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Lesser omentum

The lesser omentum is a double-layered fold of peritoneum that extends from the lesser curvature of the stomach and the proximal portion of the duodenum to the porta hepatis of the liver, serving as a key structure in the anterior wall of the lesser sac.^[1]^[2] It is divided into two main components: the hepatogastric ligament, which connects the lesser curvature of the stomach to the visceral surface of the liver, and the hepatoduodenal ligament, which links the proximal duodenum (duodenal bulb) to the liver and forms the anterior boundary of the epiploic (omental) foramen.^[1]^[3] The hepatoduodenal ligament has a free edge that contains the critical portal triad, consisting of the hepatic portal vein, proper hepatic artery, and common bile duct, while the hepatogastric ligament encloses branches of the left gastric artery and vein, as well as vagal nerve fibers and lymph nodes.^[2]^[1] Functionally, the lesser omentum provides a conduit for these essential vascular, biliary, and neural structures to reach the liver and foregut organs, while also helping to compartmentalize the peritoneal cavity by separating the greater sac from the omental bursa (lesser sac).^[1]^[2] Embryologically, it derives from the ventral mesentery of the foregut, specifically the septum transversum, and persists as the stomach rotates during development.^[4]^[1] Clinically, the lesser omentum is significant in surgical procedures involving the upper abdomen, such as gastric resections or bariatric surgeries, where access to the portal triad or lymph node dissection may be required, and its structures can be landmarks for identifying the epiploic foramen to avoid iatrogenic injury.^[2]^[4]

Anatomy

Structure and attachments

The lesser omentum is a double-layered peritoneal fold that extends from the porta hepatis of the liver to the lesser curvature of the stomach and the proximal portion of the duodenum.^[3] It forms a thin, transparent sheet of peritoneum that is continuous with the visceral peritoneum overlying the stomach, duodenum, and liver, providing a supportive mesentery in the upper abdomen.^[5] featuring a free right margin that defines key anatomical boundaries.^[1] The superior border attaches to the liver along the porta hepatis and the fissure for the ligamentum venosum, anchoring the structure posteriorly to the hepatic visceral surface.^[3] The inferior border adheres to the lesser curvature of the stomach and the first part of the duodenum.^[6] In terms of positional relationships, the lesser omentum forms the anterior boundary of the omental (epiploic) foramen, through which the greater and lesser peritoneal sacs communicate.^[5] It lies anterior to the caudate lobe of the liver and the portal structures within the hepatoduodenal region, contributing to the compartmentalization of the upper abdominal cavity without enclosing specific contents in this configuration.^[7]

Divisions

The lesser omentum is divided into two primary ligamentous components: the hepatogastric ligament and the hepatoduodenal ligament.^[8] These divisions arise from the peritoneal structure extending between the liver and the proximal gastrointestinal tract, with the hepatogastric portion being the larger and generally thinner part, while the hepatoduodenal is smaller but thicker.^[8] The hepatogastric ligament extends from the fissure for the ligamentum venosum and the porta hepatis of the liver to the lesser curvature of the stomach.^[9] It represents the medial and leftward portion of the lesser omentum, consisting of two layers of peritoneum enclosing variable amounts of connective tissue and fat, and it contains branches of the gastric vessels.^[9]^[2] The hepatoduodenal ligament forms the thicker, free-margin portion of the lesser omentum, connecting the porta hepatis of the liver to the proximal portion of the duodenum, approximately the first 2 cm beyond the pylorus.^[7] This rightward and lateral division serves as a key surgical landmark due to its distinct structure and position, forming the anterior boundary of the omental (epiploic) foramen.^[7]^[8] The boundary between these divisions occurs at the level of the porta hepatis, where the hepatogastric ligament transitions laterally to the hepatoduodenal ligament as it extends toward the duodenum.^[7] In terms of nomenclature, the hepatogastric ligament is sometimes referred to synonymously as the gastrohepatic ligament.^[9]

