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Splenic arteriovenous fistula to maintain patency of splenorenal shunts
SCIENTIFIC PAPERS
Splenic Arteriovenous Fistula to Maintain Patency of Splenorenal Shunts
R o b e r t W. C a m p b e l l , M D , I r v i n e , C a l i f o r n i a Leo B. Be,in, MD, I r v i n e , C a l i f o r n i a J a c k I. Eimenman, b i D , I r v i n e , C a l i f o r n i a Alan B. Gazzanlga, MD, I r v i n e , C a l i f o r n i a
T h e s p l e n o r e n a l s h u n t is a n e s t a b l i s h e d p r o c e d u r e for d e c o m p r e s s i o n of e s o p h a g e a l varices d u e to p o r t a l h y p e r t e n s i o n in older children a n d a d u l t s [1,2]. H o w e v e r , l o n g - t e r m results s h o w t h a t a sign i f i c a n t n u m b e r of t h e s e s h u n t s close if t h e splenic vein is s m a l l or if t h e p r o x i m a l (hilar) p o r t i o n of t h e vein is used. A r t e r i o v e n o u s fistulas h a v e b e e n u s e d e x p e r i m e n t a l l y , a n d in s o m e cases clinically, t o p r o m o t e p a t e n c y of v e n o u s a n d a r t e r i a l grafts [3-7]. T h i s p a p e r describes our e x p e r i m e n t a l work u s i n g splenic a r t e r i o v e n o u s a n a s t o m o s e s to m a i n t a i n p a t e n c y of s p l e n o r e n a l s h u n t s a n d p r e s e n t s a clinical case r e p o r t of this technic. Material and Methods
Three groups of adult dogs weighing between 18 and 23 kg were used in this study. The dogs were anesthetized with pentobarbital (30 mg/kg) and ventilated with a Harvard respirator via an endotracheal tube. In From the Department of Surgery. University of California. Irvine, Iro
vine, California.
Reprint requests should be addressed to Dr Gazzanlga. Department of Surgery, University of California. Irvine. Irvlne, California
92664.
Volume 128, Julytl)73
group I the dogs underwent anastomosis of the end of the splenic vein to the side of the renal vein without an attempt being made to increase portal pressure. Dogs in group H underwent splenorenal shunt and (with the shunt temporarily clamped) partial ligation of the portal vein to a pressure between 30 and 35 cm H=O. Dogs in group III underwent the same shunting procedure, but a splenic arteriovenous fistula was constructed 2 to 4 cm distal to the shunt. The abdomen was explored through a transverse left upper quadrant incision. The splenic artery and vein were isolated (Figure 1), the spleen was excised, and the splenic artery was anastomosed side to side to the splenic vein (Figure 2). An arteriovenous fistula, usually about 8 m m long, was created with number 7-0 silk sutures. The distal portion of the splenic vein was then anastomosed end to side to the renal vein. (Figure 3.) Postoperatively the dogs were allowed to recover and were explored at various time intervals to determine the patency of the fistula and splenorenal shunt. Two dogs in 8roup III underwent celiac arteriography postoperatively. At the time of re-exploration, portal pressure was measured through a branch of the superior mesenteric vein and in some cases the portal vein was completely ligated. Dogs were followed until death or recovery.
3
Campbell et al
Results
Figure #. The proximal portion of the splenic vein is dissected from the hilum.
Figure 2. The splenic artery is anestomosed to the splenic vein in a side to side manner distal to the venous anastomosis.
