Golwalla’s Medicine for Students Milind Y Nadkar, Aspi F Golwalla, Sharukh A Golwalla
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GastroenterologyCHAPTER 1

Naked eye—Consistency, presence of blood, mucus, helminths. Occult blood if positive suggests – GI bleeding, growth, tuberculous lesion or inflammatory bowel disease. Some patients on aspirin, mesenteric vascular disease, vegetative forms and cysts of E. histolytica.
Microscopic—For RBCs, pus cells in bacillary dysentery and inflammatory bowel disease. Presence of ova of Ascaris or Ankylostoma.
Stool culture in selected cases of chronic infective diarrhoea and pseudomembranous colitis.
RBC count, Hb, MCV, blood film, serum iron, iron binding capacity, red cell folate, serum B12, serum albumin, serum electrolytes.
Are usually not measured, but sometimes provide useful corroborative information. In normal people, basal acid output is about 2–4 mmol/hour rising to about 10–30 mmol/hour in the hour after s.c. injection of Pentagastrin 6 mcg/kg. Pentagastrin not available nowadays (An endoscopic method for measuring gastric acid output has been developed but requires further validation). Gastric acid measurements are of diagnostic value:
  1. When a gastrinoma is suspected.
  2. An ulcer has recurred after surgery.
  3. To detect achlorhydria in case of gastric ulcer.
    Occurrence of gastric ulcer in presence of achlorhydria is indicative of malignancy since most cases of benign gastric ulcer have some acid secretion.
Multiple ulcers or ulcers in unusual locations associated with severe oesophagitis, resistant to therapy, preoperative family history of peptic ulcer disease, postoperative ulcer recurrence, basal hyperchlorhydria, unexplained diarrhoea or steatorrhoea, hypercalcaemia, prominent gastric or duodenal folds.
Plain films of abdomen. Supine and erect films are taken for diagnosis of any acute abdominal condition especially obstruction or perforation. It can also reveal changes in soft tissues produced by masses or inflammation, pneumoperitoneum, gallstones, calcification of gallbladder wall, liver calcification, urinary calculi, appendoliths.
Chest radiographs can reveal a small pneumoperitoneum, level of the diaphragm, intrathoracic conditions, e.g. pneumonia.
With advances in endoscopy, the role of barium studies has now become restricted to barium swallow for the oesophagus and small bowel enema/enteroclysis for the jejunum and ileum. Now the CT scan has also become an important modality for small bowel pathology, especially with the use of CT enteroclysis (Fig. 1). Table 1 enumerates various conditions that can be diagnosed on barium studies.
Diagnostic indications for endoscopy are listed in Table 2.
Colonoscopy is gold standard for diagnosis of colonic mucosal disease.2
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Fig. 1: Enteroclysis CT abdomenFigs.
Contraindications for colonoscopy—Perforated intestine, acute diverticulitis, deep ulcerations, severe ischemic necrosis, fulminant colitis, severe cardiac or pulmonary diseases.
Capsule endoscopy. CE is performed by ingestion of a small, disposable battery powered pill containing a metal oxide semi-conductor camera. Four light emitting diodes illuminate the lumen of the bowel.
Indications—1. Obscure GI bleeding. 2. Small bowel Crohn's disease. 3. Diagnosis of coeliac disease and its complications. 4. Screening for polyps for small bowel polyposis syndromes and small bowel tumours. 5. NSAIDs enteropathies.
Contraindications—1. Patients with known or suspected obstruction, strictures, fistulas. 2. Patients with cardiac pacemaker or other implanted electromedical devices. 3. Patients with swallowing disorders. 4. Pregnancy.
USG of GI tract
USG is an important modality in abdominal imaging.
Indications. 1. Congenital—Hypertrophic pyloric stenosis, malrotation. 2. Acute bowel pathology—Appendicitis, obstruction, intussusception, colitis, sigmoid diverticulitis. 3. Tumours. 4. Miscellaneous—Ileocaecal tuberculosis, duodenal ulcer, round worms.
Endoscopic Ultrasonography
Table 1   Conditions diagnosed on barium studies
Barium swallow
Oesophageal filling defects
Strictures (sensitivity greater than that of endoscopy)
Gastro-oesophageal reflux
Oesophageal varices
Oesophageal webs
Barium meal
Peptic ulcer
Gastric ulcer
Outlet obstruction
Disorders of gastric emptying
Barium meal with follow-through
Abdominal pain
Persistent GI bleed
Partial bowel obstruction
Crohn's disease
Small bowel enema
Same as barium follow-through
Barium enema (Double-contrast)
Narrowing of lumen
Strictures (colonic diverticulitis, Crohn's disease)
Dilatation of lumen
Obstruction, volvulus, paralytic ileus,
ulcerative colitis, megacolon, Hirschsprung's disease.
Filling defects
Diverticular disease
Displacement of colon (Hepatosplenomegaly, pelvic tumours)
With EUS, lesions located in the gut wall as well as those immediately outside it can be well seen. Endoscopic ultrasonography is useful in diagnosis of submucosal tumours and in assessing the infiltration and depth of malignancy f GGI tract, and also in detection of metastasis in nearby lymph nodes.
Indications—Cancer of oesophagus, mediastinal masses, submucosal tumours, bile duct stones, pancreatic tumours, pancreatic pseudocysts, gallbladder microlithiasis, ampullary growths. Colorectal stenting.
Contraindications for colonoscopy—Perforated intestine, acute diverticulitis, deep ulcerations, severe ischemic necrosis and fulminant colitis, severe cardiac or pulmonary diseases.3
Table 2   Diagnostic indications for endoscopy
Upper GI endoscopy
Hiatal hernia
Reflux oesophagitis
Barrett's oesophagus
Mallory-Weiss syndrome
Corrosive ingestion (Fig. 3)
Ulcers (including biopsy for H. pylori)
Menetrier's disease
Infiltration (Lymphoma)
Upper GI bleed
Gastric outlet obstruction
Post-op. stomach
Lower GI endoscopy
Radiological abnormality anastomosis
Inspection of colon
Lower GI bleed
Follow up of polyp or cancer
Some cases of colitis
(Barium enema does not adequately visualise this area).
Proctoscopy—For examination of middle and lower parts of anal canal, e.g. haemorrhoids, fissures, carcinoma of anorectal region.
Sigmoidoscopy—To evaluate rectum or sigmoid colon before anorectal surgery or in a patient in whom barium enema is indicated. (Primarily used for evaluation of diarrhoea and rectal outlet bleeding)
Mucosal biopsies can be obtained under direct vision with endoscope (oesophagus, stomach, duodenum, rectum, colon). Small intestinal biopsy can be obtained with pinch biopsy forceps. Normal histology with a well-formed villous pattern almost excludes diffuse small intestinal mucosal disease. In difficult cases, jejunal biopsy with a suction (e.g. Crosby) capsule may provide further information, and allows examination of dissecting microscopic appearances.
Oesophageal Motility
Barium swallow with video fluoroscopy:
Upper oesophageal sphincter disorders
Body motility
Non-propulsive (tertiary contractions)
Uncoordinated or weak post-swallow contractions
Upper oesophageal sphincter—Tone of the sphincter and relaxation during swallowing.
Lower oesophageal sphincter tonic pressure and relaxation.
Gastric emptying—Amount of radioisotope retained in the stomach against time, carried out following a test meal containing labelled solids and liquids with different isotopes.
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Figs. 2A and B: Carcinoma of oesophagus
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Fig 3: Oesophagitis due to corrosive ingestion
Small Intestinal Transit
Barium follow-through—Noting the time taken for contrast to reach terminal ileum (normal about 90 minutes)
Lactulose-hydrogen breath test—Measuring serial breath hydrogen samples following ingestion of a non-absorbable carbohydrate. Rise in breath hydrogen concentration suggests arrival of poorly digested carbohydrate due to fermentation by colonic bacteria.
Colonic transit. Plain radiograph of abdomen on day 5 after ingestion of different shapes of inert pellets on days 1–3. The test is useful in evaluation of chronic constipation due to slow transit.
Radionuclide imaging becomes necessary when barium studies and endoscopy are not conclusive.
  • Gastric emptying time—for gastroparesis
  • Urea breath test for diagnosis of H. pylori
  • Meckel's scan for diagnosis of Meckel's diverticulum
  • Labelled red cell scan for recurrent or obscure GI bleeding.
  • Labelled leucocyte scan for localised abscess collections in inflammatory bowel disease.
  • SeHCAT scan for diagnosis of diarrhoea (bile acid-related)
  • Triolein scan for diagnosis of malabsorption
  • Epithelial permeability test for investigation of protein-losing enteropathy.
Transfemoral triple vessel angiography (coeliac axis, superior and inferior mesenteric arteries) is used when the site of bleeding cannot be determined by endoscopy. Endoscopic ultrasonography is useful in diagnosis of submucosal tumours and in assessing the infiltration and depth of malignancy of GI tract, and also in detection of metastasis in nearby lymph nodes.
  • Abdominal masses (cysts, tumours, abscess, hepato/splenomegaly)
  • Ascites
  • Depth of invasion of tumours (endoluminal endoscopic scan)
  • Aspiration biopsy
CT Scan
  • Bowel wall thickening
  • Large colonic carcinoma
  • Depth of invasion of tumours
Apart from developmental anomalies such as tongue tie, following variations are without clinical significance:
  1. Fissured tongue (Scrotal tongue)—Deep fissures mostly in longitudinal direction.
  2. Geographical tongue (Benign migratory glossitis or the wandering rash of the tongue)—For no apparent reason the filiform papillae disappear in oval patches and leave smooth red areas which look like the boundaries of countries on a map.
  3. Median rhomboid glossitis—Rhomboidal or oval, red, slightly elevated area on the dorsum of the tongue due to failure of fusion of lateral segments of the tongue. (It may be a chronic hypoplastic candidiasis rather than a developmental anomaly).
  4. Furred tongue—Fur is formed continuously and normally removed by food and saliva. Fur is quite marked if the tongue is not used much, and in smokers.
  5. 5 Rough clean tongue—Rather large tongue with unusually well-marked fungiform papillae.
  6. Horny tongue (Crocodile or toad tongue)—Various types of cornification of the mucosa.
Acute—(i) Inflammatory. (ii) Non-inflammatory in angioedema.
Chronic—Acromegaly, myxoedema, Down's syndrome, cretinism, amyloid disease or Von Gierke's glycogen storage disease. Other rare causes are congenital arteriovenous fistula between lingual artery and vein, pachydermoperiostosis, and lymphangioma circumscripta superficialis due to hyperplasia of lymphatic vessels.
Dehydration, atrophic glossitis, wasting due to hypoglossal nerve involvement, facial hemiatrophy, or pseudobulbar palsy (small pointed compact looking tongue). In myasthenia gravis atrophy of the tongue may give rise to triple longitudinal furrowing. Bilateral atrophy (with fasciculations) in progressive bulbar paralysis.
  1. Traumatic—(a) At margins of tongue in epilepsy. (b) Ulcer of frenum (sublingual ulcer) in whooping cough. (c) Dental—opposite a carious tooth.
  2. Tuberculous ulcer—associated with pulmonary tuberculosis. It is painful and tends to occur near the tip of the tongue.
  3. Recurrent aphthous ulcers—of unknown aetiology, or at times with idiopathic steatorrhoea or ulcerative colitis. Rarely from Stevens-Johnson syndrome (erythema multiforme) and Behcet's syndrome (recurrent oral, genital and eye ulceration with neurological signs).
  4. Epitheliomatous ulcer—deep and indurated.
  5. Syphilis—(a) Primary: Indurated painless ulcer, lymphadenopathy. (b) Secondary: ‘Snail track’ ulcers with greyish slough or mucus patches and lymphadenopathy. (c) Tertiary: Often midline, punched out ulcers.
  6. Hand, foot and mouth disease—Round or ovoid ulcers anywhere on mucosa (with vesicular rash on extremities).
  1. Pale tongue in anemia. Blotting paper-like pallor with pigmented margins in Ankylostoma infection at times.
  2. Red raw, ‘angry looking’ tongue in sprue, pellagra, severe and untreated diabetes, prolonged febrile illness.
  3. White tongue
    Lichen planus—Multiple white plaque-like areas.
    White patches or flakes on tongue due to curdled milk, thrush, syphilitic patches.
    Leukoplakia denotes any persistent white patch on mucous membrane of dorsum of tongue (or lips, gums or cheek). It is mostly seen in men over 40. Predisposing factors: Local include smoking, betel nut chewing, spicy food and syphilis. Leukoplakia is a precancerous lesion. Systemic: Candidiasis, lichen ruber mucosae, SLE, papilloma, chronic kidney failure.
    Hairy leukoplakia almost exclusively occurs in patients with HIV disease. It is characterised by white, non-removable lesions particularly affecting the lateral margins and ventral aspects of the tongue. The white patches can also have a homogenous plaque like appearance. At times hairy leukoplakia can be observed in a small number of non-HIV infected immunocompromised individuals.
  4. Magenta colour—in riboflavin deficiency.
  5. Blue tongue—denotes central cyanosis.
  6. Purple tongue in polycythemia.
  7. Dark red or bluish red tongue—in polycythemia vera, riboflavin deficiency, broad spectrum antibiotics.
  8. Strawberry tongue—Red tongue with the papillae standing out as white dots in scarlet fever, Kawasaki's disease and toxic shock syndrome.
  9. Raspberry tongue—In early stages of scarlet fever, the tongue shows scattered red dots on a grey background. It is due to red fungiform papillae sparsely dotted over the grey tongue.
  10. Excessively furred tongue—(a) In all febrile conditions especially typhoid. (b) Poor oral hygiene and mouth breathing. (c) Trismus as from a carious tooth.
  11. Yellow tongue—Rarely in jaundice, or due to irritants like nitric or hydrochloric acid.
  12. Black tongue—Due to fungus infection, iron, bismuth, opium or tobacco.
  13. Slate-blue tongue—in hemochromatosis.
  14. Oral hairy tongue—Yellowish brown or black furry patches made up of hypertrophied and densely matted papillae usually from antibiotic ingestion or excessive smoking. Oral hairy tongue should be differentiated from oral hairy leukoplakia which is a white lesion caused by EB virus.
  15. 6Brownish fur with dry tongue (Parrot tongue)—in chronic kidney failure.
  16. Small red lesions in hereditary telangiectasia.
The tongue in health is moist. Dryness of the tongue may be part of general dehydration as in diarrhoea, vomiting and diabetes mellitus. It is worsened by mouth breathing. Certain atropine-like drugs may cause appearance of dry tongue and mouth. Bone-dry tongue in Sjögren's syndrome.
1. Congenital—Naevi, Peutz-Jeghers syndrome (circumoral and intraoral melanosis with intestinal polyposis), racial. 2. Acquired—(a) Malabsorption or chronic cachexia. (b) Drugs—ACTH, phenothiazines, amodiaquine. (c) Endocrine—Addison's disease, ACTH producing tumours, Albright's syndrome, polyostotic fibrous dysplasia, Nelson's syndrome (hyperpituitarism following adrenalectomy). (d) Dental amalgam. (e) Neoplastic—melanoma, acanthosis nigricans.
  1. Smooth or bald tongue (atrophic glossitis)Atrophy of papillae resulting in glossy or varnished tongue may be due to iron deficiency anemia, pernicious anemia, B complex deficiency or malabsorption.
  2. Fissured tongue—Vitamin B complex deficiency, Mongolian idiocy, acromegaly, acute glossitis, dental trauma, senility or bad oral hygiene, congenital scrotal tongue.
  3. Scarred tongue—Scars on the tongue may be traumatic, secondary to ulcers from ‘tongue-biting’ as in epilepsy.
  4. Mushroom-like tongue—Sore tongue covered with whitish slough in acid poisoning.
  1. Tremors—(a) Slow rhythmic tremor stopping on voluntary extrusion of tongue in Parkinsonism. (b) Backward and forward ‘trombone’ tremor of GPI. (c) Miscellaneous causes—multiple sclerosis, prolonged fevers, wasting diseases, senility, chronic alcoholism and excessive smoking and thyrotoxicosis.
  2. Lizard tongue (Jack-in-the-box or wormian tongue) in rheumatic chorea. After protrusion, the tongue is shot back into the mouth.
  3. Deviated tongue with tip and median raphe curving round towards the affected side in hypoglossal nerve paralysis. Also in malignant infiltration, scarification after burns or severe ulceration, facial paralysis.
  4. Immobile tongue (Paretic tongue)Bilateral lingual paralysis, advanced malignancy of tongue, bulbar palsy, syringomyelia. Sluggish and slow protrusion in mental retardation. Increasingly slow movements in myasthenia gravis.
  5. Rolling movements—in cretins, Mongols and frontal lobe tumours. In case of Mongols, cretins and in macroglossia, a part of the tongue remains permanently protruded outside the mouth.
  6. Chewing tongue—Movements of the tongue as in act of chewing in athetosis.
  7. Myotonic reaction—After a sharp tap on the protruded tongue in myotonia atrophica.
  8. Spasm of the tongue may be tonic with the tongue becoming small, rigid, conical as in anxiety and general debility, or clonic (the tongue displaying sudden jerks) as in chorea, epilepsy, habit spasm, multiple sclerosis, GPI, hysteria and stuttering.
Amyloid tongue—Enlarged tongue with mottling of dark purple areas with translucent matter as part of generalised amyloidosis.
Purpuric spots on the tongue may appear in senile purpura.
Painful tongue—Paroxysms of agonising pain in glossopharyngeal neuralgia.
Alligator tongue—Dry, thick, furrowed and irregular tongue in diabetes mellitus.
Cotton wool patches on dorsum of tongue may be seen in xerostomia in graft-versus-host disease. These are areas of amorphous keratinization as seen in lichen planus.
Truncated tongue—Rarely a tuberculous ulcer at tip of tongue with oedema of the rest of the tongue may impart a truncated, amputated look to the tongue.
Frenulated tongue in Oro-facial-digital syndrome.
Fatiguability of tongue—In myasthenia gravis weakness of muscles of the tongue leads to difficulty in articulation.
Caviar lesions—Varicosities of sublingual veins may be seen on under surface of the tongue in elderly individuals, as also in mediastinal obstruction.
Secondary deposits—Small, yellowish grey nodules rarely in medullary carcinoma of thyroid.7
Causes of stomatitis and oral ulcerations are listed in Table 3.
Dysphagia indicates a delay in the passage of solids or liquids from the mouth to the stomach.
