Gastroenterology

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chapter 30 Gastroenterology

INTRODUCTION AND OVERVIEW

The adage ‘you are what you eat’ is only partly true. In fact, you are what you eat, manage to digest and absorb across the gastrointestinal tract into the bloodstream, and which you are not intolerant of or allergic to. The gastrointestinal tract is the interface with the ingested environment, and dysfunction in the gut may affect any or every vital function.

In the process of diagnosing and formulating a management plan for patients with gastrointestinal problems, it is essential to keep in mind not just the gut symptoms, but the lifestyle factors affecting gut function, and the systemic and nutritional consequences of gut dysfunction.

COMMON PRESENTATIONS

ACUTE ABDOMINAL PAIN ^1,²

Acute abdominal pain is pain of recent onset, which can vary in severity from mild and self-limiting to severe and life-threatening. Episodes may resolve spontaneously or require medical assessment and intervention. It is important to assess the site, chronicity, severity and nature of the pain and any associated signs and symptoms.

The patient’s general condition and the urgency of intervention will need to be assessed before investigations are arranged. If the patient is haemodynamically stable and there are no signs of sepsis, judiciously selected investigations may be arranged in the community setting. In an emergency or potential emergency situation, it may well be prudent to transfer the patient to hospital and have investigations carried out there.

Nature of pain

• Visceral pain—abdominal organs are not sensitive to touch. However, stretching or distending the bowel does cause pain that is poorly localised, usually to the midline. Distension of the capsule of the liver also causes pain.

• Peritoneal pain—the parietal peritoneum has pain fibres, but the visceral peritoneum does not. Pain from inflammation of the parietal peritoneum is well-localised to the area of inflammation. It is exacerbated by movement such as coughing or respiration.

• Referred pain—referred pain is pain felt distant from the site of the problem that is causing the pain. For example, right shoulder tip pain is referred from the parietal peritoneum under the diaphragm, with these areas both innervated by somatic C4 nerves. Cardiac pain may be felt in the epigastrium, and pelvic pain in the umbilical area.

Abdominal guarding is a significant sign, due to reflex contraction of muscles in the abdominal wall in response to stimulation of pain fibres of the same dermatome.

Mechanisms of abdominal pain

Acute inflammation produces pain whose features depend on whether the organ affected is intraperitoneal or extraperitoneal. Intraperitoneal inflammation causes peritonitis that is well-localised, aggravated by sudden movement and relieved by being still. Inflammation restricted to bowel mucosa does not cause peritonism.

• Obstruction—pain tends to be colicky unless there is a complication such as secondary infection or perforation, when it becomes continuous.

• Ischaemia (including torsion)—arterial ischaemia is sudden in onset, severe and continuous. Venous ischaemia is slower in onset.

• Increased pressure in a solid organ—pain tends to be dull and constant (e.g. haemorrhage into an ovarian cyst).

Type and chronicity of pain

• Colicky—felt in the midline, associated with forceful smooth muscle contraction related to stomach (epigastric), intestine (small bowel and right hemicolon colic felt periumbilically; left hemicolon colic felt suprapubically) or uterus (suprapubic). Repetitive cyclic pattern of intense pain, then relief.

Biliary ‘colic’ is continuous rather than intermittent, in the epigastrium or RUQ.

Associated features

• Fever, nausea, vomiting, micturition difficulty, bowel habit, menstruation and gynaecological history, obstetric history, medication and supplements

• Mass, rebound tenderness, guarding, signs of dehydration or blood loss (tachycardia, hypotension, pallor, reduced level of consciousness)

GENERALISED ABDOMINAL PAIN

Severe generalised abdominal pain requires rapid and accurate assessment, resuscitation and transfer to hospital.

Signs of serious abdominal pathology include generalised peritonitis with rebound, guarding and absence of bowel sounds. Signs of shock (tachycardia, hypotension, oliguria, peripheral vasoconstriction) may be evident if there has been dehydration, haemorrhage or severe allergic reaction.

