Constipation

 Definition: infrequent passage of stool (<3 times weekly) or difficulty in defecation, with straining or discomfort.
 Epidemiology: more than 4 million people in the USA annually
 Causes of constipation
o General
 Poor diet
 Inadequate fluid intake or dehydration
 Immobility (or lack of exercise)
 Irritable bowel syndrome
 Old age
 Post-operative pain
 Hospital environment (lack of privacy, having to use a bed pan)
 Distant, squalid, or otherwise unsatisfactory toilets
o Anorectal disease
 Anal fissure
 Anal stricture
 Rectal prolapse
 Intestinal obstruction
 Colorectal carcinoma
 Strictures (eg Crohn's disease)
 Pelvic mass (eg fetus, fibroids)
 Diverticulosis (rectal bleeding is a commoner presentation)
 Pseudo-obstruction
o Metabolic/endocrine
 Hypercalcaemia
 Hypothyroidism (can cause constipation, but rare in those presenting with constipation)
 Hypokalaemia
 Porphyria
 Lead poisoning
o Drugs
 (anticipate the potential effect and give dietary advice)
 Opiate analgesics (eg morphine, codeine)
 Anticholinergics (tricyclics, phenothiazines)
 Iron
o Neuromuscular
 (slow transit with ↓propulsive activity)
 Spinal or pelvic nerve injury (eg trauma, surgery)
 Aganglionosis (Chagas' disease, Hirschsprung's disease)
 Systemic sclerosis
 Diabetic neuropathy
o Other causes
 Chronic laxative abuse (rare—diarrhoea is commoner)
 Idiopathic slow transit
 Idiopathic megarectum/colon
 Psychological.
 History:
o Frequency, nature, and consistency of the stool.
o Blood or mucus in/on the stools?
o Is there diarrhoea alternating with constipation?
o Has there been a recent change in bowel habit?
o Ask about diet and drugs.
 Examination:
o Distended abdomen, PR exam noting sphincter tone, masses, faeces.
 Investigations:
o Bloods:
2+
 FBC  Anemia, U&E  electrolytes (hypokalemia), Ca (high), TFT (high TSH and low T4). Sigmoidoscopy and biopsy of abnormal mucosa.
o Imaging:
 Barium enema if suspected colorectal malignancy.
o Invasive:
 Sigmoidoscopy and biopsy of abnormal mucosa
 Colonoscopy if suspected colorectal malignancy.
 Special investigations (eg transit studies; anorectal physiology) are occasionally needed!
 Management:
o Treat causes.
o Advise exercise and a good fluid intake (a high-fibre diet is often advised, but may cause bloating without helping constipation). Consider drugs only if these measures fail,
and try to use them for short periods only. Often, a stimulant such as senna a bulking agent is more effective and cheaper than agents such as lactulose.
o Bulking agents
 Increase faecal mass, so stimulating peristalsis.
 Taken with plenty of fluid and may take a few days to act.
 CI: difficulty in swallowing; intestinal obstruction; colonic atony; faecal impaction.
 Bran powder 3.5g 2-3 times/d with food (may hinder absorption of dietary trace elements if taken with every meal).
 Ispaghula husk, eg 1 Fybogel® 3.5g sachet after a meal, mixed in water and swallowed promptly (or else it becomes an unpleasant sludge).
 Methylcellulose, eg Celevac® 3-6 500mg tablets/12h with ;300mL water. Sterculia, eg Normacol® granules, 10mL sprinkled on food daily.
o Stimulant laxatives
 increase intestinal motility, so
 Do not use in intestinal obstruction or acute colitis.
 Avoid prolonged use as it may cause colonic atony and hypokalaemia (but there are no good long-term data).
 Abdominal cramps are an important SE.
 Pure stimulant laxatives are
 bisacodyl tablets (5-10mg at night) or suppositories (10mg in the mornings) and
 senna (2-4 tablets at night).
 Docusate sodium and danthron (=dantron) have stimulant and softening actions.
 Glycerol suppositories act as a rectal stimulant.
 Sodium picosulfate (5-10mg up to 12h beforehand) is useful for rapid bowel evacuation prior to procedures.
o Stool softeners
 are particularly useful when managing painful anal conditions eg fissure.
 Arachis oil enemas lubricate and soften impacted faeces.
 Liquid paraffin should not be used for a prolonged period (SE: anal seepage, lipoid pneumonia, malabsorption of fat-soluble vitamins).
o Osmotic laxatives
 retain fluid in the bowel.
 Lactulose, a semisynthetic disaccharide, produces osmotic diarrhoea of low faecal pH that discourages growth of ammoniaproducing organisms.
 It is useful in hepatic encephalopathy (initial dose: 30-50mL/12h). SE: bloating &Igrave; it has a limited role in the treatment of constipation.
