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Year : 2017  |  Volume : 5  |  Issue : 2  |  Page : 77-81

Primary and secondary omental infarction: A 5-year experience in a tertiary care hospital

1 Department of Radiology, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India
2 Department of General and Minimally Invasive Surgery, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Date of Web Publication26-Jul-2017

Correspondence Address:
Tahleel Altaf Shera
Department of Radiodiagnoisis, Sher-I-Kashmir Institute of Medical Sciences, Srinagar - 190 011, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ssj.ssj_19_17

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Objective: The aim of this study is to describe the computed tomography (CT) features of primary and secondary omental infarction.
Materials and Methods: Five cases of primary and seven cases of secondary omental infarction are described with emphasis on CT features. The etiology and clinical features are described with the ultimate clinical outcome.
Results: In this case series of 12 patients, five omental infarcts (42%) were classified as primary. Seven cases (58%) were postoperative with four infarcts following cesarean section, one following a total abdominal hysterectomy, one occurring after a laparoscopic ovarian cystectomy, and one occurring after laparoscopic hemicolectomy. Of the seven secondary omental infarctions, one was associated with secondary thickening of the transverse colon and one patient developed an abscess. Three patients from the secondary group and one patient from the primary group underwent omentectomy. Primary infarcts showed an ill-defined fat attenuation lesion with thin stranding located in the right upper quadrant in three and left lower quadrant in two patients. The postoperative omental infarcts showed more pronounced inflammatory change and soft tissue attenuation foci interspersed with fat density foci. They were located in the right lower quadrant in four patients, in the right upper quadrant in two patients, and in the left lower quadrant in one patient. The patients were followed to clinical resolution.
Conclusion: It is possible to distinguish primary and secondary omental infarcts on the basis of CT features. Even though, a nonsurgical cause of acute abdomen, surgical management may become necessary in patients with secondary omental infarction and secondary infection who fail to respond to antibiotics and percutaneous drainage. The majority of the secondary cases followed cesarean section in our series.

Keywords: Acute abdomen, computed tomography, omental infarction

How to cite this article:
Choh NA, Shera TA, Jabeen S, Ashraf O, Khan AM, Shaheen FA, Wani GM, Wani M, Shah M, Gojwari T, Robbani I. Primary and secondary omental infarction: A 5-year experience in a tertiary care hospital. Saudi Surg J 2017;5:77-81

How to cite this URL:
Choh NA, Shera TA, Jabeen S, Ashraf O, Khan AM, Shaheen FA, Wani GM, Wani M, Shah M, Gojwari T, Robbani I. Primary and secondary omental infarction: A 5-year experience in a tertiary care hospital. Saudi Surg J [serial online] 2017 [cited 2023 Jun 11];5:77-81. Available from: https://www.saudisurgj.org/text.asp?2017/5/2/77/211608

  Introduction Top

Omental infarction is considered a rare entity. It is a mimicker of acute cholecystitis and other causes of acute abdomen.[1],[2] With the increasing use of computed tomography (CT) in the emergency room, more cases are diagnosed preoperatively, and it appears that the disease is not as rare as previously thought. Omental infarction may be primary or may occur after surgery (secondary omental infarction). The various presumed etiologies in primary infarction of omentum are a hypercoagulable state, congestive heart failure, vasculitis, superior mesenteric artery/venous thrombosis, obesity, and marathon running.[3] Patients usually present with acute to the subacute onset of abdominal pain, palpable lump, and mild leukocytosis.[4],[5] The imaging diagnosis is extremely important because the majority of patients can be managed nonoperatively.[6],[7] Secondary omental infarction which occurs in a postoperative setting and the imaging findings of which may persist for years is also important to recognize because the imaging findings may be mistaken for some sinister pathology such as omental deposits and tumors.[1],[8]

  Materials and Methods Top

This was a retrospective observational study in a single tertiary care hospital. The aim of the current study was to evaluate CT features of cases of omental infarction and to study the differences between primary and secondary omental infarction on imaging with CT. The study group comprised 12 consecutive cases whose final diagnosis was primary or secondary omental infarction on the basis of radiological, clinical, and surgical findings over 5 years and underwent CT evaluation at our institute. Omental infarctions were defined as: (a) patients with abdominal pain and an ill-defined fat attenuation lesion centered in the area of greater omentum with stranding and inflammatory change; (b) postoperative patients with new onset abdominal pain or palpable lump with CT showing a heterogeneous lesion with fat attenuation which persists on serial follow-up imaging and fails to resolve completely. Patients with clinical or laboratory evidence of pancreatitis, suspicion of omental metastatic disease, and omental hemorrhagic contusions which resolved on follow-up imaging were excluded from the study.