• Perforated appendix—history suggestive of appendicitis: initially central colicky abdominal pain later localising to the RIF, fever, tachycardia. Tenderness and rebound in RIF. Tenderness on the right on digital rectal examination. Neutrophilia and raised C-reactive protein. Requires immediate surgical referral.

• Perforated peptic ulcer—sudden prostration with severe generalised peritoneal-type abdominal pain. Symptoms may improve after 2–6 hours. Peritonitis develops after 6–12 hours with generalised tenderness and guarding, maximal in the epigastrium, board-like rigidity, loss of bowel sounds and loss of liver dullness to percussion. Gas under diaphragm may be seen on erect abdominal X-ray. Limited gastrograffin meal may help diagnosis. Initial treatment: resuscitation, nasogastric suction, antibiotics. Urgent surgical referral.

• Perforated diverticulum—history of diverticular disease or preceding undiagnosed pain in LIF. Tenderness and rebound in LIF, gas under diaphragm in erect abdominal X-ray.

• Ruptured ectopic pregnancy—suspect in a woman of childbearing age with a late period and sudden onset of pelvic or lower abdominal pain. Symptoms and signs are maximal in the pelvis; sometimes pain is felt in region of rectum. This is sometimes reported as increase in pain when woman tries to sit down. Tender mass may be evident on vaginal examination. Shock is common. Usually elevated β-hCG levels are found and ectopic implantation seen on ultrasound at 5–6 weeks of amenorrhoea. Urgent gynaecological surgery referral.

• Ruptured solid organ—a history of trauma is usually present. Symptoms and signs will include significant blood loss and also be organ-specific.

• Ruptured aortic aneurysm—patient usually elderly with risk factors for cardiovascular disease. Pain is central, constant and radiates through to the back. Not usually signs of peritonism, as bleeding is retroperitoneal. Pulsatile mass in central abdomen. May sometimes present with sudden pain followed by shock and loss of consciousness. Surgical emergency.

• Strangulated bowel—site of pain depends on area of strangulation. Is there a history or signs of a hernia or previous abdominal surgery? May be associated signs and symptoms of small bowel obstruction. Urgent surgical referral required.

• Superior mesenteric artery thrombosis or embolism—causes massive small bowel ischaemia. Often preceded by a history of atrial fibrillation or myocardial infarction. CT scan will define the problem but should not delay urgent surgical referral.

• Ischaemic colitis—associated bloody diarrhoea, signs maximal in LIF. Colonoscopy may assist diagnosis. Urgent hospital referral, although surgery usually not required.

• Pancreatitis—check for history of alcoholic binges, gallstones, trauma or medication known to cause pancreatitis.

LOCALISED ACUTE ABDOMINAL PAIN

Right iliac fossa

… think gut and gynaecology.

CONSTIPATION

Constipation refers to difficulty in passing small, hard stools. If a patient presents with ‘constipation’, it is important to find out exactly what they mean. Question the patient about their bowel motions’ frequency, volume, colour and consistency, and the presence or absence of blood. Lifestyle factors are also an important contributor to or exacerbating factor for constipation.

While the cause of constipation may be a simple matter of diet, drug side effect or behavioural bowel habit, constipation may be an indication of a serious underlying disorder.

Aetiology

• dietary inadequacy (fibre and fluids)

• physical inactivity

• Irritable bowel syndrome

• Slow transit (may run in families)

• Pelvic floor dysfunction (woman may manually disimpact with digital pressure in vagina)

• Painful bowel motions, e.g.

• anal fissure

• strangulated haemorrhoid.

• Colon cancer

• Colonic stricture

• Abnormal myenteric plexus (Hirschsprung’s disease, Chagas’ disease)

• Perianal infection

• Anal stenosis

• Dystrophia myotonica

• Systemic sclerosis

• Crohn’s disease.

• Diabetic autonomic neuropathy

• Sacral parasympathetic damage

• Spinal cord damage

• Spinal cord disease (e.g. multiple sclerosis)

• Parkinson’s disease

• Hypothyroidism

• Hypercalcaemia

• Anorexia nervosa

Drug side effects:

• Antihypertensives

• Antidepressants

• Iron supplements.

