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Portal Venous Opacification at ERCP in Association with Multiple Hepatic Abscesses and Portal Vein Thrombosis
980
CLINICAL RADIOLOGY
doi:10.1053/crad.2000.0275, available online at http://www.idealibrary.com on
Portal Venous Opaci®cation at ERCP in Association with Multiple Hepatic Abscesses and Portal Vein Thrombosis A. R. O'CONNOR, H. CURTIS, W. K. DUNN Department of Diagnostic Imaging, Queen's Medical Centre, Nottingham, U.K.
CASE REPORT A 65-year-old man was admitted to the University Hospital, Nottingham with a 2-week history of intermittent fever, rigors and right upper quadrant pain. In the 3 days before admission, he had become jaundiced. Physical examination revealed a temperature of 398C and tenderness was elicited in the right upper quadrant of the abdomen. Laboratory evaluation demonstrated abnormal extrinsic and intrinsic liver function tests with bilirubin of 65 mmol/l. A contrast-enhanced CT examination, examination of the abdomen (Fig. 1) demonstrated multiple irregular low attenuation areas in both lobes of the liver. In some areas, these demonstrated a branching pattern. This appearance was thought to represent multiple intrahepatic abscesses associated with dilated ¯uid ®lled intrahepatic bile ducts. A low attenuation ®lling defect consistent with thrombus was present in the portal vein. No soft tissue mass was demonstrated at the porta hepatis or head of the pancreas. Doppler ultrasound examination (Fig. 2) con®rmed the absence of ¯ow within the portal vein and subsequent ultrasound guided aspiration of one of the abnormal areas in the right lobe of the liver yielded bilestained purulent material. Gallstones were not identi®ed. A provisional diagnosis of multiple intrahepatic abscesses with probable bile duct obstruction and an associated portal vein thrombosis was made. ERCP was performed to identify the cause of the possible underlying biliary obstruction. At ERCP the control radiograph was unremarkable, demonstrating neither gas nor radio-opacities in the vicinity of the biliary tree. Early ®lms revealed ®lling of a non-dilated common bile duct and a normal pancreatic duct (Fig. 3). Contrast progressed into the proximal biliary tree opacifying non-dilated intrahepatic biliary radicles and a number of irregular cavities. As the examination progressed there was ®lling of the portal vein from the region of the intrahepatic abscesses in both lobes of the liver. The portal vein ®lled retrogradely in an infero-medial direction parallel to the common bile duct (Fig. 4). An irregular ®lling defect consistent with thrombus was present in the inferior portion of the portal vein extending into the superior mesenteric and splenic veins. The portal vein opaci®cation persisted until the end of the examination although a plain radiograph obtained 4 h later demonstrated no evidence of residual contrast in the right upper quadrant. As there was no evidence of biliary obstruction, sphincterotomy was not performed. The patient was treated with appropriate antibiotic therapy and made a satisfactory initial recovery but subsequently developed severe ascites. Thirty-two days after admission he was well enough to be discharged home. He died of a myocardial infarction several months following his acute admission. Autopsy con®rmed thrombosis of the portal vein but no intraabdominal septic focus could be found.