Table 3   Causes of stomatitis and oral ulcerations
Clinical features
Local: Excessive tobacco, alcohol, spices, antibiotics, drugs (gold, iodide) Systemic: Debility, infectious disease
Red mucous membrane with increased exudate
Elimination of cause. Hexidine or iodine mouth wash. Vit. B complex
Recurrent aphthous stomatitis (RAS)
Possible etiological factors: Positive family history in 1/3. Stress, local trauma, food allergy, in association with menstrual cycles. Episodic mouth ulcers in cyclic neutropenia and HIV infection. Also Behcet's disease, and Sweet's syndrome, Coeliac disease.
Tiny shallow ulcers on erythematous base covered with a greyish white exudate
Systemic: Oral steroids Topical: Mouth washes: Sodium chlorid. Compound thymol glycerin. Antiseptics: Chlorhexidine 0.2%. Povidone iodine 1%. Kamillosan-N mouth spray t.d.s. before meals.
Tooth brushing with hydrogen peroxide sodium bicarbonate paste. Immunomodulators: Tetracycline 250 mg capsule in 10 ml water. Swirl then spit qds Triamcinolone acetonide 0.1% Paste qds.
Betamethasone 500 μg soluble tabs. swirl and swallow b.d. Beclomethasone dipropionate 100 μg. aerosol sprayed directly qds.
Infection Bacterial (Vincent's angina)Red mucous membrane with increasedexudate
Predisposing factors—pre-existing gingivitis or local trauma, tobacco use
Ulcer surface covered by a grey pseudomembranous slough demarcated from surrounding mucosa by linear erythema.
Metronidazole 200 mg tds for 3 days. After control of acute phase, oral hygiene ad surgical correction of distorted gingivae.
Increased salivation, foetid odour, spontaneous gingival bleeding, lymphadenopathy and fever.
Herpes simplex
Common in children. Severe ulceration of oral mucous membrane with fever, malaise and lymphadenopathy. Initial formation of discrete, spherical grey vesicles which rupture after few hours to form ulcers. Course 2–3 weeks.
Bed rest. Mouth washes. In severe cases acyclovir
Herpes-varicella zoster
Painful oral ulcer. Tear drop rash of chickenpox.
Symptomatic treatment
Infectious mononucleosis
Ulcers particularly on fauces.
Symptomatic treatment
Hand, foot and mouth disease
Round or oval ulcers anywhere on buccal mucosa with rash on extremities.
Symptomatic treatment
Thrush (Pseudomembranous candidiasis) Occurs in infants, debilitated adults such as heroin addicts, elderly and after antibiotic and steroid therapy. Early feature of AIDS.
White slightly raised patches resembling milk curds, easily removed leaving a raw bleeding surface.
Ketoconazole 200 mg (for children under 12, 1/4 dose). In infants 0.5% gentian violet applied tds.8
Secondary syphilis
Circular, mucous patches, often greyish white with red areola
Treatment of syphilis
Hypersensitivity, cytotoxic drugs (e.g. Methotrexate)
Stomatitis and ulceration of buccal, labial and palatal mucosa.
Symptomatic treatment
Vitamin deficienyc
Nicotinic acid deficiency
Raw red tongue in pellagra
GI disorders
Crohn's disease Coeliac disease
Blood disorders
Acute leukaemia or neutropenia
Erythema multiforme and Stevens Johnson syndrome, Lichen planus, Pemphigoid, SLE
See appropriate section
Systemic disease Neoplasia
Behcet's syndrome, HIV Carcinoma Kaposi's sarcoma
Dysphagia should be distinguished from odynophagia which is discomfort or pain on swallowing hot or cold liquids, and occasionally alcohol. In general, mechanical causes lead to dysphagia for solid foods, whereas patients with motility disorders tend to complain of non-progressive dysphagia for both liquids and solids from the onset.
Causes of dysphagia are enumerated in Table 4.
Investigation of a case of Dysphagia
  1. Age and sex—Children – Cleft palate, foreign body or diphtheritic paralysis. Young females – Hysterical spasm. 30–40 – Achalasia. Menopause – Sideropaenic dysphagia. Above 50 – Carcinoma oesophagus particularly in males.
  2. SymptomsOropharyngeal dysphagia is usually distinguished from oesophageal dysphagia by the patient's awareness of inability to initiate swallowing properly and occurrence of nasopharyngeal regurgitation, there may also be aspiration of swallowed fluid into the airway.
(1)Dysphagia—(a) Onset – Acute in foreign body, encephalitis, thrombosis of cerebellar artery or hysterical. Gradual in stricture, malignancy, achalasia, etc. Onset after shock or emotional upset common in achalasia. (b) Type of distress – (i) Difficulty in swallowing both liquids and solids particularly if there is nasal reflux suggests a neurological condition. (ii) Difficulty in transferring bolus of food from mouth to gullet is usually caused by local disorders of throat, pharynx or larynx. (iii) Sensation of food sticking retrosternally is as a rule due to oesophageal abnormalities. (c) Progress – Long history with intermittent symptoms in achalasia. Dysphagia first with solids and subsequently fluids suggestive of mechanical obstruction. (d) Position at which food sticks – may provide a guide to the site of obstruction as the lesion is either at that level or higher up. (e) Relation of distress to posture – If distress at night when patient is in reclining position and relieved in upright position, it suggests oesophageal hiatus hernia. (f) Deglutition with strangulation or cough –means central lesions of bulbar type, myasthenia gravis or disease irritating 9th or 10th cranial nerves.
(2)Pain—(i) Burning, substernal contact pain is felt when hot, acid, spicy or alcoholic material passes through the inflamed oesophagus. This symptom is virtually diagnostic of oesophagitis. (ii) A prolonged history of heartburn preceding the onset of dysphagia is suggestive of peptic stricture and, less commonly, esophageal adenocarcinoma.
(iii) Impact pain—Severe pain substernally when a bolus ‘impacts’ above a narrowed oesophagus. This type of pain together with sudden dysphagia is characteristic first symptom of encircling carcinoma, occurring less commonly with benign stricture.
(iv) Spasm pain—This is severe type of oesophageal pain usually related to muscular spasm (oesophageal colic). Causes are diffuse oesophageal spasm, achalasia, reflux oesophagitis, ‘nutcracker oesophagus’.9
Table 4   Causes of dysphagia
• Inflammatory conditions – Pharyngitis, tonsillitis, aphthous ulceration
• Foreign body – Meat bolus, bone or other objects
• Ingestion of caustic substance
1. Oropharyngeal
• Cerebrovascular accident
• Motor neuron disease
• Parkinsonism
• Myasthenia gravis
• Multiple sclerosis
• Bulbar palsy
• Polyneuropathy
• Dermatomyositis
• Candida (Fig. 4)
• Herpes
Mechanical or compressive
• Intervertebral disc degeneration
• Postcricoid carcinoma
• Thyroid enlargement
• Aortic aneurysm
• Mediastinal mass
• Mucosal webs
• Pharyngeal pouch
• Globus hystericus
2. Oesophageal
Mechanical block
• Carcinoma oesophagus or cardia (Fig. 5)
• Oesophageal stricture
• Mediastinal neoplasm
• Schatzki ring (Fig. 6)
• Zenker's diverticulum (Fig. 7)
• Aberrant great vessels (dysphagia lusoria)
• Eosinophilic oesophagitis
Muscular incoordination
• Achalasia
• Scleroderma
• Diffuse oesophageal spasm
• Chaga's disease
• Oesophagitis – peptic, monilial
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Fig. 4: Oesophageal candidiasis
(3) Regurgitation—Characteristic of long standing achalasia; can occur with stooping or straining in hiatus hernia.
(4) Hematemesis—Oesophagitis, carcinoma.
(5) Nasal twang and nasal regurgitation of fluids suggests palatal paralysis.
(6) Hoarseness of voice—Carcinoma of larynx. The presence of hoarseness may be another important diagnostic clue. When hoarseness precedes dysphagia, the primary lesion is usually laryngeal; hoarseness that occurs after the development of dysphagia may result from compromise of the recurrent laryngeal nerve by a malignancy.
III. PAST HISTORY – (a) Of swallowing corrosives or of instrumentation suggests benign stricture formation. (b) Of psychoneurotic disorder may suggest globus hystericus. (c) Of cholecystitis or peptic ulcer may point to reflex cardiospasm.
  1. Mouth and throat—For stomatitis, malignancy tongue and abnormalities of pharynx.
  2. Neck—Enlarged lymph glands, goitre, malignancy of thyroid.
  3. Chest—For evidence of aneurysm, mediastinitis or mediastinal tumour, pericarditis, marked cardiac hypertrophy, empyema, and pulmonary abscess.
  4. Nervous system—For evidence of bulbar paralysis or myasthenia gravis.
  5. 10 Spine—Cold abscess to exclude chronic retro-pharyngeal abscess.
  6. Sideropenic dysphagia—in Plummer-Vinson syndrome. Dysphagia to solids, iron deficiency, koilonychia, glossitis. Dysphagia is due to a thin web in the precricoid area. The web is formed of degenerated epithelial cells.
  7. Skinchanges in the skin may suggest a diagnosis of scleroderma or mucocutaneous diseases such as pemphigoid and epidermolysis bullosa, all of which can involve the esophagus.
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Fig. 5: Carcinoma of oesophagus
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Fig. 6: Schatzki's ring
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Fig. 7: Zenker's diverticulum
  1. Laryngoscopy—Ulceration or growth of larynx.
  2. Barium swallow—Cardiospasm, stricture, growth, congenital shortening of oesophagus, oesophageal diverticulum.
    Cineradiography with liquid barium and bread soaked in barium may give functional as well as anatomical information about the pharynx and cricopharyngeal segment.
    Videofluoroscopy to investigate chronic dysphagia. It is essentially a modified barium swallow. The three phases of swallowing are observed on a screen and videotaped.
  3. Barium meal—For hiatus hernia or peptic ulceration.
  4. X-ray chest—Mediastinal tumour, aneurysm, mitral valve disease. Evidence of lung infection from repeated aspiration in achalasia.
  5. Endoscopy is the best way to determine the cause of dysphagia because of high diagnostic accuracy and opportunity to take biopsies.
  6. Manometry—Neither radiology nor endoscopy alone can exclude a treatable motility defect which can readily be demonstrated by intraluminal manometry and pH monitoring. These measure the vigour and coordination of oesophageal muscle contraction patterns, amount of gastro-oesophageal reflux, and the relationship of symptoms to oesophageal luminal events.
  7. BiopsyIt is recommended that esophageal mucosal biopsies be obtained routinely in the evaluation of unexplained dysphagia even if endoscopically identified oesophageal mucosal lesions are absent.
  1. Treatment of dysphagia depends on both the focus and the specific etio1ogy.
  2. 11Oropharyngeal dysphagia most common1y results from functional deficits caused by neuro1ogic disorders. In such circumstances, the treatment focuses on utilizing postures or maneuvers devised to reduce pharyngea1 residue and enhance airway protection 1earned under the direction of a trained swallow therapist.
  3. Dysphagia resulting from a cerebrovascu1ar accident, Parkinson's disease and amyotrophic lateral sclerosis, may manifest with severe oropharyngea1 dysphagia, feeding by a nasogastric tube or an endoscopically p1aced gastrostomy tube may be considered.
  4. Surgical intervention with cricopharyngea1 myotomy is used in specific disorders such as the idiopathic cricopharyngea1 bar, Zenker's diverticulum and ocu1opharyngeal muscular dystrophy.
  5. The majority of causes of esophageal dysphagia are effective1y managed by means of esophageal dilatation using bougie or balloon dilators.
  6. Cancer and achalasia are often managed surgically although endoscopic techniques are availab1e for both palliation and primary therapy, respectively.
  7. Infectious etio1ogies respond to antimicrobia1 medications or treatment of the underlying immunosuppressive state.
  8. Eosinophilic esophagitis has emerged as an important cause of dysphagia that is amenab1e to treatment by elimination of dietary allergens or administration of swallowed, topically acting glucocorticoids.
Gastro-oesophageal reflux disease (GORD) is caused by recurrent reflux of gastric contents into the distal oesophagus. The pathophysiology is multifactorial, but dysfunction of the lower oesophageal sphincter (LOS) has a primary role. Motility disorders of the distal oesophagus (e.g. reduced peristaltic amplitude, decreased velocity and increased duration of peristaltic contractions) cause prolonged exposure of the oesophagus to refluxed gastric contents.
Factors which facilitate reflux are listed in Table 5.
Table 5   Factors which facilitate reflux
• Relaxed or hypotonic sphincter
Diabetes mellitus, sliding hiatus hernia, fatty meal
• Decreased LOS pressure
Prolonged gastric tube intubation, scleroderma Drugs – Anticholinergics, β-adrenergic agents, calcium channel blockers, nitrates
• Raised intra-abdominal pressure
Ascites, obesity, pregnancy
• Impaired oesophageal mucosal function
Alcohol, smoking
• Delayed gastric emptying
Pyloric obstruction, fatty foods, gastroparesis
• Increased gastric contents
Large meals, Z-E syndrome
Typical symptoms: Heartburn, acid regurgitation.
Atypical symptoms: Dysphagia, globus sensation, non-cardiac chest pain, dyspepsia or abdominal pain.
Extraesophageal symptoms: Hoarseness or sore throat, or both, sinusitis, otitis media, chronic cough, laryngitis or polyps on the vocal cords or both, dental erosions, non-atopic asthma, recurrent aspiration or pulmonary fibrosis, or both.
Sleep related GER can present with multiple awakenings. Substernal burning and/or chest discomfort, indigestion or heartburn. Other symptoms include a sour or bitter taste in the mouth, water brash, coughing or choking.
Malignancy: Oesophageal adenocarcinoma, head and neck cancer.
Barrett's oesophagus is found in 10–20% of patients with reflux oesophagitis, the squamous epithelium is injured by chronic gastro-oesophageal reflux and repair is effected by columnar instead of squamous cells Upper GI scopy (Fig. 8) can be diagnostic assisted by biopsy. This columnar epithelium may undergo malignant transformation.
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Fig. 8: Barret's oesophagus.
  1. Radiology
    Barium swallow with fluoroscopy
    Upper oesophageal sphincter disorders
    Defective opening of pharyngo-oesophageal segment
    Airway aspiration.
    Body motility
    Non-propulsive (tertiary contractions)
    Uncoordinated or weak post-swallow contractions.
    Identification of hiatus hernia, mucosal ulceration, stricture, oesophageal dilatation.
  2. Upper oesophageal endoscopy
    Indications: GI bleeding, iron deficiency anemia, progressive unintentional weight loss, progressive difficulty swallowing, persistent vomiting, epigastric mass on palpation, suspicious barium meal result or other suspicious imaging result.
  3. Manometry
    • Upper oesophageal sphincter
    • Tone of upper oesophageal sphincter and relaxation during swallowing.
    • Coordination between relaxation of upper oesophageal sphincter and contraction of the pharynx.
    • Body motility
    • Evaluation of amplitude, duration and velocity of waves.
    • Lower oesophageal sphincter tonic pressure and relaxation.
  4. Oesophageal pH testing—The ideal standard for oesophageal pH probe replacement is manometric determination EES. Newer technology monitoring of oesophageal pH using a wireless system allowing for data collection for up to 48 hours.
    • Acid reflux time
    • Number and duration of reflux episodes
    • Symptom index. (Percentage of symptom episode associated with reflux episode). Special indications—Atypical symptoms, patient unresponsive to medical therapy, preoperative assessment and follow-up of patient undergoing reflux surgery.
  5. Scintigraphy. Introduction of technetium99 (99Tc) into stomach followed by abdominal compression and radiographic counting over oesophagus. This technique can demonstrate reflux as well as provide quantitative measure of its presence.
  1. Conservative measures
    • Abstain from eating within 2 hours of bed time
    • Elevate head of bed by 6 inches
    • Sleep in left lateral decubitus position
    • Avoid—Caffeine, nicotine, alcohol, chocolate, mints, carbonated beverages, high-fat foods, tomato or citrus - based products. Avoidance of acidic foods which are inherently irritating.
    • Avoid if possible medications that can worsen GER – Anticholinergic, theophylline, prostaglandin, calcium channel blockers, alendronate.
    • Weight loss if obese (most important of all)
    • Consider nasal CRAP if OSA is present
    • Rabeprazole, esmoprazole provide superior gastric acid suppression.
  2. Acid suppression—(a) Proton pump inhibitors provide rapid symptomatic relief and healing of oesophagitis in majority of patients. (b) Prokinetic agents such as Tegaserod maleate 6 mg b.d. or Levosulpiride 50 mb.d. d. or Clebopride 0.5 mg b.d. improve motility by increasing LES pressure, accelerating oesophageal acid clearance mechanism and improving gastric emptying.
  3. If no response or relapse—Test and treat for H. pylori. Distal gastritis increases production of gastric acid. In this condition eradication of H. pylori reduces risk of acid reflux. Conversely, generalized atrophic gastritis decreases production of gastric acid, as a result H. pylori eradication may increase severity.
  4. Surgery—If persistent non-acid reflux. Antireflux surgery augments the reflux barrier by a full or partial wrap of the gastric fundus (fundoplication) around the lower oesophagus.
Achalasia (Cardiospasm, Megaesophagus) is a primary motor disorder of the oesophagus. Failure of relaxation of lower oesophageal sphincter on swallowing is a characteristic feature. Degeneration of neuronal cell bodies in the myenteric plexus is thought to be the primary abnormality.
  1. Dysphagia—is the dominant symptom. Feeling of obstruction usually of the cardia or sometimes high in the oesophagus. Sensation of food sticking in the oesophagus at first intermittent, later continuous and at every meal, and more with solids.
    zoom view
    Fig. 9: Chest radiograph showing gross enlargement of the oesophagus due to achalasia
  2. Regurgitation—In initial stages, food is regurgitated almost immediately following ingestion but as oesophagus becomes dilated, food and secretion may be retained for hours and days followed by delayed regurgitation.
  3. Chest pain—Spontaneous retrosternal pain which occurs equally during night and day, is often severe and is relieved by drinking cold water. Patients describe a squeezing, pressure-like retrosternal pain, sometimes radiating to the neck, arms, jaw, and back. Paradoxically, some patients complain of heartburn that may be a chest pain equivalent. Other sensations may be bursting feeling provoked by drinking fast, or sensation of food sticking, and heart burn by lying down or stooping.
  4. Respiratory symptoms—(a) Cough and dyspnoea due to pressure on trachea and bronchus by dilated oesophagus. (b) Aspiration may result in aspiration pneumonia, bronchiectasis or lung abscess.
  5. Asymptomatic—Occasionally the condition is discovered as a mediastinal swelling on routine chest film.
  1. Pulmonary—Fibrosis due to recurrent chest infection.
  2. Carcinoma—Commonest in mid-oesophagus due to irritation from chronic stasis oesophagitis.
  3. Malnutrition—Rare.
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Fig. 10: Barium-filled oesophagus showing distension above (arrowhead) the narrow gastro-oesophageal junction Note: The abrupt narrowing of the lower end of oesophagus (bird beaksign)
  1. Radiology—(a) Plain chest radiograph will show enlarged mediastinal shadow and oesophageal dilatation with poor emptying and air-fluid level (Fig. 9) (b) Barium swallow – Oesophageal dilatation and slow flow into the stomach across a smoothly tapered gastro-oesophageal junction (bird beak sign) (Fig. 10). Absent stomach gas bubble.
