Pictorial review
Hepatic artery aneurysm
D O'DRISCOLL, S P OLLIFF and J F C OLLIFF
Department of Radiology, University Hos...
transhepatic cholangiography (PTC) may show
biliary dilatation and ®lling defects, especially in
patients with melaena (Fi...
Figure 1. 35-year-old patient presented with a life
threatening gastrointestinal bleed 3 weeks after liver
transplantation...
(c)
(b)(a)
Figure 3. 55-year-old male with the classic triad of
epigastric pain, haemobilia and obstructive jaundice.
Endo...
(a) (b)
(c ) (d)
Figure 5. 78-year-old patient presented with renal failure. (a) Ultrasound demonstrates small kidneys and...
(a)
(e)
(c) (d)
(b)
Figure 6. 26-year-old male presented with abdomi-
nal pain following blunt abdominal trauma.
(a) Ultra...
(a) (b)
Figure 7. 19-year-old woman with polyarteritis nodosa presented with a 1-month history of increasing lethargy
and ...
Acknowledgments
The authors would like to thank the Editor of
Clinical Radiology for permission to reprint
Figure 7.
Refer...
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Hepatic artery aneurysm

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Transcript of "Hepatic artery aneurysm"

  1. 1. Pictorial review Hepatic artery aneurysm D O'DRISCOLL, S P OLLIFF and J F C OLLIFF Department of Radiology, University Hospital Birmingham NHS Trust, Queen Elizabeth Hospital, Birmingham, UK Abstract. Hepatic artery aneurysms (HAAs) are rare. A review of the English language literature from 1985 to 1995 for reports of visceral artery aneurysms showed HAA to be the most frequently reported visceral aneurysm during that decade. This increase in incidence relates to the increasing use of percutaneous diagnostic and therapeutic procedures. A second factor is the increased use of diagnostic CT scanning after blunt liver trauma. The purpose of this pictorial review is to illustrate the imaging presentation and radiological management of HAAs. Hepatic artery aneurysm (HAA) was ®rst reported at autopsy in 1809 [1]. HAAs tradition- ally represent 20% of all visceral aneurysms. 20% of all HAAs are intrahepatic. A review of the English language literature from 1985 to 1995 showed that HAA was the most frequently reported visceral artery aneurysm during that decade (103 cases) [2]. This trend is probably related to the increasing use of percutaneous diagnostic and therapeutic procedures. A second factor is the increased use of diagnostic CT scanning after blunt liver trauma. These mo- dalities have increased the detection of post- traumatic false aneurysms of intrahepatic arterial branches. 50% of all HAAs reported in that decade were intrahepatic false aneurysms and 37% of these lesions were treated by embolization. Historically, mycotic aneurysms were the most common cause of HAA, although they now account for only 4% in the recent review [2]. Atherosclerosis is present in up to 30% of such lesions, although it continues to be viewed as a secondary process. Less common causes for HAA are vasculitides, such as polyarteritis nodosa, periarterial in¯ammation caused by either chole- cystitis or pancreatitis, ®bromuscular dysplasia and cystic medial necrosis. HAAs are included among the anastomotic complications of ortho- topic liver transplantation (Figure 1) [3]. 17% of reported aneurysms in the last decade were associated with liver transplantation [2]. HAAs have also followed hepatic tumour embolization, where it is speculated that the main cause of aneurysm formation was the embolic agent [4]. The majority of patients with HAA are asymptomatic prior to rupture. Of the patients who present with clinical symptoms, abdominal pain is found in 55% and gastrointestinal haemorrhage or haemobilia occured in up to 46% of symptomatic patients [2]. Quincke described the classic triad of epigastric pain, haemobilia and obstructive jaundice, but this is only present in up to one-third of cases (Figure 3) [5]. 