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Original Report |
1
Department of Radiology, MC 2026, University of Chicago, 5841 S. Maryland
Ave., Chicago, IL 60637.
2
Department of Surgery, MC 5027, University of Chicago, Chicago, IL
60637.
Received April 24, 2000;
accepted after revision July 11, 2000.
Address correspondence to A. H. Dachman.
Abstract
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CONCLUSION. An 11% incidence of portal and mesenteric venous calcification was found in patients with cirrhosis, which was much higher than anticipated. Two (29%) of seven patients who had calcification present on CT and underwent liver transplantation died at surgery as a result of portal venous thrombosis. Thus, venous calcification seen on CT is a significant finding in patients undergoing liver transplantation.
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Abdominal CT scans were retrospectively reviewed in all patients with advanced cirrhosis undergoing evaluation for liver transplantation to determine the incidence, anatomic location, and pattern of calcification. The presence or absence of portal or mesenteric calcification among patients undergoing liver transplantation was correlated with surgical outcome.
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Twenty patients had triphasic scans, including unenhanced,
arterial-weighted (25- to 30-sec scan delay), and redistribution phase (60- to
70-sec scan delay) scans. Delayed scans (
2 min) were usually obtained for
evaluation of the renal excretory phase and often included relevant anatomy.
Thirty patients had only redistribution phase (70-sec delay) scans with
delayed scans of the kidney. Twenty patients had only unenhanced scans. Images
of all patients were reviewed with attention to the regions of the portal,
splenic, and superior mesenteric veins. Contrast-enhanced scans were obtained
using 120-150 mL of IV contrast material (Omnipaque 300; Nycomed Amersham,
Princeton, NJ) injected at 2-3 mL/sec. Scans were obtained helically on a
98000 or CTi scanner (General Electric Medical Systems, Milwaukee, WI).
Collimation ranged from 7 to 10 mm, and the pitch ranged from 1:1 to 1:4 with
the parameters optimized both for soft tissue (width, 420 H; level, 40 H) and
liver tissue (width, 150 H; level, 70 H).
The presence of calcification was determined by a retrospective review of all CT images by two observers who reviewed the films jointly. When high-density material was seen on unenhanced CT, or when high-density material was seen on both early and long delayed-phase contrast-enhanced images, calcification was considered to be present. When calcification was present, the location, extent, and pattern were analyzed. Any cases considered controversial or equivocal were tabulated as "no calcification present."
Surgical reports and clinical histories for all 70 patients were reviewed. This included review of the surgical reports in consultation with the operating surgeon to define the presence of a patent portal vein and any surgical difficulty encountered in obtaining an adequate portal venous anastomosis. If a preoperative sonogram was obtained, the interval between the abdominal CT scan, the sonogram, and the transplantation was tabulated. Additionally, the sonogram was reviewed for evidence of thrombosis of the portal, splenic, or superior mesenteric vein on gray-scale and color Doppler sonography. If spectral Doppler sonography was performed, portal venous flow direction and velocity were noted. If unenhanced radiographs were available, these were reviewed with knowledge of the abdominal CT findings to evaluate the sensitivity of unenhanced radiography in the detection of portal and mesenteric venous calcifications.
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All eight patients with calcifications visible on CT had end-stage cirrhosis: five as a result of hepatitis C, two caused by alcohol use, and one a result of hepatitis B. Seven of the eight patients with venous calcification underwent transplantation. The mean time between CT and transplantation in these eight patients was 93 days (range, 4-180 days). Six of the patients who underwent transplantation also underwent sonography, which showed a patent portal vein in five patients. One patient with a thrombosed portal vein diagnosed on sonography 5 months before surgery underwent transplantation without complication. At the time of transplantation, four patients were found to have an organized intraluminal thrombus in the portal vein despite having sonographic examinations showing patency. Two of these four patients had sonographic evaluation more than 6 months before transplantation, and only one patient underwent sonography within 1 month before transplantation. None of the eight patients with venous calcification underwent angiography or had venous thrombosis revealed on CT.
Sixty of the 62 patients who did not have portal vein calcification underwent successful liver transplantation with no portal vein thrombus discovered during the transplantation procedure.
