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Abdominal cavity

The abdominal cavity is the largest serous cavity in the human body, located within the trunk between the diaphragm superiorly and the pelvic brim inferiorly, and it houses most of the gastrointestinal tract along with essential organs such as the liver, spleen, pancreas, kidneys, and adrenal glands.^[1]^[2] This cavity is lined by the peritoneum, a thin serous membrane composed of mesothelial cells supported by fibrous tissue, which forms two layers: the parietal peritoneum adhering to the cavity walls and the visceral peritoneum covering the intraperitoneal organs, creating a potential space filled with 50 to 100 milliliters of serous fluid that minimizes friction during organ movement.^[3] The peritoneum also includes specialized folds such as the mesentery, omentum, and ligaments, which anchor organs, transmit blood vessels, nerves, and lymphatics, and divide the cavity into compartments.^[3] The abdominal cavity's boundaries include the thoracic diaphragm superiorly, the pelvic inlet inferiorly, the anterolateral abdominal wall anteriorly (comprising nine layers from skin through subcutaneous tissue, muscles, and fascia to peritoneum), and the posterior wall formed by the lumbar vertebrae, psoas and quadratus lumborum muscles, and retroperitoneal structures.^[2] Its contents are categorized as intraperitoneal (mobile organs like the stomach, jejunum, ileum, liver, gallbladder, spleen, and transverse colon) and retroperitoneal (fixed structures including the kidneys, adrenal glands, duodenum from the second part onward, pancreas head and body, ascending and descending colon, aorta, and inferior vena cava).^[2] Embryologically, these organs derive from the foregut (esophagus to proximal duodenum and derivatives like liver and pancreas), midgut (distal duodenum to proximal transverse colon), and hindgut (distal transverse colon to upper anal canal), influencing their blood supply from corresponding arteries such as the celiac trunk, superior mesenteric artery, and inferior mesenteric artery.^[2] The abdominal cavity plays a critical role in protecting and supporting visceral organs involved in digestion, excretion, circulation, and endocrine functions, with its muscular walls—primarily the external oblique, internal oblique, transversus abdominis, and rectus abdominis—facilitating respiration, posture, and intra-abdominal pressure regulation.^[2] Innervation arises from thoracoabdominal nerves (T7–T11), subcostal nerve (T12), and lumbar nerves (L1), corresponding to dermatomes that map sensory distribution from the xiphoid process (T6) to the inguinal ligament (L1).^[2]

Location and Boundaries

Anatomical Boundaries

The abdominal cavity is a large, irregularly shaped space within the trunk, bounded by distinct anatomical structures that define its extent and separate it from adjacent body regions. Superiorly, it is limited by the dome-shaped thoracic diaphragm, which forms a muscular partition separating the abdominal cavity from the thoracic cavity above; the diaphragm attaches peripherally to the xiphoid process, costal margins of ribs 7 through 12, and the vertebral column at the level of the 12th thoracic vertebra, with central tendinous attachments to structures such as the liver.^[4]^[5] This superior boundary plays a critical role in respiration, as the diaphragm contracts and descends during inspiration to increase thoracic volume while displacing abdominal contents inferiorly, and relaxes during expiration to elevate the floor of the thoracic cavity.^[4] Inferiorly, the abdominal cavity extends to the pelvic brim, also known as the pelvic inlet, which marks the transitional boundary with the pelvic cavity below; this brim is formed by the sacral promontory posteriorly, the arcuate line of the ilium laterally, and the pectineal line anteriorly, effectively dividing the abdominopelvic cavity into its abdominal and pelvic components.^[2]^[5] Anteriorly, the cavity is enclosed by the anterolateral abdominal wall, comprising multiple layers including the skin, superficial fascia, muscles such as the rectus abdominis in the midline and the external oblique, internal oblique, and transversus abdominis laterally, along with the transversalis fascia and peritoneum; these structures provide protection and support while allowing flexibility for movement.^[6]^[7] Posteriorly, the abdominal cavity is bounded by the vertebral column from the 12th thoracic to the 5th lumbar vertebra, flanked by the psoas major muscles (which originate from the lumbar vertebrae and iliac fossa) and the quadratus lumborum muscles (extending from the iliac crest to the 12th rib and lumbar transverse processes); these elements form the retroperitoneal posterior wall, contributing to structural stability and housing major vessels and nerves.^[6]^[5] Laterally, the boundaries are defined by the flanks (lumbar regions between the anterior and posterior axillary lines) and the lower ribs (7th to 12th), which integrate with the oblique and transversus abdominis muscles to complete the cylindrical enclosure of the cavity.^[6]^[5] Overall, these boundaries establish the abdominal cavity's relations to the thoracic cavity superiorly via the dynamic diaphragm and to the pelvic cavity inferiorly via the static pelvic brim, facilitating coordinated visceral function across the trunk.^[2]^[5]