  2. Endoscopy—Usually reveals a chronically inflamed oesophageal mucosa. It has minimal role.
  3. Manometry—Failure of lower oesophageal sphincter to relax on swallowing. It is the most sensitive diagnostic test.
Pharmacotherapy—Isosorbide dinitrate 5 mg sublingually before meals or nifedipine 10–20 mg have a direct relaxant effect on the muscle of lower oesophageal sphincter. They may be of value while patient is awaiting definitive treatment.
Pneumatic dilatation and extramucosal oesophagomyotomy endoscopy—The aim of both procedures is to effect partial disruption of lower oesophageal sphincter, by stretching it using an inflatable balloon positioned within the oesophageal lumen, or by surgical myotomy at the cardia (Heller's operation). The most significant complication of the operation is gastro-oesophageal reflux.
Endoscopic LES myotomy (per oral esophageal myotomy)—This technique involves the creation of a tunnel within the esophageal wall through which the circular muscle of the LES and distal esophagus are transected with electrocautery.14
Endoscopic intrasphincteric injection of botulinum toxin—As an alternative to pneumatic dilatation or surgery. It may be of advantage in elderly or frail patients. Multiple treatments are needed over a period of time, but the effect tends to last longer with successive injections.
Protrusion of the stomach above the diaphragm.
Aetiology—Most common in middle-aged, obese females. It may be congenital or due to conditions which raise intra-abdominal pressure, e.g. obesity, pregnancy, ascites or abdominal tumours, or may follow surgical operations like partial gastrectomy or vagotomy.
  1. Type I Sliding—Commonest variety. Simple upward slide of fundus of stomach with oesophago-gastric junction through the hiatus into the chest.
  2. Type II Rolling (Paraesophageal)—The oesophagogastric junction is within the abdominal cavity, but part of the gastric fundus protrudes through the hiatus into the thoracic cavity.
  3. Type III combined sliding and paraesophageal hernia.
  4. Type IV hiatal hernias, viscera other than the stomach herniate into the mediastinum, most commonly the colon.
  1. Asymptomatic
  2. Symptoms due to reflux—(a) Retrosternal chest pain or discomfort especially on stooping or lying down soon after meals. (b) Heart burn or regurgitation of acid fluid, or food on bending or stooping. Nocturnal regurgitation may cause choking attacks and aspiration pneumonia. (c) Dysphagia due to oesophageal muscle spasm, oesophagitis.
  3. Symptoms due to pressure—Either of dilated oesophagus and/or gastric pouch on surrounding structures – (a) From pressure on mediastinum – Dyspnoea, palpitation, cough, anginal pain. (b) From pressure on diaphragm – Hiccup, spasmodic pain.
  4. Symptoms due to hemorrhage—Iron deficiency anemia due to massive hematemesis or oozing from oesophageal ulcers.
  5. Symptoms due to associated diseases—Peptic ulcer at level of diaphragmatic hiatus, cholecystitis, ischemic heart disease.
    In contrast to a sliding hernia, paraesophageal hernia may lead to serious complications, especially strangulation or hemorrhagic anemia.
  1. Radiology—(a) X-ray chest – If a sliding hernia is large, it may be seen as retrocardiac shadow with fluid level. (b) Barium swallow to assess hernia size and development of complications.
  2. Endoscopy and biopsy—Mainly of value in assessment of oesophagitis and of consequent bleeding, ulceration and stricture formation.
  3. Manometry is the only sensitive method, as in absence of dilation, barium meal may be reported as normal.
A. Medical
  1. To minimise gastro-oesophageal reflux—(a) Elevate bed head by 20 cm. (b) Avoid posture precipitating reflux, e.g. bending or stooping forwards, sitting in a low chair. (c) Avoid large meals. (d) No food or drink for 3–4 hours before bedtime. (e) Reduce weight if obese. Stop non-steroidal anti-inflammatory drugs. (f) Avoid foods which provoke symptoms, e.g. pastries, coffee.
  2. Reduce gastric acidity and pepsin secretion – with ranitidine or famotidine or antacids.
B. Surgical
Surgical correction in resistant cases.
Dyspepsia refers to upper abdominal symptoms usually following intake of food which appears to arise from upper GI tract.
  1. Organic dyspepsia: Erosive oesophagitis, gastric erosions, acute or chronic gastritis, gastric ulcer, duodenal ulcer, duodenitis, malignancy (carcinoma, lymphoma). It is suspected in presence of alarm symptoms (wt. loss, anemia, bleeding or positive occult blood, loss of appetite).
  2. Functional or non-ulcer dyspepsia (see later).
  3. 15 Drug-related: Aspirin, NSAIDs, antibiotics, bisphosphonates, oestrogens, steroids, digoxin, chloroquine, iron, potassium supplements.
  4. Extra intestinal systemic disease: Diabetes mellitus, hypothyroidism, hyperparathyroidism, Addison's disease, uremia.
    Symptoms of dyspepsia can be divided into:
  5. Reflux type: Retrosternal burning, regurgitation.
  6. Ulcer type: Epigastric pain on empty stomach. Relieved with bland food, antacids or acid suppression.
  7. Dysmotility type: Postprandial fullness, distension, early satiety, nausea.
At least 3 months, with onset at least 6 months previously, of one or more of the following:
  • Bothersome postprandial fullness
  • Early satiation
  • Epigastric pain
  • Epigastric burning
  • No evidence of structural disease (including upper endoscopy) that is likely to explain the symptoms.
Postprandial Distress Syndrome
  1. Bothersome postprandial fullness, occurring after ordinary sized meals, at least several times per week AND/OR
  2. Early satiation that prevents finishing a regular meal, at least several times per week.
Table 6   Potential causes of non-ulcer dyspepsia
• Duodenogastric reflux
• Duodenitis
• Carbohydrate malabsorption (lactose, fructose, sorbitol)
• Cholelithiasis or choledocholithiasis
• Chronic pancreatitis
• Systemic disorders (diabetes, thyroid, parathyroid, hypoadrenalism, connective tissue disease)
• Intestinal parasites
• Psychiatric disorders
• Visceral hypersensitivity
• Gastric/small intestinal dysmotility
• Gallbladder/biliary dysmotility
Supportive Criteria
  1. Upper abdominal bloating, postprandial nausea or excessive belching can be present.
  2. Epigastric Pain Syndrome may coexist.
  1. Pain or burning localized to the epigastrium of at least moderate severity at least once per week AND
  2. The pain is intermittent AND
  3. Not generalized or localized to other abdominal or chest regions AND
  4. Not relieved by defecation or passage of flatus AND
  5. Not fulfilling criteria for gallbladder and sphincter of Oddi disorders.
Supportive criteria
  1. The pain may be of burning quality but without a retrosternal component.
  2. The pain is commonly induced or relieved by ingestion of a meal but may occur while fasting.
  3. Postprandial distress syndrome may coexist.
Potential causes of non-ulcer dyspepsia are listed in Table 6.
Differential diagnosis of dyspepsia s given in Table 7.
Table 7   Differential diagnosis of dyspepsia
• Non-ulcer dyspepsia
• Gastro-oesophageal reflux disease
• Peptic ulcer disease
• Medication related: non-steroidal anti-inflammatory drugs, antibiotics, iron, potassium supplements, digoxin
• Carbohydrate malabsorption (lactose, fructose, sorbitol)
• Cholelithiasis or choledocholithiasis
• Chronic pancreatitis
• Systemic disorders (diabetes, thyroid, parathyroid, hypoadrenalism, connective tissue disease)
• Intestinal parasites
• Abdominal malignancy (especially pancreatic and gastric cancer)
• Chronic mesenteric ischaemia
H. pylori is a small curved (comma shaped), highly motile Gram-negative organism that colonises only the mucus layer of the human stomach. Multiple strains of the 16 organism exist. It also has considerable genetic heterogeneity, no strains being identical.
Transmission appears to be predominantly via oral faecal route, including contaminated water supplies. Transmission by endoscopy is possible. H. pylori infection can be picked up from siblings, older children, or parents predominantly via gastro-oral route.
  1. Gastritis—Gastric infection with H. pylori is the main cause of gastritis. Infection in infancy is thought to lead to pangastritis, whereas in later childhood to predominantly central gastritis.
  2. Peptic ulcer associated with H. pylori. Only a minority of individuals infected with H. pylori develop ulcers. Risk of ulceration is increased by cigarette smoking, and by the presence of more aggressive strains of the bacterium that carry the CAGA gene and the S1 variant of the gene encoding a vacuolating toxin.
Possible mechanisms for ulcer development:
1. Bacillus secretes urease which converts into ammonia, thus alkalising the surrounding acid medium for its survival but simultaneously producing ammonia-induced mucosal damage. Production of ammonia by bacteria prevents D cells in antral glands from sensing the level of acidity, leading to inappropriate release of somatostatin and an increase in gastrin and thus excess of acid secretion. 2. Neural pathways are affected by H. pylori which results in downregulation of acid production.3. H. pylori produces inflammatory response in gastric mucosa with induction of epithelial derived cytokines. Influx of neutrophils and macrophages into gastric mucosa with release of lysosomal enzymes and leukotrienes impairs mucosal defence. 4. H. pylori expresses adhesins (OMPs like BabA), which facilitate attachment of the bacteria to gastric epithelial cells.
Role in development of MALT (mucosal associated lymphoid tissue), lymphoma, gastric adenocarcinoma, GERD and dyspepsia.
Mechanisms of gastric ulcer are less well defined, but probably include—1. Local H. pylori related inflammation leading to epithelial damage. 2. Inhibition of synthesis of protective prostaglandins by inhibition of cycloxygenase-1 by NSAIDs. 3. Bile reflux, which is increased in these patients.
Non-invasive Tests
Serology. The main use of serology is for testing dyspeptic patients in primary care and patients with known ulceration but unknown H. pylori status in secondary care. Serology may remain positive for many years after successful eradication of H. pylori and is therefore not used for checking the success of treatment.
Urea breath test is a simple, non-invasive test based on the fact that H. pylori possesses a powerful urease. It is particularly useful for checking the success of treatment. It must be performed at least 4 weeks after any proton pump inhibitors, bismuth compounds or antibiotics, if not, false-negative results may be obtained.
Biochemical basis of the urea breath test is described in Figure 11.
Stool antigen test is used as ELISA to detect presence of H. pylori antigens shed in the faeces. The main advantage of the test is in large scale epidemiological studies of acquisition of H. pylori infection in children.
Invasive Tests
Antrum Biopsy
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Fig. 11: Urea labelled with the non-radioactive isotope 13C, or very small dose of radioactive 14C, is drunk by the patient If Helicobacter pylori is present in the stomach, its powerful urease catalyses hydrolysis of urea, and labelled carbon dioxide can be detected in breath samples
Table 8   Eradication of H. pylori infection
First-line treatments
Triple therapy
1. Bismuth subsalicylate 2 tab qid plus
Metronidazole 250 mg qid plus
Tetracycline 500 mg qid
2. Omeprazole 20 mg b.d. plus
Clarithromycin 250 or 500 mg bid plus
Amoxicillin 1g b.d. or
Metronidazole 500 mg b.d.
3. Ranitidine bismuth citrate 400 mg bid plus
X 14 days
Tetracycline 500 bid plus
Clarithromycin or Metronidazole 500 mg bid
Quadruple therapy
Omeprazole 20 mg b.d.
Bismuth subsalicylate 2 tab qid
Metronidazole 250 mg qid
Tetracycline 500 mg qid
Note: An alternative to ‘blind’ second-line therapy is to culture H. pylori and be guided by antibiotic sensitivities.
  1. Biopsy urease testis based on liberation of ammonia by action of H. pylori urease. One or two biopsies are placed on a gel or into a solution containing urea with a pH indicator. A colour change is produced if the H iincreases. When H. pylori is present, the urea is hydrolysed by its urease, resulting in a colour change. Most tests are read at 24 hours.
  2. Histology—H. pylori infection can be diagnosed with special stains. Multiple biopsies should be taken from the antrum and corpus.
  3. Culture—Endoscopic mucosal biopsy specimens can be cultured for H. pylori. This is not useful as a single diagnostic test, but it enables antibiotic sensitivity testing.
Eradication of H. pylori infection is achieved by regimens given in Table 8.
Gastritis is inflammation of the gastric mucosa. It can be active or chronic. Gastritis is seldom symptomatic, but can have important clinical sequelae, principally duodenal and gastric ulceration, gastric adenocarcinoma and primary gastric lymphoma. The three important causes of gastritis are H. pylori infection, NSAIDs and autoimmunity. Classification of gastritis is given in Table 9.
Chronic gastritis is of two types—Type A and Type B
Type AAutoimmune gastritis is virtually confined to the corpus and is associated with antiparietal cell and other intrinsic factor antibodies. It may result in vitamin B12 deficiency and pernicious anemia and is a risk factor for gastric adenocarcinoma.
Table 9   Classification of gastritis
Type of gastritis
H. pylori
Multifocal atrophic
H. pylori, ± environmental insults
Special forms
NSAIDs, bile, alcohol
Radiation injury
Idiopathic, gluten, drugs
Non-infectious granulomatous
Crohn's disease, sarcoidosis, Granulomatous polyangiitis and other vasculitides
Food sensitivity
Other infections
Bacteria other than H. pylori (particularly other gastric helicobacter, mycobacteria and syphilis), viruses (cytomegalovirus), fungi (Candida spp., Histoplasma) Capsulatum and Mucoraceae
Type BH. pylori can cause antral predominant gastritis, which predisposes to gastric ulceration and distal gastric adenocarcinoma.
NSAIDs/Aspirin cause gastritis characterized by mucosal hyperplasia and oedema but little inflammatory cell infiltration. It may be associated with gastric or duodenal ulceration.
Chemical gastritis due to chemical irritation e.g. reflux of bile or duodenal contents (reflux gastritis).
Treatment—Eradication of H. pylori. Patients with pernicious anemia will require parenteral vitamin B12 supplementation on a long-term basis.
The term peptic ulcer applies to mucosal ulceration near the acid bearing regions of the gastrointestinal tract. Most ulcers occur in the stomach or proximal duodenum but they may also occur in the oesophagus (due to acid reflux), in jejunum (at site of gastrointestinal anastomosis), and rarely in relation to ectopic gastric mucosa (near a Meckel's diverticulum).18
Table 10   Causes of gastric ulcer
Causes of gastric ulcer
• H. Pylori infection
• Neoplasm (carcinoma, lymphoma, lymphosarcoma)
• Stress
• Crohn's disease
• Infections (herpes simplex, cytomegalovirus)
Causes of duodenal ulcer
Common causes
• H. pylori infection
Uncommon causes
• Zollinger-Ellison syndrome (Gastrinoma)
• Hypercalcemia
• Granulomatous diseases (Crohn's disease, sarcoidosis)
• Neoplasia (carcinoma, lymphoma, leiomyoma)
• Infections (tuberculosis, herpes simplex, cytomegalovirus)
• Ectopic pancreatic tissue
  1. Heredity and strong family history.
  2. Peptic ulceration results from digestion of the mucosa with acid and pepsin of gastric juice. Acid secretion is more important in aetiology of duodenal ulcer than gastric ulcer.
  3. Mucosal resistance (Gastric mucosal barrier). Mechanism: (a) Secretion of bicarbonate by surface epithelial cells under the influence of mucosal prostaglandins. These cells also secrete mucus that impedes diffusion of ions and molecules such as pepsin. (b) The tight intercellular junctions and surface lipoprotein level provide a mechanical barrier. (c) The submucosal area provides micronutrients and oxygen while removing toxic metabolic products of gastric epithelial cells. (d) Factors reducing mucosal resistance – Drugs like aspirin, NSAIDs, H. pylori infection, reflux of bile and intestinal contents into stomach due to poorly functioning pyloric sphincter.
    Causes of peptic ulcer are enumerated in Table 10.
    Pathogenesis of duodenal ulceration is depicted in Figure 12.
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Fig. 12: Antral inflammation leads to reduced somatostatin production and, because somatostatin has a negative feedback effect on gastrin production, this results in hypergastrinemia Gastrin acts on parietal cells, resulting in high stimulated acid production, increased duodenal acid load and the formation of protective gastric metaplasia in the duodenum, Helicobacter pylori cannot colonize the normal duodenum, but can colonize gastric metaplasia, causing inflammation and ulceration
  1. Character and intensity—Variable, usually gnawing, moderate, very mild or severe.
  2. Location and radiation—Characteristically sharply circumscribed to an area about one inch in diameter between xiphoid and umbilicus. Can occur anywhere in the abdomen, retrosternally, or with a posterior ulcer in the back.
  3. Relation to food—Rhythmic occurrence and disappearance. Pain invariably absent in morning. Pain usually comes 2–3 hours after meals and is eased by food. Characteristic nocturnal distress between 12 and 2 am. Freedom from pain for about two hours after rising. In gastric ulcer pain is precipitated by food.
  4. Aggravation and relief—Aggravated by coarse foods, alcohol, nervous tension, undue fatigue. Relief by antacids or after vomiting of acid fluid.
  5. Periodicity of pain—Most characteristic feature. Even when pain is absent, recurrent bouts of heartburn, anorexia, nausea and vomiting suggest possibility of ulcer.
    Nausea and weight loss occur more commonly in gastric ulcer patients.
Variations in Clinical Picture
  1. From high pain threshold—Little or no pain, only sensation of fullness or bloating.
  2. Increased reflex activity in gastrointestinal tract—(a) Oesophageal spasm Excessive salivation and acid regurgitation (water brash). (b) Pylorospasm Heartburn. (c) Colonic spasm Features of irritable colon syndrome Constipation, abdominal pain not related to food and most marked on left side of abdomen.
  3. 19 From complications—(a) Penetrating ulcer may cause continuous pain, pain in unusual sites such as back or shoulder and refractoriness to agents formerly yielding prompt relief. (b) Bleeding acute hematemesis or anemia due to insidious bleeding. (c) Pyloric obstruction Nausea, anorexia, loss of weight and vomiting. (d) Perforation of ulcer into lesser sac may cause back pain, malaise and fever.
  4. Postbulbar ulcer—Mostly back pain, or insidious bleeding.
  5. From associated disease—Such as gallstones or hiatus hernia.
  6. From neurosis—Multiple gastrointestinal symptoms due to anxiety.
  7. Acute and stress ulcers—Aspirin, head injury (causing ulcer by acid hypersecretion, burns and shock), reflux of duodenal contents and mucosal ischemia, severe sepsis, surgery, trauma.
