- Email: [email protected]
Gastric portal hypertension
Gastric Portal Hypertension Richard T. Stone, MD, Los Angeles, California Samuel E. Wilson, MD, Los Angeles, California Edward Passaro, Jr, MD, Los Angeles, California
most commonly Exlrahepatic portal hypertension presents as upper gastrointestinal bleeding from gastroesophageal varices [I]. The site of obstruction has influenced the choice of operation which has usually been some form of portosystemic shunt. Our experience has led us to conclude that this approach may be inadequate in some patients. We postulate that there are two distinct types of extrahepatic portal hypertension: esophageal and gastric. Each requires its own method of treatment. We contend t,hat the point of obstruction within the portal system may be of less clinical importance than the route of decompression via esophageal or gastric varices. As the following cases illustrate, gastric portal hypertension is particularly difficult to both det.ect and manage.
A mesocaval shunt was constructed with a 24 mm Dacron@ tube. At operation the pressure in the superior mesenteric vein was 38 cm HsO, decreasing to 31 cm Hz0 after shunting. The inferior vena cava pressure was 7 cm HsO. Postoperative upper gastrointestinal bleeding required transfusion of 11 units of blood. At reoperation the mesocaval shunt was patent and bleeding from gastric varices was noted. Total gastrectomy was required for control of gastric variceal bleeding. No adverse symptoms have been noted for one year after operation. Comments. The route of decompression and therefore the source of bleeding was not immediately diagnosed, even though the site of portal venous occlusion was identified. With portal and splenic vein occlusion (post splenectomy), a mesocaval shunt could not control the gastric portal hypertension and gastric variceal bleeding in this patient. Total gastrectomy was required to prevent exsanguination.
Case Reports
Case II. A thirty-eight with hepatosplenomegaly
Case I. A sixty-seven year old white female presented with a two year history of recurrent hematemesis. She did not drink alcohol and had no prior history of hepatitis or exposure to hepatotoxins. Roentgenography at another hospital had shown a hiatal hernia and nonbleeding esophageal varices. Gastric varices were not described. Hiatal herniorrhaphy with vagotomy-pyloroplasty was performed. L,iver biopsy showed a mild micronodular cirrhosis. Severe bleeding from presumed ulcer disease occurred immediately postoperatively and required partial dist,al gastrectomy with Billroth II anastomosis for control. Incidental splenectomy was also performed. Over the next two years she had three upper gastrointesinal bleeding episodes requiring transfusion. Ascites was present intermittently. Severe hematemesis resulted in transfer to our hospital. When she arrived the liver was not palpable, but moderate ascites was evident, A gastroducdenal barium study and endoscopy showed esophageal var ces, and superior mesenteric arteriography demonstrsted occlusion of the portal vein with many collateral venous channels and a dilated coronary vein. (Figure 1.)
G? the Surgical Service, VA Wadsworth Hospital Center, and the Department of Surgery, UCLA School of Medicine, Los Angeles, California. Reprint requests should be addressed to Edward Passaro. Jr. MD, Surgical Service (6911112). VA Wadsworth Hospital Center, Los Angeles, California 90073. Presented at the Forty-Ninth Annual Meeting of the Pacific Coast Surgical Association, Newport Beach, California. February 19-22, 1976.
Volume 136, July 1978
year old white female presented and jaundice. Five years previ-
Ffgure 1. Subfracfion film of venous phase angiogram showing a dilated coronary vein (dilated CV) and nonvisualizafion of the portal vein (non vis PV). This patient had severe bleeding from gastric varices.
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Stone, Wilson, and Passaro
Figure 2. Venous phase angtogram revealing a patent portal vein (PV). lBe spienc vein is not vtsuaiized. Gastric varices (G. Var) are well outlined against the gastric air bubble. Portal pressure and elevated spienic (left-sided) pressure were within normal limits at operation.
Figure 3. Subtraction study of a subsequent angiogram of the same patient as in Figure 2. A tortuous omentai vein is characteristic of spienic thrombosis. Gastric varices (G. Var) are noted to fill via the shoti gastric route. Spienectomy failed to relieve gastric variceai bleeding in this patient.
ously she had had an episode of melena. She did not drink alcohol and denied hepatotoxin exposure or prior jaundice. Intravenous cholangiography revealed no abnormalities. Subsequently, her jaundice resolved but hematemesis developed. The liver was neither enlarged nor tender, but the spleen was palpable. Liver enzyme levels and prothrombin times were within normal limits. Endoscopy revealed gastric varices, and mesenteric angiography showed a dilated portal vein and gastric varices, but the splenic vein was not visualized. At operation bleeding gastric varices were oversewn. The splenic vein was noted to be fibrotic and, although patent, was inadequate for shunting. A side-to-side portocaval shunt was constructed during arterial vasopressin infusion. The preshunt portal pressure was 21 cm HzO, and the postshunt pressure 14 cm HzO. In the postoperative period, the patient had continued gastric bleeding and expired due to cardiorespiratory problems. Autopsy revealed esophagogastric varices, congestive splenomegaly, and splenic vein obstruction. The liver showed mild hepatic fibrosis. Comments. The portacaval shunt did not stop the hemorrhage in this patient with gastric portal hypertension secondary to splenic vein occlusion. Splenectomy or total gastrectomy may have been of value.
