Analgesics
Bile acid sequestrants
Antacids (aluminum, calcium)
Calcium-channel blockers
Antiarrhythmics
Chemotherapy agents
Anticholinergic agents
Diuretics (potassium wasting)
Anticonvulsants
Iron supplements
Antihistamines
Nonsteroidal anti-inflammatory agents
Antihypertensives
Opioids
Anti-Parkinson Agents
Tricyclic antidepressants
Antipsychotics
5-HT3 receptor antagonists
Antispasmodics
Table 7.2
Medication associated with diarrhoea
Abuse of laxatives | Antihypertensives |
Antacids (magnesium) | Chemotherapy agents |
Antiarrhythmics | Cholesterol lowering agents |
Antibiotics | NSAID |
Antidiabetics | Proton pump inhibitors |
11 Neurology
Normal nerve supply is crucial for colorectal and anal function. Neuronal control of colorectal function has four levels: (a) the enteric nervous system within the bowel wall, (b) the prevertebral sympathetic ganglia, (c) the autonomic nervous system within the brain stem and spinal cord, and (d) higher cortical centers.
Disorders of the enteric nervous system may be localized to a short segment as seen in most cases of Hirschsprung’s disease or irradiation damage. More general damage to the ENS can be seen in diabetes, Chagas’ disease, chronic idiopathic pseudo-obstruction, and as paraneoplastic phenomena.
Damage to the reflex center in the sacral spinal cord or to the cauda equina is usually traumatic, iatrogenic (after neurosurgery), or congenital as in spina bifida. An interrupted reflex arch from the sacral spinal cord to the left colon, the rectum, and the anal canal results in a hypotone, flaccid left colon and rectum (Krogh et al. 2002). This is followed by reduced emptying of the rectosigmoid at defecation and severely prolonged transit through the left colon and rectum causing fecal impaction (Krogh et al. 2003).
Lesions above the reflex center in the sacral spinal cord are commonly seen after traumatic injury or spinal surgery. The result is usually increased tone and contractility of the left colon and rectum and prolonged transit throughout the colorectum.
Cerebral lesions , whether congenital, vascular, or traumatic, are associated with constipation. The exact mechanism is not fully explored but may be a combination of immobility, lack of supraspinal reflex control, and deficits.
Lesions of the central nervous system or the peripheral nerves to the anorectum may cause fecal incontinence due to a combination of reduced anorectal sensibility and lack of voluntary control of the external anal sphincter. Hence, most patients with spinal cord lesions and spina bifida as well as many with multiple sclerosis and stroke suffer from severe constipation and fecal incontinence.
Parkinson’s disease in not a disease isolated to the substantia nigra. There is also loss of dopamine in the enteric nervous system and autonomic neuropathy. The result is constipation the severity of which is closely related to the severity of the classical neurological symptoms. Dystonia of striated muscle cells is a common feature of Parkinson’s disease. Dystonia of the external anal sphincter is the cause of difficult rectal evacuation commonly seen in patients with Parkinson’s disease.