Constipation

Populations and Risk Factors

• Women affected approximately 2:1 over men; prevalence increases with age, particularly after age 65
• Sedentary lifestyle — reduced physical activity decreases colonic motility and mass movement frequency
• Low dietary fiber intake (below 25–30 g/day) reduces stool bulk and slows transit
• Inadequate fluid intake — dehydration increases colonic water reabsorption, producing dry, hard stools
• Opioid use — opioid receptors (mu-receptors) are densely distributed throughout the gut wall; activation slows peristalsis and increases water absorption (opioid-induced constipation is a distinct subtype)
• Anticholinergic medications (antidepressants, antihistamines, antispasmodics) — reduce parasympathetic drive to the colon
• Pregnancy — progesterone relaxes smooth muscle; enlarging uterus compresses the sigmoid colon and rectum
• Neurological conditions: Parkinson's disease, multiple sclerosis, spinal cord injury — disrupted descending autonomic motor control to the colon
• Hypothyroidism — reduced metabolic rate slows all smooth muscle activity including colonic motility
• Chronic stress and sympathetic dominance — sustained sympathetic activation inhibits peristalsis via splanchnic nerve input
• Habitual suppression of the urge to defecate (ignoring the gastrocolic reflex) — weakens the defecation reflex arc over time

Causes and Pathophysiology

Normal Colonic Motility

• The colon performs three types of contractile activity: haustral contractions (slow segmental mixing that maximizes water absorption), peristaltic contractions (propulsive waves moving content distally), and mass movements (powerful high-amplitude propagated contractions that move large volumes of content toward the rectum, typically occurring 1–3 times daily after meals via the gastrocolic reflex)
• The enteric nervous system (ENS) — sometimes called the "second brain" — contains approximately 100 million neurons and independently coordinates motility patterns; however, it is modulated by the autonomic nervous system
• Parasympathetic innervation (vagus nerve to proximal colon; pelvic splanchnic nerves S2–S4 to distal colon and rectum) promotes motility — increases peristalsis, stimulates secretion, and relaxes the internal anal sphincter
• Sympathetic innervation (splanchnic nerves T5–L2) inhibits motility — slows peristalsis, increases sphincter tone, and reduces secretion
• This autonomic balance is the foundation of the MT treatment rationale: shifting the client toward parasympathetic dominance directly promotes colonic motility

Slow-Transit Constipation

• Reduced frequency and amplitude of mass movements and peristaltic contractions throughout the colon
• Content moves abnormally slowly through the entire colon, allowing excessive water absorption — stools become progressively drier and harder as they remain in the colon longer
• Associated with reduced numbers of interstitial cells of Cajal (the pacemaker cells of gut motility) and diminished ENS neurotransmitter activity
• Clinically: infrequent urge to defecate, minimal urgency, diffuse abdominal fullness, hard/pellet stools (Bristol Stool Scale types 1–2)
• This subtype responds well to abdominal massage — mechanical assistance to colonic transit addresses the core deficit

Outlet Dysfunction (Dyssynergic Defecation)

• Normal colonic transit but impaired evacuation at the rectoanal level — the pelvic floor muscles and external anal sphincter fail to relax (or paradoxically contract) during attempted defecation
• Produces straining, sensation of incomplete evacuation, and rectal fullness despite the urge to defecate
• Often behaviorally learned (habitual suppression of defecation) or related to pelvic floor dysfunction
• Clinically: stool reaches the rectum normally but cannot be expelled; patient reports straining, digital assistance, or positional maneuvers
• Less directly responsive to abdominal massage than slow-transit constipation, but parasympathetic activation still supports internal sphincter relaxation

Medication-Induced Constipation

• Opioid-induced constipation (OIC): Mu-opioid receptors are densely present throughout the myenteric and submucosal plexuses of the gut wall; opioid binding reduces acetylcholine release, decreasing peristalsis; simultaneously increases non-propulsive contractions, electrolyte absorption, and sphincter tone — producing severe constipation that does not resolve with tolerance development to other opioid effects
• Anticholinergic medications: Block muscarinic receptors in the ENS, reducing parasympathetic-mediated peristalsis and secretion
• Calcium channel blockers, iron supplements, antacids (aluminum-containing): Each slows motility through distinct pharmacological mechanisms

Secondary Neurological Causes

• Parkinson's disease: Degeneration of dopaminergic neurons affects the dorsal motor nucleus of the vagus — reduces parasympathetic drive to the colon; Lewy body pathology also directly affects the ENS; constipation often precedes motor symptoms by years
• Multiple sclerosis: Demyelinating lesions in the spinal cord disrupt descending autonomic pathways; both slow-transit and outlet dysfunction patterns occur depending on lesion location
• Spinal cord injury: Loss of supraspinal control to the sacral defecation center (S2–S4); upper motor neuron bowel (injury above the conus medullaris) produces a spastic pelvic floor with retained reflex defecation; lower motor neuron bowel (conus/cauda equina injury) produces a flaccid pelvic floor with loss of reflex defecation

Signs and Symptoms

Functional Constipation (Most Common Presentation)

• Fewer than three bowel movements per week
• Hard, dry, pellet-like stools (Bristol Stool Scale types 1–2)
• Straining during defecation (>25% of attempts)
• Sensation of incomplete evacuation after defecation
• Abdominal bloating and distension, often worsening throughout the day
• Diffuse, dull abdominal discomfort — typically relieved by successful defecation or passage of gas
• Reduced appetite from prolonged fullness

