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Constipation

Constipation is a common digestive disorder characterized by infrequent bowel movements or difficulty passing stool, typically defined as fewer than three bowel movements per week, with stools that are often hard, dry, lumpy, or painful to pass.^[1]^[2] It is not a disease itself but a symptom that can arise from various underlying factors and affects people worldwide, with global prevalence estimates for functional constipation ranging from 10% to 16%; in the United States, it impacts approximately 16% of adults overall and up to 33% of those aged 60 and older.^[3]^[1] Key symptoms of constipation extend beyond frequency and include straining during defecation, a sensation of incomplete evacuation, bloating or abdominal discomfort, and in severe cases, the need for manual assistance to pass stool or a feeling of rectal blockage.^[2]^[4] When symptoms persist for three months or longer, it is classified as chronic constipation, which can significantly affect quality of life.^[2] The primary causes of constipation involve slowed movement of stool through the colon, often due to lifestyle factors such as a low-fiber diet, inadequate fluid intake, lack of physical activity, or ignoring the urge to defecate.^[2]^[4] Other contributors include certain medications (e.g., opioids, antacids containing aluminum), medical conditions like irritable bowel syndrome, diabetes, or pregnancy, and structural issues such as blockages or pelvic floor dysfunction.^[2]^[4] Risk factors for developing constipation include older age, female sex, sedentary lifestyle, and mental health conditions like depression or eating disorders.^[2] If left unmanaged, it can lead to complications such as hemorrhoids, anal fissures, fecal impaction, or rectal prolapse.^[2] Treatment typically begins with lifestyle modifications, including increasing dietary fiber intake to 25–30 grams per day, drinking more fluids, and engaging in regular exercise, which can alleviate symptoms in most cases.^[5] Over-the-counter laxatives or prescription medications may be used for short-term relief, but persistent cases require medical evaluation to rule out underlying disorders.^[5] Prevention strategies mirror these approaches, emphasizing a balanced diet, hydration, and routine physical activity to maintain regular bowel function.^[2]

Overview

Definition

Constipation is a common gastrointestinal disorder characterized by infrequent or difficult bowel movements, typically defined as fewer than three defecations per week, accompanied by symptoms such as hard or lumpy stools, excessive straining, a sensation of incomplete evacuation, or the need for manual assistance to facilitate defecation.^[6] This condition reflects a dysfunction in bowel motility or evacuation rather than a disease itself, often leading to discomfort but varying widely in severity among individuals.^[7] Normal bowel habits exhibit significant variation, with healthy adults typically experiencing anywhere from three bowel movements per day to three per week, without distress or associated symptoms.^[8] Constipation deviates from this range when it causes dissatisfaction or impairment, influenced by factors like diet, age, and cultural norms that may perceive lower frequencies as acceptable.^[9] The Rome IV criteria provide a symptom-based framework for diagnosing functional constipation, requiring at least two of the key symptoms (such as reduced frequency or straining) to be present for at least three months, with symptom onset at least six months prior, emphasizing patient-reported experiences over objective measures.^[7] Constipation can be classified as functional (also known as idiopathic or primary), arising from intrinsic abnormalities in colonic or anorectal function without an identifiable external cause, or secondary, resulting from underlying medical conditions, medications, or other extrinsic factors.^[6] It may also be distinguished as acute, which is short-term and often self-resolving or treatable upon addressing triggers, versus chronic, persisting for more than three months and potentially requiring ongoing management.^[10]

Signs and Symptoms

Constipation is characterized by a range of primary symptoms that reflect difficulties in bowel movements. Patients commonly experience hard, dry, or lumpy stools, which occur in at least 25% of defecations according to diagnostic criteria.^[6] Straining during more than 25% of defecation attempts is frequent, often accompanied by pain or discomfort when passing stools.^[2] A sensation of incomplete evacuation after bowel movements affects at least 25% of instances, leading to persistent feelings of fullness or blockage in the rectum.^[11] Bloating and abdominal discomfort or cramping are also prevalent, contributing to overall unease.^[6] Associated symptoms can further indicate the condition's presence and may signal complications. Rectal bleeding may occur due to straining or associated issues like hemorrhoids.^[2] Overflow fecal incontinence, where liquid stool leaks around hardened masses, is reported in some cases, particularly in chronic or severe constipation.^[6] Loss of appetite and nausea can accompany these issues, while fatigue may arise from ongoing discomfort and disrupted sleep.^[11] Severity is often assessed using tools like the Bristol Stool Scale, where types 1 (separate hard lumps like nuts) and 2 (sausage-shaped but lumpy) are indicative of constipation due to their hard consistency.^[12] These indicators help differentiate constipation from normal stool forms (types 3-5). In occasional constipation, symptoms like infrequent stools (fewer than three per week) and mild straining may resolve spontaneously, but chronic cases involve persistent symptoms for three months or longer, escalating discomfort.^[2] The impact on quality of life is substantial, particularly in chronic constipation, where symptoms lead to reduced physical and mental well-being comparable to other chronic conditions like irritable bowel syndrome.^[13] Patients report interference with daily activities, work productivity, and social functioning due to pain, bloating, and unpredictable bowel habits, with greater effects in persistent versus transient episodes.^[14]

Causes

Dietary and Lifestyle Factors

Dietary factors play a significant role in constipation, particularly through inadequate intake of dietary fiber, which is essential for adding bulk to stool and promoting regular bowel movements. Adults are recommended to consume 25 to 30 grams of fiber per day to maintain optimal digestive health, with intakes below 25 grams associated with increased risk of constipation due to reduced stool volume and slower transit through the colon.^[15]^[16] Low-fiber diets often result from reliance on processed foods, leading to harder, drier stools that are difficult to pass; incorporating high-fiber sources such as fruits like pears and apples (providing 5-6 grams per serving), vegetables like broccoli and carrots (around 3-5 grams per cup), and whole grains like oats and brown rice (4-8 grams per serving) can mitigate this risk by enhancing stool softness and frequency.^[17]^[18] Inadequate hydration exacerbates constipation by contributing to stool dehydration, as the colon absorbs excess water from undigested material when fluid intake is insufficient. Health authorities recommend at least 2 liters of total fluid intake daily for women and 2.5 liters for men to support hydration, with low intakes linked to harder stools and increased constipation prevalence through fluid restriction effects.^[19]^[20] Dehydration from low water consumption, often seen in busy lifestyles or hot climates, reduces colonic lubrication, making evacuation more challenging; plain water is the most effective, though other non-caffeinated beverages contribute.^[21] A sedentary lifestyle, characterized by prolonged sitting and minimal physical activity, slows colonic motility and heightens constipation risk by diminishing the mechanical stimulation needed for peristalsis. Studies indicate that moderate physical activity, such as 150 minutes per week of walking or aerobic exercise, reduces constipation incidence by up to 30-50% compared to inactive individuals, with desk-bound occupations like office work posing particular hazards due to extended sitting periods exceeding 8 hours daily.^[22]^[23] Lack of movement, common in modern work environments, correlates with delayed transit times, as evidenced in cohorts of office workers where inactivity independently predicts functional constipation.^[24] Irregular daily routines disrupt the body's circadian rhythm for bowel habits, leading to inconsistent defecation patterns and constipation. Travel and shift work, which alter sleep, meal times, and physical schedules, are associated with higher prevalence of constipation symptoms due to desynchronization of gastrointestinal motility.^[25]^[26] For instance, long-haul flights or rotating night shifts interrupt the gastrocolic reflex, often resulting in infrequent stools until routines stabilize.^[27]