Results are summarized in Table I. In g r o u p I patency of the shunt was documented in only one dog at re-exploration five months after anastomosis. Two dogs explored at three weeks had portal pressures between 8 and 12 cm H~O. Upon acute ligation of the portal vein, pressures rose to over 60 cm H20, and the dogs rapidly died. Dissection of the. anastomosis revealed complete occlusion in both cases. Three dogs explored three months after anastomosis had portal pressures between 8 and 15 cm H=O. Upon acute ligation of the portal vein the pressures rose to over 60 cm HsO and the dogs died within sixty minutes. The splenorenal shunts were thrombosed in each case. In dogs in group H there were no patent anastomoses at exploration three weeks to four months later. Completing the ligation of the portal vein in this group caused rapid demise; dissection of the anastomoses revealed obliterated shunts. Portal pressures measured at the time of ~e-exploration were only slightly elevated and the apparent initial rise with partial ligation had not persisted. In group lII each dog had an audible bruit. Celiac arteriography performed on two dogs six weeks after surgery showed patency of both the splenorenat shunt and the arteriovenous fistula. (Figure 4.) The first dog underwent laparotomy and acute ligation of the portal vein. Mesenteric venous pressure was 10 cm H20 at exploration, rose to 57 cm H20 after acute ligation, and then fell rapidly to 12 cm H20. This dog recovered and lived for one year without evidence of ascites or liver dysfunction. Cardiac output, measured at exploration with Cardio-green dye, did not change after the fistula was ligated. The second dog underwent acute ligation of the portal vein after arteriography and lived six hours. Portal pressure remained around 55 cm H20 and fell only slightly upon ligation of the splenic artery. Although the shunt TABLE !
Results of Experimental Splenorenal Shunt in Dogs
Experimental Group
Figure 3. The completed fistula and splenorenai shunt.
Group ! (Shunt only) Group 11 (shunt and partial ligation of portal vein) Group !11 (shunt with proxima! arteriovenous fistula)
Patency of Shunt
Interval
1/6
3 wk-5 mo
0/4
3 wk-4 mo
6//6
3 wk~l yr
The Amlrlcan Journal of Surgery
Arteriovenous Fistula for Splonorenal Shunt Patency
was p a t e n t , it could n o t a c c o m m o d a t e t h e e n t i r e portal flow. T h e r e m a i n i n g four dogs were explored f r o m t h r e e weeks to five m o n t h s a f t e r surgery. O n l y two of t h e s e dogs u n d e r w e n t a c u t e lig a t i o n of t h e p o r t a l vein a n d b o t h d i e d w i t h i n six h o u r s of ligation. A t p o s t m o r t e m e x a m i n a t i o n b o t h s h u n t s were p a t e n t , b u t a g a i n were n o t large e n o u g h for t h e e n t i r e p o r t a l flow. T h e t w o r e m a i n ing dogs h a d p a l p a b l e bruits, n o r m a l p o r t a l pressures, a n d p a t e n t s p l e n o r e n a l s h u n t s w h e n t h e y were sacrificed a t six m o n t h s .
Case Report The patient (MR), a forty-six year old man, entered Orange County Medical Center on September 17, 1971 with hematemesis. He had had two previous admissions for upper gastrointestinal bleeding secondary to esophageal varices, but had refused surgery. Two weeks after the bleeding was controlled, he consented to surgery. It was elected to create a splenorenal shunt because encephalopathy had developed during each bleeding episode. At surgery, the splenic vein orifice was only 9 m m at its origin and did not seem to enlarge in its course over the tail of the pancreas. The pancreas was extensively fibrotic secondary to chronic pancreatitis and attempts to dissect the vein from the pancreas caused bleeding. The proximal (hilar) portion of the vein was used to fashion a distal side to side splenic artery to splenic vein fistula (measuring 7 ram). Then the end of the splenic vein was turned into the side of the renal vein. Portal pressure before anastomosis was 35 cm H=O; after shunting with the fistula open, the pressure was 20 cm H20. With the shunt clamped and fistula open, the pressure rose to 40 cm H20. Four weeks after surgery an upper gastrointestinal series revealed marked esophageal varices. The continuous murmur of the arteriovenous fistula was clearly audible on an ultrasonic listening device, although it could not be heard with a stethoscope. A celiac arteriogram was taken because of the possibility of thrombosis of the splenic vein distal to the shunt. Figure 5 shows the catheter in the celiac artery with injection and filling of both the hepatic and splenic arteries. The proximal splenic vein and left renal vein filled through the splenic artery. It is quite obvious t h a t the arteriovenoua fistula and the splenorenal shunt were patent. Because it could not be determined from the celiac arteriogram whether the splenic vein was open distal to the fistula, a second study was performed utilizing retrograde catheterization of the left renal vein. Injection into the splenic vein showed that the vein proximal to the fistula was patent and the dye coursed toward the liver. However, it was thought that the splenic artery flow was providing a partial functional obstruction to portal decompression. It was elected to re-explore the patient and ligate the coronary vein as well as the splenic artery. With ligation of the coronary
Volume 126, July 11;73
Figure 4. Celiac arteriogram in a dog demonstrating patency of both the fistula and splenorenal shunt.