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 gastrointes- tinal haemorrhage. Extrahepatic aneurysms may rupture into the peritoneal cavity, while intra- hepatic aneurysms may rupture into the biliary tree and cause Quincke's triad. In the last decade 65% of the reported HAAs had ruptured, and the mortality rate associated with rupture was 21% [2]. An aggressive approach to management of these lesions is therefore recommended. Experience in our institution con- curs with this approach. We have seen 17 cases of HAA over the last 10 years; 12 males and 5 females with an age range of 22 to 78 years. Embolization was successful in all seven cases attempted. Imaging Curvilinear calci®cation on a plain radiograph of the right upper quadrant should raise the possibility of HAA (Figure 2). Indirect evidence may be obtained from other imaging modalities; for example upper gastrointestinal tract contrast studies may show a smooth extrinsic ®lling defect in the duodenum. Endoscopic retrograde chol- angiopancreatography (ERCP) or percutaneous Received 17 June 1998 and in ®nal form 22 April 1999, accepted 27 May 1999. Address correspondence to Dr D O'Driscoll, Cambridge & Huntingdon Breast Screening Centre, The Rosie Hospital, Robinson Way, Cambridge CB2 2SW, UK. The British Journal of Radiology, 72 (1999), 1018±1025 E 1999 The British Institute of Radiology 1018 The British Journal of Radiology, October 1999
  2. 2. transhepatic cholangiography (PTC) may show biliary dilatation and ®lling defects, especially in patients with melaena (Figure 3). MRI may show haemorrhage or aneurysm formation (Figure 4). Ultrasound and CT provide the diagnosis in most cases. On ultrasound, 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 ¯uid collection, pseudocyst or cystic tumour, especially before biopsy or drainage procedures (Figure 5). Pulsed wave and colour Doppler can be useful. Ultrasound is very useful in the follow- up of patients (Figure 6). Abdominal CT is often requested in trauma patients. Vessel wall calci®cation on unenhanced scans usually indicates arteriosclerotic change. Thrombotic deposits in the vessel lumen can be seen as discrete ring-shaped or semilunar internal areas of hypodensity. Images after intravenous contrast medium clearly demonstrate the vessel lumen (Figure 6). Accurate measurements of the diameter of an aneurysm may be obtained. An attenuation of 70 HU in the tissues surrounding the aneurysm is a sign of fresh haemorrhage. While conventional CT can demonstrate an aneurysm, the artery of origin is not always clear. Three-dimensional spiral CT may allow a de®nitive diagnosis to be made prior to angiog- raphy in some cases (Figure 7) [6]. Appropriate management of HAA requires detailed angiography. This can con®rm the diag- nosis, identify any other aneurysms (20% are multiple) [7], delineate feeding vessels (Figure 8), demonstrate any arterioportal ®stula (Figure 2) and provide the anatomical information needed for surgery or embolization (Figure 9). Small aneu- rysms with a thrombosed lumen may be dif®cult to demonstrate even on angiography (Figure 1). Treatment Improvements in the quality and availability of cross-sectional imaging have resulted in an increasing number of aneurysms being detected before rupture. This allows a thorough pre-operative assessment with consideration of all possible treatment options. Unlike aortic aneurysms, the risk of rupture relative to size is unknown. The current advice is that all cases should be considered for treatment. Treatment of a speci®c aneurysm depends on its location, the regional vascular anatomy, the aetiology of the aneurysm and any associated or coexisting conditions. Common HAAs can be treated by either surgical ligation or embolization. This is possibly owing to the considerable collateral circulation available to the liver from the gastroduodenal and right gastric arteries. Maintenance of direct antegrade ¯ow is indicated if collateral ¯ow is insuf®cient or pre-existing liver disease is present. Either aneurysmorrhaphy