Two (29%) of the seven patients with portal and mesenteric calcifications who underwent liver transplantation died during surgery. In one of these patients, abdominal CT performed 4 days before transplantation revealed a patent but calcified portal vein. Abdominal and Doppler sonography 1 month before surgery showed slow hepatopetal portal venous flow with a peak velocity of 13 cm/sec. However, at surgery it was discovered that the portal vein was thrombosed. Retrospectively, we believe that collateral formation may have been mistaken for a patent main portal vein on sonography. At surgery, the portal vein was firm to palpation and surrounded by a dense inflammatory reaction. The portal vein was transected and found to be thrombosed. The thrombus was calcified and intimately adherent to, and incorporated with, the endothelium of the vein. Attempts at thrombectomy with Fogarty catheters (Baxter Health Care, Irvine, CA) and direct intraluminal dissection of the calcified thrombus failed to reestablish patency. Proximal dissection into the superior mesenteric and splenic veins revealed extension of a dense calcified thrombus into these vessels. The inferior mesenteric vein was not identifiable. As a consequence, portal flow could not be established through conventional or heroic means, and the patient died.
A second patient with portal vein calcification died during transplantation as a consequence of portal vein thrombosis, which was discovered at surgery. After a difficult hepatectomy, the portal vein was found to be calcified and thrombosed. Thrombectomy required extensive dissection extending proximal to the confluence of the splenic and superior mesenteric veins. The calcified thrombus was densely adherent to the endothelium of the vein but was successfully removed, and portal flow was reestablished. The reperfused graft showed primary nonfunction, and the patient underwent immediate retransplantation. With reperfusion of the second graft, the patient developed cardiac instability and died.
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A review of 21 cases of portal vein calcification reported between 1940 and 1990 revealed the average age to be 53.7 years (±10.2 years) and the male-to-female ratio to be 17:4 [7]. Although most patients (81%) had portal hypertension, only 38% had evidence of cirrhosis, and 52% had normal liver function, which is comparable with findings for idiopathic portal hypertension [7]. The calcified lesions were located in the portal vein in 100% of the patients, the splenic vein in 62%, the superior mesenteric vein in 33%, and the inferior mesenteric vein in none [7]. The precise cause was not elucidated in any of the cases reviewed. These findings compare with an average age of 51.9 years with a 7:1 male-to-female ratio in our study. Additionally, the calcification was located in the portal vein in 88% of the patients, the splenic vein in 50%, the superior mesenteric vein in 50%, and the inferior mesenteric vein in none. Other than patients with portal hypertension, portal calcification has also been described in newborns and infants with congenital anomalies or umbilical vein catheters during the postnatal period [8, 9].
To our knowledge, the incidence of portal and mesenteric venous calcifications in patients with cirrhosis has not been previously reported. We found an 11% incidence, which is much higher than anticipated. This finding was not mentioned in any of the initial CT reports of the patients in our study, possibly because it was not recognized, was misinterpreted as arterial calcification, or was determined to be insignificant. During retrospective review of the few cases in which sonographic or unenhanced radiographic data were available, neither portal nor mesenteric calcification was seen. This study is limited by the small cohort size, retrospective bias, and lack of correlative angiographic examinations.
We found a high operative mortality associated with portal or mesenteric venous calcification in patients undergoing liver transplantation because of preoperatively undiagnosed thrombosis of the portal venous system. In our study, two of seven patients who had portal and mesenteric calcification and thrombosis died during liver transplantation. None of the patients who did not have venous calcification on abdominal CT and underwent liver transplantation were found to have portal vein thrombosis during surgery. This finding indicates that the presence of portal vein calcification on CT may be a sign of portal vein thrombosis, which may result in a difficult transplantation. Other factors, such as unavoidable delay between CT and transplantation and suboptimal portal venous enhancement, may have contributed to preoperatively undiagnosed portal vein thrombosis in some of the patients with portal venous calcification. However, in one patient with portal venous calcification who died during transplantation, contrast-enhanced CT performed 4 days before transplantation using a technique adequate to evaluate portal vein patency revealed no evidence of portal vein thrombosis. CT examination proved to be misleading because the patient was discovered to have a heavily calcified and thrombosed portal vein intraoperatively. This suggests that a patient who undergoes preoperative CT that shows venous calcification without portal venous thrombosis may nevertheless require an additional study, such as an angiogram, to rule out incomplete venous thrombosis and to evaluate the size and integrity of the portal vein.
The data from this study suggest that portal and mesenteric venous calcification with associated thrombosis is a significant finding and more attention should be devoted to detecting mesenteric venous calcification in patients undergoing liver transplantation. Liver transplantation has become a routine procedure for many causes of end-stage liver disease. With more than 4 million Americans infected with hepatitis C alone, it is undoubtedly going to become even more common. Detection of portal and mesenteric calcification before liver transplantation may indicate the need for further definition of the portal and mesenteric venous systems. Identification of patients at high risk may provide information for prospective planning, rational distribution of organs, and a safer operation.
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