Medical Conditions

Constipation can arise as a secondary symptom of various underlying medical conditions, particularly those affecting gastrointestinal, neurological, endocrine, and metabolic systems, as well as other systemic disorders. These conditions disrupt normal bowel motility, stool formation, or defecation processes, leading to infrequent or difficult bowel movements. Gastrointestinal disorders frequently contribute to constipation through inflammation, malabsorption, or altered motility. Irritable bowel syndrome with constipation (IBS-C) is characterized by recurrent abdominal pain associated with hard or lumpy stools and infrequent defecation, affecting up to 30% of IBS patients.^[28] Inflammatory bowel disease (IBD), including ulcerative colitis, can present with constipation during remission phases or in left-sided involvement, where dyssynergic defecation impairs stool expulsion despite resolved inflammation.^[29]^[30] Celiac disease, an autoimmune reaction to gluten, may cause constipation due to small intestine damage leading to malabsorption and altered gut transit.^[31] Neurological conditions often impair autonomic nerve function controlling colonic motility and rectal sensation, resulting in chronic constipation. Parkinson's disease slows gastrointestinal transit through dopaminergic neuron loss, affecting over 50% of patients and exacerbating with disease progression.^[2]^[32] Multiple sclerosis disrupts nerve signals via demyelination, leading to constipation in up to 70% of cases due to reduced colonic contractility and pelvic floor dysfunction.^[2]^[33] Spinal cord injuries, particularly those affecting the autonomic nervous system, cause neurogenic bowel dysfunction by interrupting sacral reflexes, resulting in constipation in nearly all patients below the injury level.^[34]^[32] Endocrine and metabolic disorders influence bowel function via hormonal imbalances or electrolyte disturbances that reduce peristalsis. Hypothyroidism decreases metabolic rate and smooth muscle activity, causing constipation as a common extrathyroidal manifestation.^[6] Diabetes mellitus leads to autonomic neuropathy, slowing gastric emptying and colonic motility, with constipation reported in 20-60% of patients depending on glycemic control.^[2]^[6] Hypercalcemia, often from hyperparathyroidism, inhibits neuromuscular excitability and fluid absorption in the gut, contributing to constipation as an early symptom.^[6]^[35] Other systemic conditions such as chronic kidney disease (CKD) and eating disorders like anorexia nervosa also secondarily induce constipation. In CKD, factors including uremia, fluid restrictions, and reduced physical activity lead to constipation prevalence rates of 30-60% among patients, worsening with disease stage.^[36] Anorexia nervosa causes delayed gastrointestinal transit and reduced caloric intake, resulting in constipation in over 80% of patients due to motility disorders and electrolyte imbalances.^[37]^[38]

Medications and Substances

Certain medications and substances can induce constipation as a side effect by interfering with gastrointestinal motility, secretion, or fluid balance. These agents are commonly prescribed for various conditions, including pain, psychiatric disorders, hypertension, and nutritional deficiencies, but their impact on bowel function often leads to reduced peristalsis or harder stools.^[4] Opioids, widely used in pain management for conditions such as chronic pain or post-surgical recovery, are among the most frequent culprits of constipation. They act primarily through agonism of mu-opioid receptors in the enteric nervous system, which inhibits acetylcholine release and reduces peristalsis, gastric emptying, and intestinal fluid secretion, resulting in delayed transit and hardened stool. This effect is peripheral to the gut and occurs even with oral administration, affecting up to 40-80% of chronic users depending on dose and duration.^[39]^[40] Anticholinergic drugs, including tricyclic antidepressants (e.g., amitriptyline) and certain antipsychotics (e.g., clozapine), contribute to constipation by blocking muscarinic acetylcholine receptors in the gastrointestinal tract, thereby decreasing smooth muscle contractility and propulsive motility. These medications are prescribed for depression, anxiety, or psychosis, and their anticholinergic burden correlates with the severity of bowel slowing, particularly in older adults or those on polypharmacy.^[41]^[42] Other pharmacological classes also promote constipation through distinct mechanisms. Calcium channel blockers, such as verapamil used for hypertension or arrhythmias, inhibit calcium influx into smooth muscle cells, relaxing intestinal contractions and delaying colonic transit. Iron supplements, taken for anemia, are associated with gastrointestinal side effects including constipation, possibly due to unabsorbed iron altering gut microbiota or directly slowing motility, though the precise pathway remains unclear. Aluminum-containing antacids, employed for heartburn relief, bind to phosphates in the gut and reduce fluid secretion, leading to firmer stools and decreased bowel frequency.^[43]^[44]^[45] Non-pharmacological substances can similarly impair bowel function. Lead poisoning, often from environmental exposure, disrupts the enteric nervous system by inhibiting neurotransmitter function and smooth muscle activity, manifesting as constipation alongside abdominal pain. Excessive caffeine intake, found in coffee or energy drinks, exerts a diuretic effect that promotes dehydration, reducing water content in the colon and hardening fecal matter. Likewise, heavy alcohol consumption induces diuresis and fluid loss, exacerbating dehydration and contributing to infrequent bowel movements.^[46]^[47]^[6]

Psychological Factors

Psychological factors play a significant role in the development and exacerbation of constipation, particularly in functional cases where no structural abnormalities are present. Stress and anxiety activate the sympathetic nervous system, which diverts blood flow away from the gastrointestinal tract to prioritize "fight-or-flight" responses, thereby slowing colonic transit and reducing gut motility.^[48] This mechanism disrupts normal peristalsis, leading to harder stools and infrequent bowel movements, as evidenced by studies showing altered autonomic nervous system activity in patients with constipation-predominant irritable bowel syndrome.^[49] For instance, acute stress responses increase noradrenaline secretion in the gut, further inhibiting motility and contributing to symptoms like bloating and discomfort.^[50] Depression is strongly associated with constipation through both direct physiological effects and indirect behavioral influences. Reduced serotonin levels in the gut, common in depression, impair neuronal signaling that promotes motility, resulting in slower transit times similar to those observed in the brain's serotonin deficits.^[51] Additionally, individuals with depression often exhibit poorer self-care practices, such as inadequate dietary fiber intake or physical inactivity, which compound motility issues.^[52] Clinical studies confirm a bidirectional link, with depression increasing the risk of chronic constipation and vice versa, independent of medication side effects.^[53] This association holds across severities, with gut microbiota dysbiosis potentially mediating the connection.^[54] Behavioral aspects, such as pelvic floor dyssynergia (also known as anismus), often stem from psychological inhibition or learned responses to stress. In anismus, involuntary contraction of pelvic floor muscles during defecation hinders evacuation, frequently linked to heightened anxiety, depression, and obsessive-compulsive traits that reinforce maladaptive straining patterns.^[55] Psychological distress, including phobias of painful defecation or trauma-related avoidance, can perpetuate this cycle, particularly in those with a history of sexual abuse or familial stress.^[55] These factors contribute to obstructed defecation without organic causes, emphasizing the role of cognitive-behavioral elements in symptom maintenance. Evidence from diagnostic frameworks like the Rome IV criteria underscores the integration of psychological factors in functional constipation, defined by recurrent symptoms such as straining, incomplete evacuation, and fewer than three bowel movements per week without evidence of structural disease.^[56] Systematic reviews indicate that psychological stress, including family conflicts and anxiety disorders, significantly predicts functional constipation in both children and adults, with odds ratios ranging from 1.6 to 3.1 across stressors like bullying or parental discord.^[57] This brain-gut axis involvement highlights the need to address mental health in managing idiopathic cases, though psychological factors alone do not define the diagnosis.^[57]