The patients were scanned using a 64 detector row CT scanner (Seimens, Somatom Sensation) after administering 80–100 ml of intravenous contrast (1–1.5 mg/kg in pediatric patients) followed by volumetric dataset acquisition in portal venous phase (60 s). The images were reconstructed using 3 mm section thickness and viewed in multiple planes on a dedicated workstation.

  Results Top

Twelve patients of omental infarction were encountered with five cases of primary and seven cases of secondary omental infarction [Table 1]. All five cases of primary omental infarction presented with acute abdominal pain (two patients with right hypochondrial pain and three patients with umbilical/left lower quadrant pain). The age varied from 28 to 50 years. In the secondary group, four patients presented with mid and lower abdominal pain which differed in character from their postoperative pain, one had a fever and two patients reported a sensation of a lump in the lower abdomen. A palpable lump was noted on examination in five patients in the secondary group.
Table 1: Demographics

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Computed tomography findings

The primary omental infarction group showed an ill-defined predominantly fatty lesion with internal stranding which varied in size from 4.5 to 7.5 cm. The lesions were located in the right hypochondrium in three patients and central/left lower abdomen in two patients [Figure 1], [Figure 2], [Figure 3], [Figure 4]. Two patients showed minimal free pelvic fluid. Four patients responded to conservative treatment. One patient was operated due to persistent pain and demonstrated torsed omentum which had to be resected. Two patients in the nonoperative group had a follow-up CT within 3 months and demonstrated the persistence of the fatty lesion, although, the lesion had reduced in size [Table 2].
Figure 1: Contrast-enhanced computed tomography in a case of primary omental infarction shows a fatty lesion with stranding anterior to transverse colon. The patient was managed conservatively

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Figure 2: Same patient showing the omental infarct in serial images

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Figure 3: Contrast-enhanced computed tomography shows a fatty omental lesion with internal stranding in a patient with sudden pain. Operative findings revealed torsion of omentum with infarction

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Figure 4: Coronal computed tomography image of same patient

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Table 2: Computed tomography findings

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The secondary omental infarction group demonstrated a heterogeneous, more dense, mass-like omental lesion (size 5.0–9.0 cm) which showed multiple central and interspersed fat attenuation foci. Two lesions were located in the mid-abdomen, two in the right lower quadrant, and four extended from the right lower quadrant to the hypogastrium [Figure 5], [Figure 6], [Figure 7]. One patient showed a collection in the fatty lesion, and one patient showed marked associated thickening of the transverse colon. Five patients showed minimal reactive free fluid in the pelvis. Three patients underwent a follow-up CT after 6 weeks and demonstrated the persistence of the lesion albeit with a change of morphology (the lesion had become better defined with increasing size of the central fatty attenuation component). Three patients were operated: one for omental abscess, one for persistent pain in whom the surgeon had a suspicion of acute appendicitis, and one patient had a discrete palpable lump, in whom the surgeon was worried about the presence of a foreign body.
Figure 5: Contrast-enhanced computed tomography shows a soft tissue lesion with central fat in a patient following cesarean section (a case of secondary omental infarction)

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Figure 6: Computed tomography shows a tumefactive lesion with central fat in a patient who presented with lump following cesarean section. Postoperative diagnosis was omental infarction with secondary hemorrhage

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Figure 7: Computed tomography in a case of secondary omental infarction shows a heterogenous lesion with central fatty component consistent with omental infarction. The lesion is denser and more tumefactive than a primary omental infarct

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In both groups, in the patients managed nonoperatively, the diagnosis of omental infarction was established on the basis of imaging features, clinical course, and clinical/radiological follow-up.