DISCUSSION
Portal vein opaci®cation at ERCP examination has been reported several times in the literature. Direct puncture of the portal vein or one of its tributaries may occur during attempted duct cannulation. This has been described in association with pancreatic carcinoma [1,2,3]. Lum et al. [4] reported direct
cannulation of the superior mesenteric vein in a patient with pancreatitis. Ricci et al. [1] noted portal venous ®lling following cannulation of a choledochoduodenal ®stula fashioned using a diathermic needle knife in a patient with pancreatic carcinoma. They reported opaci®cation in a distribution similar to the biliary tree which was rapidly washed away, presumably due to a patent portal venous system. This is in marked contrast to our case which demonstrated persistence of the contrast due to the occlusion of the origin of the portal vein. Fistulous communication with the pancreatic duct has also been reported as a cause of portal venous opaci®cation [4,5,6]. In the case of Willis et al. [5] ERCP demonstrated a stricture of the pancreatic duct with ®lling of the portal vein during contrast injection. The underlying diagnosis was pancreatitis. Interestingly portal venous obstruction was also present, being con®rmed by indirect spleno-portography. There have also been several reports of rupture of pancreatic pseudocysts into the portal venous system [4,6]. Both these cases demonstrated associated portal venous thrombosis. Acute biliary vascular ®stula has also been demonstrated by ERCP in a patient who underwent ultrasound guided biopsy of a suspected right sided hepatic mass lesion and subsequently developed severe hyperbilirubinaemia [7]. This patient also demonstrated portal venous occlusion on CT examination and ERCP demonstrated rapid escape of contrast from a peripheral right hepatic bile duct into a super-medially directed vascular space which was felt to represent a collateral portal venous vessel. In our patient, direct cannulation of the portal venous system did not occur as is clearly demonstrated in Fig. 3. The portal vein ®lled retrogradely from the multiple intrahepatic abscesses, presumably via small biliary-vascular ®stulae. Thrombosis of the portal vein prevented rapid contrast clearance. This was presumed to be secondary to portal thrombophlebitis although an underlying cause of this was never discovered. Many etiological factors in pyogenic liver abscess formation are recognized. Portal empyema is a well documented source and is often secondary to intra-abdominal sepsis. Biliary obstruction with subsequent cholangitis may also lead to intrahepatic sepsis. Trauma, direct extension from an adjacent septic focus or metastatic septic dissemination from a distant site are other causes. In our patient the etiology remains a mystery. Portal venous opaci®cation at ERCP should be suspected
981
CASE REPORTS
Fig. 1 ± Abdominal CT examination demonstrates branching low attenuation tubular structures which were subsequently aspirated to reveal purulent material (arrow). The portal vein (p) is also noted to demonstrate a ®lling defect representing thrombus formation. Contrast opaci®ed collateral vessels are noted anterior to the portal vein (curved arrow).
when unusual linear contrast extravasations are noted, particularly if parallel to the common bile duct. In our patient this was secondary to multiple hepatic abscesses but direct cannulation of a venous structure and pancreatic ®stulae should also be considered as underlying causes. Failure of the venous opaci®cation to clear rapidly raises the possibility of underlying portal venous thrombosis.
Fig. 2 ± Doppler ultrasound examination demonstrates absent signal within the portal vein (p). Hepatic arterial ¯ow is seen.
Fig. 3 ± ERCP: early ®lling of the unremarkable common bile duct (arrow), main pancreatic duct and the accessory duct. There is no ®lling of the portal vein at this stage.
REFERENCES 1 Ricci E, Mortilla MG, Conigliaro R, Bertoni G,Bedogni G, Chilovi F. Portal vein ®lling: a rare complication associated with ERCP for endoscopic stent biliary stent placment. Gastrointest Endosc 1992;38:524±525. 2 Ben-Zvi JS, Siegel JH, Yatto RY. Opaci®cation of the portal system during ERCP: demonstration of an anomalous pancreato-portal connection in a patient with pancreatic carcinoma. Gastrointest Endosc 1989;35:445±447.
Fig. 4 ± ERCP: multiple irregular intrahepatic abscess cavities are present one of which is demonstrated by an arrow. There is ®lling of the right and left portal venous radicles and the main portal vein (p). Thrombus is present in the inferior portal vein (curved arrow) extending approximately from the 11th to 12th ribs. The vein in this region has an irregular contour and is more lucent than the superior non-thrombosed portion. Linear regions of contrast opaci®cation inferior to the portal vein represent thrombosed superior mesenteric (m) and splenic (s) veins.
982
CLINICAL RADIOLOGY
3 Huibregtse K, Gish R, Tytgat GNJ. A frightening event during endoscopic papillotomy. Gastrointest Endosc 1988;34:67±68. 4 Lum C, Cho KC, Scholl DG, Sundaram NK. Portal vein opaci®cation during ERCP in patients with pancreatitis. Abdom Imaging 1998;Jan± Feb 23:81±83. 5 Willis SM, Brewer TG, Pancreatic duct-portal vein ®stula. Gastroenterology 1989 Oct 97:1025±1027.
6 Takayama T, Kato K, Katada N et al. Radiological demonstration of spontaneous rupture of a pancreatic pseudocyst into the portal system. Am J gastroenterol 1982 Jan 77:55±58. 7 Verhille MS, Munoz SJ. Acute biliary-vascular ®stula following needle aspiration of the liver. Gastroenterology 1991;101:1731±1733.