Structural and Congenital Causes

Structural and congenital causes of constipation arise from anatomical abnormalities that mechanically obstruct stool passage or impair defecation mechanics, often requiring specialized diagnostic evaluation. Obstructive lesions, such as colorectal cancer, create partial or complete blockages in the colon or rectum, leading to stool retention and symptoms like abdominal pain and bloating. These tumors typically develop in older adults and can narrow the lumen, reducing colonic transit; for instance, left-sided cancers are more likely to cause obstructive constipation due to the smaller fecal volume in the distal colon. Strictures, which are fibrotic narrowings resulting from prior inflammation, surgery, or malignancy, similarly impede flow and are identified through endoscopic visualization. Volvulus, involving the twisting of the sigmoid or cecal colon, causes acute obstruction by compromising blood supply and motility, often necessitating urgent intervention.^[58] Congenital anomalies primarily affect pediatric populations and stem from developmental defects in the gastrointestinal tract. Hirschsprung's disease, characterized by the absence of enteric ganglion cells in the distal colon, results in a lack of peristalsis and failure of the internal anal sphincter to relax, creating a functional obstruction that manifests as chronic constipation from infancy. Anal atresia, including imperforate anus, involves a congenital absence or closure of the anal opening, preventing normal stool expulsion and often presenting with delayed meconium passage in newborns. These conditions highlight the role of neural and structural integrity in bowel function, with early surgical correction typically required to alleviate obstruction.^[58]^[59] Pelvic floor disorders contribute to constipation through dyssynergic defecation or outlet obstruction, particularly in women. Rectocele, a prolapse of the anterior rectal wall into the vagina, traps stool in the pouch during straining, leading to incomplete evacuation and chronic symptoms; it is more prevalent in multiparous females due to weakened pelvic support. Rectal intussusception, where the rectum telescopes into itself, similarly hinders stool passage by altering anorectal angulation, often coexisting with other pelvic abnormalities. These issues underscore the interplay between structural integrity and coordinated muscle action in defecation.^[58] Rare structural causes include megacolon, an abnormal dilation of the colon due to chronic obstruction or underlying neuromuscular dysfunction, which exacerbates constipation by reducing effective peristalsis and increasing stool retention. In severe congenital cases, such as untreated imperforate anus or extensive Hirschsprung's, megacolon can develop secondarily, forming a toxic reservoir of hardened feces. Diagnosis of these conditions often involves imaging modalities like barium enema or MRI to delineate anatomy, guiding targeted management.^[58]^[59]

Pathophysiology

Normal Bowel Physiology

The normal bowel physiology encompasses the coordinated processes that propel, form, and expel fecal matter through the large intestine. Colonic transit begins as chyme from the small intestine enters the cecum, where it is slowly advanced via haustral contractions—rhythmic, segmental mixing movements that occur every 30 minutes and last about one minute, stimulated by distension to facilitate thorough mixing and gradual propulsion.^[60] These are complemented by peristaltic waves, including high-amplitude propagated contractions (HAPCs) that generate pressures of 80-120 mm Hg and occur approximately 6 times daily (range 2-24), propelling contents toward the rectum in a more rapid manner, contributing to overall colonic transit, which typically takes 20–56 hours.^[60]^[61]^[62] Stool formation primarily occurs in the colon through water and electrolyte absorption, reducing liquid chyme to semisolid feces. The colonic epithelium absorbs approximately 90% of the remaining water via osmosis, driven by active sodium transport through channels like ENaC and NHE3, which creates an osmotic gradient for water reabsorption.^[63] The gut microbiota, comprising trillions of bacteria such as Bacteroides and Roseburia species, plays a crucial role by fermenting undigested carbohydrates into short-chain fatty acids (SCFAs) like butyrate and propionate, which provide energy to colonocytes, enhance mucosal integrity, and contribute to stool bulk and consistency while supporting further water absorption via interactions with receptors like GPR41.^[63]^[64] The defecation reflex is initiated by rectal distension from accumulated stool, triggering the rectoanal inhibitory reflex (RAIR) that relaxes the internal anal sphincter—a smooth muscle maintained in tonic contraction by sympathetic innervation.^[60] This involuntary phase, mediated by parasympathetic fibers from S2-S4, coordinates with voluntary relaxation of the external anal sphincter—a striated muscle controlled by the pudendal nerve—alongside increased intra-abdominal pressure from the diaphragm and pelvic floor muscles to straighten the anorectal angle and expel feces.^[60]^[61] Neural and hormonal controls orchestrate these processes through the enteric nervous system (ENS), an intrinsic network with the myenteric plexus regulating motility via smooth muscle contractions and the submucosal plexus managing secretion and blood flow, supported by interstitial cells of Cajal as pacemakers for slow-wave activity.^[61] The vagus nerve provides parasympathetic input to the proximal colon, promoting peristalsis through acetylcholine release on enteric motor neurons, while hormones like motilin stimulate colonic contractions to aid propulsion of contents into the large intestine.^[61]^[65]

Mechanisms of Constipation

Constipation arises primarily from disruptions in colonic motility, defecatory mechanics, and sensory processing, leading to delayed stool transit and incomplete evacuation. These mechanisms often overlap, with slow-transit constipation (STC) characterized by reduced colonic propulsion, outlet dysfunction involving impaired pelvic floor coordination, and sensory alterations that diminish the perception of rectal fullness.^[6] Recent classifications emphasize these as core pathophysiologic categories in primary chronic constipation.^[66] Slow-transit constipation results from diminished colonic motility, often due to enteric nervous system dysfunction or smooth muscle myopathy, which impairs the propagation of peristaltic waves necessary for stool advancement. In STC, high-amplitude propagating contractions (HAPCs) are reduced or absent, leading to delayed transit, particularly in the proximal colon, as evidenced by scintigraphy and manometry studies.^[67] Nerve damage, such as decreased excitatory neurotransmitters like acetylcholine in the myenteric plexus, contributes to this hypomotility, while reductions in interstitial cells of Cajal (ICCs)—key pacemakers for slow-wave generation—exacerbate the disorder, as observed in histological analyses of colectomy specimens.^[68] Myopathic changes, including smooth muscle degeneration, further hinder contractile activity, distinguishing STC from normal physiology where coordinated contractions ensure efficient transit.^[69] Outlet dysfunction, also known as defecatory or evacuation disorder, stems from uncoordinated pelvic floor muscles that fail to relax or paradoxically contract during attempted defecation, obstructing stool passage. This incoordination, often termed dyssynergic defecation or anismus, involves the puborectalis muscle not lengthening properly, maintaining an acute anorectal angle and preventing effective evacuation.^[70] Pelvic floor dysfunction affects up to 50% of chronic constipation cases and can coexist with slow transit, amplifying retention through mechanical obstruction rather than motility alone.^[71] Structural contributors, such as rectocele or internal rectal prolapse, may compound this by altering anorectal geometry, but the primary mechanism is neuromuscular discoordination.^[72] Sensory alterations in constipation involve blunted rectal sensation, where patients experience reduced awareness of stool presence or fullness, leading to voluntary retention and overflow. This hyposensitivity arises from impaired afferent nerve signaling in the rectum, often following pelvic nerve injury or chronic distension, as demonstrated in patients with sacral nerve damage who exhibit diminished rectal compliance and urge perception.^[73] In chronic cases, this can perpetuate a cycle of incomplete evacuation, with sensory retraining needed to restore normal thresholds for defecatory urge.^[72] Such alterations contribute to about one-third of functional constipation subtypes, independent of motor deficits.^[6] Emerging research highlights gut microbiome dysbiosis as a modulator of constipation mechanisms, particularly in chronic forms, where altered bacterial composition influences motility via serotonin signaling and inflammation. Dysbiosis, often involving alterations in beneficial taxa such as decreased Lactobacillus and variable abundance of Bifidobacterium and Bacteroides, upregulates intestinal serotonin transporter (SERT) expression, decreasing luminal serotonin (5-HT) availability and thereby slowing peristalsis, as shown in fecal microbiota transplantation models from constipated patients.^[74] In chronic constipation, this imbalance correlates with prolonged transit and reduced short-chain fatty acid production, which normally stimulates colonic contractions.^[75] Additionally, low-grade inflammation in the colonic mucosa, driven by dysbiosis-induced immune activation, contributes to enteric nerve dysfunction and smooth muscle impairment in persistent cases, aligning with updated motility disorder frameworks.^[66] These insights underscore the role of microbial-immune interactions in amplifying traditional mechanisms.^[76]