Subdivisions

The peritoneal cavity within the abdominal cavity is primarily subdivided into the greater sac and the lesser sac, also known as the omental bursa.^[8]^[9] The greater sac constitutes the main, expansive portion of the peritoneal cavity, encompassing most intraperitoneal structures and extending from the diaphragm superiorly to the pelvic inlet inferiorly.^[8]^[10] In contrast, the lesser sac is a smaller, irregular space located posterior to the stomach and lesser omentum, anterior to the pancreas and duodenum, and includes a superior (hepatic) recess, a splenic recess (separated from the superior recess by the gastropancreatic fold), and an inferior (omental) recess.^[9]^[11] These two sacs communicate through the epiploic foramen, or foramen of Winslow, a small vertical opening situated posterior to the hepatoduodenal ligament (free edge of the lesser omentum), anterior to the inferior vena cava, and superior to the first part of the duodenum.^[12]^[13] This foramen serves as the sole natural passageway between the sacs, allowing for the transmission of peritoneal fluid and potential pathologic spread.^[14] Within the greater sac, further partitioning occurs along the horizontal plane via the root of the transverse mesocolon, delineating the supramesocolic (or supracolic) compartment superiorly and the inframesocolic compartment inferiorly.^[14]^[15] The supramesocolic compartment lies above the transverse mesocolon and includes spaces adjacent to the diaphragm, such as the right and left subphrenic spaces, which are potential areas bounded by the coronary and triangular ligaments of the liver and the phrenicosplenic ligament on the left.^[16]^[17] These subphrenic spaces facilitate gravitational flow of peritoneal fluid toward the right side in the supine position, contributing to sites of abscess or effusion accumulation.^[16]^[18] The inframesocolic compartment, below the mesocolon, is further divided into left and right spaces by the root of the mesentery proper, with the small intestine predominantly in the central region.^[14]^[19] Lateral to the ascending and descending colon, the paracolic gutters represent additional potential spaces that enhance fluid dynamics within these compartments.^[15]^[20] The right paracolic gutter, deeper and more continuous, extends superiorly to connect the inframesocolic space with the right subphrenic space and inferiorly to the pelvis, serving as a primary pathway for ascending or descending peritoneal fluid, infections, or hemorrhage.^[18]^[21] The left paracolic gutter is shallower, separated from the subphrenic space by the phrenicocolic ligament, and communicates less freely with the upper abdomen, directing fluid primarily toward the left inframesocolic space and pelvis.^[15]^[20] These subdivisions are structurally defined by peritoneal ligaments and folds, which act as supportive and partitioning elements.^[22] The transverse mesocolon, a broad fold attaching the transverse colon to the posterior abdominal wall, forms the key horizontal divider between supra- and inframesocolic regions.^[17]^[23] The greater omentum, a double-layered fold descending from the greater curvature of the stomach, contributes to the inferior recess of the lesser sac, while the lesser omentum connects the stomach and duodenum to the liver, framing the epiploic foramen via its hepatoduodenal portion.^[11]^[13] Additional ligaments, such as the coronary and triangular ligaments anchoring the liver, delineate subphrenic boundaries, and the phrenicocolic ligament limits left paracolic gutter continuity, collectively creating these compartmentalized spaces to compartmentalize fluid movement and organ support.^[16]^[22]

