The
Significance of Portal Vein Thrombosis After Distal Splenorenal Shunt Gongliang Jin, MD, Layton
aims of this study were to determine the incidence of portal vein thrombosis after the distal splenorenal shunt, to identify any predictive factors, and to assess the clinical significance of this complication. Preoperative and postoperative angiograms and clinical evaluation were reviewed in 124 patients who underwent distal splenorenal shunts. Total and partial portal vein thrombosis were seen on 13 (10.5%) and 22 (17.7%) postoperative angiograms, respectively. The only preoperative variable correlating with development of portal vein thrombosis was portal venous perfusion, which was significantly lower in patients with than in those without portal vein thrombosis. In six of 10 patients with postoperative pancreatitis, portal vein thrombosis developed. The frequency of early postoperative complications was significantly greater in patients with total portal vein thrombosis than in those with partial or no thrombosis. Long-term follow-up has shown no significant effects of portal vein thrombosis on late ascites, encephalopathy, or survival.
F.
Rikkers,
MD
PATIENTS AND METHODS
\s=b\ The
(Arch Surg. 1991;126:1011-1016)
addition decompression of esophagogastric varices, In objectives of the distal splenorenal shunt (DSRS) in¬ and main¬ clude of to
hepatic portal perfusion Although the ma¬ hypertension.1 lost the DSRS is gradual of flow after cause portal jor collateralization from the superior mesenteric venous cir¬ cuit to the decompressed gastrosplenic component of the portal venous system, early postoperative absence of he¬ patic portal perfusion is most frequently secondary to por¬ tal vein thrombosis (PVT). The clinical significance of PVT preservation
tenance of portal venous
after the DSRS is controversial, with some series reporting subsequent high morbidity and mortality and others find¬ ing minimal influence of this complication on the early postoperative course.2"12 The aims of this study were to determine the incidence of PVT after DSRS, to identify predictive factors, and to assess the short- and long-term clinical significance of this complication.
From January 1978 through April 1990,137 patients underwent DSRS for variceal bleeding at the University of Utah Medical Cen¬ ter, Salt Lake City; the Salt Lake City Veterans Administration Medical Center; the University of Nebraska Medical Center, Omaha; and the Omaha Veterans Administration Medical Cen¬ ter. All operations were performed by a single surgeon (L.F.R.). One hundred twenty-four patients who received both preoperative and early postoperative (1 to 3 weeks) visceral angiography and had patent portal veins on the venous phase of preoperative superior mesenteric arteriography compose the population for this study. Thirteen patients, including two with a preoperative diagnosis of PVT and 11 with incomplete preoperative or post¬ operative angiography, were excluded. During the preoperative and intraoperative evaluation, the fol¬ lowing variables were assessed in all patients: age, cause of liver disease, Child's classification, serum albumin, serum total bilir-
ubin, platelet count, prothrombin time, partial thromboplastin time, operative time, and intraoperative blood transfusion. Child's classification was determined by a scoring system as pre¬
viously described.13 Hepatic hemodynamics were assessed by visceral angiogra¬ phy, which was obtained preoperatively and in the early post¬ operative interval. An angiographie study consisted of selective superior mesenteric, splenic, and hepatic arterial injections, left renal vein opacification, and corrected sinusoidal pressure (he¬ patic venous wedge pressure minus free hepatic vein pressure). The portal perfusion grade was qualitatively assessed from the venous phase of the superior mesenteric arterial injection: grade 1, visualization of the peripheral intrahepatic radicles; grade 2, opacification of only the secondary and tertiary radicles of the portal vein; grade 3, visualization of only the main portal vein and the major left and right branches; and grade 4, absence of portal venous
the
opacification.14 The presence or absence of thrombus in
portal vein was determined on the venous phase of the su¬
perior mesenteric angiogram. Three groups of patients were identified: those with total PVT (Fig 1), patients with partial PVT (Fig 2), and those with no evidence of PVT. In the absence of portal venous opacification (grade 4), total PVT was confirmed by lack of portal vein visualization after hepatic venous wedge injection of contrast and/or lack of portal venous flow on duplex
ultrasonography.
