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COLORECTAL MOTILITY DISORDERS

Mukta Bapat*, Philip Abraham+

*Lecturer; +Professor and Head, Department of Gastroenterology, KEM Hospital, Mumbai 400 012.

INTRODUCTION

Motility disorders of the large intestine, though common, are often more puzzling to diagnose than treat. The colon, because of the relative difficulty in positioning probes in it, has remained an incompletely explored organ for motility studies. Much of the information available about motility of the colon has been extrapolated from animal studies.

Physiology

The colon is involved in salt and water exchange, storage and elimination of faeces, and supporting a microbacterial environment essential for maintenance of colonic mucosal integrity. Colonic motility affects the efficiency of these complex functions. Colonic peristalsis facilitates contact between faeces and colonic mucosa and allows efficient salt and water reclamation. The enteric nervous system (submucosal and myenteric plexus) locally co-ordinates the contraction of circular and longitudinal smooth muscles of the colon. In turn, the enteric nervous system is under the control of spinal and cortical neural signals.

Colonic movements consist of ring contractions and sleeve contractions which finally result into forward mass movement of faeces, and emptying of sigmoid colon and rectum of defaecation. Colonic dysmotility results from perturbation of neuromuscular function at any level. Dysmotility can lead to altered frequency because of altered transit time or altered rhythm of colon. This may happen primarily due to direct neurological damage such as spinal cord injuries, traumatic denervation of anal sphincter, or as a neurological manifestation of systemic disorders such as diabetes mellitus or systemic sclerosis or due to imbalance between neurotransmitters of the gut.

Colonic motility disorders result from:
1.Primary and secondary smooth muscle disorders.

2.Familial and sporadic visceral neuropathies.

3.Neurological disorders like Parkinson's disease.

4.Small intestinal diverticulosis.

5.Endocrine and metabolic disorders.

6.Drugs like opiates, tricyclics, etc.

Clinical presentation

Patients with colonic dysmotility present with diverse symptoms, common being gas bloat, abdominal fullness, pain, constipation and diarrhoea. Bacterial overgrowth in stagnant portions of the bowel may result in painful diarrhoea. Hirschsprung's disease, characterized by colonic aganglionosis, generally manifests early in life in the form of progressive constipation resulting in megacolon on barium studies. Faecal incontinence forms an important subset of rectal dysmotility. Diverticular disease is also thought to result from colonic dysmotility in the form of elevated resting and postprandial colonic luminal pressures leading to hyper-segmentation and diverticulosis.

Irritable bowel syndrome is the commonest entity resulting from dysmotility. Constipation occurs frequently in patients with diabetes mellitus who require insulin. Diarrhoea in these patients appears to be more due to small bowel electrolyte and fluid secretion than to neuropathy. Patients with scleroderma show evidence of colonic dysmotility in late stage of the disease as smooth muscle atrophies and is replaced by collagen. Bowel function is disturbed in patients with generalized neuromuscular disorders. They have colonic smooth muscle dystrophy leading to pseudo-obstruction and prolonged contraction of internal and external anal sphincters.

The decision to attribute a symptom to colonic dysmotility is made only after excluding possible non-neurological organic causes. A few guidelines may be helpful. Presence of fever, severe pain, abdominal distension (and not only gas bloat), obstipation, bleeding per rectum, weight loss, recent change in bowel habits in old age, alternating constipation and diarrhoea should alert the physician to investigate for an organic cause.

Clinical examination also helps to recognize the presence of organic disease unrelated to motility disorder. Presence of fever, anaemia, lymphadenopathy, extraintestinal manifestations of systemic diseases like systemic sclerosis or thyroid disorders, abdominal lump make a diagnosis of colonic dysmotility unlikely.

Differential diagnosis of colonic dysmotility

A.Constipation-predominant disorders:

1.Diverticular disease of colon

2.Adenocarcinoma of colon

3.Gynaecological disorders like uterine tumours, endometriosis

4.Appendicitis

5.Peptic ulcer disease

6.Cholecystitis

7.Metabolic disorders like diabetes mellitus, hypothyroidism

B.Diarrhoea-predominant disorders:

1.Infective diarrhoea

2.Ulcerative colitis

3.Pseudomembranous colitis

4.Lactose intolerance

5.Metabolic disorders like hyperthyroidism, Zollinger-Ellison syndrome, carcinoid syndrome, Addison's disease

6.Malabsorption

A systematic approach which includes detailed history, proper clinical examination including structural and functional evaluation of pelvic floor, and a set of appropriate investigations make diagnosis and management of colonic dysmotility easy.