CLINICAL RADIOLOGY
doi:10.1053/crad.2000.0275, available online at http://www.idealibrary.com on
Portal Venous Opaci®cation at ERCP in Association with Multiple Hepatic Abscesses and Portal Vein Thrombosis A. R. O'CONNOR, H. CURTIS, W. K. DUNN Department of Diagnostic Imaging, Queen's Medical Centre, Nottingham, U.K.
CASE REPORT A 65-year-old man was admitted to the University Hospital, Nottingham with a 2-week history of intermittent fever, rigors and right upper quadrant pain. In the 3 days before admission, he had become jaundiced. Physical examination revealed a temperature of 398C and tenderness was elicited in the right upper quadrant of the abdomen. Laboratory evaluation demonstrated abnormal extrinsic and intrinsic liver function tests with bilirubin of 65 mmol/l. A contrast-enhanced CT examination, examination of the abdomen (Fig. 1) demonstrated multiple irregular low attenuation areas in both lobes of the liver. In some areas, these demonstrated a branching pattern. This appearance was thought to represent multiple intrahepatic abscesses associated with dilated ¯uid ®lled intrahepatic bile ducts. A low attenuation ®lling defect consistent with thrombus was present in the portal vein. No soft tissue mass was demonstrated at the porta hepatis or head of the pancreas. Doppler ultrasound examination (Fig. 2) con®rmed the absence of ¯ow within the portal vein and subsequent ultrasound guided aspiration of one of the abnormal areas in the right lobe of the liver yielded bilestained purulent material. Gallstones were not identi®ed. A provisional diagnosis of multiple intrahepatic abscesses with probable bile duct obstruction and an associated portal vein thrombosis was made. ERCP was performed to identify the cause of the possible underlying biliary obstruction. At ERCP the control radiograph was unremarkable, demonstrating neither gas nor radio-opacities in the vicinity of the biliary tree. Early ®lms revealed ®lling of a non-dilated common bile duct and a normal pancreatic duct (Fig. 3). Contrast progressed into the proximal biliary tree opacifying non-dilated intrahepatic biliary radicles and a number of irregular cavities. As the examination progressed there was ®lling of the portal vein from the region of the intrahepatic abscesses in both lobes of the liver. The portal vein ®lled retrogradely in an infero-medial direction parallel to the common bile duct (Fig. 4). An irregular ®lling defect consistent with thrombus was present in the inferior portion of the portal vein extending into the superior mesenteric and splenic veins. The portal vein opaci®cation persisted until the end of the examination although a plain radiograph obtained 4 h later demonstrated no evidence of residual contrast in the right upper quadrant. As there was no evidence of biliary obstruction, sphincterotomy was not performed. The patient was treated with appropriate antibiotic therapy and made a satisfactory initial recovery but subsequently developed severe ascites. Thirty-two days after admission he was well enough to be discharged home. He died of a myocardial infarction several months following his acute admission. Autopsy con®rmed thrombosis of the portal vein but no intraabdominal septic focus could be found.