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Fig. 13: Barium study demonstrating duodenal ulcer
“The history is everything, the physical examination nothing”.
  1. Tenderness—Deep tenderness to the right of the middle in epigastrium. Localised over the site of lesion on deep palpation. Superficial tenderness may be present.
  2. Muscle guarding or rigidity—may be present with active ulcer or deeply penetrating ulcer.
  3. Peristaltic waves may be observed in presence of obstruction. Gastric splash may suggest gastric retention due to duodenal ulcer near pylorus.
  4. Occult blood in stools.
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Fig. 14: Barium study of gastric ulcer
  1. Endoscopy is the ideal method of diagnosing duodenal ulcer. The ulcer often appears like a severe aphthous ulcer with a creamy base.
  2. Barium meal
    Acute stage
    • Ulcer crater. Persistent pool of barium.
    • Ulcer niche. Crater jutting beyond margins, shown to be on anterior or posterior wall on rolling the patient.
    • Irritable duodenal cap seen as spasticity of the cap or a hurry of the barium as it passes through the cap (Fig. 13).
    Healing stage
    • Radiating folds. Mucosal folds radiating away from the ulcer.
    • Scarred and deformed duodenal cap (trifoliate deformity) with multiple ulcers and healing.
    Radiographic criteria for benign gastric ulcer (Fig. 14).
    • Ulcer crater extending beyond gastric wall
    • Gastric folds radiating into base of ulcer
    • Thick radiolucent collar of oedema (Hampton's line) surrounding ulcer base.
    • Smooth, regular, round or oval ulcer crater
    • 20Pliable and normally distensible gastric wall in the area of the ulcer.
    • (Up to 8% of GUs that appear to be benign by radiographic appearance are malignant by endoscopy or surgery)
    • Gastroscopy. In addition to allowing direct visualization of the mucosa, photographic documentation of a mucosal defect and tissue biopsy to rule out malignancy.
    • Tests for H. pylori. (Refer)
    • Gastric studies include measurement of basal secretion, or response to injection of histamine, pentagastrin or insulin. Not necessary for assessment of uncomplicated DU, but required only for hypersecretion when patient has continuing DU after gastric surgery.
    • Fasting plasma gastrin concentration—Elevated in Z-E syndrome. Fasting gastrin levels are usually <150 pg/mL. Virtually all gastrinoma patients will have a gastrin level >150–200 pg/mL. Inj. of Secretin in normal individuals causes fall in plasma gastrin, in Z-E syndrome there is immediate rise.
    • Hb and MCV—To exclude anemia of iron deficiency.
  1. Bleeding—Most common
  2. Perforation—Acute or chronic perforation into surrounding organs – pancreas, liver, bile duct, colon.
  3. Pyloric stenosis.
  4. Malignancy at site of ulcer.
  5. Pancreatitis due to posterior penetration of ulcer.
Table 11   Differences between gastric and duodenal ulcer
Gastric ulcer
Duodenal ulcer
Course of illness
Less remittent
More remittent
Longer duration
Shorter duration
Provokes the pain
Relieves the pain
Heart burn
Less common
More common
Relief of pain not instant
Prompt relief of pain
Anorexia, nausea
More common
Less common
Spontaneous perforation
Less common
More common
Table 12   Differentiation between chronic gastritis and peptic ulcer
Chronic gastritis
Peptic ulcer
History of repeated attacks of acute gastritis
History of ingestion of NSAIDs
Pain slight, more soreness
Pain usually severe
Pain intensified by food, no pain if meal is delayed
Food may relieve pain
Pain relatively constant
Symptoms of indigestion
Few symptoms of indigestion marked
Slight or no hemorrhage
Profuse hematemesis
Endoscopy – Patchy
Endoscopy – Ulcer with
mucosal irregularity
creamy base
  1. Gastric lesions
    1. Gastric ulcer: See Table 11 for differences between gastric and duodenal ulcer.
    2. Gastric carcinoma :Clinical features(a) Dyspeptic symptoms in patient over 45 years. (b) Daily discomfort or pain. (c) Anorexia or undue fullness after meals. (d) Vomiting of small quantities of fresh or altered blood. (e) Weight loss. (f) Unexplained anemia. (g) Previous history of chronic gastritis. (h) Family history of gastric cancer. (i) Known pernicious anaemia. (j) Presence of physical signs such as epigastric mass or jaundice suggest advanced disease. Barium meal examination is useful only for detection of mucosal abnormalities. Neoplastic infiltration causes blunting, fusion, clubbing or tapering of mucosal folds. Endoscopy and biopsy with brushing for further confirmation.
    3. Chronic gastritis: Table 12 gives differentiation between chronic gastritis and peptic ulcer.
  2. Duodenal lesions
    1. Pseudoulcer syndrome (Pyloroduodenal irritability) —Discomfort later after meals, relieved temporarily by food or antacids, and in many cases typical periodicity of remissions and relapses. Often hyperchlorhydria. X-ray studies show pylorospasm and extreme irritability of duodenal cap. No evidence of ulcer.
    2. Duodenitis—Often no pain but nausea and sensation of fullness in upper right part of abdomen. Maximum intensity several hours after ingestion of food. Symptoms are usually not intermittent but continuous. Endoscopy shows inflamed, hemorrhagic or friable duodenal mucosa.21
    3. Duodenal diverticula—Pain in epigastrium, may arise ½ to 2½ hours after meals. Not relieved by diet or antacid. Diverticula seen on barium meal X-ray.
    4. Carcinoma of duodenum—Very rare. Older patient. Symptoms of short duration and severe. No intermittency of symptoms; no relief by medical treatment. Later signs of obstruction, hemorrhage or jaundice. Mass may be felt.
  3. Gallbladder disease
    Chronic cholecystitis—Vague upper abdominal distress and fullness after meals. Belching and eructations. Intolerance of fat. Attacks of epigastric pain with tenderness over gallbladder. No occult blood in stools. Biliary colic and jaundice due to complicating gall-stones. Symptoms tend to be more irregular and less periodic. Ultrasound confirms diagnosis.
  4. Pancreatic disease
    1. Chronic calcifying pancreatitis—Upper abdominal pain continuous or intermittent, weight loss, steatorrhoea, diabetes. Jaundice due to involvement of common bile duct late manifestation. Plain radiograph of abdomen may show pancreatic calculi.
    2. Carcinoma of pancreas—Mid-epigastric pain steady and dull, or paroxysmal colicky pain. Relief from pain may be obtained by stooping or bending or lying in bed with knees tightly drawn up into the abdomen (jack-knife position). Jaundice may be present. Peripheral oedema and thrombophlebitis are recognised presentations. Weight loss and anorexia. Rapidly progressive. Evidence of metastasis in liver or elsewhere.
  5. Diseases of colon
    1. Carcinoma—Pain on right side below level of umbilicus. Lump may be palpable. No response to medical regime. Filling defect on radiography.
    2. Chronic appendicitis—Dyspepsia more or less continuous. Irregular short attacks of sharper pain. Nausea common. Vomiting. Pain worse on exertion, unrelated to ingestion of food. Pain mid-epigastric but often radiates to right iliac fossa.
    3. Ileocaecal tuberculosis—May produce reflex dyspeptic symptoms. Constipation alternating with diarrhoea. Thickening or lump in right iliac fossa.
    4. Irritable bowel syndrome—Postprandial type of pain related to meals may occur. Pain often relieved by defecation. May be accompanied by abdominal fullness, bloating or flatulence. Alternating constipation and diarrhoea in majority. Faeces characteristically ribbon-like with often excessive mucus.
  6. Superficial or radicular pain—Pain usually constant. Hyperaesthesia of abdominal skin. Flexion of abdominal wall reveals situation of pain.
  7. Functional dyspepsia—Postprandial fullness, early satiation, epigastric pain or burning in absence of causative disease to explain the symptoms.
  8. Miscellaneous
    1. Hiatus hernia—Chronic heart burn, intermittent regurgitation, dysphagia and substernal or epigastric pain aggravated by stooping or lying flat. Duodenal ulcer is often found with hiatus hernia which is also more common in women. Barium examination will show intrathoracic herniation of stomach.
    2. Ankylostomiasis—Mild but continuous epigastric pain or discomfort. Anemia. Hookworm ova in stool.
    3. Epigastric hernia—Eructations, nausea and vague abdominal discomfort. Epigastric pain may be aggravated or relieved by change of posture. Hernia in the linea alba above the umbilicus.
    4. Visceroptosis—Symptoms variable and many. Pain worse after food. Pain arises during meals and increases as more food is taken. Accompanying sensation of fullness, distension, feeling of weight or dragging in epigastrium. Discomfort persists for hours often with belching and regurgitation. Antacids without effect. Weak abdominal wall. Glenard's test – On standing behind the patient, raising lower abdomen with both hands and holding it up in that position, there may be some relief.
    5. Abdominal angina—Due to chronic intestinal ischemia. As in effort angina, the pain of intestinal ischemia develops with maximal work load following meals: (i) Occurs usually in patients over 40 years of age. (ii) Post-prandial abdominal pain, usually cramping and referred to the back, develops 20 to 30 minutes after meals and lasts 1 to 2 hours. (iii) Progressive weight loss due to anorexia and malabsorption. (iv) Constipation common, may be interrupted occasionally by steatorrhoea. (v) Central abdominal bruit with at times absent peripheral pulses. (vi) X-ray studies with barium may show puddling of barium in small bowel as a result of impaired motility. (vii) Stool – Excessive fat and often occult blood. (viii) Aortography with exposure of the film in the lateral projection will demonstrate the occlusive process in the coeliac and superior mesenteric arteries.
    6. Gastrinoma—Triad of abdominal pain, weight loss and diarrhoea.
    Medical management of peptic ulcer22
  1. Short history (less than 5 years) and few relapses.
  2. Mild symptoms.
  3. Good social and economic position.
  4. No radiological evidence of penetrating ulcer, pyloric stenosis or marked duodenal deformity.
  5. General condition unsuitable for surgery.
  6. Few chances of recovery after removal of organic lesion due to marked neurosis.
  1. Rest: Physical and mental. Rest in bed during acute phase and for one week after subsidence of pain.
    Indications for hospitalization—(i) Tarry stools or strongly positive occult blood reaction. (ii) Constant pain replacing previous ulcer rhythm. (iii) Gastric retention. (iv) Uncontrollable night pain or vomiting. (v) Suspicion of impending perforation.
  2. Diet: Bland diet. Duration of particular phase of diet will depend on severity of symptoms, constitution, response to treatment and co-operation of patient. 3-hourly feeds throughout the day – small, digestible, but of adequate caloric value form the basis of treatment.
  3. Pharmacotherapy
    See Table 13 for drug treatment of peptic ulcers.
  4. Relief from anxiety and mental stress: Ulcer symptoms get aggravated during periods of mental stress. Psychotherapy and antidepressant like Doxepin 7.5 mg/day.
  5. Avoidance of gastric irritants and stimulants— Tobacco, alcohol, coffee, tea, sour fruits, meat extracts, ulcerogenic drugs.
  1. Education of patient—(a) About recurrent nature of disease. (b) Avoid tobacco, coffee, tea, alcohol, hurried meals, raw vegetables and fruits, fried food, meat extracts, condiments and spices. (c) No emotional stress. (d) Regular hours of rest and sleep. (e) Avoid excessive fatigue. (f) Avoid drugs which might reactivate ulcers, such as aspirin, NSAIDs, steroids.
  2. Dietary management—With interval feedings. Snacks between breakfast and lunch and lunch and dinner and a glass of milk before retiring. Snacks may consist of biscuits, toast, or chapattis with or without butter, sandwiches, light cake, curds, butter milk, milk, ice cream, custard or pudding.
  3. Psychotherapy—When indicated.
  4. Preparedness—Intensified therapeutic regime on exposure to circumstances known to aggravate ulcer – (a) Acute respiratory infection. (b) Excessive work or severe fatigue. (c) Insomnia and nervous irritability due to emotional tension.
Table 13   Treatment of peptic ulcers
Drugs used for peptic ulcer
Side effects
H 2 -receptor antagonists
150 b.d. or 300 mg nocte
Headache, confusion (reversible)
40 mg b.d. or 80 mg nocte
Headache, dizziness
Aluminium hydroxide
300 mg 2–3 hours after
Constipation. Long-term use
Magnesium hydroxide
40 mg a meal
depletes body of phosphates
Alginic acid
500 mg
Laxative effect
Mucoprotective drugs
Prostaglandin analogues
Contraindicated in women of child bearing age.
200 mg qds.
Abdominal pain, diarrhoea (more useful for NSAIDs induced gastritis)
1 g qds. before meals
5 mg b.d.
Colloidal bismuth
240 mg b.d. before meals
Stains tongue and teeth
Proton-pump inhibitors
20 mg
20 mg
20 mg on empty
20 mg stomach o.d.
diarrhoea. Headache
40 mg
Skin rash
Eradication of H. pylori
(see H. pylori)
15 mg t.d.s.
Dryness of mouth.
50 mg b.d.
Blurring of vision
Given as adjuvant to H2-receptor antagonists as bedtime dose
Table 14   Indications for surgical treatment of peptic ulcer
• Pyloric stenosis
• Perforation, acute and chronic
• Recurrent bleeding or severe hemorrhage
• Evidence of penetrating or adherent ulcer
• Intractability and relapses
• Severe persistent hour-glass deformity
• Very large ulcers
• Combined gastric and duodenal ulcers
• Suspicion of malignancy
• Economic consideration
Indications for Surgical Treatment
Table 14 lists indications for surgical treatment of peptic ulcer.
Severe peptic ulcer secondary to gastric acid hypersecretion due to unregulated gastrin release from a non β-cell gastrinoma. Gastrinomas are classified into sporadic tumors (more common) and those associated with multiple endocrine neoplasia (MEN) type 1. Gastrin stimulates acid secretion through gastrin receptors on parietal cells by inducing release of histamine from ECL cells. Hypergastrinemia is responsible for the clinical manifestations of ZES.
Clinical Features
(a) Peptic ulcers with atypical locations (second part of duodenum and post bulbar (jejunum). Ulcers resistant to medical therapy, recurrence after acid-reducing surgery. Ulcers presenting with complications (bleeding, perforation or obstruction). (b) Oesophagus – Mild oesophagitis to frank ulceration and Barrett's mucosa. (c) Diarrhoea results from volume overload on small intestine, inactivation of pancreatic enzymes by acid which also damages intestinal epithelial surface. (d) Signs of hyperparathyroidism or hypophyseal or pancreatic tumour (MEN 1 syndrome).
Diagnosis: Biochemical Tests
Fasting gastrin level > 150–200 pg/mL (Normal < 150 pg/mL). If normal or elevated requires additional tests. (b)1. Gastrin provocative tests—An increase of 120 pg within 15 min of secretin injection has very high sensitivity.2. Barium meal shows coarse mucosal folds and ulcers. 3. Tumour localization—EUS and imaging of pancreas with endoscopic exploration of duodenum for primary tumours. Localization of gastrinomas by measuring the uptake of the stable somatostatin analogue 111In-pentreotide (OctreoScan) is possible. CT scan (Fig. 15), MRI to exclude metastatic disease.
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Fig. 15: Urea labelled with the non-radioactive isotope 13C, or very small dose of radioactive 14C, is drunk by the patient If Helicobacter pylori is present in the stomach, its powerful urease catalyses hydrolysis of urea, and labelled carbon dioxide can be detected in breath samples
(a) Omeprazole 60 mg/day in divided doses over 24 hours. (b) Octreotide as adjuvant therapy if peptic symptoms difficult to control with PPI. (c) Surgical resection of tumour. (d) Chemotherapy for metastasis.
Table 15 lists hormones secreted by alimentary system.
Table 16 lists causes of intestinal ulcers.
The most common malignancy of the stomach is gastric adenocarcinoma. Factors associated with gastric cancer are listed in Table 17.
Patient may present with:
  • Indigestion (most common presentation)
  • Weight loss
  • Nausea
  • Vomiting
  • Hematemesis
  • Melena
  • Profound anorexia
  • Flatulence
  • Metastatic disease—Palpable left supraclavicular node, metastatic nodules to the ovary (Krukenbergs tumour), periumbilical region (“Sister Mary Joseph node”) or peritoneal cul-de-sac (Blumer's shelf palpable on rectal or vaginal examination), ascites, jaundice, palpable abdominal mass, enlarged liver.
Table 15   Alimentary hormones
Physiological role
Stimulates acid, maintains mucosal growth, causes gastric motor activity
Stimulates pancreatic bicarbonate
Stimulates GB contraction and pancreatic enzyme secretion
Causes upper alimentary motor activity
Glucose-dependent insulin releasing hormone
Stimulates insulin release
Maintains mucosal growth. Slows intestinal transit
Pancreatic polypeptide
Inhibits GB contraction and pancreatic enzyme release
Table 16   Causes of intestinal ulcers
• Amoebiasis
• Inflammatory bowel disease
• Bacillary dysentery
• Tuberculosis
• Z-E syndrome
• Malignant ulcers
• Mesenteric artery occlusion
• Ischemic colitis
Table 17   Factors associated with gastric cancer
Genetic factors
• Family history (10% of patients)
• Blood group A
Environmental and dietary
• Salted pickles and smoked meat and fish.
• Environmental nitrates/nitrites#
• High concentration of lead and zinc in drinking water
• Cigarette smoking
• Consumption of neat spirits
• Poor-quality diets low in vitamin C and high in starch
• Workers in metal, clay and paint industries
• H. pylori$
Premalignant conditions
• Chronic atrophic gastritis
• Intestinal metaplasia
• Benign gastric ulcer
• Gastric adenomatous polyps
• Previous gastric surgery
# converted to nitrosamines by gastric bacteria.
$ high gastric pH encourages bacterial overgrowth, converting nitrites to nitrosamines.
  1. Radiology—Double contrast studies to detect mucosal abnormalities due to neoplastic infiltration.
  2. Endoscopy—Multiple biopsies from the margins and brush cytology from the base and under the edges (Fig. 16).
  3. Laparoscopy—For detection of local and peritoneal spread, and endoluminal ultrasonography for assessing local invasion and lymph node metastasis.
  4. Abdominal CT—This and delineate and show metastatic spread (Fig. 17).
Surgery—In early cases local gastric resection, in more advanced disease subtotal or total gastrectomy. Chemotherapy in patients with inoperable disease.
