Fluorodeoxyglucose-positive Splenic Infarctions are Completely Regressive Just after 4 Months.

A 55-year-old woman with newly diagnosed hepatocellular carcinoma (HCC) was hospitalized in our department for the evaluation of selective internal radiotherapy (SIRT), which consists of an angiography, an intra-arterial technetium (Tc)-99m-macroaggregated albumin application and Tc-99m sulfur colloid scintigraphy to assess liver function. Besides the modest intratumoral tracer accumulation, F-18-fluorodeoxyglucose (FDG) positron emission tomography-computed tomography (PET/CT) imaging showed two intense focal cuneiform splenic FDG accumulations which turned out to be splenic infarctions. Four months later, both hypermetabolic foci were completely regressive in the first follow-up PET/CT after SIRT. This is the first report of a complete metabolic regression of splenic infarctions within just 4 months, whereas regression on CT is commonly seen after more than 2 years.

Introduction

Even though uncommon, intensive focal splenic fluorodeoxyglucose (FDG) accumulations are mainly described to be of a malignant nature. Benign focal splenic accumulations of F-18-FDG are rarely reported. Ahmadzadehfar et al. reported a splenic lesion with a circular area of high FDG uptake with a central photopenic area that was suspected to be a necrotizing metastasis of malignant melanoma. Subsequent splenectomy revealed an infected splenic infarction.[1] In another case, a splenic sclerosing hemangioma caused a false-positive finding in FDG PET.[23] An infection with Leishmania has been reported to have shown intense focal FDG uptake.[4]

Case Report

We present the case of a 55-year-old female patient with newly diagnosed hepatocellular carcinoma (HCC) who was hospitalized in our department for selective internal radiotherapy (SIRT). This was initially planned as a two-step procedure, with the right lobe to be treated first, due to its larger disease involvement.

The patient underwent a preinterventional evaluation, which consists of an angiography, an intra-arterial Tc-99m-macroaggregated albumin (MAA) application and scintigraphy[5] and a Tc-99m-sulfur colloid scintigraphy to assess liver function.[6]

After the evaluation, the patient underwent a FDG-positron emission tomography–computed tomography (PET/CT) scan for staging, in which HCC showed a typical modest FDG accumulation and no extrahepatic tumor manifestations. Surprisingly, two intense focal cuneiform FDG accumulations were detected in the spleen [Figure 1].

Figure 1

Maximum intensity projection of the patient's initial fluorodeoxyglucose-positron emission tomography–computed tomography. Two intense, focal, cuneiform splenic lesions (blue arrows). The hepatocellular carcinoma shows typical modest fluorodeoxyglucose uptake

On CT images, these two lesions showed the typical configuration of acute infarctions with wedge-shaped subcapsular contrast defects, especially in the venous phase. These lesions were not seen in the preliminary examination 1 month ago, in which HCC was initially observed.

Retrospectively, notable findings were seen in the pre-SIRT evaluations performed on the day before PET/CT. In the Tc-99m-sulfur colloid scintigraphy, there were cuneiform photopenic areas in the spleen [Figure 2]. In the conventional angiography, the infarct area showed slightly lower contrast. In the Tc-99m-MAA scintigraphy, there was no tracer accumulation in the spleen.

Figure 2

99mTc-sulfur colloid scintigraphy: cuneiform lineal photopenic areas in the infarct regions (blue arrows). In addition, multiple hepatic photopenic lesions due to hepatocellular carcinoma are visible

In the first follow-up PET/CT 4 months after SIRT, the formerly focal hypermetabolic infarcted areas showed no increased FDG uptake anymore. However, they were still detectable on CT although smaller.

Several follow-up examinations were performed over the next 28 months without any new infarctions or other pathologic lesions in the spleen. The last follow-up CT showed a complete morphologic regression of both infarcted areas as well.

Discussion

Acute splenic infarctions are a rare differential diagnosis to the well-known metastatic etiology of most focal FDG accumulations. They can be caused by bacterial infections, coagulopathies, and hematological/oncological or cardiovascular diseases and are usually restricted to subcapsular areas of the splenic parenchyma.[7] Furthermore, an association of splenic infarctions and therapy with sorafenib for HCC has been described by a single case report,[8] whereas in the present case, no pretreatment was applied. Apart from of a slightly elevated C-reactive protein (7.4 mg/L), probably caused by the HCC itself, neither the PET/CT nor clinical or other imaging examinations revealed any sign of an infection. Coagulation parameters such as the international normalized ratio and activated partial thromboplastin time were in the normal range, and the patient had no history of cardiac disease or arrhythmia.

Splenic infarctions related to radioembolization are reported as a rare side effect.[9] Due to the lack of other risk factors as mentioned above, we assume that the infarctions were caused by the diagnostic angiography performed during the SIRT evaluation.

As the patient was asymptomatic, no therapeutic consequences resulted from the splenic infarctions. No anticoagulation was necessary, and SIRT could have been performed as scheduled 2 weeks (right liver lobe) and 6 weeks (left liver lobe) after evaluation.

Splenic infarctions can present as a focal tracer accumulation in FDG PET and are a noteworthy differential diagnosis to malignant splenic FDG accumulations.

It is worth pointing out that there has been a rapid metabolic regression at the level of unaffected splenic parenchyma, much faster than seen on CT. Within 4 months, the infarcted areas could not be metabolically distinguished from unaffected splenic tissue [Figure 3] in the PET images.

Figure 3

Long-term development of the splenic infarction: from top to bottom: fused fluorodeoxyglucose-positron emission tomography–computed tomography, venous phase of the contrast-enhanced computed tomography, and fluorodeoxyglucose-positron emission tomography. From the left to right: initial examination with typical hypermetabolic, acute splenic infarction, follow-up after 4 months with complete metabolic regression, an incomplete morphologic regression, and follow-up after 28 months with both metabolic and morphologic regression of the acute splenic infarction

To the best of our knowledge, this is the first published case of complete metabolic regression of a splenic infarction, after only 4 months.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.