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Cecum

The cecum is a blind-ending pouch that constitutes the first segment of the large intestine in humans, located in the right iliac fossa at the ileocecal junction where the terminal ileum of the small intestine empties into it via the ileocecal valve.^[1] Approximately 6 to 8 cm in length, it is a highly mobile, intraperitoneal structure without a mesentery, featuring a posteromedial attachment point for the vermiform appendix, which measures 6 to 10 cm and is often positioned retrocecally.^[1] Its primary role involves receiving undigested chyme from the small intestine and initiating the processes of water and electrolyte absorption, while serving as a reservoir for gut microbiota that perform fermentation of residual carbohydrates and fibers.^[2] Structurally, the cecum's wall consists of the same four layers as the rest of the gastrointestinal tract—mucosa, submucosa, muscularis, and serosa—with taeniae coli (longitudinal muscle bands), haustra (sacculations), and omental appendices contributing to its pouched appearance.^[1] Blood supply is provided by the ileocolic artery, a branch of the superior mesenteric artery, with venous drainage via the corresponding ileocolic vein into the superior mesenteric vein; lymphatic drainage follows the arterial path to the ileocolic nodes.^[1] Embryologically, it arises from the midgut during the fifth week of gestation as part of the primary intestinal loop, undergoing a 270-degree counterclockwise rotation by the tenth week to reach its final position.^[1] Functionally, the cecum facilitates the compaction of fecal matter by absorbing water and electrolytes, secreting bicarbonate, potassium, and chloride, and supporting microbial fermentation that produces short-chain fatty acids for energy and vitamins such as K and certain B vitamins (e.g., biotin), which are subsequently absorbed.^[2] Its microbial ecosystem also contributes to immune modulation by maintaining a balance of beneficial bacteria that protect against pathogens and support overall gut barrier integrity.^[2] Clinically, the cecum is significant in conditions like appendicitis, cecal volvulus, and as a surgical landmark in procedures such as right hemicolectomy for colonic pathologies, owing to its mobility and intraperitoneal positioning that can influence diagnostic imaging and operative approaches.^[1]

Anatomy

Gross anatomy

The cecum is a blind-ended, sac-like pouch that constitutes the proximal portion of the large intestine, positioned in the right iliac fossa of the abdomen at the junction between the terminal ileum and the ascending colon. It measures approximately 6 to 8 cm in length and 7.5 cm in diameter in adults, though these dimensions can vary slightly with body size and nutritional status. The terminal ileum enters the cecum posteromedially via the ileocecal valve, also known as the ileal papilla, which protrudes into the cecal lumen and functions to regulate flow while preventing significant reflux of contents. The appendix attaches to the posteromedial wall of the cecum, typically 2 cm inferior to the ileocecal junction, and is suspended by the mesoappendix, a fold of peritoneum continuous with the mesentery of the terminal ileum. The cecum is predominantly intraperitoneal, enveloped by peritoneum on its anterior, lateral, and inferior surfaces, which allows for some mobility, though its posterior aspect adheres more closely to the underlying structures via the parietal peritoneum. Anteriorly, it relates to the anterior abdominal wall, the greater omentum, and coils of the small intestine; inferiorly, it extends toward the pelvic brim. Posteriorly, it overlies the iliacus and psoas major muscles, the femoral nerve, genitofemoral nerve, and lateral femoral cutaneous nerve of the thigh. Laterally, it abuts the abdominal wall, while medially it adjoins the terminal ileum; in females, the right ovarian or iliac vessels and adnexa may lie adjacent to its lateral border. These relations position the cecum in close proximity to the appendix, facilitating shared vascular and supportive structures. Arterial supply to the cecum arises primarily from the ileocolic artery, a major branch of the superior mesenteric artery, which divides into superior and inferior cecal branches and also gives rise to the appendicular artery. Venous drainage parallels the arterial supply, converging into the ileocolic vein and ultimately the superior mesenteric vein, which joins the portal system. Lymphatic vessels from the cecum drain along the ileocolic artery to the ileocolic lymph nodes, then proceed to the superior mesenteric nodes and cisterna chyli. Innervation includes sympathetic fibers from the superior mesenteric plexus (via the lumbar splanchnic nerves) for vasomotor control, parasympathetic fibers from the anterior and posterior vagal trunks for secretory and motor functions, and visceral afferent fibers accompanying these pathways for sensory input. Variations in cecal morphology are common, with shapes ranging from the typical ampullary form to conical, fetal, or exaggerated types, and sizes differing across populations due to genetic factors. Positional anomalies, including a mobile cecum due to incomplete peritoneal fixation or subhepatic displacement, occur in up to 11-22% of individuals and can predispose to volvulus.