Diagnosis

Ascertain frequency, volume, colour and consistency of bowel motions and whether there has been any bleeding or mucus per rectum. Enquire about the duration of the problem and previous attempts to relieve it, such as use of laxatives, herbal therapies or dietary adjustment. Sometimes severe and chronic constipation can present with loose bowel motions and faecal leakage. Ask about associated bloating, pain or weight loss.

A full dietary history is necessary, preferably with a food diary recorded over a week.

Complete physical examination including abdominal examination and digital rectal examination is necessary, including examining for fissures, fistulae, abscesses or signs of neoplasm in the anal area. Sigmoidoscopy may be helpful. In women examine for rectocele.

Investigation

• History, diet assessment and physical examination may be all that is required to elucidate the cause of constipation.

• Further investigation will be guided by likely aetiology based on history and examination.

• Blood tests—check for anaemia (FBC), iron studies, CRP, thyroid function, serum calcium.

• Plain abdominal X-ray

• Colonoscopy—to identify or exclude cancer, Crohn’s disease or stricture

• Anorectal manometry

Therapeutics

• Treat any underlying medical cause if present, such as hypothyroidism or hypercalcaemia.

• Dietary fibre 20–30 g per day, especially fresh fruit and vegetables and whole cereals (especially oatmeal).

• Prunes may help.

• Supplement with psyllium husks or Metamucil.

• Increase water intake.

• Drink warm lemon water before meals.

• Take time to eat slowly.

• Replace or remove medications that have constipation as a side effect.

• Avoid stimulant laxatives.

• Use stool softener, such as Coloxyl.

• In high doses, magnesium exerts a laxative effect (Epsom salts or milk of magnesia) for short-term relief.

• Lactulose (osmotic laxative) is useful for chronic constipation.

• Glycerin suppositories before bowel motion may assist passage of stool.

• Enemas may be required as an occasional emergency measure.

• Establish a regular toilet routine. Hypnotherapy or behavioural therapy may assist with relaxation.

• Regular physical exercise.

• Probiotic supplement.

DIARRHOEA

Diarrhoea refers to frequent loose or watery stools. History taking should include duration and severity of symptoms and systemic features (fever, myalgia, malaise, arthralgia), and presence of blood or mucus in the stool.

Acute diarrhoea

Patient should be questioned about pain, stool frequency, colour and consistency, presence of blood, and incidence of vomiting.

• Acute watery diarrhoea is most often due to viral or bacterial gastroenteritis/enteritis or protozoal infection.

• Frothy, windy, smelly stools may indicate malabsorption of fats and/or giardiasis.

• Bloody diarrhoea may be a result of infectious colitis, drug-induced colitis, inflammatory bowel disease, ischaemic colitis or antibiotic-associated diarrhoea.

• Acute diarrhoea may be a first presentation of coeliac disease, Crohn’s disease or inflammatory bowel disease.

• History should elicit symptoms of volume depletion such as dry mouth, orthostatic hypotension, tachycardia, especially when vomiting is associated.

• Questions about systemic symptoms will include fever, malaise, myalgia and arthralgia.

• History should include recent travel, medications (especially antibiotics and vitamin supplements), dietary history, consumption of fast food or leftovers and whether other members of family or a dining group developed diarrhoea, and any history of immune deficiency.

Investigation

• General physical examination will include cardiovascular assessment, signs of toxicity (fever, tachycardia, shock), abdominal palpation for mass or tenderness, and digital rectal examination for tenderness, mass or faecal impaction.

• Patients presenting with diarrhoea will need to be assessed for volume depletion, and this is particularly important in children and the elderly.

• For minor resolving episodes of diarrhoea without systemic features, no investigations will be necessary.

• Stool examination for blood, and stool culture looking for ova, cysts and parasites, may help to target therapy in cases of severe or prolonged acute diarrhoea. However, standard stool examination can be unreliable. Special requests for identification of pathogens may need to be made for suspected Campylobacter, Clostridium difficile and toxin, Yersinia, and Cryptosporidium or amoebic dysentery.

