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Radiology
HEPATIC
ARTERY ANEURYSM CAUSING OBSTRUCTIVE JAUNDICE - Treatment by Transcatheter
Embolisation.
A 22-year-old-female patient presented with symptoms of pain in the epigastrium, jaundice and weight loss of three months, duration. She was icteric. Abdominal examination revealed a pulsatile lump in the epigastric region. Laboratory investigations revealed a raised bilirubin (Total-9.7mg%, Direct- 7.0mg %). Ultra-sonography of the showed an aneurysm on the medial aspect of the pancreas causing significant dilatation of intrahepatic biliary radicals, common hepatic ducts and common bile duct (Fig 1A &B).
A contrast enhanced CT of the abdomen showed a 4.6 x 5.2 cms, well circumscribed lesion with intense enhancement suggestive of a partially thrombosed pseudoaneurysm - probably arising from the origin of gastroduodenal artery causing extrinsic compression of common bile duct and significant dilatation of intrahepatic biliary radicals(Fig 2A,B).
MR Angiography and MRCP confirmed the same findings (FIG 3A & B).
A celiac angiogram revealed a giant pseudoaneurysm arising from the hepatic artery just beyond its origin. There was sluggish antegrade flow in the distal branches of the hepatic artery (Fig .4A). The superior mesenteric angiogram showed the accessory right hepatic artery arising from it. The aneurysm was not filling on superior mesenteric angiogram (Fig.4B).
The hepatic artery was than selectively catheterized with 5F Simmons catheter The segment of the hepatic artery bearing the pseudoaneurysm was negotiated with roadrunner wire 0.035"x180 cms (Cook Inc.) & the catheter was negotiated distal to the pseudoaneurysm over it (Fig.5A).
The hepatic artery was then embolized using three steel coils (35-5-5 ; Cook Inc) distal and proximal to the pseudoaneurysm resulting in its complete exclusion from the circulation (Fig.5B) .
Post-embolization celiac and Superior mesenteric angiogram revealed no filling of the pseudoaneurysm (Fig 5C).
Doppler examination after two days revealed no flow within the aneurysm and resolution of the intra-hepatic biliary radical dilatation (Fig 6A and B). Her serum bilirubin level fell to a total-2.0mg% (direct-1.2mg %) in two weeks.
DISCUSSION:
Hepatic artery aneurysm is a rare clinical and pathological entity. Hepatic artery aneurysms traditionally represent 20% of all visceral aneurysms The classical triad as described by Quincke of abdominal pain, hemobilia and jaundice is seen in less than one-third of cases. On occasion, patients present with an acute abdominal catastrophe due to rupture of the aneurysm into the peritoneal cavity. Hepatic artery aneurysms have been treated in many ways - ligation proximal and distal to the aneurysm, extirpation followed by vein graft implantation, endoaneurysmorrhaphy and liver lobe resection and transcatheter embolization with gel foam plugs.
Hepatic artery aneurysm represent approximately 20% of all visceral aneurysms. Extrahepatic aneurysms are four times more common than intrahepatic aneurysms. Of the extrahepatic, common hepatic account for 63%, right hepatic 28%. Left and right 4% and as in the case presented here, left hepatic artery accounts for only 5%.
Mycotic aneurysms were the most common cause of hepatic artery aneurysm, although they now account for only 4%. Atherosclerosis is present in upto 30% of such lesions. Less common causes for hepatic artery aneurysm are vasculitides, such as polyarteritis nodosa. periarterial inflammation caused by cholecystitis or pancreatitis, fibromuscular dyspalsia and cystic medial necrosis.
The majority of patients with hepatic artery aneurysms are asymptomatic prior to rupture. Of the patients who present with clinical symptoms, 60-80% of patients will present with rupture either into the peritoneum, biliary tree or gastro-intestinal tract with resultant hemoperitoneum, hemobilia or hematemesis. Approximately 70% of patients may complain of abdominal pain, usually in the right upper quadrant with radiation to back. Jaundice, either due to biliary tree compression or intraductal clot is seen in about 50% of cases. Physical examination is usually normal, although large aneurysms may be associated with a pulsatile mass or an abdominal bruit. Approximately 10% of patients present with shock following rupture or massive gastro-intestinal hemorrhage.
