Presentation
Vomiting and abdominal pain for seven days prior to admission.
Patient Data
Initial non-contrast CT reveals hypodense oblong lesion starting from the falciform ligament and extends along the round ligament to end at the umbilicus.
Follow-up study shows increasingly encapsulated, mixed fat/fluid-containing opacification of the ligamentum teres extending into the peritoneum and along the frontal surface of the liver.
This results in dilated anterior intrahepatic bile ducts and subcapsular fluid collections in the inferior left hepatic lobe and along the anterior right liver, possibly bilomas related to spread of infection and biliary injury to the biliary radicles adjacent to the falciform ligament.
Additional findings include the formation of heterogeneous liver perfusion, subcutaneous tissue edema, and bilateral pleural effusion with lung atelectasis.
Case Discussion
The case shows the typical appearance of primary infraction of the ligamentum teres hepatis.
Ligamentum teres hepatis forms part of the free edge of the falciform ligament of the liver. It connects the liver to the umbilicus. It is the remnant of the left umbilical vein.
Primary infarction of the ligamentum teres hepatis is very rare.
The pathophysiology of this disease is unclear. However, one theory suggests primary ischemic necrosis of the ligament's connective tissue, which will subsequently cause an inflammatory response similar to perigastric appendagitis and intraperitoneal focal fat infarction. Another theory considers the origin infectious, starting from the umbilicus 1.
This disease could be misinterpreted as another pathology. The patient usually presents with acute abdominal pain 2.
The diagnosis is usually made by CT, which shows a hypodense stripe between the liver (falciform ligament) and the abdominal wall with fat density that extends to the umbilicus 1.
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