Omental infarction is focal fat necrosis and inflammation resulting from disruption of vascular supply to the greater or lesser omentum. It may be primary (idiopathic) or secondary (torsion, herniation, vascular thrombosis, trauma, post-surgical). Primary omental infarction is a rare condition and may mimic acute appendicitis due to its right lower quadrant location. It is more common in obese patients and after physical activity. On CT, a focal, well-defined, fat-density inflammatory area in the omentum is typical. It is generally self-limited and resolves with conservative treatment; however, complicated cases (abscess, peritonitis) may require surgery.
Age Range
20-60
Peak Age
40
Gender
Male predominant
Prevalence
Uncommon
In primary omental infarction, spontaneous thrombosis or venous congestion develops in the vascular pedicle of the omentum — the mechanism is not fully understood but obesity (increased omental mass and vascular strain), physical activity (sudden change in venous drainage), and coagulopathy are risk factors. Vascular occlusion initiates ischemia and subsequent fat necrosis in omental adipose tissue. Necrotic fat cells undergo saponification — fatty acids are released and react with calcium to form soap. This process triggers an acute inflammatory response: neutrophil and macrophage infiltration, cytokine release. On CT, focal density increase (misty fat) results from inflammatory infiltration and edema raising the fat density. Reactive inflammation spreads as a halo in surrounding fat. A fibrotic capsule may form around the inflammatory process. In secondary omental infarction, torsion or entrapment by internal hernia applies mechanical pressure to the vascular pedicle causing ischemia.
Focal fat-density infiltration area in the omentum with a central hyperdense dot corresponding to thrombotic vessel — diagnostic combination for omental infarction.
Focal, oval or elliptical, fat-density infiltration area in the omentum. Density is higher than normal fat (-40 to -80 HU, normal omental fat -100 to -130 HU) but lower than soft tissue density. Lesion size varies between 2-10 cm and is usually well-defined. A central high-density dot (thrombotic vessel) may be visible.
Report Sentence
Focal fat-density infiltration area in the omentum is observed, consistent with omental infarction.
Thin, mildly hyperdense ring around the infarction area (ring sign). This ring represents the fibrotic/inflammatory band created by the inflammatory reaction and is specific for omental infarction. Ring sign is similar to the hyperattenuating ring in epiploic appendagitis but differs in size and location.
Report Sentence
Thin hyperattenuating ring around the infarction area (ring sign) is observed, supporting the diagnosis of omental infarction.
Small hyperdense dot at the center of the infarction area — corresponds to the thrombotic omental vessel. This finding is a direct indicator of vascular occlusion and is more common in primary omental infarction. Central dot sign is larger and more prominent than the central dot in epiploic appendagitis.
Report Sentence
Hyperdense dot at the center of the infarction area (central dot sign) is observed, consistent with thrombotic omental vessel.
Focal, oval, hyperechoic, non-compressible mass in the omental area on B-mode US. Mass is more echogenic than surrounding fat tissue and may show mildly heterogeneous internal structure. Vascularity is decreased or absent on Doppler (avascular area — supports infarction). US findings are not specific but may be incidentally detected on US performed to exclude appendicitis in thin patients presenting with right lower quadrant pain.
Report Sentence
Focal hyperechoic, avascular mass in the omental area is observed, which may be consistent with omental infarction; CT correlation is recommended.
Focal area of increased density in the omentum on non-contrast CT. Lesion density is between -40 to -80 HU (fat-soft tissue intermediate density). Non-contrast acquisition is important for evaluating intrinsic density of the infarction area; the hyperdense central dot (thrombotic vessel) is more easily detected on non-contrast images.
Report Sentence
Focal density increase in the omentum on non-contrast CT is observed, consistent with omental infarction.
Heterogeneous hyperintense signal in the omental infarction area on T2-weighted images. T2 signal is high in the acute stage due to edema and inflammation. The lesion becomes more conspicuous on fat-suppressed sequences. T2 signal may decrease in the subacute/chronic stage as fibrosis develops. MRI is complementary to CT in differentiating acute appendicitis and omental infarction.
Report Sentence
Heterogeneous hyperintense focal area in the omentum on T2-weighted images is observed, consistent with acute omental infarction.
Criteria
No underlying mechanical cause; spontaneous vascular occlusion; obesity and physical activity risk factors
Distinct Features
Located in right lower quadrant; mimics appendicitis; usually self-limited
Criteria
Vascular occlusion due to omental torsion; usually larger area involvement
Distinct Features
Whirl sign (twisting of omental pedicle) may be visible on CT; larger infarction area; higher surgical need
Criteria
Disruption of omental vascular supply after surgery; especially after bariatric and abdominal surgery
Distinct Features
Surgical history; located near surgical area; iatrogenic vascular damage
Distinguishing Feature
Omental torsion shows whirl sign (omental pedicle twisting) on CT; pure infarction lacks whirl sign
Distinguishing Feature
Mesenteric panniculitis shows diffuse density increase in mesentery, fat ring sign and pseudocapsule; omental infarction is focal and localized in omentum
Distinguishing Feature
Sclerosing mesenteritis creates mass-like fibrotic tissue at mesenteric root; omental infarction shows focal fat necrosis in omentum
Distinguishing Feature
Bacterial peritonitis shows diffuse peritoneal enhancement, ascites and septic findings; omental infarction has localized focal fat infiltration and ascites is generally absent
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
no-follow-upOmental infarction is generally self-limited and resolves in 2-4 weeks with conservative treatment (analgesia, anti-inflammatory). CT diagnosis prevents unnecessary surgery (appendectomy). Complications (abscess, peritonitis, bowel adhesions) rarely develop and require surgery. Follow-up is generally not needed; control CT is considered if symptoms persist.
Omental infarction is a self-limiting condition. Diagnosis prevents unnecessary surgery. Conservative management (pain control, NSAIDs) is sufficient. Symptoms typically resolve in 1-2 weeks.