Curvilinear calcification on a plain radiograph in the right upper quadrant should raise the possibility of hepatic artery aneurysm. Upper gastro-intestinal tract studies may show a smooth extrinsic filling defect in the duodenum. ERCP or PTC may show biliary dilatation and filling defects especially in patients with malena.
On ultrasound examination, any discrete fusiform or round hypoechoic lesion in the right upper quadrant, which may or may not be pulsatile should raise the possibility of an aneurysm. Aneurysm and pseudoaneurysm must be distinguished from a fluid collection, pseudocyst or cystic tumour, especially before biopsy or drainage procedures. Pulsed and colour Doppler may be useful.
CT findings are low attenuation mass with rim-like calcification in the periphery on plain study and enhancement on IV contrast, Thrombotic deposits in the vessel lumen can be seen as discrete ring-shaped or semilunar internal areas of hypodensity.
MR Angiography may accurately delineate the location, relation and feeding vessels of the aneurysm. MRCP may sow dilatation of intra-hepatic biliary radicals and delineate the level of obstruction.
Appropriate management of hepatic artery aneurysm requires detailed angiography. This will confirm the diagnosis, identify any other aneurysm {20% are multiple}, delineate feeding vessels, demonstrate any arterioportal fistula and provide anatomical information needed for surgery or embolization.
Treatment of specific aneurysms depends on its location, regional vascular anatomy, the etiology of aneurysm and any associated or coexisting conditions. Common hepatic artery aneurysm can be treated by either surgical ligation or embolization. This is possibly owing to considerable collateral circulation available to the liver from the gastroduodenal and right gastric arteries. Embolization is the accepted treatment of choice for intrahepatic as well as intrahepatic aneurysm and pseudo-aneurysms.
Case 20: Contributed
by Dr.Rajendra C. Mehta
Other Cases
A 22-year-old-female patient presented with symptoms of pain in the epigastrium, jaundice and weight loss of three months, duration. She was icteric. Abdominal examination revealed a pulsatile lump in the epigastric region. Laboratory investigations revealed a raised bilirubin (Total-9.7mg%, Direct- 7.0mg %). Ultra-sonography of the showed an aneurysm on the medial aspect of the pancreas causing significant dilatation of intrahepatic biliary radicals, common hepatic ducts and common bile duct (Fig 1A &B).
 |
 |
|
Fig
1A
|
Fig
1B
|
A contrast enhanced CT of the abdomen showed a 4.6 x 5.2 cms, well circumscribed lesion with intense enhancement suggestive of a partially thrombosed pseudoaneurysm - probably arising from the origin of gastroduodenal artery causing extrinsic compression of common bile duct and significant dilatation of intrahepatic biliary radicals(Fig 2A,B).
 |
 |
|
Fig
2A
|
Fig
2B
|
MR Angiography and MRCP confirmed the same findings (FIG 3A & B).
 |
 |
|
Fig
3A
|
Fig
3B
|
A celiac angiogram revealed a giant pseudoaneurysm arising from the hepatic artery just beyond its origin. There was sluggish antegrade flow in the distal branches of the hepatic artery (Fig .4A). The superior mesenteric angiogram showed the accessory right hepatic artery arising from it. The aneurysm was not filling on superior mesenteric angiogram (Fig.4B).
 |
 |
|
Fig
4A
|
Fig
4B
|
The hepatic artery was than selectively catheterized with 5F Simmons catheter The segment of the hepatic artery bearing the pseudoaneurysm was negotiated with roadrunner wire 0.035"x180 cms (Cook Inc.) & the catheter was negotiated distal to the pseudoaneurysm over it (Fig.5A).
 |
|
Fig
5A
|
The hepatic artery was then embolized using three steel coils (35-5-5 ; Cook Inc) distal and proximal to the pseudoaneurysm resulting in its complete exclusion from the circulation (Fig.5B) .
 |
|
Fig
5B
|
Post-embolization celiac and Superior mesenteric angiogram revealed no filling of the pseudoaneurysm (Fig 5C).