Microscopic anatomy

The wall of the cecum exhibits the standard four-layered structure typical of the gastrointestinal tract: mucosa, submucosa, muscularis externa, and serosa. The innermost mucosa comprises the epithelium, lamina propria, and muscularis mucosae; it is lined by a single layer of columnar epithelial cells resting on a basal lamina, with deep tubular glands known as crypts of Lieberkühn extending into the lamina propria. Unlike the small intestine, the cecal mucosa lacks villi, presenting a relatively flat surface with shorter and more widely spaced crypts that are lined by epithelial cells and contain a higher proportion of goblet cells compared to the ileum. The lamina propria is a loose connective tissue layer rich in blood vessels, lymphatics, and immune cells, while the thin muscularis mucosae consists of smooth muscle fibers oriented longitudinally and circularly.^[3]^[4]^[5] The submucosa underlies the mucosa and is composed of dense irregular connective tissue containing larger blood vessels, nerves, and lymphoid structures; in the cecum, it prominently features solitary lymphoid follicles that extend from the lamina propria. The muscularis externa includes an inner thick circular smooth muscle layer responsible for segmentation and an outer longitudinal layer that is partially condensed into three thickened bands called taeniae coli, visible microscopically as bundles of longitudinal fibers. The outermost serosa is a thin layer of connective tissue covered by mesothelium, providing peritoneal attachment except at the retroperitoneal ascending colon transition.^[3]^[4]^[6] The cecal epithelium consists of several specialized cell types integrated within the crypts and surface lining. Columnar enterocytes, the predominant cells, feature apical microvilli forming a brush border for structural support; goblet cells are interspersed abundantly, secreting mucin granules visible as clear vacuoles in histological sections; Paneth cells reside at the crypt bases with prominent secretory granules; and M cells, characterized by reduced microvilli and microfolds, overlie lymphoid follicles for antigen sampling. Aggregated lymphoid nodules, less prominent than Peyer's patches in the ileum, occur in the cecum's lamina propria and submucosa, contributing to gut-associated lymphoid tissue. Compared to the small intestine, the cecal mucosa shows a flatter architecture with absent villi and plicae circulares, reflecting adaptation to its proximal large bowel position, and contains fewer Paneth cells per crypt.^[4]^[7]^[6] In standard hematoxylin and eosin (H&E) staining, the cecal mucosa appears with basophilic crypt nuclei and eosinophilic apical cytoplasm in enterocytes, while periodic acid-Schiff (PAS) highlights magenta-staining mucin in goblet cells. Electron microscopy reveals ultrastructural details such as the glycocalyx coating microvilli on enterocytes (approximately 0.3-1 μm long), dense core granules in Paneth cells (0.5-1 μm diameter), and irregular apical pockets in M cells enveloping lymphocytes. The cecal submucosa shows collagen fibers (types I and III) in a basketweave pattern under transmission electron microscopy, with lymphoid follicles displaying high endothelial venules for immune cell trafficking. These features distinguish the cecum microscopically from distal colon segments, where crypts are longer and goblet cells more numerous.^[8]^[4]^[3]