Hematemesis indicates a site of bleeding proximal to duodenal-jejunal junction, because blood entering the gut distal to this point seldom returns to the stomach (Table 18). The colour of the blood depends on whether the blood has been in the stomach, a large volume of bright red blood suggests a rapid and sizable hemorrhage, whereas a small amount of dark blood (coffee grounds) is more suggestive of a smaller bleed that has been altered by contact with gastric acid.25
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Fig. 16: Carcinoma of stomach
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Fig. 17: Linitis plastica: stomach wall thickening
Table 18   Causes of haematemesis and melena
• Oesophageal varices
• Mallory-Weiss tear
• Oesophageal carcinoma
• Reflux oesophagitis
• Foreign body
• Peptic ulcer
• Erosive gastritis
• Portal hypertensive gastropathy
• Gastric carcinoma
• Lymphoma
• Leiomyoma
• Angiodysplasia
• Dieulafoy's erosion (ruptured ectatic submucosal artery)
• Peptic ulcer
• Erosions/duodenitis
• Vascular anomalies (AVMs)
• Hemobilia
• Polyps (including Peutz-Jeghers syndrome)
• Aortoduodenal fistula
• Mesenteric arterial occlusion
Table 19   Causes of massive upper GI bleeding
Oesophageal or gastric varices
Gastric ulcer
Duodenal ulcer
Stress ulceration
Dieulafoy's erosion
Aortoenteric fistula
Melena stools have a characteristic black, tarry appearance and foul smell. Melena occurs when more than 60 mL of blood is lost into the upper GI tract. Melena indicates that blood has been present in the GI tract for at least 14 hours (and as long as 3–5 days). Lesions in the oesophagus, stomach and duodenum are responsible for most cases, but occasionally hemorrhage into small intestine, or even the right colon can cause melena if GI transit is slow. Massive upper GI bleeding (Table 19) may result in passage of dark red stools because of rapid transit.
Dieulafoy's disease is a rare cause of massive upper GI hemorrhage in previously asymptomatic individuals. The disease is characterised by a large thickened artery which follows a tortuous course towards the surface mucosa of gastric fundus, duodenum or jejunum. At endoscopy, the appearance of arterial spurting from otherwise normal mucosa is typical.
Primary care (before hospital admission)
  • IV access with infusion of normal saline
  • Oxygen
  • Early hospitalization
Hospital management
  • Resuscitation
    Insertion of large bore cannula into a substantial vein.26
    If pulse rate > 100/min or systolic BP falls below 100 mm Hg – infusion of crystalloids such as normal saline is started.
    If blood transfusion is required, 2–4 units of whole cross-matched blood. Aim is to maintain Hb concentration of 10g/dL.
After resuscitation
  • Endoscopy must be done within 24 hours and is necessary for—Diagnosis in order to plan treatment.
    Prognosis—Endoscopic stigmata are very useful by defining risk of further bleeding.
    Investigation of upper GI bleeding
  • Vomiting or retching—Before the episode characteristic of Mallory-Weiss syndrome (Fig. 18).
  • Heart burn and regurgitation—Reflux oesophagitis.
  • Dysphagia and weight loss—Oesophageal malignancy
  • History of peptic ulcer or abdominal pain—History of peptic ulcer is useful. However, bleeding can be the first manifestation of an asymptomatic ulcer.
  • Drugs—Intake of aspirin or NSAIDs.
  • Alcohol intake—Questioning for alcohol consumption and other risk factors for chronic liver disease.
  • History of easy bleeding or bruising—Coagulation or platelet disorders.
  • Haematemesis with melena—Indicates that the source of bleeding must be proximal to the jejunum.
Rapid assessment of hemodynamic state
  • Does the patient look pale or shocked?
  • Pulse rate and BP.
  • Postural hypotension.
  • Presence of purpura or petechiae—Telangiectasia of Rendu-Osler-Weber syndrome. Palpable purpura characteristic of systemic vacuities, and perioral pigmentation of Peutz-Jeghers syndrome (uncommon causes).
  • Splenomegaly, dilated abdominal veins or ascites— Signs of portal hypertension in patients bleeding from gastric or oesophageal varices. A congested gastric mucosa (portal hypertensive gastropathy) can also be a site for GI hemorrhage in patients with liver disease.
  • Presence of jaundice—Triad of biliary colic, jaundice and melena suggests hemobilia.
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Fig. 18: Mallory-weiss tear
Blood tests
  • Hemoglobin concentration—In first few hours after a bleed is a poor indicator of blood volume loss, because dilution by extracellular fluid recruited into the intravascular space may continue for more than 24 hours Low Hb at presentation usually signifies chronic blood loss.
  • Urea and electrolytes—Elevated blood urea suggests severe bleeding.
  • Liver function tests
  • Prothrombin time
Further investigations In a few individuals endoscopy does not define the cause of bleeding, because blood in the lumen prevents adequate inspection of the mucosa. If no cause is found – endoscopy can be repeated. If there is still no diagnosis and bleeding continues –
Small bowel imaging. Capsule endoscopy is recommended as a diagnostic test after a normal endoscopic evaluation of upper and lower GI tract after a negative gastroscopy and colonoscopy in patients with obscure GI bleeding.
Labelled RBC scan can detect rates of blood loss as low as 0.1 mL/min.
Angiography/CT angiography does not detect bleeding at rates below 1mL/min, but occasionally reveals underyiing vascular abnormalities. Both investigations may fail to localise the site of hemorrhage if it is intermittent.
Procedures to stop bleeding are listed in Table 20.27
Table 20   Procedures to stop bleeding
Non-variceal hemorrhage
Variceal hemorrhage
1. Endoscopic therapy to seal the arterial defect created by the ulcer. Indications: (a) Bleeding oesophageal varices. (b) Peptic ulcer with major stigmata of recent hemorrhage. (c) Vascular malformations, including actively bleeding AVMs, gastric antral vascular ectasia and Dieulafoy's lesion. (d) Rarely, active bleeding from a Mallory-Weiss tear.
Injection: (a) Adrenaline 1:10,000 (b) Fibrin glue, a mixture of thrombin and fibrinogen (injected through separate channels) and human thrombin are effective and have a low complication rate.
Heat energy: Devices are applied directly to the bleeding point to cause coagulation and thrombosis. The heater probe is pushed firmly on to the bleeding lesion to apply tamponade and defined pulses of heat energy are then given to coagulate the vessel.
Mechanical devices—‘Endoclips’ can be applied to bleeding vessels and are the best treatment for major bleeding ulcers.
Re-bleeding after endoscopic therapy requires operative interavention.
Vasoactive drugs
20u over 20 min + 0.4u/min. infusion
2 mg every 6 hrs
50 mg bolus + 50 mg/h infusion
250 mg bolus + 250 mg/h infusion
40–400 mg/min infusion
2 mg bolus every 4-6 hours.
Modified Sengstaken Blakemore(Minessota) tube insertion(Both temporary measures)
Propranolol up to a dose to reduce pulse rate by 20% to reduce risk of rebleeding
2. Drug therapy—To reduce risk of further bleeding.
Gastric acid lowering drugs—Omeprazole 80 mg bolus followed by 8 mg/hr infusion for 72 hours.
Tranexamic acid—A antifibrinolytic agent can improve stability of the clot and reduce risk of re-bleeding.
Endoscopic treatment Injection sclerotherapy – Intravariceal injection of sclerosant (5% ethanolamine, 1% olidocanol). Complications include oesophageal ulceration, fever, pleural effusion, pericarditis. Injection of fibrin glue.
3. Emergency surgery if: (a) Active bleeding cannot be controlled by endoscopic treatment. (b) Re-bleeding follows initially successful endoscopic treatment.
Variceal bandingOesophageal band ligation. Banding obliterates varices more efficiently and has few complications, but may be more difficult to perform in patients with active bleeding.
Shunt surgery. Use of small-bore 8 mm interposition H-graft portocaval shunt reduces incidence of encephalopathy.
Devascularization surgery if failure of non-operative treatments and patients who cannot undergo shunt surgery or TIPSS.
TIPS reduces rebleeding rates compared to endoscopic therapy.
Covered stents are used to improve patency.
Table 21 lists causes of acute lower GI haemorrhage.
Initial assessment: Patients usually present with bright red rectal bleeding (signifying a distal lesion) or dark red rectal bleeding which may be mixed with mucus in case of inflammatory or neoplastic lesion.
Past history of abdominal pain and alteration of bowel habit may suggest a neoplastic lesion, diarrhoea and urgency of defecation inflammatory lesion. Radiotherapy for genitourinary malignancy can cause radiation colitis. Elderly patients with cardiovascular disease may have ischemic colitis.
Table 21   Causes of acute lower GI haemorrhage
Anorectal conditions
• Haemorrhoids
• Anal fissure
• Mucosal prolapse (Solitary rectal ulcer syndrome)
• Meckel's diverticulum
• Juvenile polyps
• Inflammatory bowel disease
• Inflammatory bowel disease
• Adenomatous polyps (Fig. 19)
• Carcinoma
28• A-V malformation
• Meckel's diverticulum
• Diverticular disease
• Angiodysplasia
• Adenomatous polyps
• Carcinoma
• Ischemic colitis
• Inflammatory bowel disease
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Fig. 19: Virtual colonoscopy showing colonic polyps
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Fig. 20: Rectosigmoid growth
History of dyspepsia, alcoholism, NSAID ingestion or weight loss may give clues to the causative lesion.
Initial Management
  1. Hospitalization if suspicion of significant bleed.
  2. Correction of hypovolemia with plasma expanders followed by blood transfusion. Central venous pressure or Swann-Ganz monitoring helps prevent over transfusion in the elderly and is a sensitive indicator of continued or recurrent bleeding.
  3. Blood for Hb, clotting screen and urea and electrolyte estimation.
Investigations—May be planned after resuscitation. Digital anorectal examination and proctosigmoidoscopy (Fig. 20) to exclude local anorectal conditions and rectal biopsy plus stool microscopy and culture. Upper GI endoscopy if a local cause is not found. Capsule endoscopy is useful in detection of small bowel lesions in Crohn's disease, non-steroidal anti-inflammatory drug enteropathies, small bowel polyposis syndromes and small bowel tumours.
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Fig. 21: Lower GI bleed: Non-enhanced CT abdomen showing rectalhaematoma
CT angiography may be helpful in locating bleeder (Figs. 21 and 22).
Emergency laparotomy if hemorrhage is massive and patient is deteriorating; this should be combined with on-table colonoscopy.
Occult GI bleeding—Bleeding that is not visible and is manifested by positive faecal occult blood (FOB) testing or iron deficiency anemia.
Physical examination findings which might provide a clue about the source or bleeding:29
Facial or oral telangiectasia can suggest hereditary telangiectasia. Acanthosis nigricans in axilla suggest possible malignancy.
Perioral pigment spots are associated with Peutz-Jeghers syndrome. Purpura or ecchymosis implies possible bleeding disorder.
False positive FOB can result from pseudoperoxidase in various foods e.g. red meat, raw broccoli, turnips, cauliflower, radishes. A sensitive, quantitative measure is estimation of faecal concentration of 51Cr-labelled RBCs.
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Fig. 22: Urea labelled with the non-radioactive isotope 13C, or very small dose of radioactive 14C, is drunk by the patient If Helicobacter pylori is present in the stomach, its powerful urease catalyses hydrolysis of urea, and labelled carbon dioxide can be detected in breath samples
Diarrhoea is decrease in consistency or increase in liquidity of stools.
Diarrhoea may be further defined as acute if <2 weeks, persistent if 2–4 weeks and chronic if >4 weeks in duration.
Table 22   Causes of acute diarrhea
• Infections
Viruses (adenovirus, astrovirus, calicivirus (e.g. rotavirus, Norwalk agent), herpes simplex virus)
Bacteria (e.g. Campylobacter spp., C. difficile, E. coli, Salmonella enteritidis, Shigella spp.)
Parasites (e.g. E. histolytica, Giardia)
• Food poisoning/toxins
Bacillus cereus
Salmonella spp.
Staphylococcus spp.
Vibrio spp.
• Drugs
Antibiotics (e.g. amoxicillin)
Antihypertensives (e.g. angiotensin converting enzyme inhibitors)
Antineoplastic drugs
Antidepressants (e.g. Fluoxetine, lithium)
CNS drugs (e.g. L-dopa, valproic acid)
Cholesterol lowering drugs
GI drugs (e.g. magnesium containing antacids, prostaglandin analogues, H2- antagonists, sulphasalazine, prokinetic drugs)
Others: Theophylline, diuretics, oral hypoglycemic drugs, thyroxine, colchicine
• Poorly absorbed sugars: Fructose, mannitol, sorbitol
• Faecal impaction
• Intestinal ischemia
Table 22 enumerates causes of acute diarrhoea.
Chronic Diarrhoea
Table 23 enumerates causes of chronic diarrhea.
Eosinophilic gastroenteritis is a non-parasitic inflammatory disease of GI tract with various degrees of eosinophilic infiltration in tubular intestinal tract and biliary tree in absence of vasculitis or significant extraintestinal tissue eosinophilia.
Investigations for assessment of acute diarrhoea
  • Spot stool specimen
    • Occult blood
    • Leucocytes
    • Ova, cysts and parasites
    • Culture and sensitivity
    • Giardia antigen
    • Clostridium difficile toxin
    • DNA probes
  • Blood tests
    • Full blood count and differential
    • Urea and electrolytes
    • ESR and C-reactive protein
    • Blood culture
  • Rigid sigmoidoscopy and biopsy
  • Plain abdominal radiograph
  • Flexible sigmoidoscopy
  • Duodenal aspirates
Table 23   Causes of chronic diarrhea
• Dietary factors
Excess ingestion of fructose, sorbitol, caffeine
• Infections
Giardia lamblia
E. histolytica
Campylobacter enteritidis
Various organisms in immunocompromised (e.g. AIDS)
• Drugs
Antacids (magnesium trisilicate)
Antihypertensives (methyldopa, propranolol)
Antibiotics (Amoxicillin, lincomycin)
Iron preparations
• Lactose intolerance
• Malabsorption
Chronic pancreatitis
Bacterial overgrowth
Short bowel syndrome
• Inflammatory bowel disease
• Radiation colitis
• Neoplasms
Pancreatic cancer
Neuroendocrine tumours (carcinoid, gastrinoma), vasoactive intestinal polypeptide secreting tumour, medullary carcinoma of thyroid).
• Idiopathic secretory diarrhoea
Microscopic colitis
Collagenous colitis
Idiopathic bile salt diarrhoea
Large - volume nonspecific secretory diarrhoea
• Endocrine disorders
Diabetes mellitus
• Functional bowel disorder
Purgative use and abuse
• Faecal incontinence
Autonomic neuropathy (e.g. diabetes)
Anorectal surgery
Latrogenic sphincter damage
History, Symptoms and Signs
  1. History – (a) Age—Early life—Parasitic, dysentery, abdominal tuberculosis, genetic or biochemical abnormalities. Middle life—Colonic carcinoma, inflammatory bowel disease, pancreatic disease, laxative abuse. (b) History of allergy. (c) Family history—In hereditary pancreatitis, multiple neoplasia with multiple carcinoma of thyroid.
  2. symptoms –
    1. Type of diarrhoea—(i) Size of stool—Large stool (with little mucus) suggests small bowel disease. Small stool (with usually excess mucus) suggests large bowel involvement. (ii) Constipation alternating with diarrhoea—Carcinoma of colon, irritable bowel syndrome, diverticulosis, laxative habit, intestinal tuberculosis. (iii) Relation to ingestion of food—If of gastric origin diarrhoea immediately after each meal. Diarrhoea recurring after certain foods suggests allergy. (iv) Time of day—Urgent desire to evacuate in morning common in steatorrhoea. Nocturnal diarrhoea suggests presence of organic disease.
    2. Chronic bloody diarrhoea with systemic upset is probably caused by ulcerative colitis, colonic Crohn's disease or infectious colitis (e.g. amoebic or bacillary dysentery). Less commonly ischemic colitis, radiation colitis or gut vasculitis (e.g. Behcet's disease, SLE, polyarteritis nodosa).
    3. Weight loss—Diarrhoea associated with anorexia and weight loss suggests significant organic disease. Diarrhoea for many years without significant weight loss or systemic upset suggests irritable bowel syndrome. Diarrhoea with weight loss in spite of good appetite suggests thyrotoxicosis.
    4. Abdominal pain—Colicky lower abdominal pain associated with bouts of diarrhoea may suggest colonic obstruction or diverticulitis. Abdominal pain with fatty diarrhoea in recurrent pancreatitis, tuberculosis or Crohn's disease.
    5. Abdominal distension—Malignant disease, Crohn's disease, intestinal tuberculosis, or irritable bowel syndrome.
    6. Rectal tenesmus—Cause in rectum or lower sigmoid. Also in ulcerative colitis or diverticulitis.
    7. Sense of urgency—To pass frequent, small stools, that may be formed, loose or even pellety in irritable bowel syndrome.
  3. 31Signs –
    1. Abdominal tenderness—Diffuse in intestinal tuberculosis, over colon with diffuse colonic lesion.
    2. Doughy feel—With abdominal tuberculosis.
    3. Abdominal bruit—May be heard with stenosis of superior mesenteric artery.
    4. Mass—Carcinoma, tumour or diverticulitis.
    5. Anal abnormalities—Fissures, perianal or ischiorectal abscesses and fistulae may present as a complication of ulcerative colitis or Crohn's disease.
  4. Type of faeces –
    1. Mucus and blood—Amoebic and bacillary dysenteries.
    2. Profuse purulent discharge—Chronic ulcerative colitis.
    3. Mucus—Irritable bowel syndrome, chronic constipation, following ingestion of strong purgatives, rarely in ulcerative colitis.
    4. Fatty stools—Voluminous, pale pasty stools in steatorrhoea.
    5. Frequent soft, non-fatty stools—Diarrhoea of gastric origin.
    6. Large fermentative stools—Sprue, nutritional deficiency states, fungus infections, intestinal carbohydrate dyspepsia.
    7. With excessive bile—Gastrointestinal hypermotility induced by vigorous purgatives or after severe gastro-enteritis, fistula between biliary tract and alimentary canal in a patient who has suffered from biliary colic attacks.
    8. Watery stools—Emotional diarrhoea, internal fistulae, reflex diarrhoea, extensive Crohn's disease, ulcerative colitis. In carcinoid syn. the secretory diarrhoea is profuse.
Differentiation of small bowel from large bowel diarrhoea is given in Table 24.