disease were noted. Hepatic enzyme levels, prothrombin time, and serum albumin levels were within normal limits. Prior upper gastrointestinal series had revealed no abnormalities, but on this admission similar studies were interpreted as showing duodenal ulcer. Endoscopy revealed only duodenitis. Vagotomy-antrectomy with Billroth I anastomosis was performed. At operation the liver was normal, but a dilated, tortuous, omental vein and a dilated gastric venous plexus were noted. The portal pressure was 26 cm HZ0 measured via an omental vein. Over the next month three episodes of hematemesis were recorded. Repeat endoscopy showed gastric varices which were not bleeding. Celiac and mesenteric angiography revealed splenomegaly, a dilated splenic artery, gastric varices, and a tortuous omental vein draining into the portal vein. The splenic vein was not visualized. (Figures 2 and 3.) During these three months, the spleen became progressively larger. An attempted therapeutic embolization of the left gastric artery was unsuccessful. At operation the splenic pulp pressure was 27 cm HzO, portal vein pressure was 19 cm HzO, and the central venous pressure was 12 cm HzO. The spleen was massively enlarged, and splenectomy was performed. Liver biopsy showed passive congestion but no cirrhosis. Postoperatively, surgical drainage of a left subphrenic abscess was necessary. Thereafter, the patient had recurrent hematemesis and melena requiring transfusion of 12 units of blood. The bleeding could not be controlled either by a Linton tube or by the use of intravenous vasopressin. Total gastrectomy was performed to prevent exsanguination. Multiple sub-
Case III. A forty-five year old white male had a three year history of intermittent melena without hematemesis. There was no history of alcoholism and no exposure to hepatotoxins. On examination none of the stigmata of liver
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The American Journal of Surgery
Gastric Portal Hypertension
~IUUM~ gastric vems were not.ed to be grossly enlarged. ‘I‘h~tpatient has had no subsequent bleeding over a one and a half year follow-up period. (‘~n~nc~nts. The diagnosis of duodenal ulcer was incorrect. The contribution of the gastric surgery in aggravating the bleeding is speculat,ive, but the progressive massive splanomegaly suggests that drainage from the splenic bed and gastric remnant was impaired. Although splenectomy is effective in many patients with sinestral portal hypertension, it did not arrest gastric variceal bleeding in this patient. The portal hypertension was compartmentalized to the gastric venous plexus and was not accompanied by ele Jated portal vein pressure. He required total gastrectomy for control of life-threatening hemorrhage. Case IV. A fifty year old white male with polycythemia vera initially underwent resection of a jejunal infarct secondary to venous thrombosis five years prior to admission. Subsequently he had two episodes of hematemesis with no SOLrce of bleeding found on investigation. There was no history of alcohol abuse, hepatitis, or exposure to hepatotoxins. Two years later, the patient presented with hematemes&;. The physical examination revealed no abnormalities, and liver enzyme levels, prothrombin time, and amylase levals were within normal limits. An upper gastrointestinal series revealed esophagogastric varices which were seen to be bleeding on endoscopy. The splenic and portal veins we:-e not seen on celiac angiography. Although splenoportography did not visualize the portal vein, the splenic vein and many collaterals to the liver were noted. Large gastric varices with smaller esophageal varices were seen. iit operation, the portal, splenic, and superior mesenteric veins were thrombosed and there were no other veins large enough to construct a shunt. The splenic artery was ligated. The liver was normal both grossly and microgcopically. On the fourth postoperative day he had exigent upper gastrointestinal bleeding requiring transfusion of 14 units of blood. At reoperation, suture ligation of large bleeding gastric varices successfully controlled bleeding. No further bleeding has occurred over a two year period. Comments. This patient’s bleeding source was not readily identified. He had angiographic evidence of portal vein thrombosis secondary to polycythemia vera which progressed to involve the splenic and superior mesenteric veins. Since a shunt was technically impossible and ligation of the splenic artery was unsuccessful in controlling bleeding, direct suture ligation of gastric varices was required. Splenoportography was essential in demonstrating tot31 occlusion of the portal venous system and the gastric varices responsible for the bleeding.
Case V. A forty-five year old white male initially presented to another hospital with melena. No history of alcot01 abuse or hepatotoxin exposure was obtained. Hepatosplenomegaly and moderate ascites were noted. Hepatic enzyme levels, prothrombin time, and serum albumin levels were within normal limits. The patient subsequently underwent splenectomy for Banti’s syndrome.
Volume 136, July 1976
Over the next five years, the patient developed intermittent melena. Endoscopy showed gastric varices but no esophageal varices. An upper gastrointestinal series and barium enema revealed no abnormalities. Angiography did not visualize the portal, splenic, or superior mesenteric veins, but portal collateral veins and gastric varices were seen. The hepatic vein pressure was 3 cm HZ0 and the wedged hepatic vein pressure was 8 cm H20. He has had multiple guaiac positive stools over the last year and has required repeated blood transfusion. Comments. A shunt could not be done because of extensive thrombosis of the portal venous system: This patient continues to have gastric portal hypertension with gastric varikeal bleeding and guaiac positive stools.
Comments Portal
hypertension
may decompress
by several
pathways,, but the route of major clinical importance is the eswphagogastric venous plexus. This decompression into the azygous-caval system occurs either via the coronary vein through the esophageal venous plexus (esophageal portal hypertension) or via the short gastric veins through the gastric venous plexus (gastric p’ortal hypertension). The portal system is not necessarily a functional syncytium [2]. Compartmentalization of the splanchnic circulation in humans has been suggested and may explain the various forms of portal hypertension [2,3]. Prior discussions of the treatment of extrahepatic portal hypertension have focused almost exclusively on the location of the obstruction [4,5]. However, the route of decompression, whether gastric or esophageal, may be of greater surgical importance, since different operations are necessary to treat portal hypertension secondary to obstruction at similar locations but decompressing via different pathways. (Figure 4.11When both the location of the obstruction and the route of direct decompression are determined, an appropriate operation may be selected. Anatomy
Portal vein thrombosis most commonly produces esophageal varices, although decompression occasionally occurs via gastric varices. Splenic vein thrombosis, a less common form of extrahepatic block, usually results in asymptomatic decompression by collateral pathways which bypass the occluded splenic vein and return blood to the portal vein [6,7]. Should these pathways be inadequate, decompression
may occur via gastric varices. Patients
with total portal system obstruction decompress either the esophageal or gastric routes. The anatomy of the portal determine whether esophageal
via
venous system may or gastric portal hy-
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Stone, Wilson, and Passaro
Figure 4. Etis important to identify by angiography both the route of decompression as well as the point of obstructlon in gastric portal hypertension. Obstruction in the splenic vein at point A could allow flow in two directions (arrows). In one instance splenectomy would be effective, whereas In the other it would not be.
pertension results [8]. Decompression usually occurs via the coronary and esophageal veins in portal vein thrombosis, but if the coronary vein is absent or occluded by thrombus, decompression will occur via alternate routes such as the gastric venous plexus. The coronary vein arises from either the portal vein or the splenic vein. This variability may account for the occurrence of gastric or esophageal hypertension in individual cases of portal vein thrombosis [9,10]. Moreover, collateralization from the mesenteric venous system to the gastric omental venous plexus can influence the major route of decompression. The effect of prior gastric resection on portal flow further complicates the venous anatomy. If the splenic vein is occluded, gastric surgery may reduce the collaterals between the spleen and the portal vein and thereby cause increased flow in the esophageal or gastric venous plexi. This effect was present in cases I and III. Distal gastric resection resulted in splenic enlargement in one patient and subsequent massive gastric variceal hemorrhage in both. The presence of “downhill varices” secondary to superior vena caval obstruction also shows that identification of the location of varices without finding both the site of block and the route of decompression could lead to an inappropriate operation
[la. Gastric portal hypertension due to the direct decompression via the gastric venous plexus may result from portal vein thrombosis, splenic vein thrombosis, or total portal system occlusion. Our five patients
76
demonstrate these various sites of occlusion in the portal system which can produce gastric portal hypertension. (Table I.)