Physiology

Digestive functions

The cecum serves as the initial reservoir for chyme delivered from the ileum through the ileocecal valve, where it begins the process of water and electrolyte reabsorption to concentrate the intestinal contents. Approximately 1.5 to 2 liters of ileal effluent enter the cecum daily, with the cecum and proximal colon absorbing up to 90% of this volume, primarily sodium, chloride, and water, through active transport mechanisms in the colonic epithelium.^[9] This absorption helps maintain fluid balance and prevents excessive water loss in feces.^[2] The ileocecal valve, a muscular sphincter at the junction of the ileum and cecum, regulates the unidirectional flow of chyme while preventing reflux of colonic contents into the small intestine. Its function is primarily governed by intraluminal pressure gradients, with higher pressure in the ileum promoting opening and higher colonic pressure facilitating closure; neural inputs from the enteric nervous system and hormonal signals, such as motilin which enhances ileal motility to aid passage, further modulate its activity.^[2] Gastrin may contribute to relaxation under certain conditions, supporting coordinated gastrointestinal transit.^[10] Resident bacteria in the cecum contribute to vitamin synthesis, producing vitamin K and certain B vitamins, including biotin and folate, which are absorbed by the host. These vitamins are generated through microbial metabolism of undigested carbohydrates and proteins, supplementing dietary intake.^[11] Haustral contractions, rhythmic segmental movements of the cecal and colonic walls, facilitate mixing of contents and slow propulsion, allowing extended contact time for absorption. The residence time in the cecum and colon typically ranges from 24 to 48 hours, promoting efficient processing.^[12] Additionally, the cecum absorbs short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate, produced by bacterial fermentation, which provide an energy source for colonocytes and influence systemic metabolism.^[13]

Microbiome interactions

The cecum functions as the initial chamber of the human large intestine where microbial fermentation of undigested carbohydrates predominantly occurs, enabling gut microbiota to convert dietary fibers into short-chain fatty acids (SCFAs) including acetate, propionate, and butyrate. These SCFAs are generated in a molar ratio of approximately 60:20:20 (acetate:propionate:butyrate) through anaerobic processes, serving as a key energy source that contributes roughly 10% to the host's daily caloric needs via absorption into the colonic epithelium.^[14]^[15] The cecal microbiome is primarily composed of bacteria from the phyla Firmicutes and Bacteroidetes, which account for over 90% of the total community and drive the fermentation of complex polysaccharides. In healthy adults, this ecosystem exhibits moderate alpha diversity, with Shannon index values typically ranging from 3 to 5, indicating a stable and resilient microbial structure that optimizes SCFA yield and metabolic efficiency.^[16]^[17] Interactions between the cecal microbiota and the host immune system occur through gut-associated lymphoid tissue in the mucosal layer, fostering immune tolerance to beneficial microbes while enhancing defenses against potential pathogens via cytokine signaling and antibody production. The cecal lumen maintains a mildly acidic pH of 5.5–6.5 and microaerobic to anaerobic conditions, creating an optimal niche for SCFA-producing anaerobes like butyrate-generating Firmicutes. Dietary factors, particularly high-fiber intake, promote increased microbial biomass and elevated SCFA output in the cecum, thereby strengthening these symbiotic dynamics.^[18]^[19]^[20]

Development

Embryonic origins

The cecum originates from the endoderm of the midgut during the fifth to sixth weeks of gestation, forming as a cecal diverticulum that arises as a swelling on the antimesenteric border of the caudal limb of the midgut loop.^[21] This diverticulum represents the primordium of both the cecum and the vermiform appendix, emerging during the period of midgut herniation into the umbilical cord.^[22] By the end of the sixth week, the diverticulum begins to elongate, establishing the foundational pouch-like structure of the cecum.^[21] As the midgut loop undergoes a 270-degree counterclockwise rotation around the superior mesenteric artery axis between weeks 6 and 10, the cecum is positioned in the right lower quadrant of the abdomen.^[23] This rotation, occurring in two phases—initially 90 degrees during herniation and an additional 180 degrees upon return to the abdominal cavity—ensures the cecum's final orientation relative to the ileum and ascending colon.^[21] Concurrently, around weeks 8 to 9, mesenchymal condensations contribute to the formation of the ileocecal valve at the junction of the ileum and cecum, creating a functional sphincter through epithelial-mesenchymal interactions.^[24] Vascular development of the cecum begins early, with the superior mesenteric artery serving as the primary supply from the somite stages onward, branching to perfuse the midgut derivatives including the cecal diverticulum.^[25] Genetic regulation involves Hox genes in hindgut patterning, alongside signaling pathways like Wnt and BMP that drive endodermal proliferation and mesenchymal-epithelial signaling for proper budding and differentiation.^[26] The vermiform appendix buds from the apex of the cecal diverticulum around week 7, initially as a uniform extension that later differentiates due to differential growth rates.