Diagnosis

Clinical History and Examination

The clinical history for constipation begins with a detailed assessment of bowel habits, including the frequency, consistency, and difficulty of defecation, such as straining or incomplete evacuation, which are common presenting symptoms.^[77] Patients should be queried about recent changes in bowel patterns, dietary intake (e.g., fiber and fluid consumption), physical activity levels, and lifestyle factors like travel or stress that may contribute to symptoms.^[78] A thorough medication history is essential, encompassing prescription drugs (e.g., opioids, antidepressants), over-the-counter remedies, and supplements, as these can induce or exacerbate constipation.^[6] The physical examination typically includes an abdominal assessment through inspection, auscultation, percussion, and palpation to detect distension, tenderness, or palpable masses suggestive of fecal loading or underlying pathology.^[79] A digital rectal examination is a critical component, evaluating anal tone, sphincter integrity, the presence of fecal impaction, rectal masses, or occult blood, while also assessing perianal skin for fissures or hemorrhoids.^[78] This bedside evaluation helps differentiate functional from organic causes and identifies immediate concerns like obstruction.^[77] Alarm symptoms in the history, such as unintentional weight loss, rectal bleeding, iron-deficiency anemia, or a family history of colorectal cancer, warrant prompt further evaluation to rule out serious conditions like malignancy or inflammatory bowel disease.^[77] New-onset constipation in patients over 50 years or accompanied by fever and abdominal pain also raises red flags for organic etiology.^[6] To quantify symptom severity, validated patient-reported outcome tools like the Patient Assessment of Constipation-Symptoms (PAC-SYM) questionnaire are employed; this 12-item instrument assesses abdominal, rectal, and stool-related symptoms over the past two weeks, aiding in tracking treatment response in clinical settings.^[80]

Diagnostic Criteria

The diagnosis of constipation relies on standardized criteria to ensure consistency and guide clinical management. The Rome IV criteria, developed by the Rome Foundation, define functional constipation as recurrent symptoms occurring for at least 3 months, with onset at least 6 months prior to diagnosis, and including at least two of the following: straining during more than 25% of defecations; lumpy or hard stools (Bristol Stool Form Scale types 1 or 2) in more than 25% of defecations; sensation of incomplete evacuation in more than 25% of defecations; sensation of anorectal blockage or obstruction in more than 25% of defecations; manual maneuvers to facilitate defecation (such as digital evacuation or pelvic floor support) in more than 25% of defecations; and fewer than three spontaneous bowel movements per week.^[81] These criteria exclude structural or organic disorders and alarm symptoms such as unintentional weight loss, rectal bleeding, or anemia.^[56] Constipation is broadly classified as functional (idiopathic) or organic (secondary) based on the presence of an underlying identifiable cause. Functional constipation lacks a clear physiological or biochemical abnormality and is diagnosed when Rome IV criteria are met after excluding secondary causes through history and basic evaluation.^[6] In contrast, organic constipation arises from specific medical conditions, such as neurological disorders, endocrine diseases, or structural abnormalities, and requires targeted investigations to confirm the etiology.^[6] This distinction is crucial, as functional cases, which comprise the majority (approximately 95% in adults), respond to conservative therapies, whereas organic forms demand etiology-specific interventions.^[6] Rome IV further delineates constipation into subtypes to refine diagnosis and treatment: functional constipation (meeting core criteria without predominant abdominal pain); irritable bowel syndrome with constipation (IBS-C, where constipation predominates alongside abdominal pain improved by defecation); opioid-induced constipation (linked to opioid use without adequate laxative prophylaxis); and functional defecation disorder (encompassing dyssynergic defecation or inadequate propulsion due to pelvic floor incoordination).^[82] Slow-transit constipation, characterized by delayed colonic motility, is often subsumed under functional constipation but may require specialized testing for confirmation.^[82] These subtypes highlight the heterogeneity of constipation, guiding subtype-specific management. Recent updates in international guidelines emphasize patient-centered outcomes. The 2023 Evidence-Based Clinical Guidelines for Chronic Constipation by the Japan Gastroenterological Association incorporate quality-of-life assessments, such as the Japanese version of the Patient Assessment of Constipation Quality of Life (PAC-QOL) questionnaire, to evaluate symptom impact alongside traditional criteria, reflecting a shift toward holistic diagnostic frameworks.^[83]

Investigations

Investigations for constipation are essential to exclude secondary causes, identify structural abnormalities, and assess functional disorders, particularly in cases with alarm symptoms such as unexplained weight loss, rectal bleeding, or anemia. These tests are not routinely required for uncomplicated chronic constipation but are recommended in a stepwise manner based on clinical suspicion and response to initial therapies.^[84] Basic laboratory evaluations form the foundation to rule out systemic contributors. Thyroid function tests are indicated to detect hypothyroidism, a common reversible cause of constipation. Serum electrolytes, including potassium and calcium levels, help identify imbalances like hypokalemia that impair colonic motility. Celiac serology, such as tissue transglutaminase IgA antibodies, is recommended when gastrointestinal symptoms suggest celiac disease, which can manifest as constipation in some undiagnosed adults. A complete blood count may also reveal anemia related to occult gastrointestinal blood loss.^[6]^[85]^[85] Imaging modalities provide visualization of colonic content and anatomy, especially when obstruction is suspected. Abdominal X-rays are a simple initial tool to evaluate fecal loading or impaction, showing retained stool in the rectosigmoid colon in many chronic constipation cases with significant retention. For red-flag presentations suggestive of malignancy or stricture, computed tomography (CT) or magnetic resonance imaging (MRI) of the abdomen and pelvis can detect tumors, inflammatory bowel disease flares, or extrinsic compressions with high sensitivity. These are particularly useful in older adults or those with progressive symptoms.^[5]^[77] Specialized physiologic tests are employed for refractory cases to differentiate subtypes like slow-transit constipation or defecatory disorders. Anorectal manometry assesses anal sphincter function, rectal sensation, and coordination, identifying dyssynergic defecation, which occurs in many patients failing laxatives. Colonic transit studies, including scintigraphy with radiolabeled markers or radiopaque marker retention tests, measure whole-gut motility; retention of more than 20% of markers after 120 hours confirms slow transit. Defecography, performed via dynamic MRI or fluoroscopy, evaluates pelvic floor dynamics and detects anatomic defects such as rectocele or intussusception during simulated defecation, guiding targeted interventions.^[86]^[84] The 2025 World Gastroenterology Organisation cascade approach advocates a tiered strategy for investigations, initiating with laboratory tests and plain radiography in red-flag scenarios, escalating to advanced anorectal and colonic assessments only after failure of conservative measures like dietary fiber and osmotic laxatives. This resource-stratified guideline emphasizes cost-effectiveness, reserving invasive tests for the 10-20% of patients with treatment-resistant disease.^[84]