Table 24   Differentiation of small bowel from large bowel diarrhoea
Small bowel diarrhoea
Large bowel diarrhoea
Timing of diarrhoea
Any time
Usually on getting up in morning
Frequency of stools
Increased frequency of small stools
Normal to increased frequency of large stools
Pain if any
Central abdominal, not relieved by defecation
Often in left iliac fossa, relieved by defecation
Watery, or pale, fatty and offensive
With mucus or fresh blood, or watery
Tests used in assessment of chronic diarrhoea
Initial Evaluation
Spot stool examination
  • Gross characteristics
  • Faecal occult blood
  • Methylene blue stain for leucocytes
  • Sudan stain for fat
  • Microscopy for ova, cysts and parasites
  • Culture and sensitivity
Quantitative stool collection
  • 3-day stool weight/volume
Blood tests
  • FBC and differential
  • Urea and electrolytes, liver biochemistry, calcium and phosphate
  • ESR, C-reactive protein
  • Thyroxine and TSH
  • Antigliadin, endomysial and reticulum antibodies
  • Amoebic serology
Rigid sigmoidoscopy and biopsy
Further Evaluation
Spot stool examination
  • Laxative screen
  • Giardia antigen
  • Acid-fast stain
  • Faecal elastase
  • Faecal chymotrypsin
  • Sulphate/phosphate/magnesium concentration
Quantitative stool collection on 100 g/fat/day
Blood tests
  • Haematinics
  • INR
  • Immunoglobulin
  • Fasting 9 a.m. cortisol
  • Fasting gut hormones
  • Alkalinization
  • Laxative screen 24-hour 5-hydroxyindole acetic acid
  • 24-hour catecholamines
  • Urinary indicans
32 Flexible sigmoidoscopy and biopsies
Gastroscopy and duodenal biopsies
  • Barium meal and follow-through
  • Small bowel enema
  • Abdominopelvic ultrasonography
  • Barium enema
  • CT of abdomen and pelvis
Breath tests
  • Lactose hydrogen breath tests
  • Glucose hydrogen breath test
  • 14C glycolic acid breath test
  • Anorectal physiology studies
Trial of empirical treatment
  • Restrictive diets (low-fat, lactose-free) (avoiding lactose for lactase deficiency or gluten for celiac sprue)
  • Metronidazole
  • Cholestyramine
  • Pancreatic enzyme supplements
  • Octreotide
Clonidine, an 2-adrenergic agonist, may allow control of diabetic diarrhoea
Constipation can be defined as infrequent or difficult passage of faeces. It can also refer to hardness of stools or feeling of incomplete evacuation. Table 25 lists various causes of constipation.
  1. Determine number of stools per week and duration of the problem. Ask about straining, pain, pressure and sense of obstruction to defecation, also consistency of stools. Note any associated complaints like abdominal pain and its location, bloating, gas and audible bowel sounds.
  2. Any symptoms that might indicate an underlying disorder (secondary constipation).
  3. Dietary and habitual fluid intake.
  4. An acute or subacute onset of constipation should raise possibility of mechanical obstruction. In female patients the number and type and difficulty of deliveries since rectocoele and pelvic problems can be associated with constipation.
Table 25   Causes of constipation
Non-GI disease
Insufficient fibre
Diverticular disease
Congenital abnormality
(e.g. Hirschsprung's disease)
Motility disturbance
Irritable bowel disease
Hirschsprung's disease
Anorectal disease
Crohn's disease
Anal fissures
Disorders of rectal evacuation
Pelvic floor dysfunction
Descending perineum syndrome
Rectal mucosal prolapse
Antacids containing aluminium or calcium
Tricyclic antidepressants
Analgesics: Opioids, NSAIDs
Calcium channel blockers: Verapamil
Antipsychotics: Risperidone
Anticholinergic: Belladona alkaloids
Antiparkinsonian drugs: Amantadine
Diabetes mellitus
Spinal or pelvic nerve injury
Cerebrovascular accident
Multiple sclerosis
Gynaecological: Pregnancy, ovarian cancer
Psychiatric disorders
  • Abdominal size and girth
  • Abdominal tenderness—Local or general
  • Organomegaly
  • Masses, including palpable left colon
  • Perianal examination for excoriations, fissures and haemorrhoids
  • Internal rectal examination—masses, gross or occult blood
  • Ask the patient strain to expel the index finger during a digital rectal examination. Motion of the puborectalis posteriorly during straining indicates proper coordination of the pelvic floor muscles.
  • Clinical examination to identify signs of an underlying medical illness, e.g. hypothyroidism.
Barium enema: To exclude obstruction if constipation of recent onset.
Water-soluble contrast media: If megarectum or megacolon is suspected.33
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Fig. 23: Colonic growth
Flexible sigmoidoscopy plus barium enema or colonoscopy alone: Particularly in patients >40 years, to exclude structural diseases such as cancer or strictures (Fig. 23). Colonoscopy alone is most cost-effective in this setting because it provides an opportunity to biopsy mucosal lesions, perform polypectomy or dilate strictures.
Anorectal physiological studies to elicit anorectal inhibitory reflex and to exclude Hirschsprung's disease to assess pelvic floor coordination.
Upper gut barium studies: To exclude pseudo- obstruction if lower bowel is dilated.
Upper gut transit studies: if patient has upper gut symptoms or surgery for constipation is contemplated.
Proctography if a large rectocoele is suspected.
Abdominal CT scan: This can identify even small masses and delineate the extent of spread and metastasis (Fig. 24).
Balloon expulsion test: A balloon-tipped urinary catheter is placed and inflated with 50 mL of water. Normally, a patient can expel it while seated on a toilet or in the left lateral decubitus position. In the lateral position, the weight needed to facilitate expulsion of the balloon is determined; normally, expulsion occurs with <200 g added
If positive, an anatomic evaluation of the rectum or anal sphincters and an assessment of pelvic floor relaxation are done.
  • Increase in dietary fibre, bulking agents such as isabgol and laxatives. If continued use of laxatives is unavoidable, rectal stimulants e.g. glycerine or bisacodyl suppository, or oral senna preparation or oral bisacodyl. 5-HT4 (serotonin4) agonists may have a role initiating peristalsis when laxatives have failed or are poorly tolerated.
  • floor coordination.
  • Surgery—Subtotal colectomy or ileorectal anastomosis as a last resort, but results unpredictable.
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Fig. 24: Carcinoma of rectum: CECT showing narrowing of rectal canal due to mass
Idiopathic megarectum and megacolon—Symptoms may be present from birth, childhood or adulthood. Aetiology is unknown.
Hirschsprung's disease has variable pattern of inheritance and the major susceptibility gene is RET proto-oncogene. It should be excluded by contrast studies of the large 34 bowel, elicitation of the recto-anal inhibitory reflex or full-thickness rectal biopsy taken 2 cm above dentate line.
Management—(a) Faecal disimpaction using enemas. Life-long laxatives may be required. (b) Behavioural therapy can improve defecatory behaviour in some. (c) Colectomy with ileorectal anastomosis achieves a normal bowel frequency in 80%.
Malabsorption is a failure of normal absorption of nutrients. Principal types of malabsorption are generalized and specific.
Generalized malabsorption affects all classes of nutrients. It usually results from small intestinal disease or conditions in other organs (Table 26). When severe, it is manifested by one or more clinical features of malabsorptive stage. Because fat absorption is most affected, excess undigested fat in the stool (steatorrhoea) is strong evidence of generalized malabsorption.
Specific malabsorption is a failure of the processes governing absorption of one class or type of nutrients, e.g. genetic or acquired failure to absorb disaccharide sugars (e.g. lactase or vitamin B12 deficiency).
  • Diarrhoea and weight loss
  • Family history may suggest coeliac disease, Crohn's disease or familial pancreatitis
  • Previous surgery may lead to short gut syndrome or create other abnormalities predisposing to bacterial overgrowth
  • Immunodeficiency may lead to frequent infections
  • Radiation treatment may cause radiation enteritis
  • Obvious heavy steatorrhoea (oily stools) may indicate pancreatic insufficiency
  • Abdominal pain though uncommon, suggests a diagnosis of pancreatitis, intestinal strictures or small intestinal ischemia
Blood Tests
Tests for Evidence of Malabsorption
  • Full blood count
  • Mean cell volume, mean corpuscular hemoglobin
  • Serum iron/total iron-binding capacity (or ferritin)
  • Vitamin B12
  • Serum (or RBC) folate
  • Prothrombin time
  • Plasma proteins
Table 26   Causes of generalized malabsorption
I. Conditions within gut lumen
A. Defective substrate hydrolysis
• Pancreatic enzyme deficiency
–Chronic pancreatitis
–Cystic fibrosis
–Cancer of pancreas
–Z-E syndrome
–Hypothyroidism (also villous atrophy)
• Enzyme inactivation
–Z-E syndrome
• Intestinal hurry
B. Lack of solubilising bile salts
(failure of micelle formation)
• Reduced bile salt synthesis
–Parenchymal liver disease
–Cholestatic jaundice
• Bile salt deconjugation
–Z-E syndrome
–Bacterial over growth
• Increased faecal loss of bile salts
–Terminal ileal disease
–Crohn's disease
C. Deficiency of certain factors
• Achlorhydria
• Lack of intrinsic factor
–Pernicious anaemia
• Increased consumption of Vit. B12 in intestine
–Blind loop or stagnant loop syndrome
D. Immunological
• Immunoproliferative small intestinal disease (IPSID)
E. Drugs (Refer to Drug-induced GI disease)
II. Conditions in gut mucosa
  (Reduced absorptive area)
• Normal mucosa
–Lactase difficile
• Abnormal mucosa
–Coeliac disease
–Tropical sprue
–Whipple's disease
III. Disorders of transport from mucosal cell
• Lymphatic obstruction
–Lymphoma (abdominal)
• Epithelial processing defect
IV. Systemic diseases
Diabetes mellitus
Collagen vascular diseases
Addison's disease
Note: Tropical sprue continues to be the commonest cause following coeliac and Crohn's disease.
Tests for Cause of Malabsorption
  • C-reactive protein, ESR
  • Immunoglobulins (hypogammaglobulinemia)
  • Endomysial and antigliadin antibodies (coeliac disease).
Small intestinal biopsy at endoscopy with punch biopsy forceps. Normal histology with well-formed villous pattern almost excludes diffuse intestinal mucosal disease. In difficult cases, endoscopic small intestinal biopsy may provide information, and allows dissecting microscopic appearance to be examined readily.
Capsule endoscopy as alternative to biopsy of small intestine to detect villous atrophy in patients suspected of coeliac disease.
  • Total or subtotal villous atrophy in coeliac disease.
  • Mucosal lesions or trophozoites in mucus layer in giardiasis.
  • Lipid-filled vacuoles distending villous epithelium in Abetalipoproteinemia.
  • PAS positive engorged macrophages filling lamina propria and dilated vacuoles in Whipple's disease.
  • Other diseases—Diffuse small bowel Crohn's disease, intestinal lymphangiectasia, diffuse intestinal lymphoma, and various allergic gastroenteropathies (e.g. soya protein intolerance) can also be diagnosed.
Barium Meal Follow-through
  • Delayed transit time
  • Abnormal small intestinal pattern:
  1. Smooth appearance of margins of barium-filled intestine.
  2. Clumping of barium (Fig. 25) or transformation of a normal feathery appearance to a ladder pattern resembling a stack of coins.
  3. Radiological anatomical abnormality in stagnant loop syndromes, small intestinal resection, Crohn's disease, systemic sclerosis.
  4. Nodular lymphoid hyperplasia suggests immunoglobulin deficiency and possibility of an enteric infection such as giardiasis. In older individuals radiology may reveal multiple diverticulae leading to bacterial overgrowth.
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Fig. 25: Fragmentation and clumping of barium in the small intestineindicating malabsorption
Physical findings in malabsorption are related to malabsorption of specific nutrients (Table 27).
Table 27   Physical findings in malabsorption
Malabsorbed nutrients
Symptoms and signs
Fat soluble vitamins
Vitamin A
Night blindness
Vitamin D
Proximal myopathy
Rickets in children
Vitamin K
Water soluble vitamins
Vitamin B1
Fluid retention
Brainstem lesions
Wernicke's encephalopathy
Vitamin C
Petechial hemorrhage
Swollen gums
Follicular congestion
Folic acid
Macrocytic anaemia36
Folic acid
Macrocytic anaemia
Vitamin B12
Microcytic anaemia
Poor wound healing
Defective taste
Muscle wasting
Peripheral oedema
Bile salts
Watery diarrhoea
  • Radiograph—Pancreatic calcification
  • Ultrasonography—(Calcification and complications, e.g. pseudocysts, duct dilatation)
  • CT—(Calcification, gland atrophy, cysts and duct dilatation)
  • ERCP or MRI
Table 28 enumerates various absorption tests.
In coeliac disease, the mucosa of small intestine is abnormal. The condition improves morphologically and symptomatically with a gluten-free diet and relapses when gluten is re-introduced. It was previously called non-tropical sprue, idiopathic steatorrhoea or primary malabsorption.
Table 28   Physical findings in malabsorption
Carbohydrate malabsorption
Hydrogen breath test
After overnight fast, basal samples taken and 50 g lactose in 200 mL in water. End-expiratory blood samples analysed at 15 or 30 min interval for 2 hours
If bacteria in upper gut, or lactose absent, increased excretion of H2 in breath. Positive test is increase of 200 ppm or more
Fat malabsorption (Pancreatic function)
Triolein test
Oral dose of labelled fat and measurement of 14CO2 in expired breath
Tests ability to digest fat
3-day faecal fat collection
Adequate amount of fat intake (70 g/d)
Normal amount of fat in stool <5 g/day. More fat excretion confirms steatorrhoea.
Tubeless test
Pancreolauryl test links a fluoresceinated probe to a carrier by a link that is sensitive to pepsin
Low proportion of ingested dye recovered from urine when luminal trypsin is reduced in pancreatic insufficiency
N-benzoyl-tyrosyl paraamino-benzoic acid test
After fasting, oral dose of 500 mg NBT-PABA is given with 250 ml water
Normal subjects excrete more than 57% in 6 hours. Test relies on hydrolysis of NBT-PABA by trypsin and subsequent excretion of paraamino-benzoic acid and its metabolites.
Ileal function
SeHCAT test scan
Patient's 7-day retention of oral dose of labelled bile acid (Se-homo-cholyltaurine) after whole body scan
Low (<7%) in extensive ileal disease or bile salt malabsorption.
Schilling test
(Vitamin B12 absorption)
Ingestion of radioactive B12 and measurement of urinary recovery
If cause of abnormal B12 absorption is gastric, it can be corrected by co-administration of B12, if cause is terminal ileum it cannot be corrected.
D-xylose absorption test
5 g D-xylose p.o. to fasting patient and urine collected at 30 min. intervals for next 5 hours.
An abnormal test (<4.5 g excretion) primarily reflects the presence of duodenal/jejunal mucosal disease, blind loop syndrome.
Tests of small bowel contamination
Uncontaminated small bowel aspirate with pre-sterilized, sheathed aspiration cannula. Aerobic and anaerobic culture of aspirate
Total aerobic and anaerobic count of 105 or more suggests bacterial overgrowth.
Table 29   Presenting features of coeliac disease
• Diarrhoea (most common)
• Infertility, recurrent miscarriage
• Lassitude
• Severe anemia and/or unexplained diarrhoea in pregnancy
• Weight loss
• Mild microcytic anaemia with persistent low serum or RBC folate
• Osteomalacia
• Aphthous ulceration
• Glossitis
• Myopathy
• Skin complains (e.g. eczema)
Presenting features of coeliac disease are given in Table 29. Patients with coeliac disease are usually short, and 60% of children are below the third centile for age. Development of secondary sex characteristics is often delayed. Delayed eruption of teeth, finger clubbing and koilonychia may be seen and oedema and ascites occur occasionally in severe cases due to hypoproteinemia.
Hematology—Mild hypochromic microcytic anemia. Blood film may show Howell-Jolly bodies, siderocytes, iiregular and crenated RBCs, Heinz bodies, microspherocytes, acanthocytes and occasionally erythroblasts.
Laboratory tests—Patients with untreated coeliac disease have IgA antigliadin, IgA antiendomysial, and IgA anti-tTG antibodies. Elevated tTg antibody titres are 90–95% sensitivity and 90–95% specificity
Bone densitometry for osteoporosis.
Endoscopic small intestinal biopsy. Classical changes are villous flattening of small intestinal mucosal epithelium, inflammation of lamina propria, reduced epithelial surface cell height, increased intra-epithelial lymphocyte count.
Radiology—With barium follow-through or small bowel enema often reveals small intestinal segmentation, dilatation and loss of the normal, fine feathery pattern of the mucosa. CT and MRI may reveal small bowel dilatation with hyposplenism, and are useful in diagnosing complicating malignancy and caseating mesenteric lymph nodes.
Diet—Gluten-free diet avoiding wheat, rye and barley products. Strict dietary restriction not only reduces the increased incidence of small intestinal T cell lymphoma, but also of autoimmune disorders including diabetes mellitus and thyroid disease. The diet is low in fibre, so regular addition of rice bran and ispaghula husks is useful. Specific dietary deficiencies (e.g. iron, folic acid, occasionally B12) should be corrected.
Corticosteroids can control coeliac disease, leading to rapid cessation of diarrhoea, weight gain and improved fat absorption. However, symptoms usually return within a few days after stopping treatment. Corticosteroids should therefore be reserved for severe illness, a coeliac crisis or otherwise unresponsive disease.
Follow-up—After a gluten-free diet for 3–4 months, a repeat small intestinal biopsy should be taken to determine whether the mucosal morphology has improved. If there is no improvement, other causes of villous atrophy (e.g. giardiasis, cow's milk allergy, HIV infection) should be excluded.
It is a malabsorption disorder seen in tropical areas and is manifested by chronic diarrhoea, steatorrhea, weight loss and nutritional deficiencies including those of both folate and cobalamin.
It is a diagnosis of exclusion as chronic diarrhea in a tropical environment is most often caused by infectious agents, including G. lamblia, Yersinia enterocolitica, C. dfificile, Cryptosporidium parvum.
Tropical sprue should not be entertained as a possible diagnosis until the presence of cysts and trophozoites has been excluded in three stool samples.
Its occurrence is not evenly distributed in all tropical areas, it is found in specific locations, like southern India, Philippines.
Aetiology—The aetiology and pathogenesis of tropical sprue are uncertain. As tropical sprue responds to antibiotics the consensus is that it may be caused by one or more infectious agents.
Klebsiella pneumonia, Enterobacter cloacae and E. coli have been implicated in some studies of tropical sprue, while other studies have favoured a role for a toxin produced by one or more of these bacteria.38
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Figs. 26A and B: Contrast CT abdomen showing lymphadenopathy (A) coronal view venous phase; (B) axial view arterial phase
Diagnosis—The diagnosis of tropical sprue is best based on an abnormal small-intestinal mucosal biopsy in an individual with chronic diarrhoea and evidence of malabsorption who is either residing or has recently lived in a tropical country.
The small-intestinal biopsy in tropical sprue does not reveal pathognomonic features but resembles and can often be indistinguishable from, that seen in celiac disease.