Postnatal development

Following birth, the human cecum experiences rapid postnatal growth, with the overall large intestine length increasing from approximately 60 cm at birth to about 120 cm by age 4-5 years, approaching adult dimensions of around 150 cm during adolescence.^[27]^[28] This expansion supports the developing digestive capacity, as the cecum transitions from a relatively small, mobile structure to a more defined pouch integral to fermentation processes. The embryonic positioning of the cecum, which often remains unfixed in early life, sets the stage for this mobility during initial growth phases.^[29] During adolescence, the cecum undergoes further elongation as part of overall colonic maturation, accompanied by the development of more prominent haustral folds that enhance segmentation and mixing of contents.^[27] Hormonal surges at puberty contribute to increased density of lymphoid tissue within gut-associated lymphoid structures, including those in the cecum, bolstering immune surveillance in response to evolving microbial challenges.^[30] In adulthood, the cecum maintains a stable size post-adolescence, but longitudinal studies indicate ongoing evolution of the cecal microbiome over the lifespan, with shifts toward greater diversity and stability influenced by diet and aging.^[31] Weaning introduces dietary and environmental influences that profoundly shape cecal function, as the shift from milk-based to solid foods alters the microbiome composition, promoting bacterial species capable of enhanced fermentation of complex carbohydrates.^[32] This maturation improves the cecum's capacity for short-chain fatty acid production, aiding energy harvest and mucosal integrity. In the elderly, reduced colonic motility due to loss of cholinergic neurons may lead to potential atrophy of cecal tissues, contributing to slower transit and altered microbial dynamics.^[33] A common postnatal variation is the mobile cecum, occurring in 10-20% of adults due to incomplete retroperitoneal fixation during early development, which can predispose to twisting or volvulus under certain conditions.^[34]^[35]^[36]

Clinical significance

Associated disorders

The cecum is susceptible to several pathological conditions, including inflammation, obstruction, and neoplastic changes. Appendicitis, primarily an inflammation of the vermiform appendix attached to the cecum, can extend to involve the cecal wall in complicated cases. Perforation occurs in 20-30% of appendicitis patients, often leading to cecal abscess formation or localized peritonitis with direct cecal involvement.^[37] Symptoms typically include migratory pain starting periumbilically and localizing to the right lower quadrant, exacerbated by peritoneal irritation.^[38] Cecal volvulus represents a mechanical obstruction due to twisting of the mobile cecum around its mesentery, compromising blood supply and causing ischemia. It accounts for approximately 1-3% of all cases of intestinal obstruction, with a notably higher incidence in pregnant individuals, where up to 10% of cecal volvulus presentations occur during gestation due to increased intra-abdominal pressure and ligamentous laxity.^[39]^[40] Inflammatory bowel disease, particularly Crohn's disease, frequently implicates the cecum as part of ileocolonic involvement, affecting around 40% of patients in this distribution. The disease manifests with discontinuous skip lesions in the cecal mucosa, leading to transmural inflammation and a propensity for fistula formation between the cecum and adjacent structures such as the small bowel or skin.^[41] Cecal diverticulitis arises from inflammation of diverticula in the cecal wall, which can progress to rupture and perforation, resulting in localized abscess or peritonitis. This condition is more prevalent in Asian populations, where right-sided colonic diverticula predominate, comprising up to 75% of diverticular cases compared to left-sided predominance in Western cohorts.^[42]^[43] Neoplastic disorders of the cecum include adenocarcinoma, which constitutes approximately 20% of all colorectal cancers and often presents at advanced stages due to its proximal location and nonspecific symptoms. Cecal carcinoid tumors, a subtype of neuroendocrine neoplasms, are rare, representing about 48% of colonic carcinoids with an overall incidence of 0.31 cases per 100,000 population annually; these tumors arise from enterochromaffin cells and may cause obstruction or carcinoid syndrome if metastatic.^[44]^[45] Ischemic colitis affecting the cecum results from hypoperfusion leading to mucosal ulceration and potential necrosis, predominantly in elderly patients with comorbidities such as atherosclerosis or hypotension. Although the left colon is more commonly involved, isolated cecal ischemia occurs in a minority of cases, often due to low-flow states and watershed vulnerability at the cecal base.^[46]^[47]

