Acute cholangitis secondary to a hepatic artery aneurysm and acute aortic dissection

Surgical Rounds®, September 2007, Volume 0, Issue 0

Jason Chiriano, Vascular Surgery Resident, Division of Vascular Surgery,

Jason Chiriano, DO

Vascular Surgery Resident

Division of Vascular Surgery

Department of General Surgery

Afshin M. Molkara, MD

Assistant Professor of Surgery

Department of General Surgery

Theodore H. Teruya, MD

Assistant Professor of Surgery

Division of Vascular Surgery

Department of General Surgery

Ahmed M. Abou-Zamzam, Jr., MD

Associate Professor of Surgery

Vascular Surgery Program Director

Division of Vascular Surgery

Department of General Surgery

Loma Linda University Medical Center

Loma Linda, CA

Introduction: Hepatic artery aneurysms (HAAs) are rare lesions of the splanchnic vasculature. These aneurysms have been linked to collagen vascular disorders, arteritis, and infection. The presentation of HAAs may be confusing because of the effects of biliary tree obstruction or bleeding.

Results and discussion: This paper reports a unique case of an HAA presenting as acute ascending cholangitis and highlights the unusual presentation of abdominal pain and obstructive jaundice caused by an HAA. This case demonstrates an association between methamphetamine use and acute aortic dissection, the combination of which likely served as a unique catalyst in forming the HAA.

Conclusion: HAAs should be considered in the differential diagnosis of any patient presenting with cholangitis and extrinsic biliary compression, especially when risk factors for aortic dissection are present.

Visceral artery aneurysms (VAAs) are extremely rare, with only small series and a few case reports published in the English-language literature.1,2 Their prevalence has been reported to be 1%, and postmortem examinations have shown an incidence between 0.098% and 10%.3 Hepatic artery aneurysms (HAAs) make up almost 20% of VAAs and are the second most common VAA, following splenic artery aneurysms (60%).1-3 Up to 22% of patients with VAAs present with rupture, and the reported mortality rate is between 8.5% and 21%.2,4

The classic triad of abdominal pain, jaundice, and gastrointestinal hemorrhage occurs in about one third of patients who present with an HAA. The incidence of these aneurysms has been rising over the last several years, most likely because of greater awareness, improved imaging techniques, and an increase in blunt and penetrating abdominal trauma cases.

The etiologies of HAAs are diverse, with most reports citing preexisting atherosclerosis as a precipitating factor. Other causes include vasculitis (primarily associated with polyarteritis nodosa and systemic lupus) and iatrogenic injury to the hepatic artery leading to the formation of pseudoaneurysms.1,2,4,5 Welling and associates cited two cases of splanchnic artery aneurysms developing in patients who had a history of chronic methamphetamine use.6 We report the case of a 57-year-old man with a history of methamphetamine abuse, who developed an HAA secondary to an aortic dissection and presented to our facility with acute cholangitis.

Case report

A 57-year-old Hispanic man with a history of chronic methamphetamine abuse presented to the emergency department with a several-day history of painless jaundice. The general surgical service evaluated the patient and recommended admission for further workup. The patient refused to be admitted and was discharged from the hospital, but he returned 3 days later, exhibiting right upper quadrant abdominal pain, fever, and jaundice. Laboratory tests were significant for a white blood cell count of 19,000/µL (normal, 4,500 to 10,000/µL), total bilirubin of 23 µmol/L (normal, 5 to 21 µmol/L), and direct bilirubin of 14 µmol/L (normal, < 3.4 µmol/L). A presumptive diagnosis of ascending cholangitis was made, and the patient was started on intravenous antibiotics.

Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated ex?ternal compression of the common bile duct (Figure 1). A common bile duct stent was placed, and a presumptive diagnosis of a Klatskin tumor was made. Cytology evaluations, however, were negative for malignancy. A computed tomography (CT) scan of the abdomen revealed a Stanford type-B aortic dissection with a 2.5-cm HAA compressing the common bile duct (Figure 2). Magnetic resonance angiography confirmed these findings (Figure 3).