The biopsy sample in tropical sprue has less villous architectural alteration and more mononuclear cell infiltrate in the lamina propria.
In contrast to those of celiac disease, the histologic features of tropical sprue manifest with a similar degree of severity throughout the small intestine and a gluten-ree ddiet does not result in either clinical or histologic improvement in tropical sprue.
Treatment—Broad-spectrum antibiotics and folic acid are most often curative. Tetracycline should be used for up to 6 months and may be associated with improvement within 1–2 weeks. Folic acid alone induces hematologic remission as well as improvement in appetite, weight gain and some morphologic changes in small intestinal biopsy.
Abdominal tuberculosis can affect the GI tract, peritoneum, lymphnodes of the small bowel mesentery (Figs. 26A and B), or solid viscera (liver, spleen, pancreas). The terminal ileum and ileocaecal region are the most common sites, possibly because of increased rate of fluid and electrolyte absorption, minimal digestive activity and abundance of lymphoid tissue followed by the jejunum and colon. Multiple sites are common.
Clinical features of abdominal tuberculosis are very variable as listed in Table 30.
Signs: Vigorous peristaltic activity or distended bowel may be noted. Tenderness usually in right lower quadrant. Muscle guarding if peritoneum is involved. In presence of ileocaecal tuberculosis a tender fixed mass may be palpated in half the cases.
  1. Clinical—Possibility of intestinal tuberculosis should be considered if – (i) Lung cavity with positive sputum. (ii) Abdominal symptoms appear in association with change of bowel habit. (iii) Temperature becomes irregular without change in lung lesion. (iv) Sudden reversal of pulmonary T.B. not explained by condition of lung lesion, or unsatisfactory clinical course in spite of adequate treatment.
  2. Radiology—Suggestive features on barium meal examination – (i) Lack of barium retention in diseased segment of ileum and/or caecum (Stierlin sign). (ii) Persistent narrow stream of barium in small bowel (String sign). (iii) Areas of small bowel obstruction manifested by dilatation and delay in emptying in association with short segments of irregularity of bowel silhouette (Fig. 27) and mucosal markings. (iv) Single filling defect in caecum in hypertrophic tuberculosis. (v) road-based ttriangular appearance of terminal inch of ileum with base towards caecum (Fleischner sign).39
    Table 30   Clinical features of abdominal tuberculosis
    Site of involvement
    Type of lesion
    Modes of presentation
    Clinical features
    Small intestine
    Diarrhoea, malabsorption, lower GI bleeding, fever. Acute int. perforation, peritonitis.
    Acute on chronic
    Acute on chronic int. obstruction
    Subacute intestinal obstruction
    Acute int. obstruction
    Ileocaecum and large intestine
    Mass, subacute int. obstruction
    Acute on chronic
    Acute on chronic int. obstruction
    Acute int. obstruction
    Lower GI bleeding, fever
    Pain, ascites, fever
    Subacute int. obst.
    Acute TB peritonitis
    Acute-on- chronic
    Acute-on-chronic int. obstruction
    Diffuse hepatic involvement as in miliary TB.
    Single or multiple tuberculomas or abscesses.
  3. Histology—Demonstration of mycobacterium tuberculosis or histological evidence of tubercles with caseation necrosis tissues for histological examination can be obtained by – (a) Percutaneous fine-needle aspiration cytology (FNAC) from an abdominal mass, or ultra-sound guided or CT-guided FNAC from enlarged lymphnodes. (b) Colonoscopic biopsy from colonic and ileocaecal lesions (Fig. 28). (c) Laparoscopic biopsy of parietal peritoneum.
  1. Diet—Bland, low in residue. Low fat diet if steatorrhoea.
  2. Anti–tuberculous therapy.
  3. Fat soluble vitamins, Vitamin C and calcium.
  4. Pancreatin 1–4 gm. after each meal if very poor absorption.
  5. Surgery: Indications—(a) Localised tuberculous involvement of hyperplastic type with marked diminution of lumen caliber. (b) Stenosis of bowel causing obstruction. (c) Perforation of tuberculous ulcer.
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Fig. 27: Colonic stricture due to tuberculosis
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Fig. 28: Ileocaecal TB
IBS consists of a group of GI symptoms particularly associated with lower bowel in absence of demonstrable organic pathology.40
Recurrent abdominal pain or discomfort for at least 3 days per month in last 3 months (with symptoms onset at least 6 months prior to diagnosis) associated with two or more of the following:
  1. Improvement after defecation
  2. Onset associated with change in frequency of stool
  3. Onset associated with change in form (appearance) of stool
Other symptoms that are not essential but support the diagnosis of IBS:
  • Abnormal stool frequency (>3 bowel movements/day or <3 bowel movements/week)
  • Abnormal stool form (lumpy/hard or loose/watery stools)
  • Abnormal stool passage (straining, urgency or feeling of incomplete bowel movement)
  • Passage of mucus
  • Bloating or feeling of abdominal distension
  1. Chronic abdominal pain with constipation
  2. Diarrhoea predominant IBS
  3. Mixed IBS: Alternating diarrhoea and constipation
  1. Pathophysiology
    1. Disturbance of GI motility—In IBS, the fasted small intestine shows subtle differences in activity, particularly under conditions of stress and during sleep.
    2. Sensory abnormalities (visceral hyperalgesia). IBS patients report discomfort at lower volume of gut distension. Such patients may suffer from ‘visceral hypersensitivity’ and the cause of the problem may be neural abnormality of the primary afferent nerves to the spinal cord, or of the intrinsic nerves of the colonic wall.
  2. Psychopathology—Patients in whom continuous pain is the major symptom suffer more from depressive symptoms, whereas those with chronic unremitting symptoms tend to have subtle personality differences and low self-esteem. Marital difficulties and childhood physical abuse are reported more commonly in chronic IBS patients.
  3. Post-infective/post-inflammatory causes—Onset of symptoms may follow an enteric infective episode (e.g. Campylobacter), and IBS-like symptoms are common in patients with coexistent inflammatory bowel disease.
  4. Abnormal regulatory physiology—Patients with IBS have been reported to exhibit exaggerated GI responses, either as intrinsic reflexes (e.g. motility response to eating or infused cholecystokinin) or to exogenously infused drugs (e.g. cholinergics) and the stress-response mediator corticotrophin-releasing hormone (CRH).
  5. Diet—Colonic fibre fermentation may be a source of perceived excess gas, and has led to suggestions of a role of abnormal colonic bacterial flora.
  • Full blood count, ESR and sigmoidoscopy in patient under 40 with classical history of IBS and without significant disturbance or significant weight loss.
  • Double-contrast barium enema or colonoscopy in patients over 40 with recent onset of symptoms to rule out malignancy.
  • Rectal biopsy in patients with diarrhoea. Changes of inflammatory bowel disease or less common types of colitis may be found in a macroscopically normal rectum.
  • In patients with chronic diarrhoea, further investigations to rule out coeliac disease, Crohn's disease and chronic GI infection e.g. giardiasis.
  1. Explanation and reassurance—Physiological explanation based on concept of ‘spasm’ of bowel. Reaction of the gut can be equated to reaction to emotion e.g. fast pulse and dry mouth to apprehension. Reassurance regarding absence of organic disease.
  2. Specific therapy—According to the predominant complain of the patient.
Dietary Measures
Dietary fibre—With supplementation with bulking agents such as coarse wheat bran or ispaghula husk in gradually increasing amount.
Exclusion diets—Lactose-free diets may be tried in individuals with unexplained, chronic, painless diarrhoea.
Drug Therapy
Antispasmodics—Mebeverine 100 mg or Pinaverium bromide 50 mg, 30 minutes before food if symptoms following meals.41
Antidiarrhoeal agents—Loperamide, codeine (long-term use may produce addiction) or diphenoxylate, if frequent loose stools.
Antidepressants—In patients with anxiety provoked symptoms.
Tegaserod—5 mg b.d. ½ hour before food if associated constipation predominant IBS.
Lubiprostone—Stimulates chloride channels in the apical membrane of intestinal epithelial cells. Chloride secretion induces passive movement of sodium and water into the bowel lumen and improves bowel function. Oral lubiprostone was effective in the treatment of patients with constipation-predominant IBS.
Linaclotide— It is a minimally absorbed 14-amino-acid peptide guanylate cyclase-C (GC-C) agonist that binds to and activates GC-C on the luminal surface of intestinal epithelium. Activation of GC-C results in generation of cyclic guanosine monophosphate (cGMP), which triggers secretion of fluid, sodium and bicarbonate. The analgesic action of linaclotide appears to be mediated by cGMP acting on afferent pain fibers innervating the GI tract. The drug has been approved for treatment of constipation in IBS-C patients. 290 μg given once daily, significantly improved abdominal pain, bloating and spontaneous bowel movement.
3. Non-drug treatment—If no response to conventional therapy. (a) Elimination diets when diarrhoea is predominant symptom in a well-motivated subject. (b) Relaxation techniques for stress management. (c) Specific biofeedback. (d) Psychotherapy. (e) Hypnotherapy.
The term Diverticulosis simply describes the presence of diverticula. Diverticulitis is the clinical syndrome resulting from inflammation of a diverticulum.
Diverticular colitis—Mucosal changes are thought to be an idiosyncratic inflammatory response to diverticulitis.
1. More common in older individuals. 2. Eating habits – Diverticulosis is less common in vegetarians than those who eat meat. Hence a diet poor in fibre is associated. 3. Factors that lead to constipation and colonic hypermotility or to a weak colonic wall may be involved.
Colonic diverticula are pulsion diverticula; they arise when the pressure within the colon is excessive and the wall is weakened as a result of ageing. The sigmoid colon is the most common site for diverticulae formation. Occasionally the descending colon, less commonly the whole colon is involved. Diverticulitis occurs when a diverticulum becomes irritated by inspissated faecal material (faecolith).
  1. Uncomplicated diverticular disease—No symptoms unless the wall changes are so severe as to cause obstruction.
  2. Rectal bleeding is uncommon but tends to be sudden and profuse. Such bleeding usually occurs in simple diverticulosis rather than diverticulitis.
  3. Diverticulitis and pericolitis are usually associated with pain and tenderness in right iliac fossa that starts suddenly. Right-sided disease can mimic acute appendicitis. Patient may become extremely ill with peritonitis or Gram-negative septicaemia.
  4. Pericolic abscess may occur in or outside the wall. Symptoms can be vague (e.g. anorexia, weakness). Abdominal and pelvic examination can reveal a tender mass.
  5. Fistulas—An untreated pericolic abscess can erode into a neighbouring hollow organ, producing a fistula. Fistulas can cause new symptoms (e.g. pneumaturia and repeated urinary infections in case of colovesical fistula, malabsorption in colojejunal fistula). In women colovaginal fistulas are more common in women who have undergone hysterectomy.
  • Barium enema. Diverticulosis is readily detected. Barium enema and colonoscopy avoided in acute condition due to risk of perforation during procedure.
  • Abdominal CT is also effective for diagnosis.
  • Colonoscopy if chronic bleeding or insidious change in bowel habit, symptoms which may be caused by cancer of sigmoid colon which can be overlooked on barium enema in presence of diverticular disease. Colonoscopy should be performed after 6 weeks after attack of diverticular disease.
  1. Symptomatic, uncomplicated diverticular disease— Treatment same as irritable bowel syndrome. High fibre diet and/or bulking agents such as ispaghula and bran. If diarrhoea is the main symptom, antidiarrhoeal drugs. Musculotropic drug like mebeverine may relieve pain. Psychological support if anxiety or depression.42
  2. Rectal bleeding—Transfusion may be required in elderly patients. Occasionally embolization of bleeding vessel best performed at time of angiography.
    Endoscopic hemostasis by adrenaline injection.
  3. Diverticulitis and pericolitis—Hospitalization with rest and analgesics, nil by mouth and antibiotics against aerobic and anaerobic bacteria (e.g. cefuroxime and metronidazole).
  4. Pericolic abscess and fistulas—CT and ultrasound imaging techniques allow abscesses to be drained percutaneously. Fistulas require surgery.
Ulcerative colitis is an inflammatory disorder of the colonic mucosa characterized by relapses and remissions. The rectal mucosa is always involved, occasionally by microscopic inflammation alone, and the disease extends proximally.
UC is classified into severity in two ways—According to extent of involvement or according to symptoms. If the disease is limited to only the rectum (proctitis), limited to rectum and sigmoid colon (proctosigmoiditis). Left sided UC involves descending colon, sigmoid colon and rectum. The term pancolitis suggests involvement of the whole colon or most of the colon. Sometimes ileum gets involved called as “Backwash ileitis”.
Potential etiological factors in UC are listed in Table 31.
Clinical Features
Presentation—Onset is usually gradual. Bloody diarrhoea is the hallmark of the disease, though proctitis may present with rectal bleeding and constipation. Urgency and crampy abdominal discomfort before defecation. Stool frequency is related to the severity of the disease. Assessment of the severity of disease is given in Table 32.
Systemic features and signs Anorexia, weight loss. Anemia, fever, tachycardia, abdominal tenderness.
Table 32   Assessment of severity
Motions per day
< 4
4 to 6
> 6
Rectal bleeding
Large quantities
> 37.8ºC on 2 of 4 days
Pulse rate
> 90 beats/min.
> 10.5 g/dl
< 10.5 g/dL
Slight rise
> 30 mm/hr.
Endoscopic appearace
Erythema, decreased vascular pattern, fine granularity
Marked erythema, coarse granularity, absent vascular markings, contact bleeding, no ulcerations
Spontaneous bleeding, ulcerations
Extra-intestinal Manifestations
Ulcerative colitis has very varied systemic manifestations as given in Table 33.
Sigmoidoscopy and rectal biopsy—The appearances can be graded as – (a) Mild: Hyperaemia and oedema. (b) Moderate: Granular mucosa with contact bleeding. (c) Severe: Ulceration, spontaneous bleeding.
Table 31   Potential etiological factors in UC
1:10 to 1:15
• Family frequency
70% of affected sib pairs suffer
• Concordance
Association with panocolitis
• Chromosomes 12, 6 and 2
Microsatellite markers
Major stress can cause flarecup or precipitation of symptoms
• 40kDA colonic protein
Tumor necrosis factor
• Cellular mechanisms
• Cytokines
• Neuroimmune
• Sulphate-reducing bacteria
• Smoking
Excess hydrogen sulphide
• Appendicectomy
Protects—Ex-smokers at most risk
• Anti-inflammatory drugs
• Dietary factors
70% before UC
Deficiency or excess of certain nutrients (1-arginine, gluten)
Table 33   Systemic manifestations of ulcerative colitis
Related to activity
Aphthous ulcers
Pyoderma gangrenosum
Erythema nodosum
Arthritis (large joints)
Unrelated to activity
Primary sclerosing cholangitis
Other liver disease
(small joints)
Ankylosing spondylitis Sweet's syndrome
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Fig. 29: Barium enema showing marked contraction and shortening of the colon (pipe stem appearance) due to long-standing ulcerative colitis
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Fig. 30: Colonoscopy in active ulcerative colitis
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Fig. 31: Descending colitis
Characteristic microscopic features are a chronic inflammatory infiltrate, glandular distortion, goblet cell depletion and crypt abscesses. The crypt architecture of the colon is distorted; crypts may be bifid and reduced in number, often with a gap between the crypt bases and the muscularis mucosae.
Some patients have basal plasma cells and multiple basal lymphoid aggregates.
Ileal changes in patients with backwash ileitis include villous atrophy and crypt regeneration with increased inflammation, increased neutrophil and mononuclear inflammation in the lamina propria and patchy cryptitis and crypt abscesses.
Plain abdominal radiography in only severe disease, to assess faecal distribution (the distal extent identifies the proximal extent of colitis in majority of patients), to exclude colonic dilatation (> 5.5 cm). It is also helpful in demonstrating proximal constipation in patients with very distal disease.
Colonoscopy vs barium enema—Typical barium enema features are as shown in Figure 29. Colonoscopy is always preferable in initial investigation of bloody diarrhoea, because it provides better mucosal definition and allows biopsies (Fig. 30). Colonoscopy however is dangerous in acute episode; flexible sigmoidoscopy after phosphate enema is then the procedure of choice.
CT abdomen can also define active colitis (Fig. 31) and its proximal extent.
Other investigations
Stool examination to exclude pathogens such as E. histolytica, Clostridium difficile, E. coli, Campylobacter spp. and Shigella spp.
Full blood count, ESR or C-reactive protein to evaluate severity.
Liver function investigation once in remission.
Differential Diagnosis
Infection—Other causes of bloody diarrhoea include Clostridium difficile, E. coli, Campylobacter spp. and Shigella spp. and E. histolytica. Cytomegalovirus should be considered in immunocompromised individuals.
Crohn's colitis—Diagnosis is achieved by considering history, endoscopic appearance, histology and contrast radiology. When features of both UC and Crohn's colitis are present, the term ‘intermediate colitis’ is best used.44
Other Possibilities
Ischemic colitis—Usually sudden onset, rectum not affected.
Microscopic colitis—Causes watery, not bloody diarrhoea. Diagnosis is made by finding chronic inflammatory infiltrate (lymphocytic colitis).
Radiation colitis—History of pelvic or abdominal node irradiation with mucosal telangiectasia.
Toxic megacolon is defined as a severe attack of colitis with total or segmental dilatation of colon (diameter of transverse colon usually > 5–6 cm) recognised by plain X-rays. Megacolon is considered if 2 or more of the following criteria. 1. Pulse >100/min. 2. Temp. >101.5ºF. 3. Leucocytosis >10,000/mm3. 4. Hypoalbuminemia < 3 gm/dL.
Rectal mucosal prolapse (solitary rectal ulcer syndrome) is distinguished from proctitis by characteristic histology showing muscularis interdigitation between the crypts.
Drug-induced NSAIDs may be identical to UC, but will not return once the drugs are withdrawn.
Management of active UC is given in Table 34.
Refractory Disease
If initial response to corticosteroids and relapse with reduction of dose to 15 mg/day or within 6 weeks of stopping corticosteroids – Azathioprine 1.5–2.5 mg/kg/day. Monitoring full blood count every 4–6 weeks. If tolerated the drug is continued for 3–5 years to prevent relapse. Methotrexate if no response to azathioprine. Cyclosporine IV in severe UC refractory to steroids. Mycophenolate mofetil is effective in maintaining remission as also Infliximab.
Tofacitinib, an oral inhibitor of janus kinases 1, 3 is effective in moderate to severe UC in clinical trials.
Indications for Surgery
(a) Emergency surgery for severe disease, toxic dilatation of colon, perforation, severe hemorrhage. (b) Elective surgery: Acute disease that fails to respond to medical treatment, frequent relapses in spite of adequate treatment, chronic disease with permanently damaged bowels, strictures, total bowel involvement with activity extending over more than 10 years.
