HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Choi, S. H. Articles by Choi, B. I. Search for Related Content PubMed PubMed Citation Articles by Choi, S. H. Articles by Choi, B. I. Social Bookmarking                      What's this? Hotlight (NEW!) What's Hotlight?

Relationship Between Various Patterns of Transient Increased Hepatic Attenuation on CT and Portal Vein Thrombosis Related to Acute Cholecystitis

¹ All authors: Department of Radiology and Institute of Radiation Medicine, Seoul National University Hospital, 28, Yongon-dong, Chongno-gu, Seoul 110-744, South Korea.

Received November 21, 2003; accepted after revision March 1, 2004.

 
Address correspondence to J. M. Lee (leejm{at}radcom.snu.ac.kr).

Abstract

Top Abstract Introduction Materials and Methods Results Discussion References

 
OBJECTIVE. We sought to investigate the prevalence of portal vein thrombosis in patients with acute cholecystitis and the relationship between portal vein thrombosis and the various patterns of transient increased hepatic attenuation on CT.

MATERIALS AND METHODS. We studied 72 of 107 patients with acute cholecystitis who, during a 3-year period, underwent dual-phase contrast-enhanced CT before percutaneous cholecystostomy or cholecystectomy. CT scans were retrospectively reviewed for the presence of portal vein thrombosis and location of the thrombi and for patterns of transient increased hepatic attenuation, which were classified as either pericholecystic, segmental, or mixed.

RESULTS. Portal vein thrombi (two in hepatic segment IV, three in the left portal vein, and one in the right posterior portal vein) were found in six (8.3%) of 72 patients, and in those patients, transient increased attenuation with a segmental (five patients) or mixed (one patient) pattern was seen on CT. The pattern of transient increased attenuation in the 54 patients without portal vein thrombosis was pericholecystic in 41 (75.9%) and mixed in 13 (24.1%). Nineteen patients had segmental distribution (segmental or mixed pattern) that in 31.6% (6/19) of the patients was associated with portal vein thrombosis. Segmental distribution was more frequently found in those patients who had acute cholecystitis with portal vein thrombosis than in those who had only acute cholecystitis (p = 0.001).

CONCLUSION. In patients with acute cholecystitis, portal vein thrombosis is not uncommon. Patterns of transient increased hepatic attenuation were found to vary, depending on the presence or absence of portal vein thrombosis.

Introduction

Top Abstract Introduction Materials and Methods Results Discussion References

 
Transient focal increased attenuation of the liver is often found on CT scans in patients with acute cholecystitis. It is well known that in such patients, curvilinear areas of transient increased attenuation are seen during the early phase of incremental dynamic CT in the liver adjacent to the gallbladder fossa [1]. Moreover, the parabiliary veins and the cystic vein of the gallbladder have been depicted on angiography as entering the liver [2]. Given that acute cholecystitis has been reported to cause hepatic arterial hyperemia and early venous drainage, the curvilinear transient enhancement near the gallbladder in patients with acute cholecystitis has also been attributed to increased blood flow from the dilated aberrant cystic vein of the diseased hypervascular gallbladder [1, 3].

Because of hepatic artery enlargement and increased relative hepatic artery perfusion in regions of portal occlusion, transient hyperattenuation may occur in the region of portal occlusion and be observed during arterial phase CT [4, 5]. Therefore, portal vein thrombosis is one potential cause of transient increased hepatic attenuation on CT. Two articles reporting adults with portal vein thrombosis related to acute cholecystitis have appeared in the literature [6, 7]. However, to our knowledge, the prevalence and CT depictions of portal vein thrombosis related to acute cholecystitis have not been studied.

The purposes of our study were to determine the prevalence of portal vein thrombosis in patients with acute cholecystitis and to investigate the relationship between portal vein thrombosis in patients with acute cholecystitis and the various patterns of transient increased hepatic attenuation on CT.