Intraperitoneal Organs

Intraperitoneal organs are those enveloped by the visceral peritoneum and suspended within the peritoneal cavity by mesenteries or omenta, allowing mobility relative to the posterior abdominal wall.^[2] These structures include major components of the digestive system, such as the stomach, liver, spleen, gallbladder, jejunum, ileum, transverse colon, sigmoid colon, cecum, and appendix.^[2] The stomach occupies the upper left portion of the abdominal cavity, primarily in the epigastric and left hypochondriac regions.^[24] It features two curvatures: the convex greater curvature along the superior aspect and the concave lesser curvature along the inferior aspect, both contributing to its J-shaped contour.^[24] At its distal end, the pyloric sphincter forms a thickened ring of smooth muscle that regulates the passage of chyme into the duodenum.^[24] The liver, the largest solid organ in the body weighing approximately 1200-1500 grams in adults, is situated predominantly in the right upper quadrant beneath the diaphragm.^[2] It is divided into four lobes: the larger right lobe, the left lobe, and the smaller caudate and quadrate lobes, separated by fissures and ligaments.^[25] The liver is anchored by the coronary ligament, which encircles its superior surface, and the triangular ligaments, including left and right components that attach it to the diaphragm.^[25] The spleen is located in the left upper quadrant, posterior to the stomach and lateral to the left kidney, within the splenorenal recess.^[26] Anatomically, it serves as a site for blood filtration through its trabecular structure and white pulp, though its primary position facilitates interactions with circulating blood elements.^[26] The gallbladder lies in a fossa on the inferior surface of the right lobe of the liver, in the right upper quadrant.^[27] It consists of three main parts: the rounded fundus projecting beyond the liver's inferior border, the elongated body that stores bile, and the tapered neck leading to the cystic duct.^[27] The jejunum and ileum form the mid and distal segments of the small intestine, respectively, suspended by the mesentery proper within the central abdominal cavity.^[2] Together, they measure approximately 6-7 meters in length, with the jejunum being thicker-walled and the ileum narrower.^[28] Both feature valvulae conniventes, permanent mucosal folds that increase surface area for absorption, more prominent and closely spaced in the jejunum than in the ileum.^[29] The transverse colon and sigmoid colon are intraperitoneal segments of the large intestine, characterized by haustra—sac-like dilations formed by contractions of the taeniae coli.^[30] The transverse colon spans horizontally across the abdomen from the right to left colic flexures, suspended by the transverse mesocolon, while the sigmoid colon forms an S-shaped loop in the left lower quadrant, attached by the sigmoid mesocolon.^[30] The cecum is a blind pouch forming the first part of the large intestine, located in the right lower quadrant of the abdomen.^[30] It is intraperitoneal and receives the ileum at the ileocecal valve, with the appendix arising from its posteromedial surface.^[30] The appendix is a worm-like tubular structure attached to the cecum, measuring about 9 cm in length, and is fully intraperitoneal, allowing mobility within the peritoneal cavity.^[31]

Retroperitoneal Structures

The retroperitoneal space contains several key organs and structures that are fixed to the posterior abdominal wall by connective tissue, lacking the mesentery that allows mobility to intraperitoneal organs.^[32] These include the kidneys, adrenal glands, portions of the duodenum and pancreas, segments of the colon, major vessels, ureters, and muscles such as the psoas major.^[33] The kidneys are paired, bean-shaped organs located retroperitoneally at the level of the T12 to L3 vertebrae, with the right kidney slightly lower than the left due to the liver's position.^[34] Each kidney is enclosed by renal fascia (Gerota's fascia), a connective tissue layer that anchors it to surrounding structures and separates it from adjacent retroperitoneal contents.^[35] At the medial hilum, the renal artery enters, the renal vein exits, and the ureter emerges, facilitating blood flow and urine drainage.^[34] The adrenal (suprarenal) glands are pyramid-shaped endocrine organs situated retroperitoneally atop each kidney, embedded in perirenal fat and enclosed by the renal fascia.^[36] Anatomically, each gland consists of an outer cortex divided into three zones—glomerulosa, fasciculata, and reticularis—and an inner medulla, though these are structurally integrated without distinct peritoneal coverings.^[36] The duodenum, the initial segment of the small intestine, has its second (descending), third (horizontal), and fourth (ascending) parts positioned retroperitoneally, fixed to the posterior wall after the first part becomes intraperitoneal.^[37] The descending part lies anterior to the right kidney and head of the pancreas, receiving the common bile and main pancreatic ducts at its posteromedial wall.^[38] The horizontal part extends leftward anterior to the abdominal aorta and inferior vena cava, crossed anteriorly by the superior mesenteric vessels.^[37] The ascending part runs superiorly along the left side of the vertebral column, related posteriorly to the left psoas major and aorta.^[37] The ascending colon extends retroperitoneally from the cecum along the right flank to the hepatic flexure, fixed by parietal peritoneum to the posterior abdominal wall.^[32] Similarly, the descending colon runs retroperitoneally down the left flank from the splenic flexure to the sigmoid, also adhered to the posterior wall, providing stability compared to the mobile transverse colon.^[32] The head, uncinate process, and body of the pancreas are retroperitoneal, with the body crossing the midline anterior to the first and second lumbar vertebrae and the tail extending toward the splenic hilum and being intraperitoneal.^[39] The body relates superiorly to the splenic artery and posteriorly to the splenic vein and superior mesenteric vessels, while the tail lies anterior to the left kidney and adjacent to the spleen via the splenorenal ligament.^[39] The abdominal aorta descends retroperitoneally in the midline posterior to the peritoneum, beginning at the aortic hiatus (T12) and bifurcating at L4 into common iliac arteries.^[40] It gives rise to major paired branches, including the renal arteries originating at the L1-L2 level, which supply the kidneys.^[40] The inferior vena cava (IVC) parallels the aorta to its right, formed by the union of common iliac veins at L5 and ascending to the diaphragm at T8, receiving the renal veins at approximately L2.^[41] The ureters are paired muscular tubes that course retroperitoneally from the renal pelves downward along the psoas major muscle, crossing the common iliac arteries at the pelvic brim before entering the bladder.^[42] Their abdominal descent positions them posterior to the peritoneum, with the gonadal vessels crossing anteriorly midway.^[42] The psoas major muscle forms a key component of the posterior abdominal wall, originating from the lumbar vertebrae and transverse processes, and descending retroperitoneally along the lateral aspect of the vertebral column to insert on the lesser trochanter of the femur.^[43] It provides structural support in the retroperitoneal space, with the ureters and major vessels related medially.^[43]

