Fig. 1. Celiac angiogram shows tortuous splenic artery with aneurysm at the splenic hilum (arrow).

Fig. 2. Transplant hepatic artery anastomotic stenosis (arrow).

 Case Reference No. CC-697-02

This patient is a 40-year-old woman with a long history of autoimmune disease, one facet of which was characterized as chronic active hepatitis. She underwent an orthotopic liver transplant in October 1996. In January 1997 she returned with abdominal pain in January 1997. An ultrasound examination and CT scan demonstrated a 1.7-cm splenic artery aneurysm with a calcified rim. Before her liver transplantation, she had portal hypertension with multiple splenic varices and a large spleen.

Viseral angiography was performed prior to splenic artery embolization. This revealed a tortuous, dilated splenic artery with an aneurysm at the splenic hilum (Fig. 1), and a moderate stenosis at the transplant hepatic artery anastomosis (Fig. 2). There are multiple pools of contrast material within the splenic parenchyma (Fig. 2).We wondered at the time whether this might be due to an arteritis.

A selective right renal DSA showed no features of arteritis (Fig. 3).

It was impossible to reach the splenic artery aneurysm with any type of catheter; therefore, the splenic artery was embolized with multiple Gianturco-Wallace coils positioned as distally as possible in the mid-splenic artery.

A conventional arteriogram (Fig. 4) following coil embolization showed opacification of the proximal splenic artery but no filling distally. The calcification in the splenic artery aneurysm was seen more clearly (arrows). 2-D time-of-flight MRA (Fig. 5) the following day showed some areas of high and low signal in the spleen, as well splenic hilum varices and a very large spleen.

Following embolization, the patient developed multiple splenic infarcts with thrombosis of some varices adjacent to the spleen. With conservative management and antibiotics she made a good recovery.

 

Fig. 3. Renal angiogram showed no signs of arteritis.

Fig. 4. Post embolization splenic angiogram. Embolization coils are seen (arrows).

Fig. 5. 2-D time-of-flight MRA shows splenomegaly and splenic varices.

Questions

1) What is the etiology of the abnormal collections of contrast material in the spleen?

2) In view of her history of arteritis, portal hypertension, and these findings, was it appropriate to proceed to splenic artery embolization?

3) It was impossible to get any closer to the splenic artery aneurysm. In view of the splenic infarction, should we have embolized more proximally?

4) Although there was no immediate indication for dilating the hepatic artery stenosis, should this be treated prophylactically?

We believe that the answer to question 1 is that the contrast collections in the spleen represent splenic peliosis secondary to many years of treatment with prednisone for the autoimmune condition. The less likely alternative (particularly in view of the normal renal arteriogram) is that this was a manifestation of an arteritis associated with a chronic active hepatitis. The liver, of course, would not show any features of peliosis only 6 months after transplantation.