or direct arterial reconstruction is recommended under these conditions. Some cases may require resection of the involved segment of liver or transplantation. Pseudoaneurysm after orthotopic liver trans- plantation is an unusual but potentially fatal complication. Liver transplant patients with extrahepatic pseudoaneurysms are not usually treated by embolization as most are due to local infection and there is a high risk of completely occluding the donor artery. Treatment for these patients remains surgical. Embolization is the accepted treatment of choice for intrahepatic aneurysms [8] (Figure 6). The role of interventional radiological techniques in the treatment of extrahepatic lesions is less well described. Endovascular stenting or embolization of the aneurysm lumen are the preferred approaches to extrahepatic HAAs, with the site and morphology of the lesion determining the particular technique. Most authors would not recommend embolization for pre-gastroduodenal artery aneurysms because depriving the liver of collateral gastroduodenal ¯ow theoretically increases the risk of hepatic necrosis [9]. Most extrahepatic HAAs described in the literature have been treated surgically [9]. Pictorial review: Hepatic artery aneurysm 1019The British Journal of Radiology, October 1999
  3. 3. Figure 1. 35-year-old patient presented with a life threatening gastrointestinal bleed 3 weeks after liver transplantation. Digital subtraction angiogram shows irregular narrowing of both donor and recipient ves- sels. No de®nite bleeding site was demonstrated. A dilated segment at the anastomosis site was identi®ed as a bleeding pseudoaneurysm at surgery (arrow). (a) (b) (c) Figure 2. 61-year-old patient presented with bleeding varices, ascites and renal failure. He had a history of injury in a foundry accident 30 years earlier. (a) Plain radiograph shows calci®cation in a hepatic aneurysm and a renal calculus. (b) CT shows a heavily calci®ed aneurysm in the right lobe of liver. There is atrophy of the right lobe and hypertrophy of the left lobe of liver. (c) Venous phase of coeliac angiogram shows portal venous ®lling (arrow) via an arterioportal ®s- tula through the aneurysm. Embolization of the feed- ing right hepatic artery relieved all symptoms. D O'Driscoll, S P Olliff and J F C Olliff 1020 The British Journal of Radiology, October 1999
  4. 4. (c) (b)(a) Figure 3. 55-year-old male with the classic triad of epigastric pain, haemobilia and obstructive jaundice. Endoscopic retrograde cholangiopancreatography con®rms the melaena to be secondary to haemobilia and shows extrinsic compression on the bile duct (arrow). Angiography con®rmed a long fusiform aneurysm of the hepatic artery. Embolization with coils produced immediate occlusion and dramatic resolution of symptoms. Figure 4. 61-year-old patient presented with an epi- sode of tachycardia and hypertension. (a) CT per- formed to exclude phaeochromocytoma demonstrates a large mixed density mass in the retroperitoneum (arrows). (b) Coronal T1 weighted MR image shows retroperitoneal mass lesion with a concentric low intensity and high intensity rim (arrow), consistent with a haematoma. (c) Coronal T1 weighted image shows an area of high signal intimately related to the common hepatic artery (arrow). Angiography con- ®rmed this was thrombus in a common hepatic artery aneurysm. Pictorial review: Hepatic artery aneurysm 1021The British Journal of Radiology, October 1999
  5. 5. (a) (b) (c ) (d) Figure 5. 78-year-old patient presented with renal failure. (a) Ultrasound demonstrates small kidneys and a right upper quadrant aneurysm (open arrows). (b) CT con®rms these ®ndings (arrow). (c) Selective angiography of the coeliac axis shows a hepatic artery aneurysm (*) and a smaller aneurysm of the coeliac axis (arrow). (d) Superior mesenteric angiography shows that the hepatic artery aneurysm (*) is also perfused via the pancreaticoduodenal and gastroduodenal vessels (arrow). D O'Driscoll, S P Olliff and J F C Olliff 1022 The British Journal of Radiology, October 1999