Investigations

1.Routine stool examination for ova, parasites, blood, leucocytes, culture.

2.Flexible sigmoidoscopy with biopsy when necessary.

3.Colonoscopy if suspicion of malignancy is high.

4.Upper GI endoscopy with small bowel biopsy when necessary (optional).

5.Barium examination of small and large bowel if endoscopic examination is not possible.

6.Investigations for aetiology in relevant setting such as blood sugar, thyroid profile, serum drug levels.

Investigations specific for motility disorders

6. Colonic transit studies : The radio-opaque marker study of colonic transit is the most widely used technique to assess colonic motility in constipated patients. This may be performed as a first specific test in patients with infrequent defaecation. Materials for transit studies are prepared by cutting small pieces of a small-caliber radio-opaque tube and placing them in a capsule. Twenty such markers are swallowed on three consecutive days and plan radiographs are obtained on the fourth and seventh days to calculate the number of markers seen in three segments of the colon, viz., right, left and rectosigmoid. Transit time can be calculated by a formula. This study can differentiate between colonic inertia and outlet obstruction as the markers will be spread evenly throughout the colon and predominantly in the rectosigmoid region, respectively.

7. Anorectal manometry : This test is performed to diagnose specific conditions like Hirschsprung's disease. Faecal incontinence can be confirmed by testing rectal sensation and compliance in cases of traumatic or atraumatic denervation of internal sphincter. A decision on colostomy closure can be guided in case of Hirschsprung's disease.

Management

Treatment of colonic dysmotility depends upon the primary condition. For example, endocrine disorders are treated by hormonal therapy. Primary motility disorders are treated according to the symptoms. Major symptoms requiring relief are abdominal pain and altered bowel habits.

Dietary therapy

This forms a first step of treatment. Increase in fiber content helps to increase the bulk of stool and lessen the intraluminal pressure, thus alleviating the pain. As fat is a potent colonic stimulant and amino acids inhibit colonic movements, alterations in fat and protein content of the diet help to decrease symptoms of hypermotility.

Pharmacotherapy

Laxatives : A variety of laxatives are available over the counter. These include stimulants like cascara and senna, emollients like liquid paraffin, bulk-forming agents like bran and ispagullah, and osmotic substances like milk of magnesia, polyethylene glycol, lactulose, sorbitol. Use of stimulant laxatives should be discouraged due to serious side effects like electrolyte imbalance and damage to enteric neurons.

Drugs useful in constipation and colonic inertia : Cisapride is an agent that stimulates colonic motility and hence is more useful in patients with colonic inertia than in those with constipation and normal transit time. It has been successful in treating colonic pseudo-obstruction and irritable bowel syndrome. Addition of a cholinergic agent may give a synergistic effect. The effect of metoclopramide and domperidone on the colon is variable.

Drugs useful in diarrhoea-predominant dysmotility : Dietary fibres improve the consistency of stool due to their hydrophilic nature and thus decrease stool content. Opiate analogues like loperamide and diphenoxylate are mainstays of treatment of uncomplicated mild diarrhoea. These drugs decrease the water content and also increase the anal sphincter pressure, and thus help to maintain continence. Antispasmodic agents are useful in symptomatic management of these patients.

Psychotropic therapy : Change in the individual's response towards the symptoms may help. Mild tranquilizers, tricyclic antidepressants, and psychotherapy in selected individuals improves the outcome of the treatment.

Surgical therapy : Hirschsprung's disease and faecal incontinence require definitive surgical correction. Surgery in the form of total colectomy and ileorectal anastomosis for severe constipation is however reserved for patients who have resistant constipation and colonic inertia without pelvic floor dysfunction.

Pelvic floor testing, biofeedback training and behavioural therapy are not yet available in Indian clinical practice. These therapies are particularly useful in patients with constipation and pelvic dysfunction.


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