Idiopathic omental infarction: managed conservatively

Abstract

We report a case of a 49-year-old woman who presented with acutely worsening episodic abdominal pain. Workup was negative but CT of the abdomen showed right upper quadrant omental fat stranding, suggestive of fat necrosis or infarct. Treatment for the patient was largely supportive with pain management and fluid resuscitation.

Background 

Omental infarction is a rare condition that has not been well studied or well characterised in the literature. Because the treatment is supportive care, early recognition can reduce patient morbidity and minimise invasive workups and unwarranted treatments. As of now, the incidence of omental infarction has yet to be accurately determined and only 400 cases have been documented in the literature to date.¹ Thus, it is important to report such cases in order to add to the limited body of knowledge.

Case presentation

The patient is a 49-year-old woman with a history of well-controlled hypertension who presented with 6 weeks of colicky abdominal pain localised to the right upper quadrant. She had previously been evaluated at another local hospital several weeks before and sent home after the workup was negative. The pain acutely worsened prompting her to return for re-evaluation. She described the pain as a constant and debilitating ‘squeezing, twisting’ that did not improve with ice, rest or over-the-counter pain medications. There did not appear to be an association with time of day, food or activity and she did not report a history of trauma to the area. She denied fever, chills, nausea or vomiting, melena or dysuria. Prior to admission she had foul-smelling stool but otherwise had been bloated and constipated up to the day of discharge. Hert medical history was significant for hypertension controlled with hydrochlorothiazide and constipation treated with docusate. Her surgical history was significant for three caesarean sections (one requiring a partial hysterectomy) over 20 years ago. Her weight was 93.3 kg (body mass index of 35.3).

Investigations

Ultrasound of the right upper quadrant: No gallbladder pathology demonstrated. Hepatic steatosis. Stable left hepatic lobe lesion suggestive of cyst.

CT abdomen/pelvis: RUQ omental fat stranding suggestive of focal fat necrosis/infarct (figures 1 and 2).

Figure 1.

CT scan axial view showing right upper quadrant echogenic focus consistent with omental fat necrosis/infarct.

Figure 2.

CT scan view showing right upper quadrant echogenic focus consistent with omental fat necrosis/infarct.

See figures 1 and 2.

X-ray abdomen: negative for signs of mechanical obstruction.

Glucose: (H) 104 mg/dL (low normal to high normal: 70 to 99).

Calcium: 9.3 mg/dL (low normal to high normal: 8.5 to 10.5).

Alkaline phosphatase: 70 Units/L (low normal to high normal: 25 to 125).

Alanine amniotransferase: 36 units/L (low normal to high normal: 7 to 52).

Aspartate aminotransferase: 26 units/L (low normal to high normal: 13 to 39).

Bilirubin direct: 0.1 mg/dL (low normal to high normal: 0.0 to 0.2).

Bilirubin total: 0.6 mg/dL (low normal to high normal: 0.0 to 1.0).

Total protein: 6.6 g/dL (low normal to high normal: 6.4 to 8.0).

Albumin: 3.9 g/dL (low normal to high normal: 3.5 to 5.0).

Lipase: 31 units/L (low normal to high normal: 7 to 59).

Lactate venous: 1.5 mmol/L (low normal to high normal: 0.5 to 2.2).

White cell count: 6.6×10⁹/L (low normal to high normal: 3.6 to 10.6).

Red cell count: 3.95×10¹²/L (low normal to high normal: 4.18 to 5.51).

Haemoglobin: 131 g/L (low normal to high normal: 134 to 170).

Hematocrit: 37.2% (low normal to high normal: 40.0 to 54.0).

Mean corpuscular volume: 94 fL (low normal to high normal: 81 to 99).

MCH: 33.0 pg (low normal to high normal: 27.0 to 34.0).

Mean corpuscular hemoglobin concentration: 35.1 GM/dL (low normal to high normal: 32.0 to 36.0).

Red cell distribution width: 14.3% (low normal to high normal: 11.5 to 14.5).

Platelet: 239×10⁹/L (low normal to high normal: 150 to 450).

Mean platelet volume: 7.7 fL (low normal to high normal: 7.0 to 12.0).

Erythrocyte sedimentation rate: 11 mm/hour (low normal to high normal: 0 to 20).

Pregnancy test urine: negative.

Urinalysis: only abnormal for 25 Leu/uL.

Differential diagnosis

• Ischaemic colitis.

• Acute cholecystitis.

• Epiploic appendagitis.

• Trauma.

• Small bowel obstruction from adhesive disease from prior surgical intervention.

• Ileus.

• Diverticulitis.

• Pancreatitis.

• Ovarian cyst.

• Ectopic pregnancy.

Treatment

Because the patient’s labs were relatively benign and not indicative of infection, treatment depended largely on the interpretation of her imaging studies. RUQ ultrasound was benign but an abdominal CT scan (figures 1 and 2) was significant for ‘right upper quadrant omental fat stranding may indicate a small focus of fat necrosis/infarct’. General surgery was consulted regarding their opinion of the imaging and agreed with the diagnosis of omental infarct. Thus, supportive care was provided including gentle fluids, advancement of her diet and pain medications (Norco 5–325 mg every 4 hours and Fentanyl patch for breakthrough pain).