Materials and Methods

Top Abstract Introduction Materials and Methods Results Discussion References

 
We identified patients who had undergone emergency percutaneous cholecystostomy or cholecystectomy because of acute cholecystitis by reviewing hospital discharge records for a 3-year period (between January 2000 and December 2002). We identified 107 patients and cross-referenced this list with radiology files to identify patients in whom CT scans had been obtained before the procedure. We found 72 (67%) of these 107 patients had CT scans, and these 72 patients (52 men and 20 women; age range, 33-89 years; mean, 65 years) were our study population. All 72 patients were hospitalized for suspected acute cholecystitis and underwent preprocedural contrast-enhanced CT after sonography. Of these 72 patients, 24 underwent emergency cholecystectomy only. Of the 48 patients who underwent percutaneous cholecystostomy, 25 subsequently underwent elective open or laparoscopic cholecystectomy, and 23 were only observed. Diagnostic aspirations were performed in all patients who underwent percutaneous cholecystostomy. The time interval between surgery or percutaneous cholecystostomy and CT examination was less than 5 days in all patients.

Patients were judged to have acute cholecystitis if pathologic examination revealed acute inflammation (n = 42); if bile cultures obtained after diagnostic aspiration of the gallbladder produced positive results (n = 11); or if symptoms markedly improved after percutaneous cholecystostomy (n = 19). Patients in whom gallstones were identified at pathologic examination (n = 45) were considered to have calculous cholecystitis. Patients in whom gallstones were not identified at pathologic examination or on preoperative sonography or CT (n = 27) were considered to have acalculous cholecystitis.

Twenty-two of the 72 patients had a primary diagnosis in addition to acute cholecystitis. Among the patients with an additional primary diagnosis, those with liver metastases (n = 2, one case of lung cancer and one case of rectal cancer), primary liver cancer (n = 5), or distal common bile duct cancer (n = 2) had various hepatic enhancement patterns of their hepatic lesions or cholangitis on CT. Therefore, we excluded those hepatic segments (3% or 17/576 segments in 22 patients) that showed varying hepatic enhancement patterns on contrast-enhanced CT, which is suggestive of primary liver cancer, metastasis, or cholangitis, from the analysis of hepatic parenchymal CT attenuation differences (Table 1). In 13 patients admitted for other primary diagnoses—including stomach cancer (n = 5), renal cell carcinoma (n = 3), congestive heart failure (n = 1), malignant melanoma (n = 1), lymphoma (n = 1), leukemia (n = 1), and systemic lupus erythematosus (n = 1)—no abnormal findings in the liver were observed other than the presumed transient increased hepatic attenuation associated with acute cholecystitis (Table 1).

For the limited and anonymous review of patient data required for this study, the institutional review board of our hospital did not require us to obtain formal approval or informed patient consent.

Because our study was retrospective, the CT examinations were performed using different scanners (Somatom Plus S or Somatom Plus 4, Siemens Medical Systems; HiSpeed Advantage CT scanner, GE Healthcare; MX 8000, Marconi Medical Systems), and the CT techniques used varied. In general, examinations were performed using a helical technique with 5-10 mm collimation, a pitch of 1.0-1.4, and reconstruction intervals of 5-10 mm. The X-ray tube voltage was 120-140 kV, and the current was 150-220 mA. During the study period, our standard protocol for dynamic CT required a total volume of 100-150 mL of nonionic IV contrast material (300-370 mg I/mL) administered by power injection at a rate of 3 mL/sec, with a scanning delay of 30-40 sec for the hepatic arterial phase and 60-80 sec for the portal venous phase.

CT scans were reviewed by two experienced abdominal radiologists who interpreted the scans in consensus without knowledge of the contents of the CT report or final diagnosis of any patient. The radiologists evaluated the scans for the presence and appearance of increased hepatic parenchymal attenuation during the hepatic arterial phase of dual-phase CT and then for the presence and the extent of portal vein thrombosis within the hepatic lesion with increased parenchymal attenuation during the portal venous phase of dual-phase CT.

Increased hepatic parenchymal CT attenuation was judged to be present during the hepatic arterial phase if the two reviewers reached a consensus interpretation of this condition without significant discrepancy, which they did in all cases. Patterns of increased hepatic parenchymal CT attenuation during the hepatic arterial phase were classified as pericholecystic (within the hepatic area adjacent to the gallbladder), segmental, or mixed (pericholecystic and segmental) [3]. The presence of peripheral wedge-shaped arterial phase areas of hyperenhancement distal to segmental thrombi was documented after the identification of portal vein thrombi on CT scans obtained during the portal venous phase. Thrombi were identified as low-attenuation, intraluminal filling defects in the veins [8]. When thrombi were identified, their specific locations were documented. These included the main portal vein, the right and left portal veins, and any segmental veins. Segmental thrombi were identified as tubular structures in the portal triad that connected to an enhanced portal venous structure located more proximally in the liver [9]. Segmental involvement was described using the Couinaud nomenclature [10].