The patient underwent selective celiac angiography, which revealed an HAA that filled almost exclusively from the false lumen of the aortic dissection (Figure 4, below right). The patient was also noted to have a 1-cm splenic artery aneurysm and a 1-cm superior mesenteric artery aneurysm. Endoluminal treatment was not possible because the HAA arose from the false lumen of the aorta and could not be accessed. Open surgical treatment was undertaken. At celiotomy, the gallbladder was found to be distended, and cholecystectomy was performed. The HAA in?volved the common hepatic artery, and there was extensive inflammation in the portal triad. The aneurysm was controlled, opened, and ligated proximally and distally. There was no sign of hepatic ischemia, and hepatic revascularization was not performed.

The patient had an uncomplicated postoperative recovery and demonstrated no signs of hepatic failure, sepsis, or recurrent jaundice. At the time of discharge, his bilirubin was normal, he tolerated a regular diet, and he had good pain control.


VAAs are rare lesions that pose a significant challenge to the vascular surgeon. The first reported case of an HAA was by Quinke in 1871.2 Approximately 20% of all VAAs are aneurysms of the hepatic artery. The etiology for HAAs is diverse, but in most reported cases these an?eurysms are associated with bacterial endocarditis. Because of the availability of better treatment modalities, the incidence of mycotic visceral aneurysms has decreased, and most aneurysms are as?sociated with atherosclerosis. Other etiologies include vasculitides, trauma, and iatrogenic causes.

The natural progression of a VAA is enlargement and eventual rupture, which results in a high mortality rate.1,2,4,6 Historically, up to 70% of these aneurysms have presented with rupture. Increased awareness of these aneurysms and improved imaging techniques have led to earlier diagnosis and treatment.1,2 In a 2003 report of 36 patients presenting with HAAs, only 14% presented with rupture, while 75% were asymptomatic at the time of diagnosis.1 Although it is difficult to predict which aneurysms will rupture, larger size and nonatherosclerotic etiologies (such as vasculitis, pancreatitis, peptic ulcer disease, autoimmune disease, or infection) are risk factors.1,3 While there have been only a few reported cases of patients presenting with obstructive jaundice, our case suggests that the presence of cholangitis should lead physicians to consider whether an HAA is present.7

Potential treatments for HAAs include endovascular and open techniques. There has been some controversy regarding when it is appropriate to manage these aneurysms expectantly. Most authors advocate treatment of any HAA larger than 2 cm, although there is no randomized, prospective data that fully support this approach.1-4 Endovascular techniques include coil embolization of the aneurysm, usually avoiding total occlusion of the artery.3,8 There have been reports of embolization failing due to migration of coils, abscess formation, and recanalization.3 The mortality rate cited for endovascular procedures has ranged from 0% to 43%.3,5,9 There has been at least one report of successful treatment of a ruptured hepatic pseudo?aneurysm using a coronary stent graft.5 Reber and associates suggest that coil embolization is the treatment of choice in high-risk patients with extrahepatic pseudoaneurysms.8 Standard open techniques include aneurysm ligation or repair with interposition grafting. Ligation is generally safe in cases where there is no significant preexisting hepatic dysfunction or portal hypertension, and this procedure avoids placement of a graft in an inflamed area that is often difficult to access.

Although Welling and associates re?ported two cases of multiple VAAs developing in patients with a history of methamphetamine abuse,6 our case is unique for two reasons. First, we think our patient's condition resulted from a hypertensive crisis secondary to his methamphetamine abuse, which led to the formation of the HAA. Second, it is likely that his splenic and superior mesenteric artery aneurysms also resulted from his methamphetamine abuse, due to the gradual weakening of the arterial walls, a condition also reported by Welling and associates.6 The separate contributions of our patient's methamphetamine abuse and his aortic dissection in the genesis of the HAA are impossible to discern.


Although cholangitis typically is at?tributed to intrinsic biliary pathology, including impacted choledocholithiasis and malignancy, physicians should be cognizant of other etiologies. HAA is a rare cause of obstructive jaundice, and HAAs are associated with high rates of morbidity and mortality due to rupture and exsanguination when they are not diagnosed and treated appropriately. Preoperative identification of an HAA as a cause of obstructive jaundice is important for successfully managing this condition.


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