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Constipation and PUD
Constipation and PUD
Constipation and PUD
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 Ì 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.