Vascular structures

The lesser omentum serves as a conduit for several key arterial and venous structures, primarily divided between its hepatogastric and hepatoduodenal components. In the hepatogastric ligament, which extends along the lesser curvature of the stomach from the porta hepatis to the esophagus, the right gastric artery and its accompanying vein course distally within the peritoneal layers to supply the pyloric region and anastomose with the left gastric vessels.^[7] The left gastric artery and vein, originating from the celiac trunk, traverse the proximal portion of the hepatogastric ligament near the esophageal hiatus, providing vascular supply to the cardia and fundus of the stomach while draining into the portal venous system.^[7] The hepatoduodenal ligament, forming the thickened free margin of the lesser omentum between the porta hepatis and the superior duodenum, contains the hepatic artery proper and the portal vein as central components of the portal triad. The hepatic artery proper, a continuation of the common hepatic artery, ascends through this ligament to deliver oxygenated blood to the liver, while the portal vein conveys nutrient-rich blood from the gastrointestinal tract and spleen, constituting approximately 75% of the liver's blood supply.^[7] These vessels are enveloped in a sheath of connective tissue within the ligament, facilitating their protected passage to the hepatic hilum.^[10] Anatomical variants of these vessels may occur, potentially altering surgical approaches. For instance, an accessory or replaced right hepatic artery arising from the superior mesenteric artery can pass through the hepatoduodenal ligament posterior to the portal vein, with a prevalence of up to 20% in cadaveric studies, necessitating preoperative imaging to avoid inadvertent injury.^[7] Similarly, an aberrant left hepatic artery may originate from the left gastric artery within the hepatogastric ligament, observed in about 23% of cases and measuring 3-5 mm in diameter.^[10] In portal hypertension, the venous structures of the lesser omentum, particularly the left gastric (coronary) vein in the hepatogastric ligament, undergo dilation to form varices, serving as portosystemic collaterals that can lead to esophageal or gastric variceal bleeding if untreated.^[11] Aberrant right gastric veins may also enlarge, potentially causing pseudolesions on imaging such as in segment IV of the liver.^[10]

Biliary, nervous, and lymphatic components

The lesser omentum, particularly its hepatoduodenal ligament component, serves as a conduit for key biliary structures, including the common bile duct, which descends within the free margin of the hepatoduodenal ligament, positioned anterior to the portal vein. This arrangement facilitates the transport of bile from the liver toward the duodenum, with the duct formed by the union of the common hepatic duct and the cystic duct. The cystic duct, originating from the neck of the gallbladder, joins the common hepatic duct just distal to the porta hepatis, also traversing the hepatoduodenal ligament to contribute to the formation of the common bile duct near the gallbladder neck.^[7]^[12]^[13] Innervation of the lesser omentum is provided by the hepatic plexus, a network of autonomic nerves that accompanies the portal triad structures within the ligament and extends into the liver's Glisson's capsule. This plexus comprises sympathetic fibers derived from the celiac plexus and parasympathetic fibers from the anterior and posterior vagus nerves, enabling regulation of biliary and hepatic functions through efferent pathways, while also carrying visceral afferent sensory fibers for pain transmission.^[14]^[15] Lymphatic vessels within the lesser omentum drain interstitial fluid from the stomach, liver, and duodenum, coalescing into collecting vessels that pass through the hepatoduodenal ligament toward nodes situated at the hepatic hilum. These nodes, positioned along the hepatic artery and portal vein, receive lymph from the portal tracts and biliary system before efferent vessels proceed to the celiac lymph nodes and ultimately the cisterna chyli.^[16]^[17]

