The falciform ligament is a double layer peritoneum derived from ventral mesentery that connects the anterior portion of the liver to the inferior diaphragm and ventral abdominal wall [2]. It contains the ligamentum teres, obliterated umbilical veins, and variable amount of extraperitoneal fat which can form fatty appendages [1,4]. The falciform ligament is supplied arterially by the left inferior phrenic and middle hepatic arteries. Venous drainage is via the left inferior phrenic vein [4,5]. Pathology of the falciform ligament is uncommon, but can include internal herniation, cystic lesions, secondary infections [1,2], and recanalization secondary to portal hypertension [6].

In rare cases, focal infraction and necrosis of the falciform ligament can occur, similar to the index case. This can be associated with torsion of the falciform ligament fatty appendages, which was first described by Beasley in 1959. The diagnosis was made histologically following laparotomy for a suspected perforated peptic ulcer [7]. In 2001, Coulier et al. described a similar case and the first CT and ultrasound findings associated with falciform ligament fatty appendage torsion and necrosis [1]. The falciform ligament is considered a rare location for intraperitoneal focal fat infarction which is more commonly described in epiploic appendages and omentum [1,2,8].

To our knowledge, there are less than twenty cases of falciform ligament torsion and/or focal infraction reported in the literature [2,4]. As in our case, inflammation/infarction of falciform ligament fat often presents with epigastric and/or right upper quadrant pain, with or without constitutional symptoms. The pain is thought to be caused by ischemia resulting from vascular torsion and venous thrombosis. Intermittent symptoms may be attributed to spontaneous untwisting of the appendage, relieving the ischemia [3]. Clinically, the presentation can mimic other diseases such as cholecystitis, perforated peptic ulcer, pancreatitis and gastroesophageal reflux [2,3].In some cases, it presents as an acute abdomen, prompting surgical intervention. Despite the reported severity of symptoms, laboratory findings are often unremarkable [3,4].

Imaging findings of falciform ligament torsion and/or infraction have been described using ultrasound, CT, and MRI [3]. Although ultrasound did not focus on perihepatic fat in our case, several sonographic findings have been described in the literature. Coulier and Lloyd et al. described a heterogenous nodule that did not move with underlying structures during respiration [1,9]. Others have described ill-defined echogenicity with associated inflammatory changes [2]. CT findings are most frequently described and often include a well circumscribed heterogenous mass with increased fatty density and inflammatory changes [2,8]. Chieng et al described an ovoid fat density with attenuated peripheral rim surrounded by inflammatory changes near the falciform ligament [4]. In the index case, fat stranding compatible inflammatory changes around the falciform ligament were seen. The difference from the provided literature may be attributable to the active inflammation resulting in a heterogenous appearance of the fat. In our case,the diagnosis was also supported by MRI which showed progressive involution of the fat necrosis along the falciform ligament and anterior perihepatic space with early encapsulation, similar to the ovoid fat density described by Chieng et al on CT.

To our knowledge, our case is only the second case to characterize focal infarction of the falciform ligament using MRI. Justaniah et al reported the use of MRI in their case series and described findings of an ovoid hypointensity on T1 and T2 weighted MR images with rim enhancement on T1-weight post gadolinium [3]. These findings are similar to our findings as we also visualized post gadolinium rim enhancement, although hyperintensity about the area of fat necrosis on T2/ SPAIR imaging suggested ongoing inflammation and edema. MR imaging confirmed the findings initially seen on CT scan. Conservative management of falciform ligament fat infarction includes nonsteroidal anti-inflammatory medication and is often effective with resolution of symptoms within several weeks [2,4]. Surgical intervention has been reported in cases for increasingly severe abdominal pain [2], diagnostic uncertainty [3,4], or lack of awareness for alternative management [2,9]. While focal infarction of the falciform ligament is rare,its presentation is non-specific mimicking a wide differential of hepatobiliary, gastroduodenal, and pancreatic diseases [3]. Imaging can be diagnostic and therefore it is important for radiologists to recognize this pathology to avoid unnecessary surgical intervention