vein, the portal pressure remained unchanged at 25 cm H20. With clamping of the splenic artery, the pressure fell to 18 cm H=O, and the splenic artery was ligated. The patient's postoperative course was benign, arid eleven months after discharge he returned to work. At that time an upper gastrointestinal series demonstrated regression of the esophageal varices.
Comments P a t e n c y of a s p l e n o r e n a l s h u n t d e p e n d s u p o n the size of t h e splenic vein, the p r e s s u r e g r a d i e n t a n d flow across t h e s p l e n o r e n a l orifice, a n d "the a b s e n c e of a n g u l a t i o n or k i n k i n g of t h e splenic vein. T h r o m b o s i s of s p l e n o r e n a l s h u n t s has" b e e n m o r e c o m m o n in children, especially those u n d e r the age of t e n years, b u t it can also occur in a d u l t s a n d h a s been a f a c t o r l i m i t i n g t h e i r use [2,8]. A r t e r i o v e n o u s fistulas h a v e b e e n used in arterial r e c o n s t r u c t i v e s u r g e r y distal to p r o s t h e t i c g r a f t insertion in order to i m p r o v e r u n - o f f a n d t h e r e b y increase flow t h r o u g h t h e graft. T h e s e s h u n t s h a v e proved, b o t h in t h e e x p e r i m e n t a l l a b o r a t o r y a n d in s o m e clinical cases, to be highly effective in m a i n t a i n i n g p a t e n c y in grafts t h a t would otherwise fail [3,5]. M a n y studies have shown t h a t synthetic and a u t o g e n o u s vein g r a f t s h a v e a s i g n i f i c a n t l y higher
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Campbel! et al
patency rate when arteriovenous fistulas are placed proximal to the venous anastomosis [7,9]. T h e fistula functions by producing a high flow rate across the graft during the period required for fibrin and possibly endothelium to cover the anastomosis and line the graft, which is probably three to four weeks. After that time the graft has stabilized and venous flow in most cases is sufficient to maintain patency without the fistula [9]. In the animal studies presented, a splenic arteriovenous fistula central to the splenorenal shunt assured patency in each case and did not alter portal pressure whether the shunt was open or closed. Several studies have shown that portal arterioyenous fistulas in normal animals will not produce elevation in portal pressure until as m u c h as four or five times the basal portal blood flow is exceeded [10]. However, if portal hypertension is created~ then small increments in portal flow will produce disproportionate increases in portal pressure [II]. Thus, a small fistula in the presence of portal hypertension without a decompressive shunt might produce hazardous elevation in portal pressures. In one animal t he portal vein was totally ligated an d portal pressure fell to normal after an initial rise. T h e splenorenal s h u n t in this dog was large enough to accommodate the entire portal flow as well as t he flow through the splenic artery fistula. Portal pressures were normal one year after ligation of the portal vein. T h e r e was no evidence of congestive heart failure or ascites. The cardiac o u t p u t was the same before and after ligation of the fistula. Acute ligation of the portal vein in three other dogs, however, proved fatal after six hours. Th e venous shunt in these animals was not
Figure 5. Celiac arteriogram in a patient demonstrating patency of the arteriovenous fistula and filling of the left renal vein.