Patients with gastric portal hypertension meet Clatworthy’s description of “good livers and bad veins” [I]. Clinically they are characterized as nonalcoholics with intermittent bleeding from gastric varices which is often well tolerated. There is no physical sign to clearly distinguish between the patients with bleeding esophageal varices and those with gastric varices. Liver function tests reveal no abnormalities. It should be stressed that in most cases initial diagnosis is very difficult. This difficulty in identifying the source of bleeding has been noted by others [12-181, and it can lead to multiple ineffective initial surgical procedures. A great deal of reliance must be placed on diagnostic studies. Endoscopy is less effective in diagnosing gastric varices than in diagnosing esophageal varices. Conventional barium studies also tend to be unrewarding. Angiography is essential for determination of the location of obstruction and the route of decompression. Angiography in the presence of a gastric air bubble more clearly outlines gastric varices. This technical feature will help to identify gastric varices which are present but difficult to visualize endoscopically. Subtraction films of angiographic studies
The American Journal of Surgery
Gastric Portal Hypertension
TABLE I
Summary of Clinical Data on 5 Patients with Bleeding Gastric Varices
A&W Case
Sex
Site of Obstruction
67/F
Portal vein
II II,
38/F 45/M
Splenic vein Splenic vein
IL
50/M
L’
45/M
Portal vein, total portal system Total portal system
Prior Operations Vagotomy-pyloroplasty/splenectomy, mesocaval shunt Portacaval shunt Vagotomy-pyloroplasty, proximal gastrectomy, splenectomy Splenic artery ligation Splenectomy
can also be helpful. Complete evaluation of these patients should include splenoportography to correctly evaluate the portal system; in particular, the patency of the splenic vein and the left-sided portal pressures. For example, in case IV it was demonstrated that splenoportography was essential to the diagnosis of splenic vein occlusion. The technic of percutaneous transhepatic portal vein cannulation may provide a valuable means of determining portal pressure, direction of blood flow, and visualization of the portal system, although we have had no experience with this method [19,20]. Treatment
EIxtrahepatic portal hypertension appears to be well tolerated, and operative intervention should not be undertaken without sound indications. In cases of exigent hemorrhage or continuing blood loss requiring intermittent blood transfusion, appropriate surgical therapy is warranted. Unsuccessful operation is invariably manifested by recurrent bleeding. Rebleeding has occurred after various surgical procedures in 13 to 92 per cent of patients with portal vein occlusion [5] and after splenectomy in 9 per cent with splenic vein occlusion [7], indicating the limitations of current surgical procedures. The concept of isolated gastric portal hypertension and the realization that it may be operative in cases of occlusion at various locations within the portal system, including isolated splenic vein thrombosis, may help to select better initial operations and reduce the postoperative rebleeding rates. 11’esophageal portal hypertension is present, a mesocaval shunt is the best shunt to effect decompression [21]. If gastric portal hypertension is present, a distal splenorenal shunt should be effective. These shunts should decompress the involved venous compartment. The location of obstruction is important because it dictates whether a shunt can be constructed or if a modified type of shunt should be used. Also, less radical procedures, such as splenectomy, for splenic vein thrombosis may be indicated
Volume 136, July 1979
Treatment
-~ Comment
Total gastrectomy
Curative
T’otal gastrectomy
Deceased Curative
Direct suture ligation of gastric varices
Curative Continues bleeding intermittently
as the initial procedure. The importance of knowing the route of decompression as well as the location of obstruction is exemplified by our first patient with isolated portal vein thrombosis. Mesocaval shunt was selected because of the location of occlusion, but was ineffective in decompressing the gastric compartment, an effect that has been noted by others [22]. When the splenic vein is patent, as in isolated portal vein thrombosis, a theoretically attractive approach would be splenorenal shunting to decompress the gastric varices. As demonstrated in case I, other shunts fail to adequately relieve gastric portal hypertension. When the splenic vein is thrombosed or the spleen absent, a splenorenal shunt cannot be constructed. Splenectomy has been thought to be curative for bleeding gastric varices secondary to splenic vein thrombosis [7,13,14,23,24], but this is not always the case. Our third patient had a thrombosed splenic vein, but splenectomy only exacerbated the gastric variceal bleeding. Our fifth patient, with total portal system occlusion and gastric portal hypertension, underwent, splenectomy but continues to bleed from gastric varices. Although it is generally believed that most patients with esophageal varices will also have gastric varices, it is unusual to have isolated gastric varices [13,25]. The presence of gastric variceal bleeding should alert the surgeon that his patient may have hypertension in the gastric venous compartment which may not be manifest in other portions of the portal system. Thus, decompressive procedures directed primarily at the portal system may be ineffective. In these patients, direct suture ligation of the gastric varices (as in case IV) or elimination of the gastric compartment by total gastrectomy will be necessary to prevent exsanguination. Direct variceal ligation [ 71 and resection for bleeding varices [26] are not new concepts. Although it is quite possible that either esophageal or mesenteric varices may subsequently develop and bleed, total gastrectomy may be the only alternative in an exsanguinating patient.
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Stone, Wilson, and Passaro
Summary Extrahepatic portal hypertension may spontaneously decompress by routes which produce gastric or esophageal portal hypertension. A syndrome of gastric portal hypertension has been identified in five patients with extrahepatic portal obstruction and gastric variceal hemorrhage. Patients were nonalcoholic with good liver function who had tolerated previous bleeding episodes well. Endoscopy and upper gastrointestinal series were not helpful in diagnosing bleeding gastric varices. The definitive diagnostic test was venous phase mesenteric arteri-
ography of the gas-distended stomach, with confirmation of the bleeding site by splenoportography. Portosystemic shunting in two patients and splenectomy in three patients failed to stop gastric variceal bleeding. Emergency total gastrectomy was required in two patients and suture ligation in a third to prevent exigent bleeding. Gastric portal hypertension should be suspected in patients with upper gastrointestinal bleeding and good liver function. Since there is no standard therapy, recurrent bleeding requiring multiple operations is common. Determination of both location of obstruction and route of decompression are prerequisites to choosing the correct operation. Portocaval shunts in two patients failed to provide effective decompression due to compartmentalization of the portal hypertension to the gastric venous bed. In patients with a patent splenic vein, a distal splenorenal shunt may be effective. However, with splenic vein occlusion splenectomy may be ineffective, and a direct approach such as total gastrectomy or variteal ligation may be necessary to prevent exsanguination. References 1. Clatworthy HW Jr: Extrahepatic 2.
3. 4.
5. 6.
7. 8.
7%
portal hypertension. Major Problems in Clinical Surgery (ChildsCG, ed). Philadelphia, WB Saunders, 1974. Warren WD, Zeppa R, Fomon JJ: Selective trans-splenic decompression of gastroesophageal varices by distal splenorenal shunt. Ann Surg 166: 437, 1967. Malt RA: Portosystemic shunts. I. N Engl J Med 295: 24, 1976. Maddrey WC, Gupta KPS, Mallik KCB, et, al: Extrahepatic obstruction of the portal venous system. Surg Gynecol O&et 127: 969. 1968. Voorhees AB Jr, Price JB Jr: Extrahepatic portal hypertension. Arch Surg 108: 338, 1974. Longstretch GF, Newcomer AD, Green PA: Extrahepatic portal hypertension caused by chronic pancreatitis. Ann lnfem bled 75: 903, 1971. Sutton JP, Yarborough DY, Richards JT: Isolated splenic vein occlusion. Arch Surg 100: 623, 1970. Liebowitz HR, Roussilot LM, Whipple AO: Bleeding Esophageal Varices: Portal Hypertension. Springfield, Charles C Thomas, 1959.