Peritoneal Anatomy

Peritoneum

The peritoneum is a serous membrane that lines the abdominal cavity and covers the intraperitoneal organs, consisting of a single layer of mesothelial cells supported by underlying fibrous connective tissue derived from mesoderm.^[3] It is divided into two principal layers: the parietal peritoneum, which adheres directly to the inner surfaces of the abdominal and pelvic walls, and the visceral peritoneum, which envelops the surfaces of abdominal organs such as the liver and intestines.^[3] The parietal peritoneum is innervated by somatic nerves from spinal segments T10 to L1, conferring sensitivity to pain, temperature, and touch in a localized manner.^[3] In contrast, the visceral peritoneum receives autonomic innervation primarily from the vagus nerve (parasympathetic) and sympathetic fibers, rendering it insensitive to pain but capable of detecting stretch, ischemia, or chemical irritation through diffuse, poorly localized sensations.^[3] Between these layers lies the peritoneal cavity, a potential space that normally contains approximately 50 to 100 mL of serous fluid secreted by the mesothelial cells to provide lubrication and facilitate smooth organ movement during respiration and digestion.^[3] The peritoneum's reflections and folds extend from the parietal layer to the visceral layer, forming supportive ligaments such as the hepatoduodenal ligament, which bounds the anterior aspect of the epiploic foramen, and the gastrohepatic ligament, which connects the stomach to the liver as part of the lesser omentum.^[3] These reflections divide the peritoneal cavity into the greater sac, the principal compartment accessed upon incision through the anterior abdominal wall, and the lesser sac (also known as the omental bursa), a smaller recess that communicates with the greater sac via the epiploic foramen.^[3] The peritoneum serves multiple functions, including mechanical support for intraperitoneal organs by anchoring them via ligaments and folds, lubrication through its serous fluid to minimize friction, and immune surveillance facilitated by resident macrophages that phagocytose pathogens and debris within the cavity.^[3]

Mesenteries and Omenta

Mesenteries and omenta are double-layered folds of peritoneum that connect abdominal organs to the posterior abdominal wall or to each other, providing structural support and pathways for vessels and nerves.^[3] These structures originate from the primitive dorsal and ventral mesenteries during embryonic development and play essential roles in organ positioning within the peritoneal cavity.^[44] The mesentery proper, also known as the small bowel mesentery or mesojejunum, is a broad, fan-shaped fold that suspends the jejunum and ileum from the posterior abdominal wall.^[3] Its root, approximately 15 cm long, extends obliquely from the duodenojejunal junction on the left side of L2 vertebra to the ileocecal junction in the right iliac fossa, crossing anterior to the aorta, inferior vena cava, and right ureter.^[45] This mesentery contains the superior mesenteric artery and vein, along with associated lymphatics and nerves, facilitating nutrient absorption and organ mobility.^[3] The transverse mesocolon is a horizontal peritoneal fold that attaches the transverse colon to the anterior surface of the pancreas and the posterior abdominal wall at the level of the second lumbar vertebra.^[44] It fuses with the posterior layer of the greater omentum and provides a conduit for the middle colic vessels, nerves, and lymphatics supplying the transverse colon.^[3] This attachment allows limited mobility of the transverse colon while maintaining its position across the abdomen.^[46] The sigmoid mesocolon is an inverted V-shaped peritoneal fold that anchors the sigmoid colon to the pelvic wall, with its apex located anterior to the left ureter at the level of the sacral promontory.^[46] The two limbs of the V extend laterally to the iliac fossae, enclosing the sigmoid and superior rectal vessels, as well as lymphatics.^[3] This configuration permits the sigmoid colon's flexibility during defecation and contains fatty tissue that supports its variable length.^[47] The greater omentum, often described as an apron-like structure, arises from the greater curvature of the stomach and descends anterior to the small intestine before folding back to fuse with the transverse colon.^[44] Composed of four layers of peritoneum with abundant adipose tissue, it extends inferiorly to the level of the umbilicus or pelvis and serves as a major site for fat storage.^[48] Additionally, its rich vascular and lymphatic network, including milky spots—specialized immune aggregates—enables it to adhere to sites of inflammation or infection, thereby limiting the spread of peritoneal infections.^[49] The lesser omentum connects the lesser curvature of the stomach and the proximal duodenum to the liver, forming two distinct ligaments: the hepatogastric ligament along the lesser curvature and the hepatoduodenal ligament at the porta hepatis.^[3] The hepatoduodenal ligament forms the anterior boundary of the omental (epiploic) foramen and encloses the portal triad, consisting of the proper hepatic artery, portal vein, and common bile duct.^[44] This structure also conveys gastric vessels and lymphatics to the liver.^[47] Collectively, mesenteries and omenta function as conduits for blood vessels, lymphatics, and nerves to the abdominal viscera, while their adipose content supports fat storage and energy homeostasis.^[3] They also contribute to compartmentalization by stabilizing organ positions, reducing friction during movement, and aiding in the isolation of pathological processes within the peritoneal cavity.^[44]