Accepted
publication April From the Department of Surgery, University of Nebraska Medical for
7, 1991.
Center, Omaha.
Read before the 98th Annual
Meeting
of the Western
Surgical
Association, Scottsdale, Ariz, November 13, 1990. Reprint requests to Department of Surgery, University of Nebraska Medical Center, 600 S 42nd St, Omaha, NE 68198-3280 (Dr Rikkers).
Indicators of postoperative morbidity were ascites severe enough to require intensive medical management, moderate or severe encephalopathy, and duration of postoperative hospital stay. Encephalopathy induced by gastrointestinal bleeding and altered mental status initially appearing just before death from hepatic failure were excluded. Operative mortality was defined as death occurring during the same hospitalization as the op¬ eration or within 30 days postoperatively for discharged patients.
Downloaded From: http://archsurg.jamanetwork.com/ by a Western University User on 06/11/2015
Table
1.—Preoperative and Intraoperative Data* Total PVT (n = 13)
(n 89) =
Sex, %M
77
77
66
38
68
56
15
18
19
Age, y
50+14
54± 12
52±11
Serum
albumin, g/L Serum bilirubin,
34 ±4
33 ±6
33 ±6
u.mol/L Platelet count, X107L
21+12
34±12
34 ±3
s
thromboplastin
time,
superior mesenteric arterioFig gram showing total thrombosis of the portal vein. Only a small rim of proximal portal vein (arrows) is opactfied. No intrahepatic portal radicles are visualized. SMV indicates superior mesenteric vein.
No PVT
Alcoholic cirrhosis, % Child's class C, %
Prothrombin time, Partial
1.— Venous phase of postoperative
Partial PVT (n = 22)
s
147 ±70
125 ±61
138 ±68
14.8 ±1.9
13.9±1.7
14.2 ±1.4
38.7±7.0
38.1+7.5
38.0±7.9
Intraoperative blood 2.6 ±2.6 2.4±1.5 transfusion, U 5.2 ±0.9 5.3 ±0.8 h time, Operative *PVT indicates portal vein thrombosis. Except for cirrhosis, and Child's class C, values are mean±SD.
2.0±1.2 5.0 ±1.2 sex,
alcoholic
RESULTS
Incidence of PVT In 35 patients, PVT developed in the early postoperative interval after DSRS, giving an overall incidence of 28.2%. Twenty-two (17.7%) of these patients had a partial PVT. The remaining 13 (10.5%) had total PVT, with three (2.4%) of these 13 also having had thrombosis of the superior mesenteric vein.
Patient Profile Table 1 compares patients with total, partial, and no PVT with respect to several preoperative and intraoperative variables. Preoperative values for age, cause of liver dis¬ ease, Child's classification, albumin, total bilirubin, plate¬ let count, prothrombin time, partial thromboplastin time, operative time, and intraoperative blood transfusion were not significantly different among the three groups. The incidence of PVT was similar in patients with alcoholic cirrhosis and nonalcoholic diseases. In 20 (28.6%) of 70 alcoholic cirrhotics and 15 (27.8%) of 54 patients without alcoholic diseases, PVT developed following DSRS. When total PVT was considered separately, the incidence was not significantly different between patients with alcoholic cirrhosis (7% [5/70]) and nonalcoholic diseases (15%
[8/54]).
Fig 2.— Venous phase of postoperative superior mesenteric arteriogram showing partial, nonocclusive thrombosis of the main portal vein (large arrow). Opacified intrahepatic portal radicles (small ar¬ rows) indicate that hepatic portal perfusion is still present. SMV in¬ dicates superior mesenteric vein; PV, portal vein.