9. Doehner GA, Ruzicka FF Jr, Hoffman G. et al: The portal venous system: its roentgen anatomy. Radiology 64: 675, 1955. 10. Douglass BE, Baggenstoss AH, Hollinshead WH: The anatomy of the portal vein and its tributaries. Surg Gpwco/ Obstet 9 1: 562, 1950. 11. Sorokin JJ, Levine SM, Moss EG, et al: Downhill varices: report of a case 29 years after resection of a substernal thyroid gland. Gastroenterology 73: 345, 1977, 12. Goldstein GB: Splenic vein thrombosis causing gastric varices and bleeding. Am J Gastroenterol58: 319, 1972. 13. Hershfield NB. Morrow ): Gastric bleeding due to spienic vein thrombosis. Can Med ASSOCJ 98: 649, 1968. 14. Khan AH, O’Reilly CJ. Avekirn VA, et al: Splenic vein thromboses, an unusual cause of gastric bleeding. Angiology 28: 725, 1977. 15. Marshall JP, Smith PD. Hoyumpa AM Jr: Gastric varices: problem in diagnosis. Am J Dig Dis 22: 947, 1977. 16. Salam AA, Warren WD: Anatomic basis of the surgical treatment of portal hypertension. Surg C/in North Am 54: 1247, 1974. 17. Salam AA, Warren WD, Tyras DH: Splenic vein thrombosis: a diagnosable and curable form of portal hypertension. Surgery 74: 961, 1973. 18. Turcotte JG, Child CG Ill: Idiopathic extrahepatic portal hypertension in adults. Am J Surg 123: 35, 1972. 19. Nabseth DC, Widrich, O’Hara ET, et al: Flow and pressure characteristics of the portal system before and after splenorenal shunts. Surgery 78: 739, 1975. 20. Widrich WC, Robbins AH, Nabseth DC, et al: Portal hypertension changes following selective splenorenal shunt surgery. Radiology 121: 295, 1976. RL, Hunt AH: Proximal gastric resection in 21. RothwellJackson the treatment of bleeding gastro-esophageal varices in patients with portal hypertension due to extrahepatic obstruction. Br J Surg 57: 487, 1970. 22. Witte CL, Ovitt TW, Witte MH, et al: Left-sided segmental portal hypertension following rnesocaval interposition shunt. Surg GynecolObstet 145: 169, 1977. 23. Turrill FL, Mikkelsen WP: Sinistral (left-sided) extrahepatic portal hypertension. Arch Surg 99: 365, 1969. 24. Yale GE, Crummy AB: Splenic vein thrombosis and bleeding esophageal varices. JAMA 217: 317, 1971. 25. Rice RP, Thompson WM. Kelvin FM, et al: Gastric varices without esophageal varices. JAMA 237: 1976, 1977. 26. Habif DV: Treatment of esophageal varices by partial esophagogastrectomy and interposed jejunal segment. Surgery 46: 212, 1959.
Discussion
William P. Mikkelsen (Los Angeles, CA): The authors would have us believe that extrahepatic portal hypertension decompresses via either the coronary azygos system which induces the esophageal varices, or via the short gastric veins which induce gastric varices. I am not convinced they have proved their point. Also, I am not certain that the term “decompress” is very appropriate. Portal hypertension, whether or not it is extrahepatic, stimulates a variety of collateral pathways, none of which is decompressing, including those that produce both esophageal and gastric varices. Usually both types coexist, and which of the varices bleed is relatively unimportant. More than twenty years ago Roy Cohn, a member of this Association, demonstrated that the bleeding varix may be on either side of the esophagogastric junction. Of the five patients presented herein, three were acknowledged to have esophageal as well as gastric varices, and in only one
The American Journal oi Surgery
Gastric Portal Hypertension
were esophageal varices emphasized to he conspicuously absent. Since the follow-up period is rather short, one wcnders how permanently effective either total gastrectomy or oversewing of gastric varices will be. Oversewing is surely a temporizing procedure. Wangensteen showed many years ago that radical subtotal gastrectomy was inefl’ectual, and our experience with the Tanner operation, which is similar, has been equally dismal. The failure of a mesocaval shunt to control bleeding in the first patient perhaps was a reflection of the inappropriate pressure reduction from 37 to only 31 cm Hz0 when the inferior caval pressure was only 7 cm HzO. The failure of the portacaval shunt to control bleeding in the second patient is difficult to assess, since she expired from multiple causes. The third patient fits our criteria for sinistral or left-sided portal hypertension. Why splenectomy did not curb the bleeding in this patient is unexplained. It was successful in all three of our patients, which we previously reported. The fourth and fifth patients were the only ones with classic extrahepatic portal hypertension with occlusicn of all available shuntable veins. One was treated by oversewing gastric varices and the other was not operated on. The portal vein was proved to be patent in the second and third patients, and failure of the portal vein to opacify on mesenteric angiography in the first patient does not establish that it was occluded. There could have been reversal of portal flow in this patient, who incidentally was ah.0 cirrhotic. Thus, in summation, as much as I admire the authors and recognize their previous important contributions to the literature and to this society, I cannot accept their current concepts or recommendations. Their patients were not all representative of extrahepatic portal hypertension as alleged. Three of the five had acknowledged esophageal as well as gastric varices, and probably just happened to bleed from the gastric side. Oversewing of varices has been notoriously ineffective, and total gastrectomy is a formidable procedure which if practiced extensively will result in Isignificant operative mortality and which, I believe, will fail to prevent subsequent esophageal varical bleeding.
Volume 136, July 1979
Edward Passaro, Jr (closing): There are a number of very important issues that Dr. Mikkelsen has raised that I would like to respond to. The first and perhaps the key is whether or not the gastric and the esophageal systems in fact can be isolated. I think they can be in certain patients, and the proof is measurement of the different pressures in the two components of the venous system. Second, we are not advocating total gastrectomy for the treatment of this disease. There is no good form of treatment, and we recognize that. We had two patients who had a gastric remnant from which they were exsanguinating. We did total gastrectomy in an heroic effort to save their lives. I think both of these patients survived because that was done. As to how long it has been effective, the follow-up period has been more than a year and a half in each instance. One of these patients has bled from other portions of the gastrointestinal tract. The other patient has not bled at all. It would appear that total gastrectomy in those instances is as effective as any other form of treatment. Dr. Mikkelsen indicates that he cannot understand why splenectorny was not effective in our third patient. That is precisely the point. Why wasn’t it effective? Why was it that we had this problem? Others have indicated it is not effective. It is our analysis that the answer is related to the route of decompression, and if you do not like the word “decompression,” use “route of flow.” It just so happens that during the period of time we were writing this, a report in Gastroenterology of so-called “downhill varices” appeared. A patient many years after the removal of a substernal thyroid developed esophageal varices. If one were to focus just on those varices, the point of the entire case would be missed. This patient had obstruction of the superior vena caval system and was decompressing; or the route of flow, if you will, was downhill through the esophageal varices, indicating the importance of the direction of flow. Obviously, any portal decompression procedure in the abdomen in such a patient would have been a disaster.