Vascular and Neural Supply

Blood Supply

The blood supply to the abdominal cavity is primarily derived from branches of the abdominal aorta, which provide arterial oxygenation and nutrient delivery to the viscera and peritoneal structures. The arterial system is organized embryologically along the foregut, midgut, and hindgut derivatives, with the celiac trunk serving as the main conduit for the foregut. The celiac trunk arises from the anterior abdominal aorta at approximately the level of the T12 vertebra and bifurcates into the left gastric artery, which supplies the cardia and lesser curvature of the stomach; the splenic artery, which courses along the superior pancreas to supply the spleen, pancreas, and greater curvature of the stomach; and the common hepatic artery, which gives rise to the proper hepatic artery for the liver and the gastroduodenal artery for the duodenum and pancreas.^[50] These branches ensure robust perfusion to foregut organs such as the esophagus, stomach, duodenum, liver, spleen, and pancreas.^[51] The midgut receives its arterial supply from the superior mesenteric artery (SMA), which originates from the anterior abdominal aorta at the L1 vertebral level and provides branches to the jejunum, ileum, cecum, appendix, ascending colon, and proximal two-thirds of the transverse colon.^[52] Key branches include the inferior pancreaticoduodenal artery (anastomosing with the gastroduodenal for duodenal supply), jejunal and ileal arteries forming arcades, and the ileocolic, right colic, and middle colic arteries for the right colon.^[53] The hindgut is supplied by the inferior mesenteric artery (IMA), arising at the L3 level, which delivers blood to the distal third of the transverse colon, descending colon, sigmoid colon, and superior rectum via its left colic, sigmoid, and superior rectal branches.^[51] This segmental organization reflects the developmental vascular patterns and supports the metabolic demands of gastrointestinal absorption and motility.^[52] In addition to the unpaired visceral branches, the abdominal aorta gives rise to paired visceral and parietal branches that supply retroperitoneal structures and the posterior abdominal wall. The paired visceral branches include the inferior phrenic arteries (arising near T12, supplying the diaphragm), middle suprarenal arteries (from the aorta at L1, supplying the adrenal glands), renal arteries (originating at L1-L2, providing blood to the kidneys), and gonadal arteries (arising at L2, supplying the gonads). The parietal branches consist of four pairs of lumbar arteries (from L1-L4, supplying the posterior abdominal wall muscles and skin) and smaller vessels like the median sacral artery near the bifurcation. These branches ensure oxygenation to non-gastrointestinal abdominal organs and structural support.^[40]^[51] Venous drainage of the abdominal cavity follows a dual pattern: the portal venous system collects nutrient-rich blood from the gastrointestinal tract and accessories for processing in the liver, while systemic veins return deoxygenated blood directly to the heart. The portal vein forms posterior to the pancreatic neck from the confluence of the superior mesenteric vein (SMV) and splenic vein, measuring approximately 8 cm in length and draining the midgut and foregut derivatives, including tributaries from the inferior mesenteric vein (via the splenic vein), gastric veins, and cystic vein.^[54] The SMV, positioned lateral to the SMA, drains the small intestine, right colon, and portions of the pancreas and stomach, while the splenic vein collects from the spleen, pancreas, and stomach fundus.^[55] This portal circulation bypasses systemic oxygenation to allow hepatic first-pass metabolism of absorbed nutrients and toxins before entering the inferior vena cava (IVC) via hepatic veins.^[56] Systemic venous return includes direct tributaries to the IVC, such as the renal veins from the kidneys and lumbar veins from the posterior abdominal wall, ensuring efficient clearance of metabolic waste.^[56] Lymphatic drainage from the abdominal cavity facilitates immune surveillance and fluid balance, converging into a central pathway that empties into the venous system. Lymph from the peritoneal cavity and viscera flows through regional nodes—celiac nodes for foregut structures, superior mesenteric nodes for midgut, and inferior mesenteric nodes for hindgut—before entering the cisterna chyli, a dilated sac located at the L1-L2 level between the aorta and right crus of the diaphragm.^[57] The cisterna chyli receives lumbar and intestinal lymph trunks, rich in chyle from the intestines, and channels it superiorly through the thoracic duct, which ascends along the spine to drain into the left subclavian vein at the jugulo-subclavian junction.^[58] This system processes up to 2-4 liters of lymph daily, absorbing fats as chylomicrons and transporting immune cells.^[57] Portosystemic anastomoses provide collateral pathways between the portal and systemic circulations, becoming clinically significant in portal hypertension where increased pressure leads to variceal dilation. Common sites include esophageal anastomoses between left gastric (portal) and azygos (systemic) veins, which can form varices prone to rupture and hemorrhage; and rectal anastomoses between superior (portal) and middle/inferior (systemic) rectal veins, resulting in rectal varices.^[59] Additional shunts occur at the paraumbilical veins (recanalizing the umbilical vein to epigastric veins) and retroperitoneal collaterals.^[60] These anastomoses, while protective in normal physiology, contribute to complications like esophageal variceal bleeding in up to 30% of cirrhotic patients, necessitating interventions such as banding or shunting procedures.^[59]