• Blood tests can give valuable information about the cause and/or the effects of the diarrhoea. These might include full blood count, ESR, iron studies, folate, vitamin B₁₂, calcium, electrolytes and thyroid function.

• Sigmoidoscopy or colonoscopy may be indicated where colitis or inflammatory bowel disease is suspected.

• Initial treatment for most cases is to support hydration and relieve symptoms (see below). Where a treatable cause of diarrhoea can be established or a presumptive diagnosis made, treatment should be targeted at the cause.

• Hospitalisation is indicated for patients with sepsis or severe dehydration.

Viral gastroenteritis/enteritis

The usual cause is infection with rotavirus or noravirus. Viral gastroenteritis/enteritis generally presents with acute onset of watery diarrhoea with or without vomiting.

Treatment

• Rehydrate with fluid and electrolyte solution, and monitor fluid balance. Use the simplest route where possible (oral) but sometimes the nasogastric or IV route may be required in emergency situations (e.g. infants) or where oral rehydration is not possible. Avoid rehydration with sweet drinks such as lemonade unless diluted to one-third to one-quarter normal strength.

• Low-fibre diet (soups, diluted fruit juice, white rice)

• Exclude lactose until diarrhoea settles.

• Exclude drinks containing sorbitol.

• Antiemetic injection if required for severe vomiting (metoclopramide or prochlorperazine), or ondansetron waters.

• Probiotic (Lactobacillus spp) particularly for prolonged and antibiotic-induced diarrhoea ³.

Prevention

• Immunisation of babies against rotavirus (responsible for 50% of children’s hospital admissions).

• Maintain strict hand washing after nappy changing and toileting. Infected individuals should avoid handling food.

Bacterial gastroenteritis

Nausea, vomiting, diarrhoea and abdominal pain are common to most. Neurological, hepatic and renal complications can also occur. Rapid onset (hours) after ingestion of contaminated food suggests a pre-formed toxin, while a longer incubation period (1–3 days) suggests a bacterial or viral cause.

Pathogens include: enterotoxigenic Escherichia coli, Campylobacter, Salmonella, Shigella, Entamoeba histolytica, Clostridium perfringens, Bacillus cereus, Vibrio parahaemolyticus.

Enterotoxigenic E. coli

A leading cause of traveller’s diarrhoea. Adheres to the gut wall and produces enterotoxins.

• Watery diarrhoea, cramping abdominal pain, nausea.

• Maintain hydration; general supportive advice.

• Norfloxacin 400 mg b.i.d. p.o. or ciprofloxacin may be used for moderate to severe symptoms. Cotrimoxazole can be used for children.

Campylobacter jejuni

A common cause of food-borne illness from contaminated milk, sick pets, poorly stored food and contaminated water.

After an incubation period of 2–6 days, symptoms include: malaise, fever, myalgia, headaches and acute diarrhoea. Stools are initially watery and progress to blood and mucus. Severe cramping abdominal pain is common.

• Stool culture with special request.

• Maintain hydration; general supportive advice.

• If symptoms fail to settle: erythromycin 500 mg q.i.d. for 7 days or norfloxacin 400 mg b.i.d for 7 days.

Salmonella

Salmonella are gram-negative bacilli that can cause a range of clinical pictures including gastroenteritis, typhoid fever, bacteraemia and localised infection.

Complications include osteomyelitis, bacteraemia, abscesses, meningitis and pneumonia.

Antibiotics are generally not advised.

If required, when disease is severe or patient is at risk of complications:

• Ciprofloxacin 500 mg p.o. b.i.d. for 2 weeks

• Probiotics.

Entamoeba histolytica

Entamoeba histolytica is a protozoan parasite that exists as an invasive trophozoite and as an infective cyst. Spread by the faecal–oral route, it can reside in asymptomatic form in the large intestine, but can become invasive, resulting in colitis, or spread to involve the liver and other organs. Transmission is person-to-person, or by contaminated food and water.