  6. 6. (a) (e) (c) (d) (b) Figure 6. 26-year-old male presented with abdomi- nal pain following blunt abdominal trauma. (a) Ultrasound shows a pulsatile hypoechoic lesion in the right lobe of the liver (arrow). Continuous wave Doppler interrogation demonstrates arterial ¯ow in this lesion. (b) CT shows a large aneurysm in the right lobe of the liver (arrowheads). (c) Selective digi- tal subtraction angiography of the right hepatic artery prior to embolization also demonstrates the hepatic artery aneurysm (*). (d) Digital subtraction arterio- gram following embolization with microcoils. (e) Ultrasound 2 weeks later shows echogenic throm- bus in the former pseudoaneurysm (arrow). Pictorial review: Hepatic artery aneurysm 1023The British Journal of Radiology, October 1999
  7. 7. (a) (b) Figure 7. 19-year-old woman with polyarteritis nodosa presented with a 1-month history of increasing lethargy and intermittent abdominal pain. An abdominal ultrasound scan was normal. (a) 3D spiral CT angiogram (shaded-surface model) demonstrating a single aneurysm (AN) of the common hepatic artery (CH) arising just proximal to the origin of the gastroduodenal artery (G). Superior mesenteric artery (SMA), right (RH) and left (LH) main hepatic arteries. (b) Conventional selective coeliac axis angiogram con®rms the aneurysm arises from the common hepatic artery. Reprinted by permission of the Editor of Clinical Radiology. Figure 8. This patient had a biliary stricture following a complicated cholecystectomy. The patient had a sig- ni®cant gastrointestinal bleed 24 h after percutaneous dilatation of the stricture. Angiography demonstrates a HAA (arrow) involving an aberrant right hepatic artery that originated from the superior mesenteric artery. This was successfully embolized and bleeding ceased. Figure 9. 61-year-old female patient with probable cirrhosis was referred with a view to liver transplanta- tion. Pre-operative angiography shows a small con- tracted liver with vascular distortion and a hepatic artery aneurysm (arrow). There was no history of trauma or liver biopsy. Liver transplantation proved therapeutic for the cirrhosis and fortuitously removed the aneurysm. D O'Driscoll, S P Olliff and J F C Olliff 1024 The British Journal of Radiology, October 1999
  8. 8. Acknowledgments The authors would like to thank the Editor of Clinical Radiology for permission to reprint Figure 7. References 1. Guida PM, Moore SW. Aneurysm of the hepatic artery. Report of ®ve cases with a brief review of previously reported cases. Surgery 1966;60:299±310. 2. Shanley CJ, Shah NL, Messina LM. Common splanchic artery aneurysms: splenic, hepatic and celiac. Ann Vasc Surg 1996;10:315. 3. Hutchinson CE, MacKinlay JV, Buckels JA. Pseudoaneurysm of transplant hepatic artery: a late presentation. Br J Radiol 1993;66:158±60. 4. Nobuya A, Naofumi M, Toshio F, Ichiro S, Kzuto A, Hisayuki A, et al. Multiple intrahepatic aneu- rysms following transcatheter embolisation. Work in progress. Radiology 1994;193:743±6. 5. Harlaftis NN, Akin JT. Haemobilia from ruptured hepatic artery aneurysm. Report of a case and review of the literature. Am J Surg 1997;133:229±32. 6. Howling SJ, Gordon H, McArthur T, Hat®eld A, Lees WR. Hepatic artery aneurysms: evaluation using three-dimensional spiral CT angiography. Clin Radiol 1997;52:227±30. 7. Kadir S, Athanasoulis CA, Ring EJ, Green®eld A. Transcatheter embolization of intrahepatic artery aneurysms. Radiology 1980;134:335±9. 8. Salam TA, Lumsden AB, Martin LG, Smith III RB. Nonoperative management of visceral aneurysms and pseudoaneurysms. Am J Surg 1992;164:215±9. 9. O'Connor PJ, Chalmers AG, Chennells PM, Lintott DJ. The radiological treatment of hepatic artery aneurysms. Clin Radiol 1995;50:792±6. Pictorial review: Hepatic artery aneurysm 1025The British Journal of Radiology, October 1999

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