6
large enough to accommodate the entire portal and fistula blood flow. In the patient presented, celiac arteriography showed that both the fistula and shunt were patent (Figure 6), but there was no reflux of dye into the portal circulation. This raised the possibility of thrombosis of the distal splenic vein, but a retrograde study of the left renal vein showed the splenic vein to be patent. Because there w a s concern that the high flow through the fistula was producing a partial functional obstruction to portal decompression a t the sp!enorenal orifice, it was decided to ligate both the splenic artery and coronary vein. The patient has done well since surgery with variceal regression documented radiographically. In this case, despite portal hypertension, the fistula, when open, did not increase portal pressure. In fact, portal pressure fell to acceptable levels. W h e n the shunt was clamped, however, the fistula did increaseportal pressure. Also, the fistula did not impose a hemodynamic load on the heart since cardiac output did not change when it was created. The splenorenal shunts were thrombosed in all but one of the animals without a fistula. In this one animal, exploration Occurred five months after creation of the shunt and it is possible that the shunt initially thrombosed and later recanalized. Partial ligation of the portal vein is not a satisfactory method for producing portal liypertension [12]. Regardless, shunt failure occurred in nine of ten animals in both groups and none occurred in the group ~vithfistulas. The advantages of creating an arteriovenous fistula just proximal to the splenorenal shunt are that the hilar portion of the vein can be used, al-
Figure 6. Retrograde injection of t h e splenic vein through the splenorenal shunt in the patient presented. A dilated coronary vein is also filled.
The American Journa| of Surgery
A r t e r t o v e n o u s Fistula f o r S p l e n o r e n a l Shunt P a t e n c y
lowing for acceptable mented at the splenic
a more rapid operation. However, an fall in portal pressure must be docusurgery and possible future ligation of artery niay be necessary.
2. Hamilton DW, Hunt AH: Extrahepatic portal obstruction.
MedJAust 1: 493, 1970. 3. Kistner RL, Vermuelen WJ: Therapeutic arteriovenous
4.
Summary From this series of animal experiments it was concluded that patency of splenorenal shunts can best be maintained by creating a distal arteriovenous fistula. Such a fistula was created distal to the splenorenal shunt in one patient. Because of persistent varices the splenic artery was ligated five weeks later, at which time angiographic studies showed the shunt and fistula to be patent. The patient is doing well eleven months later, with radiographic documentation of variceal regression. This technic m a y be suitable when the peripheral portion of the splenic vein must be used or when, as in children, the vein is small.
5. 6. 7. 8. 9. 10.
11.
References 12. 1. Trusler GA, Morris FR, Mustard WT: Portal hypertension in childhood. Surgery 52: 664, 1962.
Volume 126, July 1973
fistula In management of severe ischemia of the extremities. Surg C/in NAmer 50: 291. 1970. Levin PM, Rich NM, Hutton JE, Barker WF, Zeller JA: Rote of arterlovenous shunts in venous reconstruction. AmerJ Surg 122: t83, 1971. Blaisdell FW, Lira RC, Hall AD, Thomas AM: Reconstruction of small arteries with an arterJovenous fistula. Arch Sutg 92: 206, 1966. Johnson V, EIseman B: Evaluation of arteriovenous shunt to maintain patency of venous autograft. Amer J Surg 118: 915, 1969. Mitsuoka H, Howard JM: Experimental grafting of the inferior vena cava. Cardiovasc Surg 9: 190. 1968. Ltnton RR: A splenorenal or a portocaval shunt? Surg Gynec Obstet 121: 117, 1965. Yamaguchi A, Eguchi S, Iwasaki T, Asano K: The influence of arteriovenous fistulae on the devascularized llmb. JAMA 190: 109, 1965. Siderys H. Judd D, Herendeen JL, Kilman JW, Waldhausen JA: The experimental production of elevated portal pres.~ure by increasing portal flow. Surg Gynec Obstet 120: 514, 1965. Sato T, Koyama K, Watanabe K, Kimura S: Experimental portal hypertension in adult dogs and puppies. Surg Gynec Obstet 115: 327, 1962. Walker R, Allen MS: A comparison of experimental portal hypertension in adult dogs and puppies. Surg Gynec Obstet 115: 327, 1962.