79
most commonly Exlrahepatic portal hypertension presents as upper gastrointestinal bleeding from gastroesophageal varices [I]. The site of obstruction has influenced the choice of operation which has usually been some form of portosystemic shunt. Our experience has led us to conclude that this approach may be inadequate in some patients. We postulate that there are two distinct types of extrahepatic portal hypertension: esophageal and gastric. Each requires its own method of treatment. We contend t,hat the point of obstruction within the portal system may be of less clinical importance than the route of decompression via esophageal or gastric varices. As the following cases illustrate, gastric portal hypertension is particularly difficult to both det.ect and manage.
A mesocaval shunt was constructed with a 24 mm Dacron@ tube. At operation the pressure in the superior mesenteric vein was 38 cm HsO, decreasing to 31 cm Hz0 after shunting. The inferior vena cava pressure was 7 cm HsO. Postoperative upper gastrointestinal bleeding required transfusion of 11 units of blood. At reoperation the mesocaval shunt was patent and bleeding from gastric varices was noted. Total gastrectomy was required for control of gastric variceal bleeding. No adverse symptoms have been noted for one year after operation. Comments. The route of decompression and therefore the source of bleeding was not immediately diagnosed, even though the site of portal venous occlusion was identified. With portal and splenic vein occlusion (post splenectomy), a mesocaval shunt could not control the gastric portal hypertension and gastric variceal bleeding in this patient. Total gastrectomy was required to prevent exsanguination.
Case Reports
Case II. A thirty-eight with hepatosplenomegaly
Case I. A sixty-seven year old white female presented with a two year history of recurrent hematemesis. She did not drink alcohol and had no prior history of hepatitis or exposure to hepatotoxins. Roentgenography at another hospital had shown a hiatal hernia and nonbleeding esophageal varices. Gastric varices were not described. Hiatal herniorrhaphy with vagotomy-pyloroplasty was performed. L,iver biopsy showed a mild micronodular cirrhosis. Severe bleeding from presumed ulcer disease occurred immediately postoperatively and required partial dist,al gastrectomy with Billroth II anastomosis for control. Incidental splenectomy was also performed. Over the next two years she had three upper gastrointesinal bleeding episodes requiring transfusion. Ascites was present intermittently. Severe hematemesis resulted in transfer to our hospital. When she arrived the liver was not palpable, but moderate ascites was evident, A gastroducdenal barium study and endoscopy showed esophageal var ces, and superior mesenteric arteriography demonstrsted occlusion of the portal vein with many collateral venous channels and a dilated coronary vein. (Figure 1.)
G? the Surgical Service, VA Wadsworth Hospital Center, and the Department of Surgery, UCLA School of Medicine, Los Angeles, California. Reprint requests should be addressed to Edward Passaro. Jr. MD, Surgical Service (6911112). VA Wadsworth Hospital Center, Los Angeles, California 90073. Presented at the Forty-Ninth Annual Meeting of the Pacific Coast Surgical Association, Newport Beach, California. February 19-22, 1976.
Volume 136, July 1978
year old white female presented and jaundice. Five years previ-
Ffgure 1. Subfracfion film of venous phase angiogram showing a dilated coronary vein (dilated CV) and nonvisualizafion of the portal vein (non vis PV). This patient had severe bleeding from gastric varices.
73
Stone, Wilson, and Passaro
Figure 2. Venous phase angtogram revealing a patent portal vein (PV). lBe spienc vein is not vtsuaiized. Gastric varices (G. Var) are well outlined against the gastric air bubble. Portal pressure and elevated spienic (left-sided) pressure were within normal limits at operation.
Figure 3. Subtraction study of a subsequent angiogram of the same patient as in Figure 2. A tortuous omentai vein is characteristic of spienic thrombosis. Gastric varices (G. Var) are noted to fill via the shoti gastric route. Spienectomy failed to relieve gastric variceai bleeding in this patient.
ously she had had an episode of melena. She did not drink alcohol and denied hepatotoxin exposure or prior jaundice. Intravenous cholangiography revealed no abnormalities. Subsequently, her jaundice resolved but hematemesis developed. The liver was neither enlarged nor tender, but the spleen was palpable. Liver enzyme levels and prothrombin times were within normal limits. Endoscopy revealed gastric varices, and mesenteric angiography showed a dilated portal vein and gastric varices, but the splenic vein was not visualized. At operation bleeding gastric varices were oversewn. The splenic vein was noted to be fibrotic and, although patent, was inadequate for shunting. A side-to-side portocaval shunt was constructed during arterial vasopressin infusion. The preshunt portal pressure was 21 cm HzO, and the postshunt pressure 14 cm HzO. In the postoperative period, the patient had continued gastric bleeding and expired due to cardiorespiratory problems. Autopsy revealed esophagogastric varices, congestive splenomegaly, and splenic vein obstruction. The liver showed mild hepatic fibrosis. Comments. The portacaval shunt did not stop the hemorrhage in this patient with gastric portal hypertension secondary to splenic vein occlusion. Splenectomy or total gastrectomy may have been of value.
