Chronic constipation is common, but Slow Transit Constipation (STC) is a distinct and often severe subtype of functional constipation. STC is characterized by a physical delay in the movement of waste through the large intestine, or colon. This delay causes significant discomfort and reduces the quality of life. Understanding the physiological failure that defines STC is crucial for effective management.
Defining Slow Transit Constipation
Slow Transit Constipation is fundamentally a motility disorder where the colon’s ability to generate propulsive force is impaired. The large intestine relies on rhythmic, muscular contractions, known as peristalsis, to move stool toward the rectum for elimination. In STC, this coordinated movement is significantly reduced or absent, causing waste material to linger abnormally long. This delayed passage allows excessive water absorption, resulting in hard, dry feces that are difficult to pass.
STC differs from other forms of chronic constipation. Normal transit constipation involves appropriate stool speed, but patients still experience symptoms like hard stools. Defecation disorders relate to a lack of coordination in the pelvic floor muscles, preventing the final expulsion of stool. STC is defined by a measurable, generalized sluggishness throughout the entire colon.
Underlying Causes of Impaired Motility
The physical cause of STC lies in a breakdown of the system that regulates colonic movement. The colon’s motor function is coordinated by the enteric nervous system (ENS), often called the “brain of the gut,” and specialized pacemaker cells called the Interstitial Cells of Cajal (ICCs). ICCs are responsible for generating the electrical slow waves that lead to muscular contractions.
In many STC cases, there is an underlying abnormality in this neuromuscular apparatus. This may manifest as an enteric neuropathy, involving damage or abnormal neurons in the ENS, or as a myopathy, which is a weakness or degeneration of the smooth muscle wall of the colon. A reduction in the number of ICCs has also been observed in the colon tissue of some patients.
These abnormalities lead to a reduction in High-Amplitude Propagating Contractions (HAPCs), the powerful mass movements that propel content over long distances. When the cause cannot be identified, the condition is termed idiopathic colonic inertia. Secondary causes, such as neurological diseases (Parkinson’s), systemic conditions (diabetes), or medications (opioids and antidepressants), can also disrupt the ENS and mimic STC.
Diagnostic Procedures and Testing
Confirming a diagnosis of STC requires objective testing to measure how quickly waste moves through the colon and to rule out other causes of constipation. The primary tool is the Colonic Transit Study, most commonly performed using radiopaque markers, often called the Sitz Marker Study.
For this test, the patient swallows a capsule containing small, radio-dense markers visible on X-ray. Abdominal X-rays are taken on specific days, typically five days after ingestion, while the patient refrains from taking most laxatives. If more than 20% of the markers remain in the colon after five days, the transit time is considered prolonged, confirming slow colonic transit.
A Colonic Manometry study may be performed for patients with severe symptoms who have not responded to medical therapy. This procedure involves inserting a specialized catheter into the colon to measure pressure changes and muscular contractions. Manometry helps characterize the physiological problem by measuring the frequency and force of contractions, sometimes differentiating between neuropathy and myopathy. Furthermore, tests like Defecography or Anorectal Manometry assess the function of the rectum and pelvic floor, ensuring the delay is not an outlet obstruction mimicking STC.
Comprehensive Management Strategies
The management of STC follows a stepwise approach, starting with conservative measures and progressing to aggressive pharmacological and surgical options for refractory cases. The initial approach focuses on optimizing stool volume and consistency. Standard lifestyle changes often have limited success in true STC. Dietary fiber supplementation may be attempted but can sometimes worsen symptoms like bloating if the colon is severely dysfunctional. Therefore, increasing fluid intake and using osmotic laxatives like polyethylene glycol are preferred to soften the stool.
When initial steps fail, the focus shifts to prescription medications designed to actively stimulate the colon.
Prokinetic Agents
These drugs enhance gastrointestinal motility by increasing the strength and frequency of contractions. Prucalopride, a selective serotonin 5-HT4 receptor agonist, is an example that stimulates the colonic mass movements often absent in STC.
Secretagogues and Stimulants
Secretagogues increase the secretion of fluid into the intestinal lumen, softening the stool and accelerating transit. Examples include linaclotide and lubiprostone, which are approved for chronic constipation. Stimulant laxatives, such as bisacodyl or sodium picosulfate, are also used as they directly stimulate the nerves and muscles of the colon to induce motility.
For patients whose condition is refractory and debilitating despite exhaustive medical therapy, subtotal colectomy with ileorectal anastomosis is the definitive surgical option. This major procedure involves removing the entire colon, leaving only the rectum, and connecting the end of the small intestine (ileum) directly to the rectum. The goal is to eliminate the non-functional organ responsible for the transit delay. While surgery can significantly relieve the infrequency of bowel movements, it is associated with risks such as fecal incontinence and small bowel obstruction, and is reserved for the most severe cases.