7
Splenic Arteriovenous Fistula to Maintain Patency of Splenorenal Shunts
R o b e r t W. C a m p b e l l , M D , I r v i n e , C a l i f o r n i a Leo B. Be,in, MD, I r v i n e , C a l i f o r n i a J a c k I. Eimenman, b i D , I r v i n e , C a l i f o r n i a Alan B. Gazzanlga, MD, I r v i n e , C a l i f o r n i a
T h e s p l e n o r e n a l s h u n t is a n e s t a b l i s h e d p r o c e d u r e for d e c o m p r e s s i o n of e s o p h a g e a l varices d u e to p o r t a l h y p e r t e n s i o n in older children a n d a d u l t s [1,2]. H o w e v e r , l o n g - t e r m results s h o w t h a t a sign i f i c a n t n u m b e r of t h e s e s h u n t s close if t h e splenic vein is s m a l l or if t h e p r o x i m a l (hilar) p o r t i o n of t h e vein is used. A r t e r i o v e n o u s fistulas h a v e b e e n u s e d e x p e r i m e n t a l l y , a n d in s o m e cases clinically, t o p r o m o t e p a t e n c y of v e n o u s a n d a r t e r i a l grafts [3-7]. T h i s p a p e r describes our e x p e r i m e n t a l work u s i n g splenic a r t e r i o v e n o u s a n a s t o m o s e s to m a i n t a i n p a t e n c y of s p l e n o r e n a l s h u n t s a n d p r e s e n t s a clinical case r e p o r t of this technic. Material and Methods
Three groups of adult dogs weighing between 18 and 23 kg were used in this study. The dogs were anesthetized with pentobarbital (30 mg/kg) and ventilated with a Harvard respirator via an endotracheal tube. In From the Department of Surgery. University of California. Irvine, Iro
vine, California.
Reprint requests should be addressed to Dr Gazzanlga. Department of Surgery, University of California. Irvine. Irvlne, California
92664.
Volume 128, Julytl)73
group I the dogs underwent anastomosis of the end of the splenic vein to the side of the renal vein without an attempt being made to increase portal pressure. Dogs in group H underwent splenorenal shunt and (with the shunt temporarily clamped) partial ligation of the portal vein to a pressure between 30 and 35 cm H=O. Dogs in group III underwent the same shunting procedure, but a splenic arteriovenous fistula was constructed 2 to 4 cm distal to the shunt. The abdomen was explored through a transverse left upper quadrant incision. The splenic artery and vein were isolated (Figure 1), the spleen was excised, and the splenic artery was anastomosed side to side to the splenic vein (Figure 2). An arteriovenous fistula, usually about 8 m m long, was created with number 7-0 silk sutures. The distal portion of the splenic vein was then anastomosed end to side to the renal vein. (Figure 3.) Postoperatively the dogs were allowed to recover and were explored at various time intervals to determine the patency of the fistula and splenorenal shunt. Two dogs in 8roup III underwent celiac arteriography postoperatively. At the time of re-exploration, portal pressure was measured through a branch of the superior mesenteric vein and in some cases the portal vein was completely ligated. Dogs were followed until death or recovery.
3
Campbell et al
Results
Figure #. The proximal portion of the splenic vein is dissected from the hilum.
Figure 2. The splenic artery is anestomosed to the splenic vein in a side to side manner distal to the venous anastomosis.