Innervation

The innervation of the abdominal cavity encompasses autonomic, enteric, and somatic components that regulate visceral functions, gastrointestinal motility, and sensory perception of the abdominal wall and organs. The autonomic nervous system provides sympathetic and parasympathetic inputs to the viscera, while the enteric nervous system handles intrinsic control of the gut, and somatic nerves supply the abdominal musculature.^[61] Sympathetic innervation originates from preganglionic fibers in the thoracic spinal cord (T5-L2), traveling via the greater (T5-T9), lesser (T10-T11), and least (T12) thoracic splanchnic nerves, which synapse in the celiac, superior mesenteric, and inferior mesenteric ganglia or plexuses. These postganglionic fibers distribute to abdominal organs, mediating vasoconstriction, inhibition of motility and secretion, and transmission of visceral pain signals that can refer to somatic dermatomes. For instance, sympathetic fibers from the celiac plexus innervate foregut derivatives like the stomach and liver, while those from the superior mesenteric plexus supply midgut structures such as the small intestine; additionally, the renal plexus, derived from celiac and lumbar splanchnic nerves, innervates the kidneys, and direct splanchnic fibers supply the adrenal glands.^[62]^[63] Parasympathetic innervation to the abdominal cavity arises primarily from the vagus nerve (cranial nerve X), which forms anterior and posterior trunks that innervate foregut and midgut organs up to the distal transverse colon, promoting peristalsis, glandular secretion, and vasodilation. The hindgut, including the distal colon and rectum, receives parasympathetic input from pelvic splanchnic nerves (S2-S4), which synapse in intramural ganglia and enhance motility and defecation reflexes. These fibers lack the extensive pre- and postganglionic distinction seen in sympathetics, as most synapses occur within the organ walls; parasympathetic supply to the kidneys is limited, with primary regulation being sympathetic.^[61]^[62] The enteric nervous system, an intrinsic network embedded in the gastrointestinal tract wall, autonomously coordinates digestion and absorption through myenteric (Auerbach's) plexuses between the longitudinal and circular muscle layers, which primarily control motility, and submucosal (Meissner's) plexuses in the submucosa, which regulate secretion, blood flow, and mucosal activity. Comprising millions of neurons, it integrates extrinsic sympathetic and parasympathetic inputs but functions semi-independently, often referred to as the "second brain" for its reflexive capabilities.^[64] Somatic innervation of the abdominal wall derives from ventral rami of spinal nerves, with the lower intercostal nerves (T7-T11) supplying the upper and middle regions, including the rectus abdominis, external oblique, internal oblique, and transversus abdominis muscles, as well as overlying skin. The subcostal nerve (T12) innervates the lower lateral wall, while the iliohypogastric (L1) and ilioinguinal (L1) nerves provide sensory and motor supply to the lower anterior wall, mons pubis, and proximal thigh, contributing to proprioception and cutaneous sensation. These nerves pierce the abdominal muscles to reach the skin, forming dermatomes that map pain localization.^[65]^[63] Visceral pain pathways in the abdominal cavity involve afferent fibers traveling with sympathetic nerves to the spinal cord (T5-L2), where they synapse in the dorsal horn and project to higher centers, often resulting in poorly localized, cramping pain due to convergence with somatic inputs. Referred pain occurs when visceral afferents activate the same spinal segments as somatic nerves, such as appendiceal inflammation referring pain to the umbilicus via T10 dermatomes, initially presenting as periumbilical discomfort before localizing to the right lower quadrant upon parietal involvement.^[31]^[66]