 Magnesium salts (eg magnesium hydroxide; magnesium sulfate) are useful when rapid bowel evacuation is required. Sodium salts (eg Microlette® and
Micralax® enemas) should be avoided as they may cause sodium and water retention.
 Phosphate enemas are useful for rapid bowel evacuation prior to procedures.
o What if laxatives don't help?
 A multi-disciplinary approach:
 Behaviour therapy, psychological support, habit training ± sphincter-action biofeedback may help.
 5HT4 agonists, which induce peristalsis by systemic rather than luminal means, are under trial (tegaserod and prucalopride: neither currently licensed in UK).
 Complications: Hemorrhoids, anal fissure, diarrhea, fecal incontinence, PR bleed, rectal prolapse, faecal impaction, uterine hernia, and uterine prolapse.
 Prognosis: deaths from Constipation: 29 deaths in the USA 1982-85.
Peptic Ulcer Disease
 Definition: Gastric and duodenal ulcers caused commonly by H. Pylori infection
 Epidemiology: 50-60% of adults worldwide, duodenal ulcers are more common
 Causes of PUD:
o H. Pylori infection
o Smoking
o NSAIDs
o Zollinger-Ellison
o Steroids
o Hypercalcemia
 Risk factors: Smoking, NSAIDs, Steroids, Blood group O
 Pathology:

o
o “Gastric ulcers are found in any part of the stomach, but are most commonly seen on the lesser curve. Most duodenal ulcers are found in the
duodenal cap; the surrounding mucosa appears inflamed, haemorrhagic or friable (duodenitis). Erosions are superficial mucosal defects,
whereas in a peptic ulcer there is a break in the superficial epithelial cells penetrating down to the muscularis mucosa at the site of the
ulcer; there is a fibrous base and an increase in inflammatory cells. H. pylori-induced gastritis is present, confined to the antrum in DU disease
but also involving the body in gastric ulcer disease.”
 History:
o Epigastric pain;
 Duodenal ulcers, worse at night and when the patient is hungry
 Gastric ulcers; worse when eating
 Relieved by antacids
o Nausea & Vomiting  relieves pain
o Heartburn
o Anorexia and weight loss; particularly gastric ulcers
o Perforation: septic patient with acute abdomen and signs of peritonism (guarding, rigidity, tenderness)
 Examination:
o PR exam noting sphincter tone, masses, faeces.
 Investigations:
o Non-invasive methods
 13C Urea breath test. This is a quick and easy way of detecting the presence of H. pylori and is used as a screening test. The
measurement of 13CO2 in the breath, after ingestion of 13C urea, requires a mass spectrometer, which is expensive, but the test
is very sensitive (97%) and specific (96%). The breath test is also used to demonstrate eradication of the organism following
treatment.
 Serological tests detect IgG antibodies and are reasonably sensitive (90%) and specific as serology.
 Stool test. A specific immunoassay using monoclonal antibodies for the qualitative detection of H. pylori antigen is widely
available. The overall sensitivity is 96% with a specificity of 97%. It is useful in the diagnosis of H. pylori infection and for
monitoring efficacy of eradication therapy. (Patients should be off PPIs for 1 week but can continue with H2 blockers.)
o Invasive (endoscopy)
 Rapid urease test. Gastric biopsies are added to a urea solution containing phenol red. If H. pylori are present, the urease enzyme
splits the urea to release ammonia which raises the pH of the solution and causes a rapid colour change.
 Culture. Biopsies obtained can be cultured on a special medium, and sensitivities to antibiotics can be ascertained.
 Histology. H. pylori can be detected histologically on routine (Giemsa) stained sections of gastric mucosa obtained at endoscopy.
 Management:
o Stopping smoking
o Triple therapy for 1 week with antibiotics and PPIs continued for 6 weeks:
 omeprazole 20 mg + metronidazole 400 mg and clarithromycin 500 mg (all twice daily)
 omeprazole 20 mg + clarithromycin 500 mg and amoxicillin 1 g (all twice daily).
o Surgical therapy:
 Considered when there is
 Recurrent uncontrolled bleeding
 Perforations
 Partial gastrectomy or vagotomy
 Complications of surgery:
 Dumping syndrome
 Diarrhoea
 Nutritional deficiencies: anemia, iron def., vit B12, folate def.
 Anorexia
 Complications: haemorrhage (emergency, cross-match 6 Units, 2 14G IV lines, loads of fluids, get the surgeons involved!), perforation (treat with NG suction,
IV fluids and Cefuroxime 1.5g/TDS + Metronidazole 500mg/TDS refer for urgent surgery), gastric outlet obstruction (due to oedema surrounding the ulcer)
 Prognosis: 0.1% death rate, usually good.