Results are summarized in Table I. In g r o u p I patency of the shunt was documented in only one dog at re-exploration five months after anastomosis. Two dogs explored at three weeks had portal pressures between 8 and 12 cm H~O. Upon acute ligation of the portal vein, pressures rose to over 60 cm H20, and the dogs rapidly died. Dissection of the. anastomosis revealed complete occlusion in both cases. Three dogs explored three months after anastomosis had portal pressures between 8 and 15 cm H=O. Upon acute ligation of the portal vein the pressures rose to over 60 cm HsO and the dogs died within sixty minutes. The splenorenal shunts were thrombosed in each case. In dogs in group H there were no patent anastomoses at exploration three weeks to four months later. Completing the ligation of the portal vein in this group caused rapid demise; dissection of the anastomoses revealed obliterated shunts. Portal pressures measured at the time of ~e-exploration were only slightly elevated and the apparent initial rise with partial ligation had not persisted. In group lII each dog had an audible bruit. Celiac arteriography performed on two dogs six weeks after surgery showed patency of both the splenorenat shunt and the arteriovenous fistula. (Figure 4.) The first dog underwent laparotomy and acute ligation of the portal vein. Mesenteric venous pressure was 10 cm H20 at exploration, rose to 57 cm H20 after acute ligation, and then fell rapidly to 12 cm H20. This dog recovered and lived for one year without evidence of ascites or liver dysfunction. Cardiac output, measured at exploration with Cardio-green dye, did not change after the fistula was ligated. The second dog underwent acute ligation of the portal vein after arteriography and lived six hours. Portal pressure remained around 55 cm H20 and fell only slightly upon ligation of the splenic artery. Although the shunt TABLE !
Results of Experimental Splenorenal Shunt in Dogs
Experimental Group
Figure 3. The completed fistula and splenorenai shunt.
Group ! (Shunt only) Group 11 (shunt and partial ligation of portal vein) Group !11 (shunt with proxima! arteriovenous fistula)
Patency of Shunt
Interval
1/6
3 wk-5 mo
0/4
3 wk-4 mo
6//6
3 wk~l yr
The Amlrlcan Journal of Surgery
Arteriovenous Fistula for Splonorenal Shunt Patency
was p a t e n t , it could n o t a c c o m m o d a t e t h e e n t i r e portal flow. T h e r e m a i n i n g four dogs were explored f r o m t h r e e weeks to five m o n t h s a f t e r surgery. O n l y two of t h e s e dogs u n d e r w e n t a c u t e lig a t i o n of t h e p o r t a l vein a n d b o t h d i e d w i t h i n six h o u r s of ligation. A t p o s t m o r t e m e x a m i n a t i o n b o t h s h u n t s were p a t e n t , b u t a g a i n were n o t large e n o u g h for t h e e n t i r e p o r t a l flow. T h e t w o r e m a i n ing dogs h a d p a l p a b l e bruits, n o r m a l p o r t a l pressures, a n d p a t e n t s p l e n o r e n a l s h u n t s w h e n t h e y were sacrificed a t six m o n t h s .
Case Report The patient (MR), a forty-six year old man, entered Orange County Medical Center on September 17, 1971 with hematemesis. He had had two previous admissions for upper gastrointestinal bleeding secondary to esophageal varices, but had refused surgery. Two weeks after the bleeding was controlled, he consented to surgery. It was elected to create a splenorenal shunt because encephalopathy had developed during each bleeding episode. At surgery, the splenic vein orifice was only 9 m m at its origin and did not seem to enlarge in its course over the tail of the pancreas. The pancreas was extensively fibrotic secondary to chronic pancreatitis and attempts to dissect the vein from the pancreas caused bleeding. The proximal (hilar) portion of the vein was used to fashion a distal side to side splenic artery to splenic vein fistula (measuring 7 ram). Then the end of the splenic vein was turned into the side of the renal vein. Portal pressure before anastomosis was 35 cm H=O; after shunting with the fistula open, the pressure was 20 cm H20. With the shunt clamped and fistula open, the pressure rose to 40 cm H20. Four weeks after surgery an upper gastrointestinal series revealed marked esophageal varices. The continuous murmur of the arteriovenous fistula was clearly audible on an ultrasonic listening device, although it could not be heard with a stethoscope. A celiac arteriogram was taken because of the possibility of thrombosis of the splenic vein distal to the shunt. Figure 5 shows the catheter in the celiac artery with injection and filling of both the hepatic and splenic arteries. The proximal splenic vein and left renal vein filled through the splenic artery. It is quite obvious t h a t the arteriovenoua fistula and the splenorenal shunt were patent. Because it could not be determined from the celiac arteriogram whether the splenic vein was open distal to the fistula, a second study was performed utilizing retrograde catheterization of the left renal vein. Injection into the splenic vein showed that the vein proximal to the fistula was patent and the dye coursed toward the liver. However, it was thought that the splenic artery flow was providing a partial functional obstruction to portal decompression. It was elected to re-explore the patient and ligate the coronary vein as well as the splenic artery. With ligation of the coronary
Volume 126, July 11;73
Figure 4. Celiac arteriogram in a dog demonstrating patency of both the fistula and splenorenal shunt.
