Torsion of the greater omentum is defined as a twist of the organ in its longitudinal axis around a narrow pedicle. It may be classified as primary or secondary.

In primary or idiopathic torsion, a redundant, mobile segment of omentum rotates around a proximal fixed point in the absence of any associated intra-abdominal pathology. This was first described by Eitel in 1899, but it remains a relatively rare condition, with fewer than 200 cases reported in the literature. Although the precise cause is unknown, both predisposing and precipitating factors in the pathogenesis of the condition can be identified.

Factors which predispose to torsion include anatomical abnormalities of the omentum itself, such as accessory omentum, bifid omentum, irregular accumulations of omental fat in the obese, and a narrowed omental pedicle. The normal anatomical arrangement of the omental vessels may also give rise to torsion. The omental veins are larger, longer, and more tortuous than the arteries and this redundancy allows venous kinking and obstruction, thereby providing a fixed point around which a self-perpetuating torsion may occur. The higher incidence of torsion on the right is related to the greater size and mobility of the right side of the omentum.

Factors that precipitate torsion are those which cause displacement of the omentum. These include blunt trauma to the abdomen, coughing and straining, heavy exertion, sudden change in body position, and hyperperistalsis from overeating.

Secondary torsion is more common than the primary type and is associated with pre-existing abdominal pathology. The omentum usually twists between two fixed points, with its distal edge attached directly or by adhesions to cysts, tumours, foci of intra-abdominal inflammation, postsurgical wounds or scarring, internal hernia, or external hernial sacs. The majority of cases occur in patients with inguinal herniae. The precipitating factors of primary torsion also initiate secondary torsion.

The omentum twists a variable number of times around a pivotal point, usually in a clockwise direction. The venous return is compromised and the distal omentum becomes congested and oedematous. The resultant haemorrhagic extravasation stimulates an aseptic peritonitis with a characteristic accumulation of serosanguinous fluid in the peritoneal cavity. As the torsion proceeds, arterial occlusion leads to acute haemorrhagic infarction and eventual necrosis of the omental segment. If the mass is not excised it becomes atrophic and fibrotic and, on rare occasions, the pedicle may even auto-amputate.

Omental torsion usually occurs in the fourth or fifth decades of life. Men are affected twice as often as women and the majority of patients are overweight. The signs and symptoms reflect the underlying localized peritonitis. As the affected segment is usually on the right, the sudden onset of pain, with rebound tenderness and guarding is also usually right-sided, and is often mistaken for acute appendicitis or even acute cholecystitis or twisted ovarian cysts. The clinical features are not usually sufficient to allow an accurate preoperative diagnosis. This is of little consequence, as the clinical findings warrant laparotomy even in the absence of definitive diagnosis. The finding of free serosanguinous fluid in association with a normal appendix, gallbladder, pelvic organs, and bowel should alert the surgeon to the possibility of omental torsion.

The condition only becomes clinically apparent once vascular thrombosis of the omental vessels has occurred and is irreversible even if the omentum is derotated. Treatment consists of resection of the affected portion of omentum. Any disease process associated with secondary torsion also requires correction. Although omental torsion is not life-threatening, segmental omentectomy reduces morbidity and removed inflammatory tissue which may later serve as a focus of intra-abdominal adhesions. Postoperative recovery is usually rapid and morbidity is minimal.

In childhood, omental cysts are usually caused by development abnormalities of lymphoid tissue, such as obstruction of lymphatic channels or by growth of congenitally misplaced lymphatic tissue. They are variously called chylous cysts, cystic hygromas, or cystic lymphangiomas, and are benign. They vary greatly in size, the smallest being only a few centimetres in diameter, and can be unilocular or multilocular. Histologically the cysts contain many foamy macrophages, giving the fluid a milky appearance, and each cyst has an endothelial lining similar to cystic hygroma of the neck.

Omental cysts of mesothelial origin occur almost exclusively in adult life, usually in women under the age of 50 years. Although they are benign, local recurrence often occurs after surgical excision. They appear as large, multicystic masses similar to cystic lymphangiomas, but histologically they are lined by flattened or cuboidal mesothelial cells and the cyst fluid is clear, containing mucopolysaccharides. Although the aetiology is unknown there is no association with asbestos exposure.

As with dermoid cysts elsewhere in the body, omental dermoid cysts are lined with squamous epithelium and may contain epithelial structures such as hair and teeth.

Omental pseudocysts are caused by fat necrosis or abdominal trauma with haematoma formation. They are lined with fibrous tissue and contain bloodstained fluid.

Many omental cysts are small and asymptomatic and may only be discovered incidentally at laparotomy or autopsy. Large cysts may present with diffuse abdominal distension or as a smooth, mobile, palpable mass in the lower midline. Characteristically they are non-tender unless complicated by torsion of the omentum or intestinal obstruction. Plain radiographs of the abdomen may demonstrate a soft tissue shadow and barium studies may show displacement of bowel. The differential diagnosis includes mesenteric, peritoneal, or retroperitoneal cysts and tumours, but the diagnosis is usually made at laparotomy. Treatment consists of surgical excision of the cyst.

The vast majority of omental neoplasms are metastatic carcinomas arising from ovary, gastrointestinal tract, or pancreas, and these are often associated with abdominal ascites. The rare diffuse malignant mesothelioma of the peritoneum which is associated with exposure to fibrous minerals such as asbestos also consistently involves the omentum.

Primary solid tumours of the omentum are exceptionally rare and may be benign or malignant. The majority are of smooth muscle origin and histologically may be of spindle-cell or epithelioid types. Malignant potential is difficult to predict from the histology but approximately one-third are frankly malignant. Before making a diagnosis of primary smooth muscle tumour of the omentum, leiomyosarcoma of the uterus or gastrointestinal tract giving rise to omental metastases must be carefully excluded. Other rare primary omental tumours include fibroma, fibrosarcoma, lipoma, and liposarcoma. Infantile myxoid hamartoma, found in infants under 1 year old, consists of multiple nodular lesions which show histological resemblance to myxoid liposarcoma; the clinical course is invariably benign.

Benign primary tumours of the omentum, when sufficiently large, present with a palpable abdominal mass or diffuse distension and require surgical excision. Malignant primary omental tumours are highly invasive and often present late with involvement of adjacent organs. Radical surgical excision of both the omentum and the involved organs may be required but often palliative surgery is the only treatment option.

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Morson BC, Dawson IMP, Day DW, Jass JR, Price AB, Williams GT. Morson and Dawson's Gastrointestinal pathology. 3rd edn. London: Blackwell, 1990.

Stout AP, Hendry J, Purdie FJ. Primary solid tumours of the great omentum. Cancer 1963; 16: 231–43.