disease were noted. Hepatic enzyme levels, prothrombin time, and serum albumin levels were within normal limits. Prior upper gastrointestinal series had revealed no abnormalities, but on this admission similar studies were interpreted as showing duodenal ulcer. Endoscopy revealed only duodenitis. Vagotomy-antrectomy with Billroth I anastomosis was performed. At operation the liver was normal, but a dilated, tortuous, omental vein and a dilated gastric venous plexus were noted. The portal pressure was 26 cm HZ0 measured via an omental vein. Over the next month three episodes of hematemesis were recorded. Repeat endoscopy showed gastric varices which were not bleeding. Celiac and mesenteric angiography revealed splenomegaly, a dilated splenic artery, gastric varices, and a tortuous omental vein draining into the portal vein. The splenic vein was not visualized. (Figures 2 and 3.) During these three months, the spleen became progressively larger. An attempted therapeutic embolization of the left gastric artery was unsuccessful. At operation the splenic pulp pressure was 27 cm HzO, portal vein pressure was 19 cm HzO, and the central venous pressure was 12 cm HzO. The spleen was massively enlarged, and splenectomy was performed. Liver biopsy showed passive congestion but no cirrhosis. Postoperatively, surgical drainage of a left subphrenic abscess was necessary. Thereafter, the patient had recurrent hematemesis and melena requiring transfusion of 12 units of blood. The bleeding could not be controlled either by a Linton tube or by the use of intravenous vasopressin. Total gastrectomy was performed to prevent exsanguination. Multiple sub-
Case III. A forty-five year old white male had a three year history of intermittent melena without hematemesis. There was no history of alcoholism and no exposure to hepatotoxins. On examination none of the stigmata of liver
74
The American Journal of Surgery
Gastric Portal Hypertension
~IUUM~ gastric vems were not.ed to be grossly enlarged. ‘I‘h~tpatient has had no subsequent bleeding over a one and a half year follow-up period. (‘~n~nc~nts. The diagnosis of duodenal ulcer was incorrect. The contribution of the gastric surgery in aggravating the bleeding is speculat,ive, but the progressive massive splanomegaly suggests that drainage from the splenic bed and gastric remnant was impaired. Although splenectomy is effective in many patients with sinestral portal hypertension, it did not arrest gastric variceal bleeding in this patient. The portal hypertension was compartmentalized to the gastric venous plexus and was not accompanied by ele Jated portal vein pressure. He required total gastrectomy for control of life-threatening hemorrhage. Case IV. A fifty year old white male with polycythemia vera initially underwent resection of a jejunal infarct secondary to venous thrombosis five years prior to admission. Subsequently he had two episodes of hematemesis with no SOLrce of bleeding found on investigation. There was no history of alcohol abuse, hepatitis, or exposure to hepatotoxins. Two years later, the patient presented with hematemes&;. The physical examination revealed no abnormalities, and liver enzyme levels, prothrombin time, and amylase levals were within normal limits. An upper gastrointestinal series revealed esophagogastric varices which were seen to be bleeding on endoscopy. The splenic and portal veins we:-e not seen on celiac angiography. Although splenoportography did not visualize the portal vein, the splenic vein and many collaterals to the liver were noted. Large gastric varices with smaller esophageal varices were seen. iit operation, the portal, splenic, and superior mesenteric veins were thrombosed and there were no other veins large enough to construct a shunt. The splenic artery was ligated. The liver was normal both grossly and microgcopically. On the fourth postoperative day he had exigent upper gastrointestinal bleeding requiring transfusion of 14 units of blood. At reoperation, suture ligation of large bleeding gastric varices successfully controlled bleeding. No further bleeding has occurred over a two year period. Comments. This patient’s bleeding source was not readily identified. He had angiographic evidence of portal vein thrombosis secondary to polycythemia vera which progressed to involve the splenic and superior mesenteric veins. Since a shunt was technically impossible and ligation of the splenic artery was unsuccessful in controlling bleeding, direct suture ligation of gastric varices was required. Splenoportography was essential in demonstrating tot31 occlusion of the portal venous system and the gastric varices responsible for the bleeding.
Case V. A forty-five year old white male initially presented to another hospital with melena. No history of alcot01 abuse or hepatotoxin exposure was obtained. Hepatosplenomegaly and moderate ascites were noted. Hepatic enzyme levels, prothrombin time, and serum albumin levels were within normal limits. The patient subsequently underwent splenectomy for Banti’s syndrome.
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Over the next five years, the patient developed intermittent melena. Endoscopy showed gastric varices but no esophageal varices. An upper gastrointestinal series and barium enema revealed no abnormalities. Angiography did not visualize the portal, splenic, or superior mesenteric veins, but portal collateral veins and gastric varices were seen. The hepatic vein pressure was 3 cm HZ0 and the wedged hepatic vein pressure was 8 cm H20. He has had multiple guaiac positive stools over the last year and has required repeated blood transfusion. Comments. A shunt could not be done because of extensive thrombosis of the portal venous system: This patient continues to have gastric portal hypertension with gastric varikeal bleeding and guaiac positive stools.
Comments Portal
hypertension
may decompress
by several
pathways,, but the route of major clinical importance is the eswphagogastric venous plexus. This decompression into the azygous-caval system occurs either via the coronary vein through the esophageal venous plexus (esophageal portal hypertension) or via the short gastric veins through the gastric venous plexus (gastric p’ortal hypertension). The portal system is not necessarily a functional syncytium [2]. Compartmentalization of the splanchnic circulation in humans has been suggested and may explain the various forms of portal hypertension [2,3]. Prior discussions of the treatment of extrahepatic portal hypertension have focused almost exclusively on the location of the obstruction [4,5]. However, the route of decompression, whether gastric or esophageal, may be of greater surgical importance, since different operations are necessary to treat portal hypertension secondary to obstruction at similar locations but decompressing via different pathways. (Figure 4.11When both the location of the obstruction and the route of direct decompression are determined, an appropriate operation may be selected. Anatomy
Portal vein thrombosis most commonly produces esophageal varices, although decompression occasionally occurs via gastric varices. Splenic vein thrombosis, a less common form of extrahepatic block, usually results in asymptomatic decompression by collateral pathways which bypass the occluded splenic vein and return blood to the portal vein [6,7]. Should these pathways be inadequate, decompression
may occur via gastric varices. Patients
with total portal system obstruction decompress either the esophageal or gastric routes. The anatomy of the portal determine whether esophageal
via
venous system may or gastric portal hy-
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Stone, Wilson, and Passaro
Figure 4. Etis important to identify by angiography both the route of decompression as well as the point of obstructlon in gastric portal hypertension. Obstruction in the splenic vein at point A could allow flow in two directions (arrows). In one instance splenectomy would be effective, whereas In the other it would not be.
pertension results [8]. Decompression usually occurs via the coronary and esophageal veins in portal vein thrombosis, but if the coronary vein is absent or occluded by thrombus, decompression will occur via alternate routes such as the gastric venous plexus. The coronary vein arises from either the portal vein or the splenic vein. This variability may account for the occurrence of gastric or esophageal hypertension in individual cases of portal vein thrombosis [9,10]. Moreover, collateralization from the mesenteric venous system to the gastric omental venous plexus can influence the major route of decompression. The effect of prior gastric resection on portal flow further complicates the venous anatomy. If the splenic vein is occluded, gastric surgery may reduce the collaterals between the spleen and the portal vein and thereby cause increased flow in the esophageal or gastric venous plexi. This effect was present in cases I and III. Distal gastric resection resulted in splenic enlargement in one patient and subsequent massive gastric variceal hemorrhage in both. The presence of “downhill varices” secondary to superior vena caval obstruction also shows that identification of the location of varices without finding both the site of block and the route of decompression could lead to an inappropriate operation
[la. Gastric portal hypertension due to the direct decompression via the gastric venous plexus may result from portal vein thrombosis, splenic vein thrombosis, or total portal system occlusion. Our five patients
76
demonstrate these various sites of occlusion in the portal system which can produce gastric portal hypertension. (Table I.)