Management

Prevention Strategies

Preventing constipation involves adopting lifestyle and dietary habits that promote regular bowel movements and mitigate common risk factors. Increasing dietary fiber intake to 25-30 grams per day through sources such as fruits, vegetables, whole grains, and legumes is recommended, as it adds bulk to stool and facilitates its passage through the intestines.^[5] This amount aligns with guidelines for adults, with gradual increases over several weeks to minimize side effects like bloating and gas.^[5] Complementing fiber with adequate hydration—aiming for 2-3 liters of fluids daily, primarily water—enhances its laxative effects by softening stool consistency.^[87] Meta-analyses of randomized controlled trials indicate that such dietary fiber interventions can significantly reduce the incidence and symptoms of constipation, with improvements in bowel frequency observed in up to 50% of cases in some studies.^[88] Regular physical activity is another cornerstone of prevention, with guidelines recommending at least 150 minutes of moderate-intensity aerobic exercise per week, such as brisk walking or swimming, to stimulate intestinal motility and reduce transit time.^[89] Systematic reviews of cohort studies confirm that moderate to high levels of physical activity are associated with a lower risk of constipation, potentially through enhanced gut peristalsis and overall metabolic health.^[22] Establishing consistent toilet routines, including responding promptly to the defecation urge and designating fixed times for bowel movements (e.g., after meals), further supports regularity by training the body's natural gastrocolic reflex. For high-risk groups, tailored strategies are particularly important. Travelers, who may face disruptions from altered diets, dehydration, and immobility, can prevent constipation by prioritizing hydration—drinking at least 8-10 glasses of water daily and limiting caffeine and alcohol intake to counteract dry cabin air and jet lag effects.^[90] In the elderly, where reduced mobility and medication use heighten vulnerability, routine monitoring during health check-ups, combined with encouragement of daily light exercise and fiber-rich meals, helps maintain bowel function proactively.^[91] These measures address underlying dietary and lifestyle factors, such as low fiber consumption, that contribute to constipation risk.^[87]

Conservative and Non-Pharmacological Treatments

Conservative and non-pharmacological treatments form the cornerstone of managing mild to moderate constipation, emphasizing lifestyle modifications and targeted therapies to improve bowel motility and function without relying on medications. These approaches are particularly effective for functional constipation and outlet obstruction types, such as dyssynergic defecation, by addressing underlying neuromuscular and behavioral factors. Evidence supports their use as first-line interventions, often yielding sustained benefits when combined with patient education on bowel habits.^[86] Biofeedback therapy is a specialized pelvic floor training technique designed to retrain dysfunctional defecation patterns in patients with dyssynergia, where inadequate coordination between abdominal and pelvic muscles hinders evacuation. This non-invasive method uses visual or auditory feedback from sensors to guide patients in relaxing the puborectalis muscle and synchronizing abdominal pressure during straining, typically over 6-8 sessions. Systematic reviews indicate success rates of approximately 60-80% in improving symptoms for outlet dysfunction, with one meta-analysis reporting 63% clinical improvement compared to alternative therapies. Long-term efficacy persists in about 70% of responders, making it superior to laxatives for this subtype.^[92]^[93]^[94] Physical therapies offer accessible options to stimulate gastrointestinal motility and alleviate constipation symptoms through manual or mind-body techniques. Abdominal massage involves rhythmic clockwise strokes over the colon pathway, performed for 10-15 minutes daily, which enhances peristalsis and reduces transit time. A 2023 meta-analysis of randomized trials demonstrated superior efficacy in increasing defecation frequency and improving stool consistency compared to no intervention, with effects lasting up to three months post-treatment. Yoga incorporates poses such as spinal twists, forward bends, and inversions to promote abdominal compression and relaxation, thereby facilitating bowel movement; systematic reviews of exercise interventions, including yoga, show significant symptom relief and quality-of-life improvements in functional constipation. Acupuncture, often using electroacupuncture at points like ST25 and CV6, modulates autonomic nervous system activity to boost colonic contractions. Recent meta-analyses from 2023-2024 confirm its effectiveness in elevating treatment response rates by 20-30% over sham controls, particularly in elderly patients with functional constipation, with minimal adverse effects.^[95]^[96]^[97] Enemas and suppositories provide targeted relief for acute fecal impaction or rectal evacuation difficulties, serving as short-term adjuncts in conservative management. Glycerin suppositories draw water into the rectum to soften stool and trigger the defecation reflex within 15-30 minutes, while saline or mineral oil enemas lubricate and flush the lower bowel. Clinical guidelines recommend their use for refractory cases after lifestyle measures fail, noting safety in adults when limited to occasional administration to avoid dependency or mucosal irritation. These interventions clear impactions in over 80% of suitable patients but are not intended for chronic daily use.^[98]^[99]^[5] Structured exercise protocols enhance colonic propulsion by increasing intra-abdominal pressure and stimulating peristalsis, with low-impact activities proving most accessible for constipation relief. Walking for 20-30 minutes daily at a moderate pace has been shown in cohort studies to reduce constipation prevalence by promoting gut motility, with benefits evident within weeks of consistent practice. More intensive routines, such as aerobic exercises or yoga sequences performed 3-5 times weekly, further shorten transit time and improve evacuation completeness. These protocols overlap with prevention strategies by fostering habitual physical activity, which sustains long-term bowel regularity.^[22]^[100]^[101]

Pharmacological Treatments

Pharmacological treatments for constipation primarily involve laxatives that target different aspects of bowel function, such as increasing stool bulk, drawing water into the colon, or stimulating peristalsis. These agents are selected based on the severity and type of constipation, with over-the-counter options often used first-line for mild cases and prescription medications for chronic idiopathic constipation (CIC). Guidelines from the American College of Gastroenterology (ACG) and American Gastroenterological Association (AGA) recommend starting with fiber supplements or osmotic laxatives before escalating to stimulants or novel agents.^[102] Bulk-forming laxatives, such as psyllium and methylcellulose, work by absorbing water in the intestines to increase stool volume and soften consistency, thereby promoting easier passage. Psyllium, derived from the husks of Plantago ovata seeds, swells upon hydration to form a gel-like mass that enhances colonic transit. Methylcellulose, a semisynthetic cellulose derivative, similarly retains water and adds bulk without fermenting in the gut, making it suitable for patients with bloating.^[103] These agents are typically dosed at 5-10 grams daily with ample fluids, with side effects including abdominal discomfort if hydration is inadequate; they are considered safe for long-term use in most adults.^[104] Osmotic laxatives draw water into the bowel lumen to soften stool and stimulate defecation. Polyethylene glycol (PEG, also known as macrogol) is a high-molecular-weight polymer that is poorly absorbed and effective for both acute and chronic constipation, with dosing of 17 grams daily in adults.^[105] Lactulose, a non-absorbable disaccharide, is metabolized by colonic bacteria to produce osmotically active acids, though it may cause more gas than PEG.^[105] Long-term studies confirm PEG's safety, showing no significant electrolyte disturbances or dependency in extended use, outperforming lactulose in tolerability.^[106] Common side effects for both include bloating and diarrhea, with caution advised in renal impairment to avoid hypermagnesemia if magnesium-based osmotics are considered.^[102] Stimulant laxatives promote colonic motility by irritating the mucosa or stimulating enteric nerves. Bisacodyl, a diphenylmethane derivative, is activated in the colon to increase peristalsis and secretion, dosed at 5-15 mg orally or rectally as needed.^[107] Senna, an anthraquinone from Cassia plants, similarly enhances propulsive activity after bacterial metabolism in the gut, typically administered as 15-30 mg at bedtime.^[108] These are recommended for short-term use in CIC when osmotics fail, per ACG/AGA guidelines, due to potential side effects like cramping and electrolyte imbalance with prolonged use.^[109] Newer pharmacological agents target specific receptors for refractory CIC. Prucalopride, a selective 5-HT4 receptor agonist, enhances serotonin-mediated colonic motility, dosed at 2 mg daily; analyses confirm cardiovascular safety and efficacy in increasing spontaneous bowel movements.^[110] Linaclotide, a guanylate cyclase-C agonist, stimulates chloride and bicarbonate secretion to increase intestinal fluid, administered at 145 mcg daily; trials demonstrate sustained symptom relief in adults with CIC, with side effects primarily diarrhea.^[111] Plecanatide, a similar guanylate cyclase-C agonist dosed at 3 mg or 6 mg daily, is approved for CIC and IBS-C, offering comparable efficacy with once-daily dosing.^[112] These agents are reserved for cases unresponsive to traditional laxatives, offering improved quality of life without the habituation risks of stimulants.^[102] Overall, treatment selection should consider individual factors like comorbidities, with monitoring for side effects such as dehydration or imbalances.^[104]