  Discussion Top

Omental infarction is a rare cause of acute abdomen with acute to sub-acute pain that may be localized to the right upper quadrant or right or left lower quadrant.[4] The patients may also complain of nausea, vomiting, fever, and diarrhea.[7] The diagnosis used to be missed clinically, but with the widespread use of CT as a primary modality for acute abdominal pain, more cases are being diagnosed preoperatively and managed conservatively. Omental infarction was traditionally labeled as with or without torsion, a distinction which was immaterial because of the same treatment required in either case.[6]

Primary omental infarction is a hemorrhagic infarction that is thought to arise from kinking of veins and vascular compromise due to the precarious blood supply to the right side of the omentum and due to its greater length and mobility on the right.[3],[4] Torsion of the omentum may be due to anatomical variants like a bifid omentum; vascular variants that predispose to venous obstruction and congenital attachment abnormalities. Omental cysts, masses, or scars may predispose to secondary torsion. Primary omental infarction may also be secondary to obesity, overeating, marathon running, congestive heart failure, and hypercoagulable states.[1],[4],[6],[7] One of our patients in the primary group was obese, and three were females. None of the patients had any evidence of hypercoagulable state or a collagen vascular disease. One of the patients in this group demonstrated omental torsion intraoperatively. All other patients improved on conservative treatment. All CT scans were obtained within 48 h of presentation. The CT morphology of an oval, predominantly fat attenuation mass with a whorled pattern of stranding internally was seen in all patients.[2],[9] We did not encounter any difficulty in differentiating these lesions from epiploic appendagitis or diverticulitis.[10] The minimal free fluid was noted in the pelvis in two cases. Although many of the features typical for omental infarction may be demonstrated on noncontrast images, the contrast was administered in all the patients due to the nonspecific presenting signs and symptoms, and hence that other differentials may also be evaluated.

Secondary omental infarction has been described after colonic resection, gastrectomy, or pelvic surgeries by both open and laparoscopic approaches.[8],[11],[12],[13],[14],[15] This entity needs to be distinguished from omental contusions which are a result of operative trauma and resolve completely on follow-up. Postoperative omental infarction has been morphologically classified into four subtypes: Type I – ill-defined, heterogeneous, fat attenuation lesion; Type II – well-defined fat attenuation lesion with rim enhancement; Type III – well-defined heterogeneous lesion with fat component; and Type IV – well-defined heterogeneous lesion without a fat component.[12] There is a good likelihood of mistaking such lesions as omental deposits in the surveillance imaging of cancer patients, and thus, familiarity with this entity is of paramount importance. The lesions become denser and more well defined on follow-up imaging. When previous CT imaging is not available, biopsy may be needed to definitively rule out a malignant infiltration of the omentum.[8] The likely mechanism of postoperative omental infarcts is venous thrombosis, artery ligation, kinking due to adhesions, etc., Six out of our seven cases of secondary omental infarction followed pelvic surgery (four cesarean sections, one total abdominal hysterectomy and one laparoscopic cystectomy). The indications of repeat imaging were the new onset of pain (four patients), palpable lump (four patients), and fever (two patients). All the patients were imaged within 48 h of presentation and within 3 weeks after surgery. The lesions were denser with central and interspersed fat attenuation as compared to the primary group (in which the lesions were predominantly fatty with stranding within the lesion). Three patients were operated; one with a clinical suspicion of acute appendicitis, one with a firm, palpable lump where there was concern for a retained foreign body, and one in which a collection was noted within the omental lesion. In all three cases, omentectomy was done and the diagnosis of omental infarct was confirmed. The reason for the denser appearance of the secondary infarcts may be due to a predominant component of venous obstruction and secondary hemorrhagic infarction. Four out of seven cases of secondary infarction followed a cesarean section. The reasons may be a hypercoagulable state during the postpartum period as well as mechanical distortion of the omentum due to a gravid uterus. Anatomical factors like a large omentum hanging down into pelvis may also contribute. We strongly feel that secondary infarction after cesarean section, in particular, may be more common and is missed because very few patients are imaged in the postoperative period, and the pain arising from omental infarction may be erroneously attributed to the surgery. It is pertinent to mention that none of the patients of postcesarean omental infarction had a pfannensteil incision, increasing the possibility of omental incarceration during suturing of fascia pfannenstiel.