Portal Venous Hemodynamics preoperative portal perfusion grade was signifi¬ cantly greater (worse portal perfusion) in patients with total PVT (2.3±0.6, n 13, P
Significance of Portal Vein Thrombosis After Distal Splenorenal Shunt Gongliang Jin, MD, Layton
aims of this study were to determine the incidence of portal vein thrombosis after the distal splenorenal shunt, to identify any predictive factors, and to assess the clinical significance of this complication. Preoperative and postoperative angiograms and clinical evaluation were reviewed in 124 patients who underwent distal splenorenal shunts. Total and partial portal vein thrombosis were seen on 13 (10.5%) and 22 (17.7%) postoperative angiograms, respectively. The only preoperative variable correlating with development of portal vein thrombosis was portal venous perfusion, which was significantly lower in patients with than in those without portal vein thrombosis. In six of 10 patients with postoperative pancreatitis, portal vein thrombosis developed. The frequency of early postoperative complications was significantly greater in patients with total portal vein thrombosis than in those with partial or no thrombosis. Long-term follow-up has shown no significant effects of portal vein thrombosis on late ascites, encephalopathy, or survival.
F.
Rikkers,
MD
PATIENTS AND METHODS
\s=b\ The
(Arch Surg. 1991;126:1011-1016)
addition decompression of esophagogastric varices, In objectives of the distal splenorenal shunt (DSRS) in¬ and main¬ clude of to
hepatic portal perfusion Although the ma¬ hypertension.1 lost the DSRS is gradual of flow after cause portal jor collateralization from the superior mesenteric venous cir¬ cuit to the decompressed gastrosplenic component of the portal venous system, early postoperative absence of he¬ patic portal perfusion is most frequently secondary to por¬ tal vein thrombosis (PVT). The clinical significance of PVT preservation
tenance of portal venous
after the DSRS is controversial, with some series reporting subsequent high morbidity and mortality and others find¬ ing minimal influence of this complication on the early postoperative course.2"12 The aims of this study were to determine the incidence of PVT after DSRS, to identify predictive factors, and to assess the short- and long-term clinical significance of this complication.
From January 1978 through April 1990,137 patients underwent DSRS for variceal bleeding at the University of Utah Medical Cen¬ ter, Salt Lake City; the Salt Lake City Veterans Administration Medical Center; the University of Nebraska Medical Center, Omaha; and the Omaha Veterans Administration Medical Cen¬ ter. All operations were performed by a single surgeon (L.F.R.). One hundred twenty-four patients who received both preoperative and early postoperative (1 to 3 weeks) visceral angiography and had patent portal veins on the venous phase of preoperative superior mesenteric arteriography compose the population for this study. Thirteen patients, including two with a preoperative diagnosis of PVT and 11 with incomplete preoperative or post¬ operative angiography, were excluded. During the preoperative and intraoperative evaluation, the fol¬ lowing variables were assessed in all patients: age, cause of liver disease, Child's classification, serum albumin, serum total bilir-
ubin, platelet count, prothrombin time, partial thromboplastin time, operative time, and intraoperative blood transfusion. Child's classification was determined by a scoring system as pre¬
viously described.13 Hepatic hemodynamics were assessed by visceral angiogra¬ phy, which was obtained preoperatively and in the early post¬ operative interval. An angiographie study consisted of selective superior mesenteric, splenic, and hepatic arterial injections, left renal vein opacification, and corrected sinusoidal pressure (he¬ patic venous wedge pressure minus free hepatic vein pressure). The portal perfusion grade was qualitatively assessed from the venous phase of the superior mesenteric arterial injection: grade 1, visualization of the peripheral intrahepatic radicles; grade 2, opacification of only the secondary and tertiary radicles of the portal vein; grade 3, visualization of only the main portal vein and the major left and right branches; and grade 4, absence of portal venous
the
opacification.14 The presence or absence of thrombus in
portal vein was determined on the venous phase of the su¬
perior mesenteric angiogram. Three groups of patients were identified: those with total PVT (Fig 1), patients with partial PVT (Fig 2), and those with no evidence of PVT. In the absence of portal venous opacification (grade 4), total PVT was confirmed by lack of portal vein visualization after hepatic venous wedge injection of contrast and/or lack of portal venous flow on duplex
ultrasonography.