vein, the portal pressure remained unchanged at 25 cm H20. With clamping of the splenic artery, the pressure fell to 18 cm H=O, and the splenic artery was ligated. The patient's postoperative course was benign, arid eleven months after discharge he returned to work. At that time an upper gastrointestinal series demonstrated regression of the esophageal varices.
Comments P a t e n c y of a s p l e n o r e n a l s h u n t d e p e n d s u p o n the size of t h e splenic vein, the p r e s s u r e g r a d i e n t a n d flow across t h e s p l e n o r e n a l orifice, a n d "the a b s e n c e of a n g u l a t i o n or k i n k i n g of t h e splenic vein. T h r o m b o s i s of s p l e n o r e n a l s h u n t s has" b e e n m o r e c o m m o n in children, especially those u n d e r the age of t e n years, b u t it can also occur in a d u l t s a n d h a s been a f a c t o r l i m i t i n g t h e i r use [2,8]. A r t e r i o v e n o u s fistulas h a v e b e e n used in arterial r e c o n s t r u c t i v e s u r g e r y distal to p r o s t h e t i c g r a f t insertion in order to i m p r o v e r u n - o f f a n d t h e r e b y increase flow t h r o u g h t h e graft. T h e s e s h u n t s h a v e proved, b o t h in t h e e x p e r i m e n t a l l a b o r a t o r y a n d in s o m e clinical cases, to be highly effective in m a i n t a i n i n g p a t e n c y in grafts t h a t would otherwise fail [3,5]. M a n y studies have shown t h a t synthetic and a u t o g e n o u s vein g r a f t s h a v e a s i g n i f i c a n t l y higher
S
Campbel! et al
patency rate when arteriovenous fistulas are placed proximal to the venous anastomosis [7,9]. T h e fistula functions by producing a high flow rate across the graft during the period required for fibrin and possibly endothelium to cover the anastomosis and line the graft, which is probably three to four weeks. After that time the graft has stabilized and venous flow in most cases is sufficient to maintain patency without the fistula [9]. In the animal studies presented, a splenic arteriovenous fistula central to the splenorenal shunt assured patency in each case and did not alter portal pressure whether the shunt was open or closed. Several studies have shown that portal arterioyenous fistulas in normal animals will not produce elevation in portal pressure until as m u c h as four or five times the basal portal blood flow is exceeded [10]. However, if portal hypertension is created~ then small increments in portal flow will produce disproportionate increases in portal pressure [II]. Thus, a small fistula in the presence of portal hypertension without a decompressive shunt might produce hazardous elevation in portal pressures. In one animal t he portal vein was totally ligated an d portal pressure fell to normal after an initial rise. T h e splenorenal s h u n t in this dog was large enough to accommodate the entire portal flow as well as t he flow through the splenic artery fistula. Portal pressures were normal one year after ligation of the portal vein. T h e r e was no evidence of congestive heart failure or ascites. The cardiac o u t p u t was the same before and after ligation of the fistula. Acute ligation of the portal vein in three other dogs, however, proved fatal after six hours. Th e venous shunt in these animals was not
Figure 5. Celiac arteriogram in a patient demonstrating patency of the arteriovenous fistula and filling of the left renal vein.