All scans were reviewed on a PACS (Marotech) monitor, which allows rapid manual cine evaluation through the liver and upper abdomen, thus enabling the physicians to easily identify intraluminal filling defects and to associate them with the portal venous system. Reviewing on a PACS also allows window and level settings of images of the hepatic parenchyma to be easily changed.

The relationship between the presence of portal vein thrombosis and a transient increased hepatic attenuation pattern was examined using Fisher's exact test. A p value of less than 0.05 was considered a statistically significant difference. All statistical analyses were performed using the Statistical Package for the Social Sciences software package (version 10.0, SPSS).

Results

Top Abstract Introduction Materials and Methods Results Discussion References

 
Sixty (83.3%) of the 72 patients with acute cholecystitis showed transient increased attenuation within the hepatic area (pericholecystic or segmental distribution) on CT scans obtained during hepatic arterial phase. Portal vein thrombi were found in six (8.3%) of the 72 patients with acute cholecystitis, and these six patients had no other clinical problems except acute cholecystitis. Table 2 lists the locations of the portal vein thrombi as well as the locations and appearances of transient hepatic parenchymal hyperattenuation in six patients with portal vein thrombosis (Figs. 1A, 1B, 1C, 2A, 2B, 3A, 3B). All patients with portal vein thrombosis had segmental distribution (segmental [n = 5] or mixed [n = 1]) of transient increased hepatic attenuation. Wedge-shaped areas of hyperenhancement distal to or corresponding to the segmental location of the thrombus were identified in two patients with segmental portal vein thrombosis. This finding was often subtle and was identified only using manually adjusted narrow window and level settings. Such areas of hyper-enhancement were not present on any of the scans on which thrombi were not identified.

View larger version (92K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —62-year-old woman with portal vein thrombosis related to acute cholecystitis in segment IV of liver. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (arrows) with segmental distribution in segment IV.

View larger version (70K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —62-year-old woman with portal vein thrombosis related to acute cholecystitis in segment IV of liver. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (arrows) with curvilinear appearance in pericholecystic gallbladder fossa of liver.

View larger version (107K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —62-year-old woman with portal vein thrombosis related to acute cholecystitis in segment IV of liver. CT scan obtained during portal venous phase shows occlusive thrombus (arrowhead) with low attenuation in segment IV.

View larger version (102K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2A. —76-year-old woman with portal vein thrombosis related to acute cholecystitis in segments VI and VII of liver. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (arrows) with segmental distribution in segments VI and VII.

View larger version (121K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2B. —76-year-old woman with portal vein thrombosis related to acute cholecystitis in segments VI and VII of liver. CT scan obtained during portal venous phase reveals occlusive thrombi (arrowheads) with low attenuation in segments VI and VII.

View larger version (88K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3A. —69-year-old woman with portal vein thrombosis related to acute cholecystitis in left portal vein. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (arrows) with lobar distribution in left lobe of liver.

View larger version (104K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3B. —69-year-old woman with portal vein thrombosis related to acute cholecystitis in left portal vein. CT scan obtained during portal venous phase reveals occlusive thrombus (arrowhead) with low attenuation in left portal vein.

Of the 54 patients without portal vein thrombosis, 41 (75.9%) had a pericholecystic pattern of transient increased attenuation within the hepatic area adjacent to the gallbladder (Fig. 4), and 13 (24.1%) had a mixed pattern (Fig. 5A, 5B). Of the 13 patients with a mixed pattern, six showed transient increased attenuation within hepatic segments IV (segmental pattern) and V (pericholecystic pattern), and seven showed such attenuation within segments II, III, IV (all three, segmental pattern) and V (pericholecystic pattern) (Table 3). A total of 19 patients had segmental transient increased hepatic attenuation, and 13 of these patients did not have portal vein thrombosis. Therefore, segmental transient increased hepatic attenuation was associated with portal vein thrombosis in 31.6% of the patients. The segmental distribution—including segmental (n = 5) or mixed (n = 1) pattern—of transient increased hepatic attenuation adjacent to the gallbladder on CT was more frequently found in the patients with portal vein thrombosis (p = 0.001). However, the pericholecystic transient increased hepatic attenuation (n = 1) was less frequently found in these patients (p = 0.0001).