Accepted
publication April From the Department of Surgery, University of Nebraska Medical for
7, 1991.
Center, Omaha.
Read before the 98th Annual
Meeting
of the Western
Surgical
Association, Scottsdale, Ariz, November 13, 1990. Reprint requests to Department of Surgery, University of Nebraska Medical Center, 600 S 42nd St, Omaha, NE 68198-3280 (Dr Rikkers).
Indicators of postoperative morbidity were ascites severe enough to require intensive medical management, moderate or severe encephalopathy, and duration of postoperative hospital stay. Encephalopathy induced by gastrointestinal bleeding and altered mental status initially appearing just before death from hepatic failure were excluded. Operative mortality was defined as death occurring during the same hospitalization as the op¬ eration or within 30 days postoperatively for discharged patients.
Downloaded From: http://archsurg.jamanetwork.com/ by a Western University User on 06/11/2015
Table
1.—Preoperative and Intraoperative Data* Total PVT (n = 13)
(n 89) =
Sex, %M
77
77
66
38
68
56
15
18
19
Age, y
50+14
54± 12
52±11
Serum
albumin, g/L Serum bilirubin,
34 ±4
33 ±6
33 ±6
u.mol/L Platelet count, X107L
21+12
34±12
34 ±3
s
thromboplastin
time,
superior mesenteric arterioFig gram showing total thrombosis of the portal vein. Only a small rim of proximal portal vein (arrows) is opactfied. No intrahepatic portal radicles are visualized. SMV indicates superior mesenteric vein.
No PVT
Alcoholic cirrhosis, % Child's class C, %
Prothrombin time, Partial
1.— Venous phase of postoperative
Partial PVT (n = 22)
s
147 ±70
125 ±61
138 ±68
14.8 ±1.9
13.9±1.7
14.2 ±1.4
38.7±7.0
38.1+7.5
38.0±7.9
Intraoperative blood 2.6 ±2.6 2.4±1.5 transfusion, U 5.2 ±0.9 5.3 ±0.8 h time, Operative *PVT indicates portal vein thrombosis. Except for cirrhosis, and Child's class C, values are mean±SD.
2.0±1.2 5.0 ±1.2 sex,
alcoholic
RESULTS
Incidence of PVT In 35 patients, PVT developed in the early postoperative interval after DSRS, giving an overall incidence of 28.2%. Twenty-two (17.7%) of these patients had a partial PVT. The remaining 13 (10.5%) had total PVT, with three (2.4%) of these 13 also having had thrombosis of the superior mesenteric vein.
Patient Profile Table 1 compares patients with total, partial, and no PVT with respect to several preoperative and intraoperative variables. Preoperative values for age, cause of liver dis¬ ease, Child's classification, albumin, total bilirubin, plate¬ let count, prothrombin time, partial thromboplastin time, operative time, and intraoperative blood transfusion were not significantly different among the three groups. The incidence of PVT was similar in patients with alcoholic cirrhosis and nonalcoholic diseases. In 20 (28.6%) of 70 alcoholic cirrhotics and 15 (27.8%) of 54 patients without alcoholic diseases, PVT developed following DSRS. When total PVT was considered separately, the incidence was not significantly different between patients with alcoholic cirrhosis (7% [5/70]) and nonalcoholic diseases (15%
[8/54]).
Fig 2.— Venous phase of postoperative superior mesenteric arteriogram showing partial, nonocclusive thrombosis of the main portal vein (large arrow). Opacified intrahepatic portal radicles (small ar¬ rows) indicate that hepatic portal perfusion is still present. SMV in¬ dicates superior mesenteric vein; PV, portal vein.
Portal Venous Hemodynamics preoperative portal perfusion grade was signifi¬ cantly greater (worse portal perfusion) in patients with total PVT (2.3±0.6, n 13, P