Colectomy with temporary ileostomy and ileoanal pouch construction is operation of choice.
Table 34   Management of active UC
Mild attack
Moderate attack
Severe attack
Prednisolone oral
20 mg/d x 1 month
40 mg/d x 1 week
15 mg/d x 1 week
30 mg/d x 1 week
Hydrocortisone 400 mg iv/day
10 mg/d x 1 week
Then as for
Rectal hydrocortisone.
5 mg/d x 1 week
mild attack
Fluids IV
Potassium supplements
Corticosteroid enema
Prednisolone phosphate 20 mg in saline od or bd or Hydrocortisone 100 mg od
As for mild attacks
Metronidazole 500 mg 6 hourly iv Thromboembolism prophylaxis Toxic dilatation – Treat medically for 12–24 hrs, if no improvement (pulse, stool frequency, diameter)–Colectomy
5-ASA products
Alternative to corticosteroids
Continue unchanged
2 g/day
Or Olsalazine
1.2–2.4 g/day
for 6 weeks
Mesalazine enema
1 g in 100 mL saline
A non-specific granulomatous inflammation involving sharply demarcated single or multiple areas of the intestine, and probably a non-specific pathological response to a variety of exciting agents.
It can affect any part of the GI tract, but most commonly affects the terminal ileum or the ileocaecal region.
Genetic factors: About 15–20% of patients with Crohn's disease have one or more family members (usually a first degree relative) with either Crohn's disease or ulcerative colitis. Mutations in the CARD15 (NOD2) gene on chromosome 16 have been found in about one-third of patients with Crohn's disease and are particularly associated with ileal disease. Genes within the HLA region (chromosome 6p) appear to influence colonic involvement and the presence of extraintestinal manifestations.
Smoking: Smokers are more likely to develop the disease than non-smokers. Also the disease has a more unfavourable course in smokers.45
Table 35   Clinical features of Crohn's disease
Disease site
Clinical features
Abdominal pain
Obstructive symptoms
Mass in right iliac fossa
Acute ileitis (uncommon)
Rectal bleeding
Perianal disease
Extra intestinal manifestations
Other sites
Mouth, stomach, duodenum affected (rarely)
Infective organisms: Mycobacterium paratuberculosis has been found in tissue of a small number of patients with Crohn's disease.
Diet: High intake of refined sugar and low intake of fibre from fruits and vegetables have been reported in patients with Crohn's disease.
Immune mechanisms: There is evidence that the normal mechanisms for down-regulating mucosal immune response are impaired in patients with Crohn's disease.
Clinical Features
Clinical features of Crohn's disease depend on the site of disease as enumerated in Table 35. Table 36 lists the extra-intestinal manifestations of Crohn's disease.
  • Strictures—More common in small intestine. May cause obstructive symptoms.
  • Fistulas—may develop between loops of bowel adjacent to the bladder or vagina. Pneumaturia and recurrent urinary infections indicate fistula into the bladder. Passage of flatus or feculent vaginal discharge signifies a vaginal fistula.
  • Perianal disease—Fissures, fistulas and abscesses. Fleshy skin tags with violaceous hue common.
  • Carcinoma of intestine—may complicate long standing colonic disease.
  • Secondary amyloidosis in long standing cases.
Table 36   Extra-intestinal manifestations
Related to disease activity
• Aphthous ulceration
• Erythema nodosum
• Pyoderma granulosum
• Acute arthritis (large joint, transient)
• Eye complications: Conjunctivitis, episcleritis, uveitis
Unrelated to disease activity
• Sacroiliitis (usually asymptomatic)
• Ankylosing spondylitis
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Fig. 32: A) Small bowel enema in Crohn's disease of terminalileum The lumen is narrowed and there is fissure ulceration (arrows); (B) Combination of transmural thickening and spasm produces the classical ‘string sign’ in the terminal ileum
  1. Stool examination to exclude known pathogens.
  2. Sigmoidoscopy and rectal biopsy: Patients with small bowel involvement may show histological evidence of rectal inflammation; this may show features of Crohn's disease (e.g. focal inflammation, granulomata).
  3. Imaging
    1. Small bowel enema (enteroclysis) and an air-contrast barium enema—Crohn's disease often leads to separation of bowel loops, a normal (Fig. 32A) and ulcerated terminal ileum and in advanced cases the string sign (Fig. 32B).
    2. Indium 111-labelled or 99 technetium-HMPAO-labelled leucocyte scans may also be helpful in demonstrating extent of inflammation if barium radiology is equivocal.
    3. Ultrasonography may be helpful in patients with a palpable abdominal mass in order to differentiate an inflammatory mass from an abscess.
    4. CT is often more useful and may show thickened loops of affected intestine.
    5. MRI is the procedure of choice for investigating complex perianal disease.
    6. Colonoscopy is useful for histological confirmation and for assessing extent of colonic involvement and for obtaining ileal biopsy specimens. Flexible sigmoidoscopy is safer because of higher risk of bowel perforation.
Table 37 enlists the differentiating features between ulcerative colitis and Crohn's disease.46
Table 37   Differentiating features between ulcerative colitis and Crohn's disease
Ulcerative colitis
Crohn's disease
Smokers (more severe)
Family history
Clinical Features
Bloody diarrhoea
Not so common
Abdominal lumps
Perianal disease
Signs of malabsorption
Rectal involvement
Fine ulceration
Double contour
‘Rose-thorn’ ulcers
Cellular infiltrate
Neutrophils, plasma cells, eosinophils
Lymphocytes, plasma cells, macrophages
Crypt abscesses
Special features
Granulomas, Aphthous ulcer
Histiocyte lined fissures
Loss of vascular pattern, contact bleeding, ulceration and spontaneous bleeding
Deep longitudinal ulcers, skip lesions
Rectal involvement
Very rare
May occur
Differential Diagnosis
Small intestinal disease—(a) Tuberculosis: Colonoscopy with multiple biopsy may be helpful and laparotomy may detect serosal tubercles. (b) Microscopic colitis is characterised by chronic watery diarrhoea and histopathologically by typical microscopic abnormalities in an otherwise macroscopically normal colonic mucosa. Collagenous and lymphocytic colitis are the two common forms of microscopic colitis. (c) Other conditions include intestinal lymphoma, carcinoid, α-chain disease, actinomycosis, amyloidosis, Behcet's disease and carcinoma.
  1. General measures—Well-balanced diet with high fibre content. Low-fat, low-residue diet if steatorrhoea or strictures. Vitamin supplements. Rest in bed during acute phase with liquid diet. If anemia, iron by injection, or B12 and folic acid if megaloblastic anaemia. Codeine sulphate, diphenoxylate or loperamide helps to reduce bowel looseness.
  2. Drug treatment
    Aminosalicylates—Sulphasalazine1 g t.d.s. orally in active colonic disease. Mesalazine delayed release 400 mg t.d.s. for maintenance therapy.
Corticosteroids—are beneficial in active disease. (a) Local therapy—Hydrocortisone suppositories for disease of rectosigmoid colon, foam or liquid enema for more proximal disease od or bd × 3–6 weeks. Prednisolone 0.25–0.75 mg/kg to maximum of 60 mg for 4 months. (b) Systemic treatment—Parenteral corticosteroids e.g. Hydrocortisone 100 mg. IV 8-hourly useful for inducing remission in severely ill patients with acute Crohn's colitis.
Metronidazole—400 mg t.d.s. if associated sepsis (e.g. in relation to fistulas or perianal disease or bacterial overgrowth of small intestine with resulting steatorrhoea).
Immunosuppressive agents—Azathioprine 2.5 mg/kg/day or 6-mercaptopurine 1.5 mg/kg/day may be used if other therapy has failed and surgical treatment is inappropriate. Regular blood count should be done to detect bone marrow suppression. Cyclosporine has rapid onset of action. IV injection at a dose of 2–4 mg/kg/day induces clinical improvement within a week. Prophylaxis against Pneumocystis jiroveci pneumonia is administered in all patients on the drug.
Immunotherapy—Infliximab (an IgG1 chimeric antibody to tumour necrosis factor). Single infusion of 5mg/kg i.v. Two-thirds of patients with chronic active disease resistant to corticosteroids and immunosuppression respond as also 50% with fistulas. Regular infusions every few months for maintenance. Side-effects are uncommon but include activation of latent tuberculosis, and appearance of antibodies to dsDNA with occasional manifestations of lupus-like syndrome.47
Natalizumab is a recombinant humanized IgG4 anti body against α4-integrin that has been shown to be effective in induction and maintenance of patients with CD. It has been approved since February 2008 for the treatment of patients with CD refractory or intolerant to anti-TNF therapy. Side effect is progressive multifocal leukoencephalopathy (PML). The most important risk factor for development of PML is exposure to the John Cunningham (JC) polyomavirus.
Vedolizumab, leukocyte trafficking inhibitor, monocloal antibody directed against α4β7 integrin, is indicated for patients who have had an inadequate response or lost response to or were intolerant of a TNF blocker or immunomodulator or had an inadequate response or were intolerant to or demonstrated dependence on glucocorticoids. It is an option for patients who are JC antibody positive since it does not cross the blood-brain barrier.
Ustekinumab, a fully human IgG 1 monoclonal antibody, blocks the biologic activity of IL-12 and IL-23, shows efficacy in moderate to severe CD in clinical trials.
Surgical Management
  • Intestinal obstruction
  • Perforation
  • Failure to respond to medical therapy.
  • Complications such as fistulas and perianal disease.
Limited resections, stricturoplasty or end-to-end anastomosis as necessary. Split ileostomy to isolate colon in case of fistulas and perianal disease.
AMI is usually caused by superior mesenteric artery (SMA) embolization or thrombosis (Fig. 33), non-occlusive mesenteric ischemia or acute mesenteric venous thrombosis. Rare causes include vasculitis, fibromuscular dysplasia, dissection, trauma and rupture of a mesenteric aneurysm.
Emboli can originate from the heart or aorta. Most emboli lodge distal to origin of middle colic artery.
Thrombosis of SMA or coeliac axis occurs as a result of underlying mesenteric atherosclerotic stenosis progressing to occlusion, usually at the origin of the vessel.
Non-occlusive mesenteric ischemia develops in patients in a low cardiac output state, particularly in presence of digoxin or vasoconstrictors. Mesenteric vasoconstriction results in segmental vasospasm of secondary and tertiary branches of the SMA.
Mesenteric venous thrombosis may be secondary to infection, hypercoagulability states, cirrhosis, splenomegaly, malignancy, trauma or pancreatitis. Bowel oedema, impaired venous drainage and increased plasma viscosity reduce arterial inflow and may lead to bowel infarction.
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Fig. 33: Abdominal angiography showing celiac and superior messenteric artery thrombus
Clinical Features and Diagnosis
Classically AMI presents with acute onset of abdominal pain disproportionate to the physical signs. Central abdominal pain. GI emptying may occur, with emesis and bloody diarrhoea.
Laboratory Findings
These include leucocytosis, acidosis, hyperkalemia and raised hematocrit, LDH, SGOT and creatine kinase occur later.
CT angiography is sensitive for mesenteric occlusion. It also identifies non-vascular causes of acute abdominal pain. CT angiography with three dimensional reconstruction may show the vascular anatomy and pathology in sufficient detail for diagnosis and operative treatment.
Acute SMA embolism—Balloon embolectomy, usually with patch angioplasty of the SMA. For chronic proximal occlusion or stenosis, bypass grafting. Resection of infarcted bowel after revascularization.48
Acute SMA thrombosis—Replacement of a bypass graft to the SMA distal to the occlusive segment. Thrombolytic therapy is considered in acute thrombosis with no clinical signs of peritonitis.
Non-occlusive mesenteric ischemia—Any metabolic cause can be identified and corrected. The SMA is selectively catheterized and vasodilating agents such as papaverine given.
Mesenteric vein thrombosis—Fluid resuscitation and systemic anticoagulation. Thrombolysis in patients with no signs of peritonitis.
Clinical Features
Classical symptom is abdominal pain after eating (also termed ‘mesenteric angina’). Diarrhoea secondary to malabsorption may occur. Patients become fearful of eating and thus lose weight. On physical examination an epigastric bruit may be heard. Signs of multifocal atherosclerosis are usually present.
Lateral views on MDCT/MR aortography are the best means of demonstrating visceral occlusive lesions. Duplex scanning can document presence of stenosis in the visceral arteries.
Mesenteric stenting—percutaneous angioplasty stent replacement in those with a suitable vascular anatomy offer long term relief from pain.
Table 38   Categories of adverse effects of drugs on GI tract
Causative drug
Heart burn
Anticholinergic agents, tricyclic antidepressants. phenothiazines
Oesophagitis, candida oesophagitis, strictures
Tetracycline, bisphosphonates Immunosuppressive drugs NSAIDs
Pot chloride, quinidine (particularly slow-release preparations)
Dyspepsia and gastro-duodenal ulcers GI tract
NSAIDs, co-prescription of corticosteroids, warfarin, aspirin
Nausea and vomiting
Gut damage including ulceration
Locally irritant - Iron, NSAIDs, theophylline, and pharmacologically metronidazole
Disturb intestinal flora (e.g. C. difficile) Antagonising anti-peristaltic
Act via CNS: Levodopa, bromocriptine, opiates, digoxin, chemotherapeutic agents
adrenergic stimulation
Cephalosporins, β-blockers
Direct irritant action on colon
Bile acids
Stimulation of intestinal
secretion and motility
Constipation induced abdominal pain
Antimuscarinic drugs: atropine, tricyclic antidepressants, opiates.
Drug-induced mega colon from enteric neurotoxicity
Vincristine or possibly laxatives
Bloating and occasionally impaction
Dietary fibres in excessive amounts
Inflammation of the colon
Mefenamic acid, penicillamine, antibiotics, oral gold.
Small intestinal disease Coeliac disease Folate deficiency
Colchicine, biguanides, laxatives, salicylates. Sulfasalazine and phenytoin cause folate malabsorption.
Drug effects on GI tract (Table 38) can be considered in four categories:
  1. Due to pharmacological mode of action—Adverse drug reactions can occur as a predictable result of a drug's mode of action. For instance, anticholinergic agents (e.g. antidepressants) reduce oesophageal sphincter pressure resulting in reflux and heartburn, they also reduce colonic transit resulting in constipation.
  2. Impairment of GI defences—example NSAIDs act principally by inhibiting prostaglandin synthesis.
  3. Direct injury to GI tract—example oesophageal damage by potassium preparation, gastroduodenal ulcer by cytotoxic drugs, and ulceration and colitis associated with oral gold.
  4. Changes in colonic bacterial flora.
There are several syndromes that depend on lie. These may involve obvious secondary gain for example the malingerer who seeks compensation for disability. Alternatively, there may be no obvious motive, as in Munchausen's syndrome. The physician must be alert to complaints of abdominal pain, constipation, diarrhoea or vomiting when the tests are negative and the observed behaviour of the patient does not fit the complaint. The linking phenomena in such cases include elaborate, fantastic, deliberate fabrication of disease, often by someone with medical knowledge, and inexplicable, intractable and often hazardous compulsion to undergo treatment.
Munchausen syndrome is a type of factious disease characterised by simulated disease, pathological lying (often elaborate and fantastic), and wandering from place to place and hospital to hospital.
  • Abdominal: Patients travel to various hospitals undergoing repeated operations, only to discharge themselves against advice (even with wounds still healing and iv drips in place).
  • Bleeding: Characterised by bleeding symptoms: Anticoagulant subtype, anemia subtype, pretended bleeding subtype.
  • Neurological: Patients present with unusual often convincing fits, spells, faints and anesthesia
  • Miscellaneous: Pyrexia, dermatological, endocrine
  • Munchausen syndrome-by-proxy: A form of child abuse in which a parent or carer feigns illness in a child.
Oral Manifestations of Systemic Disease
Coeliac disease occasionally produces oral ulceration, glossitis and/or angular stomatitis.
Allergic gingivostomatitis and cheilitis—Altered taste, burning or discomfort may occur as a result of food allergy to various foods, flavourings, preservatives and dental materials. In severe cases of food allergy, ulceration may occur.
Inflammatory bowel disease—Crohn's disease can manifest as tags, ulcers and/or mucosal granulomatosis leading to swelling or cobble-stoning. Ulcerative colitis may produce aphthae, chronic ulceration or pyostomatitis vegetans, which is characterized by deep fissuring and micropustules.
Behcet's syndrome is the association of orogenital ulceration with ocular disease.
Hematological disease—Hematinic deficiency may cause glossitis or ulceration. Leukemia and lymphoma may cause infections, ulcers, purpura or gingival swelling.
Genodermatoses with characteristic oral manifestations include – (a) Rendu-Osler-Weber disease with mucocutaneous telangiectasiae that are prone to spontaneous hemorrhage. (b) Cowen's syndrome characterized by circumoral and submucosal soft tissue nodules (trichilemmomas). (c) Peutz-Jeghers syndrome with mucocutaneous freckling and intestinal polyposis.
Skin manifestations of GI disease are listed in Table 39.
Causes of Immune Deficiency
  • Defects in production of secretory IgA
  • Genetic defects
  • 50Iatrogenic cellular immune deficiency (Total body irradiation or chemotherapy)
  • HIV infection
Common Infections of the Intestines Associated with Immune Deficiency
Table 39   Skin manifestations of GI disease
GI disorder
Erythema nodosum
Inflammatory bowel disease
Pyoderma gangrenosum
Inflammatory bowel disease
Bleeding disorders
Mucocutaneous pigmentation
Peutz-Jeghers syndrome
Acanthosis nigricans
GI malignancy
  • Giardia lamblia. Mainly acquired from water, but can occur in homosexual males as a result of sexual activity.
  • Cryptosporidiosis is associated with chronic diarrhoea, wasting and death.
  • Microsporidiosis with chronic diarrhoea and wasting
  • Bacterial diarrhoea (Shigella, salmonella and campylobacter).
  • Mycobacterium avium intracellulare. Diarrhoea is a late manifestation of HIV infection.
  • Cytomegalovirus infection in patients with severe immune suppression causes bloody diarrhoea, sometimes associated with toxic dilatation and colonic perforation.
Common Infections of the Oesophagus
  • Oesophageal candidiasis causes pain on swallowing.
  • CMV of oesophagus produces hemorrhagic oesophagitis.
  • Ulcers of unknown aetiology similar to aphthous ulcers in appearance.
Gastroparesis means incomplete or partial paralysis of the stomach. It is a disorder of delayed gastric emptying in absence of mechanical obstruction. Causes-peptic ulcer disease, endocrine disorders, (thyroid, diabetes, parathyroid, collagen vascular disease), psychogenic causes.