Interventional and Surgical Options

Interventional and surgical options are reserved for patients with chronic constipation refractory to conservative and pharmacological management, particularly those with structural abnormalities or severe motility disorders. According to the 2024 American Society of Colon and Rectal Surgeons (ASCRS) clinical practice guidelines, such interventions require prior evaluation of colonic motility and transit, as well as anorectal physiology testing, to confirm eligibility and exclude functional etiologies.^[66] Patient selection emphasizes individuals with isolated slow-transit constipation or outlet dysfunction who have failed medical therapy, with conditional recommendations due to variable outcomes and risks like infection and incontinence.^[66] Minimally invasive procedures target specific dysfunctions, such as sphincter hypertonicity or nerve-mediated motility issues. Botulinum toxin (Botox) injections into the puborectalis and external anal sphincter muscles are conditionally recommended by the ASCRS for outlet dysfunction constipation caused by nonrelaxing puborectalis, aiming to reduce spasm and facilitate defecation.^[66] In a study of children with chronic idiopathic constipation and anal fissures, intrasphincteric Botox injections (100 units) led to symptom resolution in 70% of cases, with increased stool frequency and reduced laxative use, and no major complications reported over 6 months.^[113] Sacral nerve stimulation (SNS), involving implantation of a device to modulate sacral nerves, has been explored for refractory constipation, particularly slow-transit types. However, evidence from randomized trials shows mixed results: one small study (n=2) reported a 150% increase in bowel movements and symptom relief, while a larger crossover trial (n=59) found no significant improvement in bowel frequency or bloating, with common adverse events including implant-site pain (32%) and infections (12%).^[114] The ASCRS guidelines do not endorse SNS for constipation due to insufficient evidence.^[66] Surgical interventions address structural or congenital causes. For severe slow-transit constipation confirmed by scintigraphy, subtotal colectomy with ileorectal anastomosis is conditionally recommended after failed medical therapy, removing the non-functioning colon to restore transit.^[66] A systematic review of 31 studies (n=1,407 patients) reported median satisfaction rates of 67% (retrospective) to 90% (prospective), with increased bowel frequency (median 4 per day) but persistent issues in 9% due to recurrent constipation; complications included small-bowel obstruction (median 18%, reoperation 14%), diarrhea (14%), and incontinence (14%), with mortality up to 6%.^[115] Outcomes are poorer in patients with coexisting psychiatric conditions or untreated rectal disorders.^[115] For rectal prolapse contributing to obstructed defecation, ventral mesh rectopexy fixes the rectum to the sacrum, often laparoscopically, to correct intussusception and improve evacuation. In a series of 42 patients, rectopexy with sigmoid resection reduced constipation prevalence from 43.6% to 25.6% (p<0.001), decreased rectosigmoid transit time from 21.1 to 12.7 hours (p<0.001), with a 7.1% complication rate, no mortality, and zero recurrences at 54-month follow-up.^[116] In congenital cases like Hirschsprung's disease, where aganglionosis causes functional obstruction, pull-through surgery removes the aganglionic segment and anastomoses healthy bowel to the anus, typically via minimally invasive transanal approach. This procedure, indicated post-biopsy confirmation, allows most children to pass stool normally, though 10-30% experience post-operative constipation managed with fiber, fluids, and laxatives; complications include enterocolitis (first-year risk) and incontinence.^[117] Overall, surgical success varies by etiology, with ASCRS emphasizing multidisciplinary assessment to mitigate risks like infection (5-10%) and new-onset incontinence (up to 14%).^[66]

Complications and Prognosis

Potential Complications

Untreated or severe constipation can lead to a range of acute complications, primarily affecting the anorectal region. Fecal impaction occurs when hardened stool accumulates in the rectum and colon, preventing normal passage and potentially causing abdominal pain, bloating, and urinary retention.^[2] This condition is particularly common in individuals with chronic constipation and can result in overflow incontinence, where liquid stool leaks around the impacted mass, mimicking diarrhea.^[118] Hemorrhoids, or swollen veins in the anus and lower rectum, often develop from repeated straining during bowel movements, leading to pain, itching, and bleeding.^[2] Chronic constipation heightens the risk of more persistent anorectal and colonic issues. Anal fissures, which are small tears in the lining of the anus, arise from the passage of hard stools or excessive straining, causing sharp pain and potential bleeding during defecation.^[11] In severe cases, prolonged impaction may contribute to volvulus, a twisting of the colon that obstructs bowel contents and blood flow, or stercoral perforation, where impacted feces erode the intestinal wall, leading to peritonitis.^[119] Systemic complications can emerge, especially in vulnerable populations such as the elderly. Electrolyte disturbances, including hypokalemia and hypomagnesemia, may result from dehydration associated with reduced fluid intake or vomiting due to bowel obstruction from constipation.^[119] In older adults, severe constipation increases the risk of aspiration pneumonia, often through overflow incontinence or associated immobility leading to gastroesophageal reflux and inhalation of gastric contents.^[119] Rare but serious complications include bowel obstruction from massive fecal loading, toxic megacolon characterized by severe colonic dilation and potential perforation, and cardiovascular strain. Straining during defecation can cause transient spikes in blood pressure, triggering events such as arrhythmias, acute coronary syndrome, or syncope in susceptible individuals.^[120] These risks underscore the importance of addressing constipation to prevent escalation to life-threatening conditions.^[121]