Patients with gastric portal hypertension meet Clatworthy’s description of “good livers and bad veins” [I]. Clinically they are characterized as nonalcoholics with intermittent bleeding from gastric varices which is often well tolerated. There is no physical sign to clearly distinguish between the patients with bleeding esophageal varices and those with gastric varices. Liver function tests reveal no abnormalities. It should be stressed that in most cases initial diagnosis is very difficult. This difficulty in identifying the source of bleeding has been noted by others [12-181, and it can lead to multiple ineffective initial surgical procedures. A great deal of reliance must be placed on diagnostic studies. Endoscopy is less effective in diagnosing gastric varices than in diagnosing esophageal varices. Conventional barium studies also tend to be unrewarding. Angiography is essential for determination of the location of obstruction and the route of decompression. Angiography in the presence of a gastric air bubble more clearly outlines gastric varices. This technical feature will help to identify gastric varices which are present but difficult to visualize endoscopically. Subtraction films of angiographic studies
The American Journal of Surgery
Gastric Portal Hypertension
TABLE I
Summary of Clinical Data on 5 Patients with Bleeding Gastric Varices
A&W Case
Sex
Site of Obstruction
67/F
Portal vein
II II,
38/F 45/M
Splenic vein Splenic vein
IL
50/M
L’
45/M
Portal vein, total portal system Total portal system
Prior Operations Vagotomy-pyloroplasty/splenectomy, mesocaval shunt Portacaval shunt Vagotomy-pyloroplasty, proximal gastrectomy, splenectomy Splenic artery ligation Splenectomy
can also be helpful. Complete evaluation of these patients should include splenoportography to correctly evaluate the portal system; in particular, the patency of the splenic vein and the left-sided portal pressures. For example, in case IV it was demonstrated that splenoportography was essential to the diagnosis of splenic vein occlusion. The technic of percutaneous transhepatic portal vein cannulation may provide a valuable means of determining portal pressure, direction of blood flow, and visualization of the portal system, although we have had no experience with this method [19,20]. Treatment
EIxtrahepatic portal hypertension appears to be well tolerated, and operative intervention should not be undertaken without sound indications. In cases of exigent hemorrhage or continuing blood loss requiring intermittent blood transfusion, appropriate surgical therapy is warranted. Unsuccessful operation is invariably manifested by recurrent bleeding. Rebleeding has occurred after various surgical procedures in 13 to 92 per cent of patients with portal vein occlusion [5] and after splenectomy in 9 per cent with splenic vein occlusion [7], indicating the limitations of current surgical procedures. The concept of isolated gastric portal hypertension and the realization that it may be operative in cases of occlusion at various locations within the portal system, including isolated splenic vein thrombosis, may help to select better initial operations and reduce the postoperative rebleeding rates. 11’esophageal portal hypertension is present, a mesocaval shunt is the best shunt to effect decompression [21]. If gastric portal hypertension is present, a distal splenorenal shunt should be effective. These shunts should decompress the involved venous compartment. The location of obstruction is important because it dictates whether a shunt can be constructed or if a modified type of shunt should be used. Also, less radical procedures, such as splenectomy, for splenic vein thrombosis may be indicated
Volume 136, July 1979
Treatment
-~ Comment
Total gastrectomy
Curative
T’otal gastrectomy
Deceased Curative
Direct suture ligation of gastric varices
Curative Continues bleeding intermittently
as the initial procedure. The importance of knowing the route of decompression as well as the location of obstruction is exemplified by our first patient with isolated portal vein thrombosis. Mesocaval shunt was selected because of the location of occlusion, but was ineffective in decompressing the gastric compartment, an effect that has been noted by others [22]. When the splenic vein is patent, as in isolated portal vein thrombosis, a theoretically attractive approach would be splenorenal shunting to decompress the gastric varices. As demonstrated in case I, other shunts fail to adequately relieve gastric portal hypertension. When the splenic vein is thrombosed or the spleen absent, a splenorenal shunt cannot be constructed. Splenectomy has been thought to be curative for bleeding gastric varices secondary to splenic vein thrombosis [7,13,14,23,24], but this is not always the case. Our third patient had a thrombosed splenic vein, but splenectomy only exacerbated the gastric variceal bleeding. Our fifth patient, with total portal system occlusion and gastric portal hypertension, underwent, splenectomy but continues to bleed from gastric varices. Although it is generally believed that most patients with esophageal varices will also have gastric varices, it is unusual to have isolated gastric varices [13,25]. The presence of gastric variceal bleeding should alert the surgeon that his patient may have hypertension in the gastric venous compartment which may not be manifest in other portions of the portal system. Thus, decompressive procedures directed primarily at the portal system may be ineffective. In these patients, direct suture ligation of the gastric varices (as in case IV) or elimination of the gastric compartment by total gastrectomy will be necessary to prevent exsanguination. Direct variceal ligation [ 71 and resection for bleeding varices [26] are not new concepts. Although it is quite possible that either esophageal or mesenteric varices may subsequently develop and bleed, total gastrectomy may be the only alternative in an exsanguinating patient.
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Stone, Wilson, and Passaro
Summary Extrahepatic portal hypertension may spontaneously decompress by routes which produce gastric or esophageal portal hypertension. A syndrome of gastric portal hypertension has been identified in five patients with extrahepatic portal obstruction and gastric variceal hemorrhage. Patients were nonalcoholic with good liver function who had tolerated previous bleeding episodes well. Endoscopy and upper gastrointestinal series were not helpful in diagnosing bleeding gastric varices. The definitive diagnostic test was venous phase mesenteric arteri-
ography of the gas-distended stomach, with confirmation of the bleeding site by splenoportography. Portosystemic shunting in two patients and splenectomy in three patients failed to stop gastric variceal bleeding. Emergency total gastrectomy was required in two patients and suture ligation in a third to prevent exigent bleeding. Gastric portal hypertension should be suspected in patients with upper gastrointestinal bleeding and good liver function. Since there is no standard therapy, recurrent bleeding requiring multiple operations is common. Determination of both location of obstruction and route of decompression are prerequisites to choosing the correct operation. Portocaval shunts in two patients failed to provide effective decompression due to compartmentalization of the portal hypertension to the gastric venous bed. In patients with a patent splenic vein, a distal splenorenal shunt may be effective. However, with splenic vein occlusion splenectomy may be ineffective, and a direct approach such as total gastrectomy or variteal ligation may be necessary to prevent exsanguination. References 1. Clatworthy HW Jr: Extrahepatic 2.
3. 4.
5. 6.
7. 8.
7%
portal hypertension. Major Problems in Clinical Surgery (ChildsCG, ed). Philadelphia, WB Saunders, 1974. Warren WD, Zeppa R, Fomon JJ: Selective trans-splenic decompression of gastroesophageal varices by distal splenorenal shunt. Ann Surg 166: 437, 1967. Malt RA: Portosystemic shunts. I. N Engl J Med 295: 24, 1976. Maddrey WC, Gupta KPS, Mallik KCB, et, al: Extrahepatic obstruction of the portal venous system. Surg Gynecol O&et 127: 969. 1968. Voorhees AB Jr, Price JB Jr: Extrahepatic portal hypertension. Arch Surg 108: 338, 1974. Longstretch GF, Newcomer AD, Green PA: Extrahepatic portal hypertension caused by chronic pancreatitis. Ann lnfem bled 75: 903, 1971. Sutton JP, Yarborough DY, Richards JT: Isolated splenic vein occlusion. Arch Surg 100: 623, 1970. Liebowitz HR, Roussilot LM, Whipple AO: Bleeding Esophageal Varices: Portal Hypertension. Springfield, Charles C Thomas, 1959.