Symptoms range from mild diarrhoea to fulminating amoebic dysentery with fever, profuse bloody diarrhoea and abdominal pain and tenderness.

Complications include perforation, strictures, amoeboma and involvement of other organs, such as liver abscess.

• Stool culture

• Indirect haemagglutination assay

• Liver ultrasound.

• Metronidazole 600–800 mg t.d.s. for 6–10 days plus diloxanide furoate 500 mg t.d.s. for 10 days.

Clostridium perfringens

A common food-borne pathogen with an incubation period of 8–24 hours. Usually the result of eating contaminated meat or poultry.

• Watery diarrhoea, cramping abdominal pain

• Usually resolves after 24 hours.

Hydration and supportive treatment.

Bacillus cereus

A form of food poisoning, usually related to ingestion of contaminated fried rice or rice that is cooked then improperly refrigerated, although a wide variety of foods have been implicated. Infection is associated with two distinct syndromes: a vomiting syndrome (ingestion of a pre-formed toxin) and a diarrhoeal syndrome resulting from the production of an enterotoxin.

Usually self-limiting over 20–36 hours, but will respond to quinolones if necessary.

Yersinia enterocolitica

Transmission is via the faecal–oral route through contaminated food and water and by person-to-person transmission. Symptoms include diarrhoea and vomiting. Bloody diarrhoea is more common in children than adults, and infection usually resolves after 2 weeks.

• Stool culture or serology.

• Antibiotic treatment is usually not required.

• If required, cotrimoxazole or one of the quinolones is usually effective.

Giardiasis

Giardia lamblia is a flagellated protozoon. The cystic form is shed in the stool and can survive in the environment. Transmission is through contaminated food or water, or person-to-person contact.

Infection is characterised by colicky abdominal pain, pasty or frothy foul-smelling stools that may be paler than usual, anorexia, malaise and excess flatus. May present as an acute diarrhoeal illness or chronic diarrhoea. Blood in the stool and fever are not features of giardiasis. Symptoms may resolve after 1–3 weeks but can persist for many months.

Diagnosis

Usually made clinically, as stool examination is not very sensitive.

Treatment

• Therapeutic trial of tinidazole 500 mg × 4 stat or metronidazole 400 mg p.o. t.d.s. for 7 days

• Probiotic (Lactobacillus spp).

Pseudomembranous colitis

Pseudomembranous colitis is usually due to overgrowth of Clostridium difficile. This may be a result of antibiotics when a probiotic is not co-prescribed. Features include profuse watery diarrhoea, cramping abdominal pain and tenesmus ± fever within days or weeks of taking an antibiotic.

Treatment

• Cease the offending antibiotic

• Metronidazole 400 mg p.o. t.d.s. for 7–10 days plus a probiotic; OR

• Vancomycin 125 mg p.o. q.d. for 10 days plus a probiotic.

A probiotic supplement (Lactobacillus spp and Saccharomyces boulardii) has been shown to prevent antibiotic-associated diarrhoea.⁴ The S. boulardii strain is used to restore microbial balance and inhibit C. difficile proliferation.⁵

Traveller’s diarrhoea

Common in visitors to developing countries. The most common pathogen is enterotoxigenic E. coli, although other pathogens can be responsible, including Shigella (10%), Salmonella (5%), Campylobacter (3%), Yersinia (2%), G. lamblia (4%), E. histolytica (1%), Cryptosporidium (3%) and viruses (3%).¹

Onset is abrupt, with up to six bowel movements a day, lasting for 3–4 days in most cases. Symptoms may be more severe, with profuse watery diarrhoea. Blood in the stool suggests invasive disease.

Treatment

• Maintain fluid and electrolyte intake. If rehydration sachets are not available, add one teaspoon of sugar and a pinch of salt to a 250 mL glass of filtered, boiled or bottled water. Soups with added salt and diluted fruit juices and low-fibre bland foods until diarrhoea settles.

• Norfloxacin 400 mg p.o. b.i.d. for 3 days for suspected bacterial gastroenteritis.