Prognosis

The prognosis for functional constipation is generally favorable, with most patients experiencing significant improvement or resolution through lifestyle modifications such as increased dietary fiber intake, adequate hydration, and regular physical activity. Holistic approaches, including these non-pharmacological interventions, lead to symptom relief in the majority of cases, though a small subset of adults may remain severely affected despite treatment. For instance, biofeedback therapy, often combined with lifestyle changes, achieves resolution in 80% to 95% of patients with defecatory disorders, highlighting the potential for high success rates when compliance is maintained.^[6]^[122] In secondary constipation, outcomes are highly dependent on addressing the underlying cause, with variable success rates tied to the severity of the primary condition. For example, in advanced cancer patients, where constipation affects 50% to 90% due to opioids, tumor effects, or immobility, prognosis is often poor without aggressive management, as symptoms may persist or worsen alongside disease progression. Effective treatment of the root cause, such as adjusting medications or managing metabolic disturbances, can improve bowel function, but chronicity remains a challenge in palliative settings.^[123]^[124] Chronic constipation carries a notable risk of recurrence, estimated at 10% to 15% following initial treatment success, particularly when dietary compliance lapses or in cases with prolonged symptom duration. Quality-of-life metrics, such as SF-36 scores, reveal significant impairments in physical and mental health domains among affected individuals, with constipated patients scoring lower than non-constipated controls across multiple studies. Prognostic factors include older age, female gender, and delayed intervention, which correlate with worse long-term outcomes and higher persistence rates—up to 30% of childhood cases extending into adulthood. Recent 2025 data on microbiome-based therapies, including fecal microbiota transplantation, show promising results with pooled remission rates of approximately 51% and improvement in 65% of chronic cases, potentially enhancing long-term prognosis by restoring gut flora balance.^[6]^[125]^[126]^[127]

Epidemiology

Prevalence and Distribution

Constipation is a common gastrointestinal disorder affecting approximately 14% of the global adult population.^[84] This prevalence is notably higher among women, with a female-to-male ratio of about 2:1, as evidenced by multiple population-based studies.^[128] The condition's occurrence shows significant regional variations, with rates of 16-20% reported in Western countries such as the United States and parts of Europe, often linked to dietary patterns lower in fiber, while lower prevalence—around 10-13%—is observed in regions with traditionally high-fiber diets, including many Asian countries.^[84] In contrast, some African populations exhibit higher rates, up to 32% among older adults, highlighting the influence of socioeconomic and dietary factors.^[129] Prevalence trends indicate an increase associated with aging populations, where rates can reach 33% in adults over 60 years old due to factors like reduced mobility and medication use.^[1] Recent 2024 data also reveal a pediatric prevalence of approximately 12%, particularly in regions like Asia, underscoring the condition's impact across age groups.^[130] Regarding etiology, about 90-95% of constipation cases are classified as functional, lacking an identifiable organic cause, while the remaining 5-10% stem from underlying organic conditions such as neurological disorders or structural abnormalities.^[131]

Risk Factors and Demographics

Constipation exhibits notable demographic patterns, with prevalence consistently higher among females than males, at a ratio of approximately 2.2:1 across North American populations.^[132] This disparity is linked to hormonal influences, including elevated progesterone levels during pregnancy and postpartum periods, which reduce gastrointestinal motility and elevate risk. Advancing age also correlates strongly with increased susceptibility, particularly beyond 65 years, where symptoms affect roughly 34% of women and 26% of men.^[133] Socioeconomic factors play a significant role, as lower income levels are associated with inadequate dietary fiber intake, heightening constipation risk through suboptimal nutrition.^[134] Regional differences further stratify vulnerability; for instance, in certain populations like those in China, rural residents face higher rates (up to 14.1% in the elderly) compared to urban dwellers (12%), potentially due to variations in lifestyle and access to healthcare.^[135] Comorbid conditions substantially amplify risk, with diabetic patients experiencing constipation in up to 50% of cases, driven by autonomic neuropathy and impaired colonic motility.^[136] Similarly, opioid users report prevalence rates of 40% to 60%, as these medications directly inhibit intestinal peristalsis.^[39] Emerging research from 2024 and 2025 underscores the role of gut microbiome dysbiosis in constipation pathogenesis, where imbalances—often triggered by antibiotic exposure—disrupt microbial diversity and colonic function, emerging as modifiable risk factors.^[137]^[138]

History

Historical Understanding

In ancient times, the concept of constipation was intertwined with early medical theories of bodily imbalance and internal decay. Around 400 BCE, Hippocrates, often regarded as the father of Western medicine, described constipation within the framework of humoral theory, positing that health depended on the balance of four bodily fluids—blood, phlegm, yellow bile, and black bile—and that stagnation in the bowels could lead to an excess of black bile, causing systemic illness akin to early notions of autointoxication from putrefying waste.^[139] This view echoed even older ideas from ancient Egypt, as documented in the Ebers Papyrus (c. 1550 BCE), which attributed diseases to the poisoning of the body by decomposing intestinal matter.^[140] By the 19th century, medical understanding shifted toward an overemphasis on intestinal "toxins," framing constipation as the "disease of civilization" due to modern diets low in fiber and sedentary lifestyles. Physicians like Charles Bouchard popularized the autointoxication hypothesis in the 1880s, arguing that retained fecal matter released harmful substances like ptomaines into the bloodstream, potentially causing up to 90% of chronic diseases, which spurred widespread use of aggressive purges, enemas, and cathartics to ensure daily evacuations.^[140] This toxin-centric perspective, influenced by emerging microbiology, often led to unnecessary and harmful interventions, as the theory lacked empirical support beyond observational fears of putrefaction.^[141] In the early 20th century, psychological interpretations gained traction, influenced by Sigmund Freud's psychoanalytic theory, which linked constipation to fixation in the anal stage of psychosexual development, where excessive retention during toilet training fostered "anal-retentive" traits like orderliness and obstinacy, sometimes pathologized as contributing to neuroses.^[142] Concurrently, laxative overuse exploded, with patent medicines such as Carter's Little Liver Pills dominating markets amid autointoxication hype, as surgeons like William Arbuthnot Lane even advocated colectomies to remove "toxic" colons, performing hundreds between 1908 and 1925 before the practice was discredited for high mortality.^[141] A pivotal shift occurred in the 1950s, when medical consensus began recognizing functional types of constipation—chronic conditions without identifiable organic causes or toxin involvement—emphasizing dietary and lifestyle factors over autointoxication, as seen in analyses like the 1957 "constipation syndrome" framework that highlighted nutritional deficiencies rather than universal poisoning.^[143] This marked a departure from earlier misconceptions, contrasting with modern definitions that focus on symptom-based criteria like infrequent bowel movements without red flags for underlying pathology.^[6]

