably close to the overall figure since 25 (81%) of 31 reported cases of intestinal varices were located in the colon." Several mechanisms have been proposed to explain the formation of submucosal varices in the small intestine and colon. In patients without cirrhosis, a congenital anomaly of the venous system has been suggested by both Lopata and Berlin1" and Levy et al." Such a vascular anomaly has never been observed clinically, so this explanation remains conjectural. Mesenteric vein thrombosis or obstruction is a plausible reason for localized intestinal venous hyperten¬ sion. Burbige et ab noted varices formed at the splenic flexure due to splenic vein thrombosis, a consequence of previous pancreatitis. Congestive heart failure with chronic passive congestion of the liver and mesenteric venous hypertension was thought to have produced conges¬ tion, hyperemia, and marked dilation of the submucosal

Fig 1.—Case 3. Cecal wall. Submucosa is filled with massively dilated venous channels (hematoxylin-eosin, original magnifica¬ tion x10).

4. Barium enema illustrates varices in cecum.

Fig 2.—Case

cecal veins in a patient who died after four episodes of lower intestinal bleeding.•" Although this etiology has not been confirmed in other patients with colonie varices, it may have been a contributory cause of the mesenteric venous hypertension in our second patient. Surgeons have been reluctant to ascribe the bleeding of colonie and jejunal varices to portal hypertension, primari¬ ly because severe rectal bleeding rarely occurs from the frequently observed hemorrhoidal varices of the cirrhotic. Nevertheless, of the 15 patients with colonie varices collected by Doberneck and Janovski,'"' ten had cirrhosis and one had fibrosis of the portal vein. Portal hyperten¬ sion, therefore, presumably existed in at least 11 of their patients; in seven, manometry confirmed the increased mesenteric venous pressure. Portal hypertension second¬ ary to cirrhosis appears to be responsible for the formation of intestinal varices in all six of our patients. Four of the six had no variceal involvement of the gastroesophageal junction. The absence of esophageal var¬ ices in patients with portal hypertension and colonie varices is best explained by a lack of collateral communica¬ tion from the portal and coronary veins to the azygous vein. This lack of collaterals has been noted previously.'" The management of patients with intestinal varices has been marred by both incorrect preoperative diagnosis and subsequent operation for upper GI tract bleeding of unknown cause.' In some patients, bleeding esophageal varices, suspected preoperatively, were not found at oper¬ ation, and the source of bleeding was not readily identified by the surgeon. Bleeding intestinal varices should be considered in every patient with known liver disease and suspected portal hypertension who has lower gastrointesti¬ nal bleeding. It is imperative that the location and cause of bleeding be found prior to operation. Absence of upper gastrointestinal bleeding is confirmed by passing a nasogastric tube into the stomach or by gastroduodenoscopy. Gastroduodenoscopy, extended to the fourth portion of the

Fig 3.—Case 6. Visceral angiography shows patent splenic and portal vein, with dilation and varices (arrow) of inferior mesenteric vein.

Fig 4.—Case 6. Postoperative splenic arteriogram shows patency of splenorenal shunt, flow into vena cava, and absence of inferior mesenteric varices.

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Table 2—Clinical

Reports

of Treatment of Intestinal Varices1

No. of Cases

Site

Treatment

Small intestine

Portasystemic Cecum and

Sigmoid

ascending

Outcome 1 alive, 1 died 5 alive up to 2 yr 1 alive, 2 died 5 died Alive at 1 mo

Medical colon

colon and rectum

shunt

(ligation

failed in

one)

Medical

Resection Portacaval shunt Medical Portasystemic shunt Resection or other procedure

17

duodenum, may be a worthwhile examination for small intestinal varices; it established the diagnosis in one of our patients. Evaluation should begin with sigmoidoscopy because rectosigmoid varices are quite easily identified by this method. Wagner et al," however, cautioned that if air is insufflated through the sigmoidoscope, the intraluminal

pressure may collapse the varices to such an extent that they become invisible. Colonoscopy is of limited value during the bleeding period, but after cessation of hemor¬ rhage and adequate bowel preparation, varices of the cecum and ascending colon may be identified. On barium enema, if the colon is free of blood clots and fecal material, varices appear as radiolucencies of the colon wall. Again, if the barium is instilled with increased pressure, the varices may be compressed and not visual¬ ized. The postevacuation film is likely to be the most informative. On occasion, varices of the duodenum and the first portion of the jejunum have been identified on sequential barium examination of the small bowel.-1 Barium studies should not be done on the actively bleeding patient, since residual barium may confound subsequent

angiography.

