Omental infarction is a rare cause of acute abdomen resulting from vascular compromise of the greater omentum. It is a condition where the omentum, a fatty tissue that surrounds the abdominal organs, experiences a disruption in its blood supply, leading to tissue ischemia. Because of the rich vasculature of the greater omentum, anastomoses reorganise the vascularisation, which explains the mostly benign course of omental infarction. This condition can mimic other common causes of acute abdomen, delaying diagnosis. The reported incidence is less than 4 per 1000 cases of appendicitis. Up until now, approximately 400 patients with omental infarction have been published.
Causes of Omental Infarction
Omental infarction is the result of vascular obstruction and ends in tissue ischaemia. The causes of omental infarction can be broadly classified into primary and secondary.
Primary Omental Infarction
A diagnosis of primary or ‘idiopathic’ OI is made when no discernable aetiology is found. Primary omental infarction occurs when there is no underlying condition causing the infarction. The classic location of primary omental infarction is in the right lower quadrant medial to the ascending colon or cecum. The vascular compromise occurs along the right edge of the greater omentum where the arterial supply is usually tenuous. Sometimes it is the result of kinking of venous channels in the inferior part of the greater omentum in the pelvis. Primary omental infarction is usually seen in the right lower quadrant. Pathogenesis relating to blood supply disruption in idiopathic OI is unknown. In view of a preponderance for right side presentations, it has been suggested that the right half of the omentum consists of anatomically altered vasculature, less tolerant of spontaneous venous stasis and thrombosis secondary to stretching of omental veins.
Secondary Omental Infarction
Secondary omental infarction is located at the site of initial insult. Secondary causes for OI include hypercoagulability, vasculitides, polycythaemia, and for omental torsion, cysts, tumours, and adhesions. Secondary torsions are seen more frequently and these are associated with previous laparotomy, attachment of the omental tissue to tumours, presence of intra-abdominal scar tissue, cysts or intra-abdominal inflammation. Both primary and secondary omental torsion result in venous stasis, followed by formation of an omental thromboembolism, which may lead to omental infarction.
Risk Factors
Obesity is a known risk factor for omental infarction. The theory behind this is that fat accumulation within the omentum occludes blood supply to the distal parts of the omentum in addition to making it more susceptible to torsion. A raised body mass index has been of particular interest, on the back of cases reporting idiopathic OI in obese children.
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Symptoms of Omental Infarction
Patients will present with a sudden onset of cramps/abdominal pain or a 'stitch'. The most common symptoms of omental infarction are non-specific: acute abdominal pain in the right lower quadrant, anorexia, nausea, vomiting, diarrhoea and fever. Omental infarction usually presents as right-sided abdominal pain although seldom causing left-sided abdominal pain and even epigastric pain. The dominion of right-sided abdominal pain in omental infarction has been attributed to right segmental infarction as a result of the tenuous blood vessels in this part of the omentum as well as its longer size and higher mobility in comparison to the left side which subjects it to torsion.
Understanding abdominal innervation helps to decipher clinical presentation. Parietal peritoneum of the anterior abdominal wall shares somatic innervations with muscle and skin adjacently overlying. Irritation will therefore precipitate localised tenderness and muscle contraction, guarding, through efferent pathways, via afferent connections on the parietal peritoneum.
Diagnosis of Omental Infarction
Historically, omental infarction was diagnosed only intraoperatively during surgery for presumed appendicitis or other causes of acute abdomen. Laboratory tests are non-specific as well: elevated leucocytes and slightly elevated levels of C reactive protein (CRP). Therefore, omental infarction cannot be distinguished from other diagnoses without the help of imaging techniques. But with the increase in the use of imaging, especially abdominal computed tomography (CT) scan in the work-up for acute abdomen, more cases of omental infarction are being diagnosed preoperatively. The diagnosis is usually inferred from abdominal CT scan which shows a localised inflammatory-appearing mass of omentum.
Imaging Techniques
A diagnostic tool that can distinguish between the top differential diagnoses is the CT scan. Expanded access to CT imaging over the last twenty years has coincided with improved recognition of omental pathology radiographically. The characteristic signs of omental infarction at CT are a well-circumscribed, non-enhancing, fatty mass with heterogeneous attenuation and focal fat stranding surrounding the lesion. Localised fat density lesions are seen in OI. Concentric linear strands, or the ‘whirl’ sign, and hyperattentuated streaky infiltration have both been described in omental torsion.
In a case report, ultrasound showed some induration of the intra-abdominal fat adjacent to the anterior abdominal wall at the painful location. The CT scan showed an area of slightly heterogeneous fatty tissue with a maximum diameter of 4.7 cm, which was surrounded by some fat stranding in the left ventral margin near the ventral abdominal wall.
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Differential Diagnosis
Composing a differential diagnosis is one of the first goals when a patient presents at the ED with acute abdominal pain. In the case of left-sided omental infarction, the CT scan showed omental fat stranding nearby the sigmoid and descending colon. These structures showed a few diverticula, but the fat induration was not typically located around these diverticula, which excluded the diagnosis of acute diverticulitis. No intra-abdominal free air was seen, which excluded abdominal perforation. A normal appendiceal lumen and wall, without fat stranding around the appendix, excluded acute appendicitis.
Treatment of Omental Infarction
Currently, conservative management and surgery are the only treatment options for omental infarction with no consensus as to the best treatment modality. This has also led to the observation that omental infarction is a self-limiting condition which can be managed conservatively.
Conservative Management
Arguments in favour of conservative medical management are the often self-resolving character of omental infarction, especially since omental infarction is described to be self-limiting (proven with CT) even after 1-3 years follow-up, as well as the safety and effectiveness of conservative treatment, which protects patients from unnecessary surgical intervention. Conservative management includes analgesics, anti-inflammatory medication and fluid management. General consensus holds OI and omental torsion as principally self limiting conditions, and this is supported by CT imaging data at 1-3 years follow up.
In a reported case, the patient was treated conservatively with analgesia, anti-inflammatory medication and fluid management, coupled with daily monitoring of blood inflammatory markers. An increase in these markers and/or unresolved pain will have indicated surgical intervention. As it happens, his pain resolved and the patient was discharged without complication, a total of nine days from onset of initial symptoms. At the outpatient clinics, she reported that within 3 days, she was completely free of complaints and her LDH levels returned to normal again.
Surgical Intervention
Arguments in favour of surgical intervention are a shorter length of hospitalisation compared with conservative treatment (2 vs 4 days), which will be supported by patients and will save money. In addition, (laparoscopic) treatment is favoured by some because it allows for confirmation of the radiological findings. The use of minimally invasive surgery in the management of idiopathic omental torsion: The diagnostic and therapeutic role of laparoscopy. In tandem there are general anaesthetic and surgical risks to consider with any surgical intervention.
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Management Recommendations
After CT imaging diagnosis, Itenburg et al. advocate close monitoring of a patient in the first 24-48 h, refraining from considering surgery until deterioration in any symptom, sign or clinical marker. To what extent a change is significant enough to precipitate surgery is an arbitrary judgement. Nevertheless prudence can potentially avoid unnecessary surgery, such as in our patient, circumventing its associated risks.
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