Constipation

Primary constipation:

Due to disordered regulation of colonic and anorectal neuromuscular functions as well as brain-gut neuroenteric function. Primary constipation includes slow transit constipation and evacuation disorders (dyssynergic defecation).
Multiple possible aetiologies have been proposed for irritable bowel syndrome-constipation (IBS-C) that include genetic, environmental, social, biological, and psychological factors.[23]

Secondary constipation:

Results from a plethora of factors such as metabolic disturbances (hypercalcaemia, hypothyroidism), drugs (e.g., opioids, calcium-channel blockers, antipsychotics, tricyclic antidepressants), neurological disorders (parkinsonism, spinal cord lesions, diabetes mellitus), and primary diseases of the colon (stricture, cancer, anal fissure, proctitis).
While there is a definite association between rectocele and constipation, causality or the direction of causality is not entirely clear. It is unclear if rectocele causes constipation or constipation predisposes to rectocele formation.

Pregnancy-associated constipation:

Constipation during pregnancy is mainly attributed to hormonal, drug-related, and physiological changes.[21][22] Increased progesterone levels may be the cause of slowed gastrointestinal motility in the first trimester, while pressure of the gravid uterus on the rectosigmoid colon may lead to obstruction in the last trimester.[21][22]

Slow transit constipation (STC) is related to primary dysfunction of colonic smooth muscle (myopathy) or its innervation (neuropathy), or both.[24] Studies have confirmed that patients with STC exhibit significantly impaired phasic colonic motor activity, and gastrocolonic and morning waking responses, although the diurnal variation of colonic motility is preserved.[24][25] Periodic motor activity in the rectosigmoid area is increased, serving as a brake for colonic food propulsion.[25] Additionally, there is a significant decrease not only in the number of high-amplitude propagated contractions (HAPC) but also in the velocity of propagation and amplitude, leading to premature abortion of these waves in patients with constipation.[24][25][26]

Dyssynergia seems to be an acquired behavioural disorder of defecation in two-thirds of adult patients with difficult defecation, stemming from faulty toilet training, behavioural problems, or parent-child conflicts.[3] In a prospective study, most patients with dyssynergic defecation showed the inability to coordinate the abdominal, rectoanal, and pelvic floor muscles during attempted defecation.[3][27] Failure of rectoanal coordination consisted of either paradoxical anal contraction, inadequate anal relaxation, or impaired rectal/abdominal propulsive forces.[3] Additionally, two-thirds of these patients exhibit rectal hyposensitivity.[3]

Types of constipation

Primary: due to disordered regulation of colonic and anorectal neuromuscular functions as well as brain-gut neuroenteric function. Using symptom-based criteria, an international panel of experts has classified constipation into:[5][6][7]

Functional defecation disorders:
- Dyssynergic defecation: paradoxical contraction or inadequate relaxation of the pelvic floor muscles during attempted defecation[8]
- Slow transit constipation: inadequate defecatory propulsion (inadequate propulsive forces during attempted defecation)
- Irritable bowel syndrome-constipation (IBS-C).

Secondary: constipation secondary to another condition such as diet, drugs, pregnancy, or behavioural, endocrine, metabolic, neurological, and primary diseases of the colon (stricture, cancer, anal fissure, proctitis).[9]

Pathophysiology

Classification

Types of constipation