• Tinidazole or metronidazole for suspected giardiasis.

• Antiemetic for severe vomiting (metoclopramide).

• Loperamide (Imodium®) can be used two caps stat then one after each unformed stool to a maximum of eight per day.

• Small amounts of low-fibre food until diarrhoea settles.

• Avoid alcohol, coffee, raw fruit and vegetables and wholegrain cereals until diarrhoea settles.

• Medical assistance should be sought in the event of bloody diarrhoea, persisting severe symptoms, abdominal pain or high fever, and special caution should be exercised with children, the frail elderly and immunocompromised individuals.

Prevention

• Drink filtered or bottled water only.

• When travelling, avoid tap water, ice in drinks, dairy products, peeled fruit, uncooked vegetables and salads, and raw seafood.

• Safe food storage and preparation

• Antibiotic prophylaxis is not routinely recommended.

Herbs and supplements for diarrhoea ⁶

• Bilberry—astringent activity, traditional use in acute non-specific diarrhoea. Approved by Commission E for this indication.⁷

• Chamomile—used to relieve stomach cramps, dyspepsia and flatulence. A study of chamomile and pectin in children aged between 6 months and 5.5 years with diarrhoea showed reduced duration and severity of diarrhoea.⁸ Approved by Commission E for gastrointestinal spasms and inflammatory diseases of the gastrointestinal tract.⁷

• Colostrum—bovine colostrum is derived from cow’s milk. Hyperimmune bovine colostrum is produced by immunising cows with either specific pathogens or their antigens. It has been shown to be highly effective in prophylaxis and treatment of infectious diarrhoea caused by rotavirus.⁹

Dose: 100 mL t.d.s. for 3 days with bovine colostrum from cows immunised with the four serotypes of human rotavirus.

• Goldenseal—used traditionally as an antidiarrhoeal agent. Much of the research has been done on the chief constituent, berberine. Supplements should be standardised to contain at least 8 mg/mL of berberine and 8 mg/mL of hydrastine. It acts by decreasing intestinal activity and inhibiting toxin formation from microbes.

Ciguatera fish poisoning

Results from ingestion of a fish containing a neurotoxin (ciguatoxin) that originates in algae living in tropical waters, particularly the Pacific and Caribbean. Ciguatoxin is very heat resistant, so ciguatoxin-laden fish cannot be detoxified by conventional cooking. Symptoms start within 5 minutes to 30 hours of ingestion: nausea, vomiting, diarrhoea, photophobia, blurred vision, ataxia and paraesthesiae. Bradycardia, hypotension and heart block may occur. There is no proven effective treatment or antidote for ciguatera poisoning. The symptoms can last from weeks to years, and in extreme cases as long as 20 years, often leading to long-term disability.¹⁰ Most people do recover slowly over time. Often patients recover but redevelop symptoms in the future. Relapses can be triggered by consumption of nuts, alcohol, fish or fish-containing products, chicken or eggs, or by exposure to fumes such as those of bleach and other chemicals. Exercise is also a possible trigger.¹¹

Chronic diarrhoea

Frequent or urgent passing of unformed stools for more than a month can be referred to as chronic diarrhoea. It should be distinguished from faecal incontinence or tenesmus.

Diagnosis

History and investigations are directed at finding a treatable cause of chronic diarrhoea.

• Patient should be questioned about pain, stool frequency and timing, colour and consistency, and presence of blood, flatus or mucus.

• A history of travel to developing countries, even several months or years before, may assist diagnosis.

• A comprehensive dietary history should be ascertained, including all foods, alcohol, soft drinks, fruit juices and milk.

• Medication history, including antibiotics and antacids, herbs and supplements.

• Inquire specifically about weight loss, mouth ulceration, joint pain, visual problems and emotional health.

• Family history may suggest suspicion of coeliac disease, inflammatory bowel disease or bowel cancer.

Physical examination should be comprehensive, bearing in mind the possibility that diarrhoea could be a result of local gastrointestinal inflammation or infection, gastrointestinal manifestation of systemic disease such as thyrotoxicosis or an adverse drug effect, or that the diarrhoea will have systemic and nutritional consequences such as malabsorption, anaemia, dehydration or nutritional deficiencies.