DISCUSSION
Portal vein opaci®cation at ERCP examination has been reported several times in the literature. Direct puncture of the portal vein or one of its tributaries may occur during attempted duct cannulation. This has been described in association with pancreatic carcinoma [1,2,3]. Lum et al. [4] reported direct
cannulation of the superior mesenteric vein in a patient with pancreatitis. Ricci et al. [1] noted portal venous ®lling following cannulation of a choledochoduodenal ®stula fashioned using a diathermic needle knife in a patient with pancreatic carcinoma. They reported opaci®cation in a distribution similar to the biliary tree which was rapidly washed away, presumably due to a patent portal venous system. This is in marked contrast to our case which demonstrated persistence of the contrast due to the occlusion of the origin of the portal vein. Fistulous communication with the pancreatic duct has also been reported as a cause of portal venous opaci®cation [4,5,6]. In the case of Willis et al. [5] ERCP demonstrated a stricture of the pancreatic duct with ®lling of the portal vein during contrast injection. The underlying diagnosis was pancreatitis. Interestingly portal venous obstruction was also present, being con®rmed by indirect spleno-portography. There have also been several reports of rupture of pancreatic pseudocysts into the portal venous system [4,6]. Both these cases demonstrated associated portal venous thrombosis. Acute biliary vascular ®stula has also been demonstrated by ERCP in a patient who underwent ultrasound guided biopsy of a suspected right sided hepatic mass lesion and subsequently developed severe hyperbilirubinaemia [7]. This patient also demonstrated portal venous occlusion on CT examination and ERCP demonstrated rapid escape of contrast from a peripheral right hepatic bile duct into a super-medially directed vascular space which was felt to represent a collateral portal venous vessel. In our patient, direct cannulation of the portal venous system did not occur as is clearly demonstrated in Fig. 3. The portal vein ®lled retrogradely from the multiple intrahepatic abscesses, presumably via small biliary-vascular ®stulae. Thrombosis of the portal vein prevented rapid contrast clearance. This was presumed to be secondary to portal thrombophlebitis although an underlying cause of this was never discovered. Many etiological factors in pyogenic liver abscess formation are recognized. Portal empyema is a well documented source and is often secondary to intra-abdominal sepsis. Biliary obstruction with subsequent cholangitis may also lead to intrahepatic sepsis. Trauma, direct extension from an adjacent septic focus or metastatic septic dissemination from a distant site are other causes. In our patient the etiology remains a mystery. Portal venous opaci®cation at ERCP should be suspected
981
CASE REPORTS
Fig. 1 ± Abdominal CT examination demonstrates branching low attenuation tubular structures which were subsequently aspirated to reveal purulent material (arrow). The portal vein (p) is also noted to demonstrate a ®lling defect representing thrombus formation. Contrast opaci®ed collateral vessels are noted anterior to the portal vein (curved arrow).
when unusual linear contrast extravasations are noted, particularly if parallel to the common bile duct. In our patient this was secondary to multiple hepatic abscesses but direct cannulation of a venous structure and pancreatic ®stulae should also be considered as underlying causes. Failure of the venous opaci®cation to clear rapidly raises the possibility of underlying portal venous thrombosis.
Fig. 2 ± Doppler ultrasound examination demonstrates absent signal within the portal vein (p). Hepatic arterial ¯ow is seen.
Fig. 3 ± ERCP: early ®lling of the unremarkable common bile duct (arrow), main pancreatic duct and the accessory duct. There is no ®lling of the portal vein at this stage.
REFERENCES 1 Ricci E, Mortilla MG, Conigliaro R, Bertoni G,Bedogni G, Chilovi F. Portal vein ®lling: a rare complication associated with ERCP for endoscopic stent biliary stent placment. Gastrointest Endosc 1992;38:524±525. 2 Ben-Zvi JS, Siegel JH, Yatto RY. Opaci®cation of the portal system during ERCP: demonstration of an anomalous pancreato-portal connection in a patient with pancreatic carcinoma. Gastrointest Endosc 1989;35:445±447.
Fig. 4 ± ERCP: multiple irregular intrahepatic abscess cavities are present one of which is demonstrated by an arrow. There is ®lling of the right and left portal venous radicles and the main portal vein (p). Thrombus is present in the inferior portal vein (curved arrow) extending approximately from the 11th to 12th ribs. The vein in this region has an irregular contour and is more lucent than the superior non-thrombosed portion. Linear regions of contrast opaci®cation inferior to the portal vein represent thrombosed superior mesenteric (m) and splenic (s) veins.
982
CLINICAL RADIOLOGY
3 Huibregtse K, Gish R, Tytgat GNJ. A frightening event during endoscopic papillotomy. Gastrointest Endosc 1988;34:67±68. 4 Lum C, Cho KC, Scholl DG, Sundaram NK. Portal vein opaci®cation during ERCP in patients with pancreatitis. Abdom Imaging 1998;Jan± Feb 23:81±83. 5 Willis SM, Brewer TG, Pancreatic duct-portal vein ®stula. Gastroenterology 1989 Oct 97:1025±1027.
6 Takayama T, Kato K, Katada N et al. Radiological demonstration of spontaneous rupture of a pancreatic pseudocyst into the portal system. Am J gastroenterol 1982 Jan 77:55±58. 7 Verhille MS, Munoz SJ. Acute biliary-vascular ®stula following needle aspiration of the liver. Gastroenterology 1991;101:1731±1733.