Diagnostic and therapeutic approaches

Diagnosis of cecal disorders primarily relies on imaging modalities to visualize structural abnormalities. Computed tomography (CT) scanning serves as the gold standard for detecting cecal volvulus, where the characteristic "whirl sign" indicates mesentery torsion around the ileocolic vessels, confirming the diagnosis with high specificity.^[48] For cecal diverticulitis, CT identifies key features such as colonic wall thickening exceeding 4 mm, pericolic fat stranding, and inflamed diverticula, enabling accurate staging and differentiation from other conditions.^[49] Ultrasound is particularly useful in evaluating suspected appendicitis involving the cecum, demonstrating a non-compressible appendix with a diameter greater than 6 mm as a diagnostic criterion with sensitivity approaching 90%.^[50] Endoscopic evaluation through colonoscopy allows direct visualization of the cecum for biopsy in cases of inflammatory bowel disease (IBD) or tumors, facilitating histopathological confirmation. Skilled operators achieve cecal intubation rates exceeding 95% during screening procedures, ensuring comprehensive assessment of the region.^[51] Non-invasive biomarkers complement imaging; fecal calprotectin levels above 50 μg/g indicate active cecal inflammation, such as in Crohn's disease, with high negative predictive value for ruling out IBD.^[52] Carcinoembryonic antigen (CEA) serves as a serum biomarker for monitoring cecal malignancy post-treatment, with elevations signaling potential recurrence in colorectal cancer patients.^[53] Therapeutic approaches for cecal pathologies emphasize targeted interventions based on the underlying condition. Laparoscopic appendectomy is the preferred surgical method for acute appendicitis, offering success rates over 95% and reduced morbidity compared to open procedures.^[54] For cecal cancer, right hemicolectomy provides curative intent, with 5-year survival rates exceeding 90% for stage I and approximately 80-90% for stage II disease following resection.^[55] Pharmacotherapy plays a key role in managing inflammatory conditions; uncomplicated cecal diverticulitis is typically managed conservatively with bowel rest, hydration, and analgesia, without routine antibiotics; antibiotics such as ciprofloxacin combined with metronidazole are reserved for complicated cases or immunocompromised patients.^[56] In Crohn's disease affecting the cecum, biologic agents like infliximab are employed to induce and maintain remission by targeting tumor necrosis factor-alpha, often in combination with immunomodulators.^[57] Recent advances in diagnostic imaging include artificial intelligence (AI)-assisted CT interpretation for gastrointestinal disorders, which enhances specificity by 15-20% in detecting abnormalities like cecal inflammation or masses through automated feature recognition and reduced false positives.^[58] These AI tools integrate deep learning algorithms to analyze volumetric data, improving overall diagnostic efficiency in clinical settings.^[59]

History

Etymology

The term "cecum" derives from the Latin caecum, meaning "blind" or "hidden," specifically as part of the phrase intestinum caecum, translating to "blind gut" or "blind intestine," which describes the structure's pouch-like form with a closed end that does not directly communicate with other intestinal segments.^[60]^[61] This nomenclature reflects the anatomical feature's blind-ended nature at the junction of the small and large intestines.^[62] The Latin term is a direct translation of the Ancient Greek typhlon enteron (τυφλὸν ἔντερον), where typhlon means "blind" and enteron refers to "intestine," a phrase appearing in early medical writings, including those attributed to Hippocrates in the 5th century BCE.^[63]^[64] These Hippocratic texts used typhlon to denote the cecum's obscured or non-penetrating pouch, influencing subsequent Greco-Roman anatomical descriptions.^[64] The word entered English in the early 18th century, with its first recorded use around 1721 in anatomical contexts to refer to the colonic pouch.^[60]^[61] Historical synonyms in English included "blind pouch" or "blind gut," emphasizing the same structural characteristic, while the British spelling variant "caecum" persists in some modern texts, retaining the original Latin form.^[65] The term has influenced related anatomical nomenclature, such as "ileocecal," which combines "ileum" (from Latin ileum, denoting the terminal small intestine) and "cecum" to describe the junction and valve between them. Standardization occurred in 1895 with the Basel Nomina Anatomica (BNA), which officially adopted intestinum caecum as the Latin term for the structure, establishing a uniform international nomenclature for anatomy.^[66] This convention helped resolve variations in earlier texts and remains foundational in modern terminologia anatomica.^[66]