Clinical Aspects

Ascites

Ascites refers to the pathological accumulation of fluid in the peritoneal cavity, defined as more than 25 mL of serous fluid that leads to abdominal distension.^[67]^[68] This condition most commonly arises as a complication of liver disease but can stem from various systemic disorders.^[69] The primary causes of ascites include portal hypertension, often due to liver cirrhosis or portal vein thrombosis, which accounts for approximately 80% of cases.^[68] Hypoalbuminemia, resulting from conditions such as nephrotic syndrome or malnutrition, contributes by reducing plasma oncotic pressure.^[68] Malignancy, particularly peritoneal carcinomatosis from ovarian, gastric, or pancreatic cancers, leads to about 10% of cases through direct invasion or lymphatic obstruction.^[68] Infectious etiologies, such as tuberculous peritonitis, are less common but significant in endemic regions, causing exudative ascites via peritoneal inflammation.^[68] Pathophysiologically, ascites formation involves an imbalance in Starling forces across the peritoneal membrane, where increased hydrostatic pressure from portal hypertension exceeds the counteracting oncotic pressure, favoring fluid transudation into the peritoneal space.^[70] In cirrhosis, splanchnic vasodilation and sodium retention further exacerbate this disequilibrium, leading to renal hypo-perfusion and activation of the renin-angiotensin-aldosterone system.^[68] For non-portal hypertensive causes, such as malignancy or infection, local factors like lymphatic blockage or exudation predominate.^[68] Clinically, patients present with progressive increase in abdominal girth, unexplained weight gain, and discomfort from distension.^[68] Dyspnea may occur due to diaphragmatic elevation reducing lung expansion, particularly in severe cases.^[71] On physical examination, shifting dullness is a key sign, detected by percussion revealing a change in dullness location when the patient shifts position, indicating free fluid.^[72] Diagnosis begins with clinical suspicion, confirmed by imaging such as ultrasound or computed tomography (CT) to visualize fluid accumulation.^[68] Diagnostic paracentesis is essential, with analysis of ascitic fluid using the serum-ascites albumin gradient (SAAG); a SAAG greater than 1.1 g/dL indicates portal hypertension-related ascites, while lower values suggest other causes like malignancy or infection.^[73] Fluid cell count, culture, and cytology further differentiate etiologies.^[73] Treatment focuses on addressing the underlying cause, alongside symptomatic management with sodium restriction (typically 2 g/day) and diuretics such as spironolactone (initially 100 mg daily) combined with furosemide (40 mg daily) in a 100:40 mg ratio to mobilize fluid effectively in up to 90% of cases.^[74] Large-volume paracentesis (>5 L) provides rapid relief for tense ascites, with albumin infusion (6-8 g/L removed) to prevent circulatory dysfunction.^[75] For refractory ascites unresponsive to medical therapy, transjugular intrahepatic portosystemic shunt (TIPS) placement reduces portal pressure and controls fluid buildup in select patients with preserved liver function; emerging options as of 2025 include the alfapump system, an implantable device for automated ascites removal, showing efficacy in clinical trials for recurrent cases.^[76]^[77]