View larger version (130K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4. —74-year-old man with acute gangrenous cholecystitis. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (thick solid arrow) with curvilinear appearance in pericholecystic gallbladder fossa of liver. Note intraluminal gas collection (thin solid arrow) in gallbladder fundus and pericholecystic infiltration (open arrow).

View larger version (122K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5A. —62-year-old man with gallbladder empyema. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (arrows) with lobar distribution in left lobe of liver.

View larger version (108K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5B. —62-year-old man with gallbladder empyema. CT scan obtained during hepatic arterial phase shows transient increased hepatic attenuation (solid arrow) with curvilinear appearance in pericholecystic gallbladder fossa of liver. Note pericholecystic fluid collection (open arrow).

Discussion

Top Abstract Introduction Materials and Methods Results Discussion References

 
In our study, the frequency of transient increased hepatic attenuation on hepatic arterial phase CT images was 83.3% (60/72 patients), which is higher than the frequency of such attenuation in the healthy adults (3%) [3]. Portal vein thrombosis was found in six (8.3%) of 72 patients with acute cholecystitis. Transient increased hepatic attenuation can occur in patients with acute cholecystitis with or without portal vein thrombosis. All patients with portal vein thrombosis had transient increased hepatic attenuation with a segmental pattern, and the portal vein thrombus was always in the segment with transient increased hepatic attenuation. One of the six patients exhibited not only a segmental but also a pericholecystic pattern of transient increased hepatic attenuation. Of the 66 patients without portal vein thrombosis detectable on CT, 54 (82%) had pericholecystic (n = 41) or mixed (n = 13) transient increased hepatic attenuation. None of these patients had purely segmental transient increased hepatic attenuation. These results suggest that acute cholecystitis contributes to transient increased hepatic attenuation on contrast-enhanced CT scans and that there is a difference in the hemodynamic mechanism of transient increased hepatic attenuation in patients with portal vein thrombosis related to acute cholecystitis and in patients with acute cholecystitis only.

Transient increased attenuation in the liver has been frequently observed in the patients with gallbladder disease on dynamic CT, MRI, angiography, or CT arterioportography [1, 3, 11-13]. Increased venous drainage attributed to hyperemia associated with acute cholecystitis is one cause of the transient increased attenuation of the liver, according to Matsui et al. [2]. Ito et al. [3] also reported various patterns of transient increased hepatic attenuation in patients with gallbladder diseases, including chronic cholecystitis, gallbladder cancer, and adenomyomatosis, in addition to pericholecystic hepatic enhancement. Those researchers suggested that increased cystic venous drainage might contribute to transient increased hepatic attenuation. Moreover, CT angiography has shown that the cystic veins that emerge from the body or fundus of the gallbladder flow mainly into the subsegmental portal branches or sinusoids of segment IV or V and that the veins that emerge from the neck of the gallbladder flow into the more proximal portal branches [13]. This fact correlates well with the results of our study in that we found that the main hepatic areas with transient increased hepatic attenuation were segments IV and V. Because of these variations in the termination of the cystic vein, transient increased hepatic attenuation could possibly appear in these segments in a variable fashion in addition to appearing in the liver parenchyma around the gallbladder fossa [3]. However, in patients with acute cholecystitis who had portal vein thrombosis, another hemodynamic mechanism that induces transient increased hepatic attenuation might play an important role. We believe that in the patients with portal vein thrombosis, hepatic arterial hyperperfusion of the involved hepatic segments is responsible for segmental distribution of transient increased hepatic attenuation [14-18]. In addition, the pericholecystic transient increased hepatic attenuation, which was thought to be caused by increased venous drainage through a direct vascular channel between the liver and the gallbladder, was found in only one of the patients with portal vein thrombosis. These results suggest that the thrombi associated with acute cholecystitis can obliterate various vascular channels between the gallbladder and the liver, as was described earlier.