The management of omental infarction includes expectant observation. The indications of surgery are a severe pain (in the primary group) and abscess formation, fever, and pain (in the secondary group). Conventionally, omentectomy has been performed in such cases which can also be done laparoscopically.[16],[17],[18] The radiologist, by suggesting the diagnosis, can increase the confidence of the surgeon in more expectant management.[2],[3],[19],[20]

  Conclusion Top

The diagnosis of primary omental infarction is straightforward (predominantly fatty lesions within the omentum with central stranding) and should be managed conservatively. Secondary omental infarction may be more common than thought and is probably missed. It is more common after a cesarean section (probably due to hypercoagulable state of the postpartum period as well as the mechanical distortion of the omentum due to a gravid uterus). In the absence of a pathological confirmation, follow-up CT features are sufficiently diagnostic for secondary omental infarction. The denser and more heterogeneous appearance of postoperative omental infarction may be due to predominant venous obstruction and hemorrhagic type of infarction.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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Wiesner W, Kaplan V, Bongartz G. Omental infarction associated with right-sided heart failure. Eur Radiol 2000;10:1130-2.  Back to cited text no. 5
Grattan-Smith JD, Blews DE, Brand T. Omental infarction in pediatric patients: Sonographic and CT findings. AJR Am J Roentgenol 2002;178:1537-9.  Back to cited text no. 6
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Kerr SF, Hyland R, Rowbotham E, Chalmers AG. Postoperative omental infarction following colonic resection. Clin Radiol 2012;67:134-9.  Back to cited text no. 8
Kim J, Kim Y, Cho OK, Rhim H, Koh BH, Kim YS, et al. Omental torsion: CT features. Abdom Imaging 2004;29:502-4.  Back to cited text no. 9
van Breda Vriesman AC. The hyperattenuating ring sign. Radiology 2003;226:556-7.  Back to cited text no. 10
Park KE, Chung DJ, Kim W, Hahn ST, Lee JM. Secondary omental infarction related to open and laparoscopic-assisted distal gastrectomy: Report of two cases. Korean J Radiol 2011;12:757-60.  Back to cited text no. 11
Oh JY, Cho JH, Kang MJ, Lee JH, Kwon HJ, Nam KJ, et al. Omental infarction caused by laparoscopy-assisted gastrectomy for gastric cancer: CT findings. Clin Radiol 2011;66:966-73.  Back to cited text no. 12
Schwartzman GJ, Jacobs JE, Birnbaum BA. Omental infarction as a delayed complication of abdominal surgery. Clin Imaging 2001;25:341-3.  Back to cited text no. 13
Paspulati RM, Dalal TA. Imaging of complications following gynecologic surgery. Radiographics 2010;30:625-42.  Back to cited text no. 14
Phillips RW, Peterson CM. Infarction of the omentum after cesarean section. A case report. J Reprod Med 1988;33:382-4.  Back to cited text no. 15
Cianci R, Filippone A, Basilico R, Storto ML. Idiopathic segmental infarction of the greater omentum diagnosed by unenhanced multidetector-row CT and treated successfully by laparoscopy. Emerg Radiol 2008;15:51-6.  Back to cited text no. 16
Nubi A, McBride W, Stringel G. Primary omental infarct: Conservative vs. operative management in the era of ultrasound, computerized tomography, and laparoscopy. J Pediatr Surg 2009;44:953-6.  Back to cited text no. 17
Itenberg E, Mariadason J, Khersonsky J, Wallack M. Modern management of omental torsion and omental infarction: A surgeon's perspective. J Surg Educ 2010;67:44-7.  Back to cited text no. 18
Park TU, Oh JH, Chang IT, Lee SJ, Kim SE, Kim CW, et al. Omental infarction: Case series and review of the literature. J Emerg Med 2012;42:149-54.  Back to cited text no. 19
Miguel Perelló J, Aguayo Albasini JL, Soria Aledo V, Aguilar Jiménez J, Flores Pastor B, Candel Arenas MF, et al. Omental torsion: Imaging techniques can prevent unnecessary surgical interventions. Gastroenterol Hepatol 2002;25:493-6.  Back to cited text no. 20


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]

  [Table 1], [Table 2]

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