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large enough to accommodate the entire portal and fistula blood flow. In the patient presented, celiac arteriography showed that both the fistula and shunt were patent (Figure 6), but there was no reflux of dye into the portal circulation. This raised the possibility of thrombosis of the distal splenic vein, but a retrograde study of the left renal vein showed the splenic vein to be patent. Because there w a s concern that the high flow through the fistula was producing a partial functional obstruction to portal decompression a t the sp!enorenal orifice, it was decided to ligate both the splenic artery and coronary vein. The patient has done well since surgery with variceal regression documented radiographically. In this case, despite portal hypertension, the fistula, when open, did not increase portal pressure. In fact, portal pressure fell to acceptable levels. W h e n the shunt was clamped, however, the fistula did increaseportal pressure. Also, the fistula did not impose a hemodynamic load on the heart since cardiac output did not change when it was created. The splenorenal shunts were thrombosed in all but one of the animals without a fistula. In this one animal, exploration Occurred five months after creation of the shunt and it is possible that the shunt initially thrombosed and later recanalized. Partial ligation of the portal vein is not a satisfactory method for producing portal liypertension [12]. Regardless, shunt failure occurred in nine of ten animals in both groups and none occurred in the group ~vithfistulas. The advantages of creating an arteriovenous fistula just proximal to the splenorenal shunt are that the hilar portion of the vein can be used, al-
Figure 6. Retrograde injection of t h e splenic vein through the splenorenal shunt in the patient presented. A dilated coronary vein is also filled.
The American Journa| of Surgery
A r t e r t o v e n o u s Fistula f o r S p l e n o r e n a l Shunt P a t e n c y
lowing for acceptable mented at the splenic
a more rapid operation. However, an fall in portal pressure must be docusurgery and possible future ligation of artery niay be necessary.
2. Hamilton DW, Hunt AH: Extrahepatic portal obstruction.
MedJAust 1: 493, 1970. 3. Kistner RL, Vermuelen WJ: Therapeutic arteriovenous
4.
Summary From this series of animal experiments it was concluded that patency of splenorenal shunts can best be maintained by creating a distal arteriovenous fistula. Such a fistula was created distal to the splenorenal shunt in one patient. Because of persistent varices the splenic artery was ligated five weeks later, at which time angiographic studies showed the shunt and fistula to be patent. The patient is doing well eleven months later, with radiographic documentation of variceal regression. This technic m a y be suitable when the peripheral portion of the splenic vein must be used or when, as in children, the vein is small.
5. 6. 7. 8. 9. 10.
11.
References 12. 1. Trusler GA, Morris FR, Mustard WT: Portal hypertension in childhood. Surgery 52: 664, 1962.
Volume 126, July 1973
fistula In management of severe ischemia of the extremities. Surg C/in NAmer 50: 291. 1970. Levin PM, Rich NM, Hutton JE, Barker WF, Zeller JA: Rote of arterlovenous shunts in venous reconstruction. AmerJ Surg 122: t83, 1971. Blaisdell FW, Lira RC, Hall AD, Thomas AM: Reconstruction of small arteries with an arterJovenous fistula. Arch Sutg 92: 206, 1966. Johnson V, EIseman B: Evaluation of arteriovenous shunt to maintain patency of venous autograft. Amer J Surg 118: 915, 1969. Mitsuoka H, Howard JM: Experimental grafting of the inferior vena cava. Cardiovasc Surg 9: 190. 1968. Ltnton RR: A splenorenal or a portocaval shunt? Surg Gynec Obstet 121: 117, 1965. Yamaguchi A, Eguchi S, Iwasaki T, Asano K: The influence of arteriovenous fistulae on the devascularized llmb. JAMA 190: 109, 1965. Siderys H. Judd D, Herendeen JL, Kilman JW, Waldhausen JA: The experimental production of elevated portal pres.~ure by increasing portal flow. Surg Gynec Obstet 120: 514, 1965. Sato T, Koyama K, Watanabe K, Kimura S: Experimental portal hypertension in adult dogs and puppies. Surg Gynec Obstet 115: 327, 1962. Walker R, Allen MS: A comparison of experimental portal hypertension in adult dogs and puppies. Surg Gynec Obstet 115: 327, 1962.
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