Slow-Transit vs. Outlet Dysfunction

Chronic Constipation Consequences

• Hemorrhoids from chronic straining
• Anal fissures from passage of hard, large stools
• Fecal impaction — particularly in elderly or immobile patients
• Rectal prolapse from chronic excessive straining
• Paradoxical diarrhea (overflow incontinence around impacted stool) — may be misinterpreted as diarrhea

Assessment Profile

Subjective Presentation

• Chief complaint: "I haven't been able to go" or "I feel backed up"; reports infrequent bowel movements, bloating, abdominal fullness, straining; may report reliance on laxatives; ask specifically about Bristol Stool Scale type, frequency, and duration of symptoms
• Pain quality: Dull, diffuse abdominal discomfort; cramping associated with ineffective peristaltic attempts; sensation of pressure or fullness in the lower abdomen and rectum; pain is typically relieved by successful defecation
• Onset: Often gradual and chronic; may be acute following surgery (postoperative ileus), medication changes (especially opioid initiation), immobilization, or travel; ask about recent dietary changes, fluid intake changes, and new medications
• Aggravating factors: Sedentary behavior, dehydration, low-fiber diet, stress (sympathetic dominance), ignoring the urge to defecate, opioid or anticholinergic medication use, travel or disruption of routine
• Easing factors: Physical activity (stimulates mass movements via the gastrocolic reflex), adequate hydration and fiber, warm beverages (particularly in the morning — stimulates the gastrocolic reflex), relaxation and parasympathetic-dominant states, abdominal self-massage
• Red flags: Sudden onset constipation in a previously regular individual over age 50 → colorectal cancer screening referral; bloody stools or rectal bleeding → medical referral; unexplained weight loss with constipation → medical referral; severe constant abdominal pain (not relieved by defecation or gas passage) → rule out bowel obstruction — do not treat; fever with abdominal pain and constipation → medical referral; progressive constipation with neurological symptoms (weakness, sensory changes) → neurological referral

Observation

• Local inspection: Abdominal distension (visible bloating, particularly in the lower abdomen); surgical scars (prior abdominal surgery increases adhesion risk and may indicate postoperative ileus history); note any ostomy appliances
• Posture: Guarded posture with trunk flexion to reduce abdominal discomfort; reduced thoracolumbar extension; may hold or support the abdomen; chronic constipation patients may adopt a posture that compresses the abdomen
• Gait: Typically normal; severely distended patients may move cautiously; observe for neurological gait abnormalities if secondary neurological causes are suspected (Parkinsonian shuffling gait, spastic or ataxic gait in MS, wheelchair use in SCI)

Palpation

• Tone: Abdominal wall musculature may be guarded (voluntary protective contraction) or chronically hypertonic from sustained discomfort; rectus abdominis and obliques may be tender to palpation; periumbilical tone often increased; paraspinal muscles (thoracolumbar junction T10–L2) may be hypertonic from viscerosomatic reflex — the thoracolumbar sympathetic outflow to the colon originates here, and chronic visceral irritation produces segmentally related somatic muscle guarding
• Tenderness: Palpable tenderness along the course of the colon — ascending colon (right flank), hepatic flexure (right upper quadrant), transverse colon (epigastric/umbilical region), splenic flexure (left upper quadrant — often the most tender point due to the acute angle of the flexure), descending colon (left flank), and sigmoid colon (left lower quadrant); colonic loading palpation — loaded colon segments palpate as firm, tubular, and tender; fullness in the sigmoid region is particularly significant as it indicates stool accumulation proximal to the rectum
• Temperature: Normal; no local temperature changes expected; warmth in the abdomen would suggest inflammatory pathology (appendicitis, diverticulitis, IBD flare) rather than functional constipation — investigate further before proceeding with abdominal massage
• Tissue quality: Abdominal fascia may be restricted and inelastic, particularly in chronic constipation with habitual guarding; adhesions from prior abdominal surgery may produce localized areas of reduced fascial mobility; visceral mobility may be assessed as reduced — the ascending and descending colon normally have limited mobility but the transverse colon and sigmoid should have some glide

Motion Assessment

• AROM: Trunk rotation and lateral flexion may be restricted by abdominal guarding or distension; forward flexion may be limited by discomfort from increased intra-abdominal pressure; hip flexion may compress the abdomen and provoke discomfort; deep breathing (diaphragmatic excursion) may be reduced — assess rib expansion as an indirect marker of diaphragmatic mobility
• PROM / end-feel: Trunk PROM may reveal an elastic-muscular end-feel from abdominal wall guarding rather than a capsular or bony restriction; passive hip flexion bringing the knee toward the chest may provoke abdominal discomfort; palpate abdominal wall tension during passive trunk rotation to assess guarding
• Resisted testing: Generally normal; no specific weakness pattern expected; resisted trunk flexion may provoke abdominal discomfort but should not produce weakness; any focal weakness suggests a neurological cause requiring further investigation

Special Test Cluster

If neurological signs are present (new weakness, sensory changes, gait disturbance), add a neurological screening (DTRs, Babinski, dermatomal sensation) to evaluate for secondary neurological cause (SCI, MS, Parkinson's).

Differential Assessment