Portal vein thrombosis is a condition that is either caused by or associated with a variety of factors and diseases [8, 19-22]. The condition includes various infectious and inflammatory processes, such as the invasion or compression of the vein by a tumor (usually a hepatocellular carcinoma or pancreatic adenocarcinoma), hypercoagulable states, and mechanical manipulation [8, 19-22]. However, in our patients with portal vein thrombosis, no other clinical conditions known to cause portal vein thrombosis were found. In patients with acute cholecystitis and portal vein thrombosis, the portal vein thrombosis may have been the result of an inflammation or of an infection reaching the cystic vein. Two possible paths of infection are proposed: a connection between the cystic vein and the hepatic sinusoid or a connection between the cystic and portal veins. In cases in which a connection between the cystic vein and the hepatic sinusoid plays an important role in portal vein thrombosis, a direct spread of infection and inflammation from the gallbladder to the portal vein is the main cause of thrombosis. Small portal vein thrombi are believed to play an important role in cases in which a connection between the cystic and portal veins provides an infectious and inflammatory path in portal vein thrombosis. Thus, portal vein thrombosis associated with acute cholecystitis could be present in hepatic segments II, III, and VII as well as in pericholecystic hepatic segments (segments IV and V).

We recognize that our study has limitations. Patients with portal vein thrombosis did not undergo follow-up CT after cholecystectomy or percutaneous cholecystostomy for the evaluation of changes in portal vein thrombosis. Only one patient received follow-up sonography, which showed the absence of portal vein thrombosis. We were unable to find any factors other than acute cholecystitis predisposing patients with portal vein thrombosis to the disease. Moreover, patients improved clinically after undergoing cholecystectomy or percutaneous cholecystostomy and were discharged without clinical problems. Our study is likely to have a selection bias because we included patients with acute cholecystitis who were referred for CT evaluation. Some patients judged to have acute cholecystitis did not undergo CT before treatment but had sonography instead. CT is required to reveal complications related to cholecystitis, such as gallbladder perforation with pericholecystic abscess or emphysematous cholecystitis [23, 24]. Although we do not know the indications that led to our patients being referred for CT, it is possible that those patients who were the most ill tended to receive these referrals.

In summary, portal vein thrombosis associated with acute cholecystitis is not rare, and patterns of transient increased hepatic attenuation on CT scans vary, depending on the presence or absence of portal vein thrombosis. Segmental distribution, which includes segmental and mixed patterns, of transient increased hepatic attenuation was also observed on the scans of patients with acute cholecystitis and without portal vein thrombosis, but we believe that the hemodynamic mechanism underlying segmental transient increased hepatic attenuation in such patients without portal vein thrombosis differs from those with portal vein thrombosis. Increased hepatic arterial blood flow through the parabiliary plexus may be responsible for the transient increased hepatic attenuation in the patients with portal vein thrombosis. Segmental transient increased hepatic attenuation in patients referred for acute cholecystitis is strongly suggestive of portal vein thrombosis, and a meticulous search for portal vein thrombi is warranted. Every patient with portal vein thrombosis associated with acute cholecystitis had transient increased hepatic attenuation in either a segmental pattern or segmental and pericholecystic patterns.

References

Top Abstract Introduction Materials and Methods Results Discussion References

 