Embryology

Developmental origin

The lesser omentum originates from the ventral mesogastrium, an early embryonic fold of mesoderm that forms between the developing foregut (including the stomach and duodenum) and the liver primordium within the septum transversum.^[18]^[19] This structure arises as a double layer of visceral peritoneum suspending the primitive gut tube and anchoring it to the anterior abdominal wall during the initial stages of gastrointestinal development.^[20] Formation of the lesser omentum occurs primarily between weeks 4 and 5 of gestation, coinciding with the outgrowth of the hepatic diverticulum into the ventral mesentery.^[18]^[21] As the liver bud expands, it divides the ventral mesogastrium into distinct components: the hepatogastric ligament develops from the attachment to the lesser curvature of the stomach, while the hepatoduodenal ligament forms from the connection to the proximal duodenum.^[20]^[19] The positioning of the lesser omentum is influenced by the rotation of the midgut and stomach, which begins around week 5 and establishes its final orientation at the porta hepatis.^[21] During this 90-degree clockwise rotation of the stomach, the ventral mesogastrium is reshaped and pulled toward the liver, defining the omentum's attachments.^[21] A notable persistent structure within the lesser omentum is the ligamentum venosum, which represents the obliterated remnant of the fetal ductus venosus and lies along the free margin of the lesser omentum in the fissure for the ligamentum venosum.^[18]^[20] Congenital variations of the lesser omentum are uncommon and primarily involve structural defects or anomalous positioning of its components, often arising during embryonic development from the ventral mesogastrium. One such rare anomaly is a congenital fissure or defect in the hepatogastric ligament associated with intestinal malrotation, which can result in internal herniation of the small intestine. These defects are typically incidental findings during imaging or surgery and have a low incidence, with case reports highlighting their association with congenital weaknesses in the peritoneal folds.^[22] Anomalous positioning within the portal triad, particularly in the hepatoduodenal ligament, represents another key variation, such as a replaced right hepatic artery originating from the superior mesenteric artery and typically coursing posteriorly along the common bile duct. This variant alters the standard arrangement where the hepatic artery typically lies to the right of the bile duct, potentially complicating hepatobiliary procedures if unrecognized. Vascular anomalies of this type occur in approximately 10-20% of the population, with the replaced right hepatic artery specifically noted in about 10-13% of cases, and are usually detected via preoperative CT angiography or intraoperative exploration.^[23] Cystic biliary malformations, including choledochal cysts, are congenital lesions that can involve the extrahepatic bile ducts within the hepatoduodenal ligament. These are rare, with an overall incidence of 1 in 100,000 to 150,000 individuals, and can manifest as fusiform or saccular expansions. Diagnosis often relies on ultrasound, MRCP, or CT imaging, which reveal the cystic structures and their relation to the portal triad components.^[24]

Function

Structural support

The lesser omentum functions primarily as an anchoring structure, connecting the lesser curvature of the stomach and the proximal portion of the duodenum to the liver, which stabilizes these organs relative to one another and maintains their positions within the upper abdomen.^[25] This attachment, mediated by the hepatogastric and hepatoduodenal ligaments, prevents excessive displacement of the stomach and duodenum during peristaltic movements and respiratory excursions, ensuring coordinated gastrointestinal function.^[1] By tethering these viscera, the lesser omentum contributes to the overall mechanical integrity of the foregut, allowing limited mobility while resisting undue torsion or migration.^[26] In addition to its anchoring role, the lesser omentum delineates the anterior boundary of the lesser sac (omental bursa), a key peritoneal recess posterior to the stomach, thereby aiding in the compartmentalization of the peritoneal cavity and facilitating the separation of abdominal spaces.^[25] This boundary formation supports the structural organization of the upper abdomen, where the lesser omentum acts as a partition that integrates with surrounding peritoneal folds to contain and direct intra-abdominal pressures.^[7] Unlike the greater omentum, which exhibits greater mobility and extends broadly to envelop lower abdominal viscera for protective coverage, the lesser omentum remains more fixed in position, emphasizing targeted stability in the hepatogastric region rather than diffuse peritoneal support.^[27]

Conduit for vessels and ducts

The lesser omentum serves as a critical conduit for the portal triad, which comprises the hepatic artery, portal vein, and common bile duct, all bundled within its hepatoduodenal ligament to ensure coordinated delivery of oxygenated blood, nutrient-rich venous blood, and bile to and from the liver. This arrangement optimizes hepatobiliary flow by minimizing the distance and protecting these structures as they traverse from the duodenum and stomach toward the porta hepatis.^[7]^[28] In addition to vascular elements, the lesser omentum facilitates lymphatic drainage and neural transit from foregut-derived organs such as the stomach, duodenum, and liver to the systemic circulation. Lymphatic vessels and nodes, including hepatic and gastric varieties, course through its layers, enabling the collection and transport of interstitial fluid and immune cells from these regions. Branches of the vagus nerve also travel within the hepatogastric portion, providing parasympathetic innervation that integrates with broader autonomic pathways.^[1]^[29] This conduit role underpins key physiological processes, including nutrient absorption via the portal vein, which channels postprandial blood from the gastrointestinal tract to the liver for metabolic processing, and bile excretion through the common bile duct, which delivers hepatic secretions to the duodenum for lipid emulsification. The vagal fibers support gastric motility and secretion, ensuring efficient foregut function. Collectively, these pathways promote seamless hepatogastrointestinal integration.^[7]^[1] The lesser omentum harbors mesenchymal stem cells (MSCs) that contribute to local tissue repair, though their density and regenerative capacity are less pronounced compared to those in the adipose-rich greater omentum. These MSCs, capable of differentiating into multiple lineages and modulating inflammation, aid in wound healing and vascular support within the upper abdominal compartment.^[30]