Advances in Treatment

In the mid-20th century, the understanding of constipation shifted toward dietary interventions, with the popularization of fiber therapy during the 1960s and 1980s largely attributed to Denis Burkitt's dietary fiber hypothesis. Burkitt, observing lower rates of constipation and related gastrointestinal disorders in rural African populations consuming high-fiber diets, proposed that low dietary fiber intake in Western societies led to reduced stool bulk, prolonged transit time, and increased intraluminal pressures, thereby contributing to constipation.^[144] This hypothesis, building on earlier work by researchers like Hugh Trowell, spurred clinical recommendations for increased intake of soluble and insoluble fibers from sources such as fruits, vegetables, and whole grains, which were shown to soften stools and improve bowel frequency in multiple observational studies.^[145] By the 1980s, fiber supplementation became a cornerstone of non-pharmacological management, influencing public health campaigns and reducing reliance on harsher laxatives.^[146] The 1990s marked advancements in diagnostic standardization and osmotic therapies. The Rome criteria, first established in the early 1990s for functional gastrointestinal disorders and refined in Rome II (1999) to include specific diagnostic thresholds for functional constipation—such as fewer than three defecations per week and straining during at least 25% of attempts—provided a consensus framework for identifying idiopathic cases, facilitating more targeted research and treatment.^[147] Concurrently, polyethylene glycol (PEG)-based laxatives, such as PEG 3350, were introduced in the late 1990s, offering an effective, well-tolerated osmotic agent that draws water into the colon to promote defecation without significant electrolyte imbalances, as demonstrated in pivotal trials showing superior efficacy over traditional lactulose.^[148] FDA approval of PEG 3350 for constipation in 1999 solidified its role as a first-line therapy.^[149] From the 2000s to the 2020s, pharmacological innovations expanded options for refractory cases, particularly with prokinetics like prucalopride, a selective 5-HT4 receptor agonist approved in Europe in 2009 for chronic idiopathic constipation. Clinical trials established its ability to enhance colonic motility, increasing spontaneous bowel movements by up to 30% compared to placebo, with a favorable safety profile minimizing cardiac risks associated with earlier agents.^[150] More recently, in 2024 and 2025, emerging microbiome modulators, including probiotics, postbiotics, and fecal microbiota transplantation (FMT), have shown promise in clinical studies by restoring gut dysbiosis linked to slow-transit constipation; for instance, multi-strain probiotics improved stool consistency and frequency in randomized trials,^[151] while postbiotics like Probio-Eco alleviated symptoms in double-blind studies by modulating short-chain fatty acid production.^[152] Neuromodulation techniques, such as sacral nerve stimulation, have also advanced through ongoing trials, with 2024 data indicating significant reductions in constipation severity and improved quality of life in patients with slow-transit disorders after six months of therapy.^[153] Guideline evolution has paralleled these developments, providing structured approaches to care. The Rome III criteria, published in 2006, refined diagnostic criteria for functional constipation by emphasizing symptom duration and excluding structural causes, influencing global practice.^[154] Building on this, the 2023 Evidence-Based Clinical Guidelines for Chronic Constipation by the Japanese Gastroenterological Association incorporated evidence for prokinetics and microbiome interventions in stepwise management.^[83] Most recently, the 2025 World Gastroenterology Organisation (WGO) Global Guideline introduced a cascade model tailored to resource availability, recommending fiber and osmotic laxatives as initial steps in low-resource settings, escalating to prokinetics and neuromodulation in high-resource contexts, thereby promoting equitable, evidence-based treatment worldwide.^[84]

Special Populations

Children and Adolescents

Constipation affects 5–30% of children worldwide, with the majority of cases classified as functional constipation characterized by withholding behaviors such as voluntary stool retention due to pain or fear during defecation.^[155]^[131]^[156] In children and adolescents, these behaviors often emerge during developmental stages, leading to cycles of harder stools and further avoidance.^[157]^[158] Common causes in this population include challenges during toilet training, where children may resist bowel movements due to discomfort or anxiety, and cow's milk intolerance, which can lead to harder stools and perianal irritation.^[159]^[160]^[161] Excessive consumption of cow's milk may also contribute by displacing fiber-rich foods in the diet.^[162] Diagnosis typically relies on the Rome IV pediatric criteria, which for children aged 4 years and older include two or fewer defecations per week, at least one episode of fecal incontinence per week in toilet-trained children, stool retention history, painful or hard bowel movements, large stools in the rectum or toilet, or large fecal mass in the rectum.^[163]^[56]^[164] To rule out organic causes like Hirschsprung's disease, a barium enema is often used as a screening tool, revealing characteristic findings such as a narrow distal rectum transitioning to a dilated proximal colon.^[165]^[166]^[167] Treatment begins with polyethylene glycol (PEG) as the first-line osmotic laxative, which is safe, effective for disimpaction and maintenance, and well-tolerated in children over 6 months.^[168]^[169]^[170] For cases involving pelvic floor dyssynergia, biofeedback therapy shows efficacy, with 2024 reviews reporting success rates of approximately 80% in improving symptoms and continence.^[171]^[172]^[173] Despite these approaches, gaps persist, including underdiagnosis in school-aged children due to limited screening in educational settings and reliance on parental reports.^[155]^[174] Emerging 2025 trials on pediatric neuromodulation, such as sacral neuromodulation, are exploring its role as an adjuvant for refractory cases, showing preliminary promise in improving bowel function without invasive surgery.^[175]^[176]^[177]

Elderly and Pregnant Individuals

Constipation is particularly prevalent among elderly individuals, with a reported prevalence of 15% to 30% among those over 60 years worldwide, varying due to inconsistent diagnostic criteria such as Rome IV.^[178] In older adults, risk factors include physical inactivity, polypharmacy with medications like opioids and anticholinergics, and comorbidities such as diabetes, Parkinson's disease, or pelvic floor disorders.^[178] ^[179] Symptoms typically involve fewer than three bowel movements per week, hard or lumpy stools, straining, and a sensation of incomplete evacuation, which can lead to complications like fecal impaction if unmanaged.^[179] Management in the elderly begins with lifestyle modifications, including increasing dietary fiber to 25–30 grams daily from sources like fruits, vegetables, and whole grains, alongside adequate fluid intake and moderate exercise such as walking.^[178] ^[179] If these are insufficient, osmotic laxatives like polyethylene glycol (17 g/day) or lactulose (15 g/day) are recommended as first-line pharmacological options due to their efficacy and safety profile in short-term use.^[178] Stimulant laxatives such as bisacodyl (5–10 mg) may be added for refractory cases, while biofeedback therapy shows 70%–80% success for defecatory disorders; evaluation includes history, digital rectal exam, and tests like anorectal manometry only for persistent symptoms.^[178] Alarm symptoms like rectal bleeding or weight loss warrant further investigation to rule out organic causes.^[178] In pregnant individuals, constipation affects 11% to 38% of women, primarily due to elevated progesterone levels that relax intestinal smooth muscle and prolong transit time, compounded by increased water absorption, reduced physical activity, iron supplements, and uterine pressure in later trimesters.^[180] Symptoms mirror those in the general population, including infrequent stools and discomfort, but may exacerbate conditions like hemorrhoids.^[180] First-line interventions emphasize non-pharmacological approaches: gradually increasing dietary fiber to 25 grams daily via fruits (e.g., apples, raspberries), vegetables, whole grains, beans, nuts, and seeds, paired with sufficient water intake and light exercise to promote bowel regularity without risking dehydration.^[181] ^[180] If needed, safe laxatives include bulk-forming agents like psyllium, stool softeners such as docusate (no increased malformation risk in studies of 116–473 exposures), and osmotic options like polyethylene glycol for short-term use, as they exhibit minimal systemic absorption and no association with congenital anomalies.^[180] Stimulant laxatives like senna are generally safe short-term (odds ratio for malformations 0.64) but should be avoided long-term to prevent electrolyte imbalances; consultation with a healthcare provider is essential for personalized management.^[180]

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Evidence indicates that dysbiosis of gut microbiota may contribute to functional constipation and constipation-type irritable bowel syndrome.Abstract · Introduction · Gut Microbiota in Functional... · Gut Microbiota in Irritable...
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Physical exam · check your blood pressure, temperature, and heart rate · check for dehydration · use a stethoscope to listen to sounds in your abdomen · check your ...
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[PDF] Comparison of Polyethylene Glycol 3350+Electrolytes vs ...
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[PDF] Biofeedback Is Superior to Laxatives for Normal Transit Constipation ...
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NCT04713085 | Sacral Neuromodulation in Children and Adolescents
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Current Treatment Options for Children with Functional Constipation ...
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The first line of therapy for constipation includes increasing dietary fibre and water intake and moderate amounts of daily exercise. If these are ineffective, ...
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Eating more foods with fiber can help fight constipation. Fiber is found in fruits, vegetables, whole grains, beans, nuts, and seeds.