1. Yamashita K, Jin MJ, Hirose Y, et al. CT finding of transient focal increased attenuation of the liver adjacent to the gallbladder in acute cholecystitis. AJR1995; 164:343 -346[Abstract/Free Full Text]
2. Matsui O, Takashima T, Kadoya M, et al. Staining in the liver surrounding gallbladder fossa on hepatic arteriography caused by increased cystic venous drainage. Gastrointest Radiol1987; 12:307 -312[Medline]
3. Ito K, Awaya H, Mitchell DG, et al. Gallbladder disease: appearance of associated transient increased attenuation in the liver at biphasic, contrast enhanced dynamic CT. Radiology1997; 204:723 -728[Abstract/Free Full Text]
4. Oliver JH III, Baron RL. Helical biphasic contrast-enhanced CT of the liver: technique, indications, interpretation, and pitfalls. Radiology1996; 201:1 -14[Abstract/Free Full Text]
5. Baron RL, Oliver JH III, Dodd GD III, Nalesnik M, Holbert BL, Carr B. Hepatocellular carcinoma: evaluation with biphasic, contrast-enhanced, helical CT. Radiology1996; 199:505 -511[Abstract/Free Full Text]
6. Harch JM, Radin RD, Yellin AE, Donovan AJ. Pylethrombosis: serendipitous radiologic diagnosis. Arch Surg1987; 122:1116 -1119[Abstract/Free Full Text]
7. Kidney DD, Forino MT, Cohen AJ, Hunter V. Case report: portal venous thrombosis in acute cholecystitis. CT, ultrasound, Doppler and power Doppler findings. Clin Radiol1998; 53:459 -461[Medline]
8. Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med2001; 345:1683 -1688[Free Full Text]
9. Baker ME, Remzi F, Einstein D, et al. CT depiction of portal vein thrombi after creation of ileal pouchanal anastomosis. Radiology2003; 227:73 -79[Abstract/Free Full Text]
10. Dodd GD III. An American's guide to Couinaud's numbering system. AJR 1993;161:574 -575[Free Full Text]
11. Matsui O, Takahashi S, Kadoya M, et al. Pseudolesion in segment IV of the liver at CT during arterial portography: correlation with aberrant gastric venous drainage. Radiology1994; 193:31 -35[Abstract/Free Full Text]
12. Loud PA, Semelka RC, Kettritz U, Brown JJ, Reinhold C. MRI of acute cholecystitis: comparison with the normal gallbladder and other entities. Magn Reson Imaging1996; 14:349 -355[Medline]
13. Sugita M, Ryu M, Satake M, et al. Intrahepatic inflow areas of the drainage vein of the gallbladder: analysis by angio-CT. Surgery 2000;128:417 -421[Medline]
14. Ternberg JL, Butcher HR Jr. Blood-flow relation between hepatic artery and portal vein. Science1965; 150:1030 -1031[Abstract/Free Full Text]
15. Itai Y, Matsui O. Blood flow and liver imaging. Radiology1997; 202:306 -314[Free Full Text]
16. Itai Y, Moss AA, Goldberg HI. Transient hepatic attenuation difference of lobar or segmental distribution detected by dynamic computed tomography. Radiology1982; 144:835 -839[Free Full Text]
17. Matsui O, Takashima T, Kadoya M, et al. Segmental staining on hepatic arteriography as a sign of intrahepatic portal vein obstruction. Radiology1984; 152:601 -606[Abstract/Free Full Text]
18. Choi BI, Chung JW, Itai Y, Matsui O, Han JK, Han MC. Hepatic abnormalities related to blood flow: evaluation with dual phase helical CT. Abdom Imaging1999; 24:340 -356[Medline]
19. Cohen J, Edelman RR, Chopra S. Portal vein thrombosis: a review. Am J Med 1992;92:173 -182[Medline]
20. Plemmons RM, Dooley DP, Longfield RN. Septic thrombophlebitis of the portal vein (pylephlebitis): diagnosis and management in the modern era. Clin Infect Dis1995; 21:1114 -1120[Medline]
21. Valla DC, Condat B. Portal vein thrombosis in adults: pathophysiology, pathogenesis, and management. J Hepatol 2000;32:865 -871[Medline]
22. Sheen CL, Lamparelli H, Milne A, Green I, Ramage JK. Clinical features, diagnosis, and outcome of acute portal vein thrombosis. Q J Med 2000;93:531 -534
23. Lamki N, Raval B, St. Ville E. Computed tomography of complicated cholecystitis. J Comput Assist Tomogr1986; 10:319 -324
24. Varma DGK, Faust JM. Computed tomography of gangrenous acute postoperative acalculous cholecystitis. J Comput Assist Tomogr 1988;12:29 -31

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				E. Altun, R. C. Semelka, J. Elias Jr, L. Braga, V. Voultsinos, J. Patel, N. C. Balci, and J. T. Woosley Acute Cholecystitis: MR Findings and Differentiation from Chronic Cholecystitis Radiology, July 1, 2007; 244(1): 174 - 183. [Abstract] [Full Text] [PDF]

This Article Abstract Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Choi, S. H. Articles by Choi, B. I. Search for Related Content PubMed PubMed Citation Articles by Choi, S. H. Articles by Choi, B. I. Social Bookmarking                      What's this? Hotlight (NEW!) What's Hotlight?