Clinical significance

Surgical relevance

The lesser omentum serves as a critical landmark in hepatobiliary surgery, particularly through its hepatoduodenal ligament component, which is clamped during the Pringle maneuver to control hepatic bleeding by temporarily occluding inflow to the liver via the portal triad.^[7] This technique, involving compression of the hepatoduodenal ligament—the free edge of the lesser omentum containing the portal vein, hepatic artery, and common bile duct—reduces blood loss during liver resections or trauma management, with studies showing effective inflow occlusion in intermittent applications.^[31] Access to the portal triad is facilitated by opening the lesser omentum during procedures such as cholecystectomy, where the hepatoduodenal ligament is dissected to expose and isolate the cystic structures for safe gallbladder removal, minimizing risks of bile duct injury. Similarly, in liver transplantation, the lesser omentum is mobilized and divided to allow precise anastomosis of the portal vein, hepatic artery, and bile duct, addressing variations in vascular anatomy that occur in up to 20% of cases and ensuring graft viability.^[32] In laparoscopic surgery, the thin, avascular nature of the lesser omentum enables straightforward visualization and dissection, particularly in bariatric procedures like gastric bypass, where it is incised along the lesser curvature to mobilize the stomach for pouch creation without compromising accessory vessels.^[33] This approach reduces operative time and postoperative complications compared to open techniques. Historically, the lesser omentum was described in Gray's Anatomy (1918 edition) as a duplicature of peritoneum extending from the stomach's lesser curvature to the liver's porta hepatis, emphasizing its role in enclosing key vessels.^[34] Modern preoperative planning benefits from ultrasound and MRI, which delineate the lesser omentum's contents and attachments to guide surgical access and avoid iatrogenic injury.^[35]

Pathological conditions

The lesser omentum is rarely affected by torsion or infarction, conditions that arise due to the mobility of its free margins, leading to vascular compromise and presenting as acute abdominal pain mimicking other surgical emergencies.^[36] Torsion typically occurs in the gastrohepatic or hepatoduodenal portions, with infarction resulting from thrombosis or twisting that occludes blood supply, often requiring prompt surgical intervention to prevent necrosis.^[37] These vascular pathologies are exceedingly uncommon, with fewer than 20 reported cases of primary lesser omental torsion in the literature.^[36] Metastatic involvement of the lesser omentum is a frequent complication in advanced malignancies, particularly gastric and peritoneal carcinomatosis, where tumor cells spread directly through its peritoneal surfaces or lymphatics.^[38] In pancreatic cancer, especially of the head, the lymph nodes within the hepatoduodenal ligament—a key component of the lesser omentum—are commonly affected, with metastatic rates exceeding 50% in regional nodal stations such as those along the common hepatic artery.^[39] This involvement contributes to disease staging and prognosis, often manifesting as nodular masses or lymphadenopathy detectable on imaging.^[40] Cysts and abscesses in the lesser omentum can arise from parasitic infections, such as hydatid cysts caused by Echinococcus granulosus, which may form isolated lesions within its folds, leading to mass effect or rupture.^[41] Inflammatory abscesses, often secondary to adjacent infections like perforated peptic ulcers or amebic liver disease, localize in the lesser omental bursa and present with fever, pain, and sepsis.^[42] Biliary-related pathologies, including those associated with choledochal cysts in the hepatoduodenal ligament, can result in cystic dilatations or inflammatory collections that distort the lesser omentum's structure.^[43] Diagnostic approaches for lesser omental pathologies primarily rely on cross-sectional imaging, with computed tomography (CT) serving as the modality of choice for identifying torsion (e.g., whirl sign), masses, or fluid collections due to its high sensitivity for omental diseases.^[44] Magnetic resonance imaging (MRI) provides additional soft-tissue characterization, particularly for cystic or neoplastic lesions, while biopsy is often performed laparoscopically to confirm malignancy or infection in ambiguous cases.^[44]

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