Outcome and follow-up

One week after discharge the patient was seen at a follow-up outpatient appointment. Her pain had improved and was well controlled on Tylenol and Naproxen. She had not felt the need to revisit the emergency department for her pain. At 3 weeks after discharge, she continued to note improvement of RUQ pain.

Discussion

A major challenge to the diagnosis of omental infarction is that it can mimic the classic presentation of an acute abdomen.² Based on patients' symptoms, they most commonly fit the picture of peritonitis. Laboratory values can show a non-specific inflammatory response.³ Omental infarctions caused by inguinal hernias can present with acute pain in the scrotum rather than an acute abdomen. As described in our patient, the symptoms of omental infarction were mistaken for more common causes of right sided abdominal pain initially such as acute cholecystitis. The differential diagnosis typically includes appendicitis, perforation, diverticulitis, small bowel obstruction due to adhesive disease and ischaemic colitis. Gynaecological aetiologies must be considered as well, including rupture of ovarian cysts and ectopic pregnancies.

The number of new omental infarction cases per year is unknown; however, approximately 400 cases have been documented in the literature. The condition is seen most often in children and men aged 40–50 years. The classic presentation is abdominal pain that is sudden in its onset, non-radiating and most frequently located over the right quadrants. Right-sided abdominal pain has been seen in roughly 88% of all presentations and is likely attributed to the greater omentum’s increased length and mobility on the right side relative to the left.⁴ Associated symptoms such as changes in bowel habits and nausea are uncommon.

The greater omentum is peritoneum that has been folded twice, composed of fibrous, adipose and lymphatic tissues that attaches to the greater curvature of the stomach and duodenum. It travels inferiorly to blanket the lower visceral organs by shielding around the majority of the intestines. Its primary role is to prevent the spread of infection within the abdomen.

There are two main categories of omental infarctions primary and secondary.⁵ In both types infarction can take place with or without torsion of the greater omentum. Causes of omental infarction result from thrombosis, venous stasis and haemorrhagic necrosis that are subsequently demonstrated through histological evidence of venous congestion, thrombosis, haemorrhage and fat cell necrosis.⁶ Primary omental infarction occurs spontaneously and has thus been labelled as idiopathic segmental infarction of the greater omentum (ISIGO). Risk factors for ISIGO include malformation, differences in fat distribution and redundant omental veins.⁷ It is thought that the torsion leading to infarction is due to wedging of the greater omentum between the abdominal wall and the liver as a result of localised trauma, intense exercise, environmental vibrations and increased intra-abdominal pressure after coughing or excessive straining. Secondary omental infarction have specific aetiologies including inflammatory conditions and neoplasms that create adhesions between the omentum and pathological tissues.⁴ Omental strangulation can also be caused by entrapped inguinal hernias that are often discovered during reparative surgeries.

Traditionally, omental infarctions were diagnosed during surgery. However, new advancements in imaging techniques have allowed for the diagnosis to be determined outside of surgery such as in our case. CT scans are the imaging studies of choice. Greater omental pathologies can be divided into four categories caking(the displacement of omental adipose tissue by soft tissue), fat stranding, cystic masses and discrete nodules.⁸ The most common finding on imaging is fat stranding that is not proportional to the level of bowel wall thickening. Differential diagnoses for this particular finding include diverticulitis and appendicitis.⁹ Besides CT scans, ultrasound techniques may prove beneficial in diagnosis and can be used for the exclusion of cholelithiasis. The typical finding on ultrasound for an omental infarction will be an appearance of non-compressible and large echogenic mass in the omental fat.¹⁰

Today there are two main strategies in the management of omental infarction, conservative and laparoscopic excision. Classical laparotomy is no longer performed due to its invasiveness compared with the conservative or laparoscopic approach. There is currently no preference based on literature in the choice of management, thus it should be decided based on the individual as well as the imaging and clinical findings. Conservative management includes oral analgesic medications, anti-inflammatory medications and antibiotics. The advantage of early surgical intervention is the reduced incidence of necrosis, abscess formation and adhesion formation. Laparoscopic surgery can also decrease the patients' time in the hospital. A disadvantage of conservative management is that symptoms can persist for weeks with the mean time of resolution being 13.5 days.¹¹ However, there are the natural risks of laparoscopic surgery including complications with anaesthesia, intraoperative hazards and postoperative morbidity. In patients who are non-operative candidates due to comorbidities and conservative management remains a preferable option. In our case report, a conservative approach lead to symptom resolution.

Learning points.

• Omental infarction should be included in the differential diagnosis list of acute abdominal pain in order to prevent unnecessary surgical interventions.

• Traditionally, omental infarctions were diagnosed during surgery. New advancements in imaging techniques have allowed for the diagnosis and it is important to be aware of imaging findings consistent with the diagnosis.

• This disease appears to be a self-limited course, treated with conservative care including pain control and fluids.

• Unnecessary operations, consultations and treatments can be avoided in cases where omental infarction is diagnosed by imaging studies.