 |
|
Fig
5C
|
Doppler examination after two days revealed no flow within the aneurysm and resolution of the intra-hepatic biliary radical dilatation (Fig 6A and B). Her serum bilirubin level fell to a total-2.0mg% (direct-1.2mg %) in two weeks.
 |
 |
|
Fig
6A
|
Fig
6B
|
DISCUSSION:
Hepatic artery aneurysm is a rare clinical and pathological entity. Hepatic artery aneurysms traditionally represent 20% of all visceral aneurysms The classical triad as described by Quincke of abdominal pain, hemobilia and jaundice is seen in less than one-third of cases. On occasion, patients present with an acute abdominal catastrophe due to rupture of the aneurysm into the peritoneal cavity. Hepatic artery aneurysms have been treated in many ways - ligation proximal and distal to the aneurysm, extirpation followed by vein graft implantation, endoaneurysmorrhaphy and liver lobe resection and transcatheter embolization with gel foam plugs.
Hepatic artery aneurysm represent approximately 20% of all visceral aneurysms. Extrahepatic aneurysms are four times more common than intrahepatic aneurysms. Of the extrahepatic, common hepatic account for 63%, right hepatic 28%. Left and right 4% and as in the case presented here, left hepatic artery accounts for only 5%.
Mycotic aneurysms were the most common cause of hepatic artery aneurysm, although they now account for only 4%. Atherosclerosis is present in upto 30% of such lesions. Less common causes for hepatic artery aneurysm are vasculitides, such as polyarteritis nodosa. periarterial inflammation caused by cholecystitis or pancreatitis, fibromuscular dyspalsia and cystic medial necrosis.
The majority of patients with hepatic artery aneurysms are asymptomatic prior to rupture. Of the patients who present with clinical symptoms, 60-80% of patients will present with rupture either into the peritoneum, biliary tree or gastro-intestinal tract with resultant hemoperitoneum, hemobilia or hematemesis. Approximately 70% of patients may complain of abdominal pain, usually in the right upper quadrant with radiation to back. Jaundice, either due to biliary tree compression or intraductal clot is seen in about 50% of cases. Physical examination is usually normal, although large aneurysms may be associated with a pulsatile mass or an abdominal bruit. Approximately 10% of patients present with shock following rupture or massive gastro-intestinal hemorrhage.
Curvilinear calcification on a plain radiograph in the right upper quadrant should raise the possibility of hepatic artery aneurysm. Upper gastro-intestinal tract studies may show a smooth extrinsic filling defect in the duodenum. ERCP or PTC may show biliary dilatation and filling defects especially in patients with malena.
On ultrasound examination, any discrete fusiform or round hypoechoic lesion in the right upper quadrant, which may or may not be pulsatile should raise the possibility of an aneurysm. Aneurysm and pseudoaneurysm must be distinguished from a fluid collection, pseudocyst or cystic tumour, especially before biopsy or drainage procedures. Pulsed and colour Doppler may be useful.
CT findings are low attenuation mass with rim-like calcification in the periphery on plain study and enhancement on IV contrast, Thrombotic deposits in the vessel lumen can be seen as discrete ring-shaped or semilunar internal areas of hypodensity.
MR Angiography may accurately delineate the location, relation and feeding vessels of the aneurysm. MRCP may sow dilatation of intra-hepatic biliary radicals and delineate the level of obstruction.
Appropriate management of hepatic artery aneurysm requires detailed angiography. This will confirm the diagnosis, identify any other aneurysm {20% are multiple}, delineate feeding vessels, demonstrate any arterioportal fistula and provide anatomical information needed for surgery or embolization.
Treatment of specific aneurysms depends on its location, regional vascular anatomy, the etiology of aneurysm and any associated or coexisting conditions. Common hepatic artery aneurysm can be treated by either surgical ligation or embolization. This is possibly owing to considerable collateral circulation available to the liver from the gastroduodenal and right gastric arteries. Embolization is the accepted treatment of choice for intrahepatic as well as intrahepatic aneurysm and pseudo-aneurysms.