Key anatomical discoveries

The earliest documented recognition of intestinal structures resembling the cecum dates to ancient Greek biological works, such as those of Aristotle in the 4th century BCE, who identified the cecum among sections of the intestines, with further descriptions of blind-ending pouches at the junction of the small and large intestines appearing in early medical texts.^[67]^[68] During the Renaissance, significant progress in visualizing the cecum occurred with Andreas Vesalius's 1543 publication of De humani corporis fabrica libri septem, which provided the first accurate illustrations of the cecum as a dilated pouch and its associated vermiform appendix as a small blind diverticulum, correcting prior misconceptions from Galen and advancing precise anatomical depiction through direct human cadaver dissection.^[69] In the early 20th century, British surgeon Sir William Arbuthnot Lane advanced understanding of cecal mobility, proposing in the 1900s that an unfixed or "mobile" cecum contributed to "chronic intestinal stasis," a condition he linked to delayed fecal transit and systemic toxicity, influencing surgical interventions like colectomy to fix the cecum.^[70] A pivotal surgical milestone came in 1886 when American pathologist Reginald H. Fitz published his seminal paper "Perforative Inflammation of the Vermiform Appendix," identifying appendiceal perforation as a primary cause of cecal-related peritonitis and advocating early appendectomy, which spurred the procedure's adoption despite earlier isolated attempts.^[71] The introduction of barium enema radiography in the 1910s revolutionized cecal imaging, enabling radiographic visualization of structural anomalies such as cecal volvulus through contrast filling of the colon, with early applications confirming the "bird's beak" sign indicative of twisting and obstruction.^[72] In the mid-20th century, fiberoptic colonoscopy, developed in the 1960s, allowed direct endoscopic visualization of the cecal interior, facilitating detailed assessment of its mucosal lining and orifice during routine and diagnostic procedures.^[73] By the 1980s, computed tomography (CT) scans correlated these findings with external anatomy, confirming cecal positional variations and diverticular involvement in conditions like ascending colon diverticulitis through cross-sectional imaging.^[74]

Other animals

In herbivores

In herbivorous animals, particularly hindgut fermenters such as horses and rabbits, the cecum is markedly enlarged to serve as a primary site for the microbial breakdown of cellulose and other indigestible plant fibers that cannot be digested by mammalian enzymes. This adaptation allows for the retention of fibrous digesta, promoting prolonged exposure to symbiotic bacteria and protozoa that hydrolyze complex polysaccharides. In horses, the cecum accounts for a significant portion of the gastrointestinal tract volume, averaging 33 liters in a 500 kg adult, while the combined hindgut (cecum and colon) comprises approximately two-thirds of the total digestive capacity.^[75]^[76] Similarly, in rabbits, the cecum represents up to 40-60% of the gastrointestinal volume, enabling efficient processing of high-fiber diets typical of lagomorphs.^[77] Microbial fermentation within the herbivore cecum converts plant fiber into short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, which are readily absorbed across the cecal wall to provide essential energy. In equines, these volatile fatty acids generated from cecal and colonic fermentation supply 60-70% of the animal's total maintenance energy requirements, underscoring the cecum's role in sustaining herbivores on low-nutrient, fibrous forage.^[78] Rabbits exhibit analogous fermentation dynamics, where cecal microbes produce SCFAs that contribute substantially to daily caloric needs, often estimated at 10-20% from volatile fatty acids alone, complementing foregut digestion.^[79] This process not only extracts calories from otherwise indigestible material but also supports overall metabolic homeostasis in hindgut-dependent species. Structural adaptations in the cecum and associated regions enhance fermentation efficiency and minimize risks during digestion. In horses, the large colon's spiral loop and robust mesenteric attachments stabilize the hindgut, preventing displacement or volvulus that could disrupt cecal function amid the animal's athletic movements.^[80] In lagomorphs like rabbits, coprophagy facilitates nutrient recycling; soft cecal pellets (cecotrophs), rich in microbial proteins and vitamins, are reingested directly from the anus, allowing a second pass through the small intestine for enhanced absorption of B vitamins and amino acids produced during fermentation.^[81] Variations across herbivorous species illustrate the cecum's tailored role in digestion. In rabbits, the gastrointestinal tract contents can comprise up to 20% of total body weight during peak fermentation cycles, with the cecum accounting for 40-60% of the gastrointestinal volume, enabling selective retention of fine particles for microbial action while expelling coarser fiber.^[82] In elephants, another hindgut fermenter, the cecum measures up to 1.5 meters in length and, despite occupying a minor proportion of the vast gastrointestinal tract (total intestine ~20-33m), serves as the main fermentation chamber, with the extensive colon also contributing to fiber degradation in this megaherbivore.^[83]^[84] Evolutionary adaptations link cecal enlargement to dietary pressures from fibrous vegetation. Among perissodactyls (odd-toed ungulates) like horses and rhinos, a prominently expanded cecum evolved to accommodate prolonged microbial processing of coarse, low-quality forage, reflecting selective advantages in open grasslands.^[85] In contrast, many artiodactyls (even-toed ungulates), such as ruminants, developed smaller ceca due to foregut fermentation in the rumen, which preempts the need for hindgut specialization despite similar reliance on fibrous diets; this divergence highlights convergent evolutionary solutions to herbivory across ungulate orders.^[86]