Peritonitis

Peritonitis is an inflammation of the peritoneum, the serous membrane lining the abdominal cavity and covering the abdominal organs, typically resulting from infection or chemical irritation. It is classified into primary and secondary types. Primary peritonitis, also known as spontaneous bacterial peritonitis, occurs without an identifiable intra-abdominal source and is often associated with conditions like cirrhosis that lead to ascites, allowing bacterial translocation into the peritoneal fluid. Secondary peritonitis arises from a breach in the gastrointestinal tract or other organs, such as perforation due to appendicitis or diverticulitis, leading to contamination of the peritoneal cavity.^[78]^[79]^[78] Common causes include bacterial infections, with Escherichia coli and Bacteroides fragilis being frequent pathogens in secondary cases due to their prevalence in gut flora. Chemical peritonitis can result from the leakage of irritants like gastric acid from peptic ulcer perforation or bile from biliary tract rupture, provoking a sterile inflammatory response. Fungal peritonitis, less common, typically affects immunocompromised individuals and may involve species like Candida albicans, often in the context of peritoneal dialysis or systemic immunosuppression.^[79]^[80]^[81]^[82] In pathophysiology, irritants trigger peritoneal irritation, eliciting an exudative inflammatory response characterized by neutrophil influx and fluid accumulation. This leads to fibrin deposition, which can wall off the infection but may also promote abscess formation if unresolved; the greater omentum aids in localizing the process by adhering to inflamed sites and containing bacteria. Progression can result in systemic effects like sepsis if the inflammatory cascade overwhelms host defenses.^[83]^[84]^[85]^[86] Symptoms manifest as severe abdominal pain, often diffuse and worsening with movement, accompanied by board-like abdominal rigidity due to peritoneal irritation. Physical examination reveals rebound tenderness, where pain intensifies upon sudden release of pressure, along with fever, tachycardia, and signs of systemic inflammation such as nausea and vomiting. In advanced cases, patients may exhibit lethargy or altered mental status from peritonitis-induced sepsis.^[78]^[87]^[88] Diagnosis involves laboratory tests showing elevated white blood cell count indicative of infection, often with a left shift toward neutrophils. Imaging, such as upright abdominal X-rays, detects free intraperitoneal air signaling perforation, while ultrasound or CT scans identify fluid collections or abscesses. Paracentesis of peritoneal fluid for culture and analysis confirms the etiology; if diagnosis remains unclear, exploratory laparotomy may be necessary for direct visualization and source identification.^[89]^[89]^[89] Treatment prioritizes source control and antimicrobial therapy, beginning with broad-spectrum intravenous antibiotics targeting common gram-negative (e.g., E. coli) and anaerobic (e.g., Bacteroides) organisms, adjusted based on culture results. Surgical intervention, such as laparotomy, is essential for secondary peritonitis to repair perforations and drain abscesses. Supportive measures include intravenous fluids for hemodynamic stability, nasogastric tube decompression to reduce bowel distension, and pain management; in primary cases linked to cirrhosis, additional paracentesis may be performed.^[89]^[79]^[89]

Trauma and Surgical Considerations

The abdominal cavity is vulnerable to both blunt and penetrating trauma, each presenting distinct mechanisms and injury patterns. Blunt trauma typically results from high-energy impacts, such as motor vehicle accidents involving seatbelt injuries, leading to solid organ lacerations like those of the spleen or liver due to deceleration forces or compression against the spine.^[90] Penetrating trauma, conversely, is often caused by gunshot wounds or stab injuries, which directly violate the peritoneal cavity and frequently damage hollow viscera such as the small bowel or colon.^[91] Common injuries in abdominal trauma include splenic rupture, which is the most frequent solid organ injury in blunt mechanisms, often graded by the American Association for the Surgery of Trauma (AAST) scale to assess severity.^[92] Liver lacerations represent another prevalent blunt injury, while bowel perforation is more typical in penetrating cases, potentially leading to contamination if undetected.^[90] Initial assessment relies on the Focused Assessment with Sonography for Trauma (FAST) ultrasound to rapidly detect free intraperitoneal fluid suggestive of hemorrhage, followed by computed tomography (CT) scanning in hemodynamically stable patients for detailed injury characterization and grading.^[93] Management strategies prioritize hemodynamic stability, with non-operative approaches favored for low-grade injuries in stable patients, involving close observation, serial imaging, and angioembolization if needed, achieving success rates exceeding 90% for splenic and hepatic injuries.^[94] Operative intervention, indicated for hemodynamic instability or peritonitis, typically involves exploratory laparotomy via a midline incision to provide rapid access for hemorrhage control and visceral inspection.^[95] Laparoscopic techniques have emerged as an adjunct for diagnostic evaluation and select repairs in stable penetrating trauma, reducing incision size and recovery time while identifying diaphragmatic or hollow viscus injuries.^[96] In severe cases, damage control surgery is employed to address the lethal triad of hypothermia, acidosis, and coagulopathy, involving abbreviated procedures such as perihepatic packing for hemorrhage control, bowel resection without anastomosis, and temporary abdominal closure to mitigate risks like evisceration.^[97] A key complication is abdominal compartment syndrome, arising from edema and resuscitation fluids post-damage control, which elevates intra-abdominal pressure and impairs organ perfusion, necessitating decompressive laparotomy if pressures exceed 20 mmHg with physiologic compromise.^[98] Historically, abdominal trauma management centered on mandatory exploratory laparotomy since the early 20th century to exclude occult injuries, but post-1980s advancements in imaging and selective non-operative paradigms, alongside the adoption of laparoscopy in the 1990s, shifted toward minimally invasive and observation-based strategies, decreasing unnecessary operations by up to 50% in stable patients.^[96]

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