9. Doehner GA, Ruzicka FF Jr, Hoffman G. et al: The portal venous system: its roentgen anatomy. Radiology 64: 675, 1955. 10. Douglass BE, Baggenstoss AH, Hollinshead WH: The anatomy of the portal vein and its tributaries. Surg Gpwco/ Obstet 9 1: 562, 1950. 11. Sorokin JJ, Levine SM, Moss EG, et al: Downhill varices: report of a case 29 years after resection of a substernal thyroid gland. Gastroenterology 73: 345, 1977, 12. Goldstein GB: Splenic vein thrombosis causing gastric varices and bleeding. Am J Gastroenterol58: 319, 1972. 13. Hershfield NB. Morrow ): Gastric bleeding due to spienic vein thrombosis. Can Med ASSOCJ 98: 649, 1968. 14. Khan AH, O’Reilly CJ. Avekirn VA, et al: Splenic vein thromboses, an unusual cause of gastric bleeding. Angiology 28: 725, 1977. 15. Marshall JP, Smith PD. Hoyumpa AM Jr: Gastric varices: problem in diagnosis. Am J Dig Dis 22: 947, 1977. 16. Salam AA, Warren WD: Anatomic basis of the surgical treatment of portal hypertension. Surg C/in North Am 54: 1247, 1974. 17. Salam AA, Warren WD, Tyras DH: Splenic vein thrombosis: a diagnosable and curable form of portal hypertension. Surgery 74: 961, 1973. 18. Turcotte JG, Child CG Ill: Idiopathic extrahepatic portal hypertension in adults. Am J Surg 123: 35, 1972. 19. Nabseth DC, Widrich, O’Hara ET, et al: Flow and pressure characteristics of the portal system before and after splenorenal shunts. Surgery 78: 739, 1975. 20. Widrich WC, Robbins AH, Nabseth DC, et al: Portal hypertension changes following selective splenorenal shunt surgery. Radiology 121: 295, 1976. RL, Hunt AH: Proximal gastric resection in 21. RothwellJackson the treatment of bleeding gastro-esophageal varices in patients with portal hypertension due to extrahepatic obstruction. Br J Surg 57: 487, 1970. 22. Witte CL, Ovitt TW, Witte MH, et al: Left-sided segmental portal hypertension following rnesocaval interposition shunt. Surg GynecolObstet 145: 169, 1977. 23. Turrill FL, Mikkelsen WP: Sinistral (left-sided) extrahepatic portal hypertension. Arch Surg 99: 365, 1969. 24. Yale GE, Crummy AB: Splenic vein thrombosis and bleeding esophageal varices. JAMA 217: 317, 1971. 25. Rice RP, Thompson WM. Kelvin FM, et al: Gastric varices without esophageal varices. JAMA 237: 1976, 1977. 26. Habif DV: Treatment of esophageal varices by partial esophagogastrectomy and interposed jejunal segment. Surgery 46: 212, 1959.
Discussion
William P. Mikkelsen (Los Angeles, CA): The authors would have us believe that extrahepatic portal hypertension decompresses via either the coronary azygos system which induces the esophageal varices, or via the short gastric veins which induce gastric varices. I am not convinced they have proved their point. Also, I am not certain that the term “decompress” is very appropriate. Portal hypertension, whether or not it is extrahepatic, stimulates a variety of collateral pathways, none of which is decompressing, including those that produce both esophageal and gastric varices. Usually both types coexist, and which of the varices bleed is relatively unimportant. More than twenty years ago Roy Cohn, a member of this Association, demonstrated that the bleeding varix may be on either side of the esophagogastric junction. Of the five patients presented herein, three were acknowledged to have esophageal as well as gastric varices, and in only one
The American Journal oi Surgery
Gastric Portal Hypertension
were esophageal varices emphasized to he conspicuously absent. Since the follow-up period is rather short, one wcnders how permanently effective either total gastrectomy or oversewing of gastric varices will be. Oversewing is surely a temporizing procedure. Wangensteen showed many years ago that radical subtotal gastrectomy was inefl’ectual, and our experience with the Tanner operation, which is similar, has been equally dismal. The failure of a mesocaval shunt to control bleeding in the first patient perhaps was a reflection of the inappropriate pressure reduction from 37 to only 31 cm Hz0 when the inferior caval pressure was only 7 cm HzO. The failure of the portacaval shunt to control bleeding in the second patient is difficult to assess, since she expired from multiple causes. The third patient fits our criteria for sinistral or left-sided portal hypertension. Why splenectomy did not curb the bleeding in this patient is unexplained. It was successful in all three of our patients, which we previously reported. The fourth and fifth patients were the only ones with classic extrahepatic portal hypertension with occlusicn of all available shuntable veins. One was treated by oversewing gastric varices and the other was not operated on. The portal vein was proved to be patent in the second and third patients, and failure of the portal vein to opacify on mesenteric angiography in the first patient does not establish that it was occluded. There could have been reversal of portal flow in this patient, who incidentally was ah.0 cirrhotic. Thus, in summation, as much as I admire the authors and recognize their previous important contributions to the literature and to this society, I cannot accept their current concepts or recommendations. Their patients were not all representative of extrahepatic portal hypertension as alleged. Three of the five had acknowledged esophageal as well as gastric varices, and probably just happened to bleed from the gastric side. Oversewing of varices has been notoriously ineffective, and total gastrectomy is a formidable procedure which if practiced extensively will result in Isignificant operative mortality and which, I believe, will fail to prevent subsequent esophageal varical bleeding.
Volume 136, July 1979
Edward Passaro, Jr (closing): There are a number of very important issues that Dr. Mikkelsen has raised that I would like to respond to. The first and perhaps the key is whether or not the gastric and the esophageal systems in fact can be isolated. I think they can be in certain patients, and the proof is measurement of the different pressures in the two components of the venous system. Second, we are not advocating total gastrectomy for the treatment of this disease. There is no good form of treatment, and we recognize that. We had two patients who had a gastric remnant from which they were exsanguinating. We did total gastrectomy in an heroic effort to save their lives. I think both of these patients survived because that was done. As to how long it has been effective, the follow-up period has been more than a year and a half in each instance. One of these patients has bled from other portions of the gastrointestinal tract. The other patient has not bled at all. It would appear that total gastrectomy in those instances is as effective as any other form of treatment. Dr. Mikkelsen indicates that he cannot understand why splenectorny was not effective in our third patient. That is precisely the point. Why wasn’t it effective? Why was it that we had this problem? Others have indicated it is not effective. It is our analysis that the answer is related to the route of decompression, and if you do not like the word “decompression,” use “route of flow.” It just so happens that during the period of time we were writing this, a report in Gastroenterology of so-called “downhill varices” appeared. A patient many years after the removal of a substernal thyroid developed esophageal varices. If one were to focus just on those varices, the point of the entire case would be missed. This patient had obstruction of the superior vena caval system and was decompressing; or the route of flow, if you will, was downhill through the esophageal varices, indicating the importance of the direction of flow. Obviously, any portal decompression procedure in the abdomen in such a patient would have been a disaster.
79