The essential diagnostic test is selective mesenteric In five of our six patients, the venous phase of the mesenteric arteriogram clearly outlined the varices. One should not expect, however, to see contrast material extravásate into the bowel lumen, as the concentration at

angiography.

10

7

alive, 1 died, 2 unknown

4 alive (2 rebled) 1 alive, 2 died

4

3

the venous level is usually too diluted for visualization within the gut. Splenoportography has not been helpful in demonstrating colonie varices. We treated three patients with transfusion and intraarterial infusion of vasopressin into the superior mesenter¬ ic artery; one died of continued hemorrhage and liver failure. One patient with cecal varices had a right hemicolectomy that controlled bleeding, but died of hepatic failure. The remaining two patients had successful decom¬ pression of left colonie and duodenojejunal varices, respec¬ tively, by portasystemic shunts. This small number of patients by itself is, of course, insufficient to draw thera¬ peutic conclusions, but when added to the 27 previously reported cases, it permits some tentative recommendations (Table 2). Medical management is indicated initially and should employ vasopressin infusion early, since no tamponade techniques are applicable. Local control of small intes¬ tinal varices by suture ligation or segmental resection has been attempted on nine occasions, failing in eight, with seven deaths. All ten patients in whom portacaval shunt has been done survived for up to two years. On the basis of this collected experience, we would propose that bleeding from intestinal varices, severe enough to require operation, should be treated by portasys¬ temic shunt. '

D.

Byrnes provided editorial assistance.

References 1. Stone

RT, Wilson SE, Passaro E Jr: Gastric portal hypertension. Am J

Surg 136:73-78,

1978. 2. Perchik L, Max TC: Massive hermorrhage from varices of the duodenal a loop in cirrhotic patient. Radiology 80:641-644, 1963. 3. Shearburn EW, Cooper DR: Duodenal varices treated by portacaval shunt. Arch Surg 93:425-427, 1966. 4. Rosen H, Silen W, Simon M: Selective portal hypertension with isolated duodenojejunal varices. N Engl J Med 277:1188-1190, 1967. 5. Feldman M Jr, Smith VM, Warner CG: Varices of the colon. JAMA 179:729-730, 1962. 6. Levy JS, Hardin JH, Shipp H, et al: Varices of cecum as an unusual cause of gastrointestinal bleeding. Gastroenterology 33:637-640, 1957. 7. Case 40102, Case records of the Mass General Hospital. Engl J Med 250:434-438, 1954. et a al: Colon varices, complication of 8. Burbige EJ, Tarder G, Carson S, pancreatitis with splenic vein thrombosis. Am J Dig Dis 23:752-755, 1978. N

9. Hirsch F, Pirout A: Varices due colon gauche. Arch Mal Appar Dig 52:73-82, 1963. 10. Lopata HI, Berlin L: Colon varices: A rare cause of lower gastrointestinal bleeding. Radiology 87:1048-1050, 1966. 11. Wagner M, Kiselow MC, Keats WL, et al: Varices of the colon. Arch Surg 100:718-720, 1970. 12. Adson MA, Fulton RE: The ileal stoma and portal hypertension. Arch Surg 112:501-504, 1977. 13. Hamlyn AN, Lunzer MR, Morris JS, et al: Portal hypertension with

varices in unusual sites. Lancet 2:1531-1534, 1974. 14. Eade MN, Williams JA, Cooke WT: Bleeding from an ileostomy caput medusae. Lancet 2:1166-1168, 1969. 15. Doberneck RC, Janovski NA: Isolated bleeding from colonic varices in patients with liver disease. Am J Dig Dis 15:834-841, 1970. 16. Fleming RJ, Seaman WB: Roentgenographic demonstration of unusual extraesophageal varices. Am J Roentgenol 103:281-290, 1968.

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Massive lower gastrointestinal bleeding from intestinal varices.

Massive Lower Gastrointestinal From Intestinal Varices Samuel E. Wilson, MD; Richard T. Stone, MD; John P. Christie, MD; Edward Passaro, Jr, \s=b\ L...
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