In non-herbivores

In carnivores such as cats and dogs, the cecum is notably reduced in size, typically comprising a small portion of the total gastrointestinal tract length, often described as a short, comma-shaped structure in cats and a relatively long but spiraled sac in dogs that nonetheless represents minimal overall capacity relative to the small intestine.^[87]^[88] This diminished size correlates with their protein-rich diets, where the cecum plays a limited role in microbial fermentation, primarily serving for water absorption and electrolyte reabsorption rather than significant breakdown of fibrous materials.^[89]^[90] In omnivorous species like pigs and humans, the cecum exhibits a moderate size that supports opportunistic digestion of dietary fiber through microbial activity, with the pig cecum being relatively large and distinct compared to the human counterpart.^[91] The cecal microbiome in these animals adapts to dietary variations, shifting in composition—for instance, higher fiber intake promotes increased abundance of fermentative bacteria such as those producing short-chain fatty acids, enhancing nutrient salvage from mixed diets.^[92] Unique adaptations appear in certain non-herbivores; for example, the cecum is vestigial in phocid seals, present only as a rudimentary structure at the ileocolic junction with negligible functional contribution.^[93] In piscivorous cetaceans like dolphins, the cecum is absent, with water and electrolyte absorption concentrated in the colon to efficiently process high-protein, low-fiber marine prey.^[94]^[95] In captive carnivores fed diets high in carbohydrates—deviating from their natural protein-dominant intake—cecal microbiome dysbiosis can occur, characterized by overgrowth of certain bacterial groups like Firmicutes, potentially leading to altered cecal function and digestive imbalances.^[96]^[97] Evolutionarily, strict carnivores exhibit a smaller cecum alongside shorter overall gut transit times, typically ranging from 10 to 24 hours in cats and dogs, facilitating rapid processing of easily digestible animal matter in contrast to the extended retention in fiber-dependent species.^[98]^[99]^[100]

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In this review, we will discuss various aspects of the mesenchymal–epithelial interactions observed during digestive epithelium development and differentiationMissing: ileocecal valve
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Parsons [1908] noted that the U-shaped cecum is almost always present in the later months of fetal life and in the early postnatal period. He believed that the ...
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[7] A mesentery torsion around the ileocolic vessels, as seen on a CT scan, is described as a "whirl sign" and is considered pathognomonic for diagnosing a ...Cecal Volvulus · Epidemiology · PathophysiologyMissing: ultrasound thickening diameter
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in human anatomy, "the pouch at the beginning of the colon," 1721, from Latin intestinum caecum "blind gut," from neuter of caecus "blind, hidden," from Proto- ...
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