Abdominal palpation, rectal examination and examination of stool are essential.

Diagnostic clues:

• Tenesmus suggests rectal involvement.

• Small-volume frequent stools suggest large bowel disease.

• Steatorrhoea (pale, bulky, greasy, floating stools) suggests small bowel or pancreatic disease.

• Large-volume watery stools suggest small bowel disease or laxative overuse.

• Bright red blood suggests local anal bleeding, or rectal or low colonic disease.

• Altered blood, or blood mixed with stool, suggests problems higher in the colon.

• Weight loss suggests an underlying organic disease, malabsorption, colon cancer or thyrotoxicosis.

• Arthritis or sacroiliitis suggests inflammatory bowel disease or hypogammaglobulinaemia.

• Central abdominal pain suggests small bowel origin.

• Iliac fossa pain suggests large bowel origin.

• Diarrhoea waking the patient from sleep at night, or blood in stools, excludes functional bowel disease.

• Skin rash may suggest coeliac disease (dermatitis herpetiformis) or inflammatory bowel disease (erythema nodosum or erythema multiforme).

• Abdominal bloating is non-specific.

• Diarrhoea in association with certain food types suggests food intolerance or reaction (e.g. milk and lactose intolerance, gluten and coeliac disease, sorbitol in chewing gum or drinks).

• Sexual history may lead to HIV testing, with diarrhoea a common symptom.

Diagnostic possibilities:

• Coeliac disease (see p. 392)

• Giardiasis (see p. 372)

• Irritable bowel syndrome (see p. 389)

• Inflammatory bowel disease (see p. 390)

• Crohn’s disease (see p. 390)

• Dietary intolerance

• Malabsorption

• Overuse of laxatives.

Therapeutics

Identify and treat any underlying cause.

• Probiotic—Lactobacillus acidophilus and/or bifidobacteria taken as powder or in capsules helps normalise bowel flora.

• Bovine colostrum is a component in some probiotic supplements and helps treat some kinds of infectious diarrhoea.

• Maintain hydration.

• Maintain nutrition. Rice or barley water, fresh vegetable juices, miso broth, or other clear broths with added Celtic sea salt help restore fluid and electrolyte balance.

• Avoid coffee, chocolate, dairy products and strong spices.

• Multivitamin supplement.

• Protein supplement may be necessary for malabsorption.

Herbs

• Blackberry leaf (Rubus fruticosus) or raspberry leaf (Rubus idaeus) teas.

• Bilberry (Vaccinum myrtillus) also has astringent properties (4 g per day in divided doses).

• Agrimony (Agrimonia eupatorium) is a traditional remedy for diarrhoea. Usual dosage is about ½ teaspoon per day.

For relieving gut inflammation:

• Quercetin (250–500 mg 2–4 times per day) to be taken with bromelain as this improves its digestion. They commonly come together in formulas and bromelain is also an anti-inflammatory. (Caution: Commission E states that hypersensitivity to bromelain can cause diarrhoea.)

• Chamomile (Matricaria recutita) tea.

• Marshmallow root (Althea officinalis) as cold-water tea.

• Slippery elm powder (Ulmus fulva) or marshmallow root powder (A. officinalis). Plants containing berberine can be used for infectious diarrhoea. These include barberry (Berberis vulgaris) 250–500 mg three times per day, goldenseal (Hydrastis canadensis) 250–500 mg three times per day and Oregon grape (Berberis aquifolium) 250–500 mg three times per day.

ALTERNATING DIARRHOEA AND CONSTIPATION

Consider irritable bowel syndrome, carcinoma of colon, diverticular disease, giardiasis, food intolerance.

FAECAL INCONTINENCE

Faecal incontinence, or involuntary leakage of faecal material, is thought to occur in about 10% of adults but is reported in only one in eight cases.¹² It can cause severe restriction of social interaction and lifestyle, and is a common precipitant for admission to residential aged care.

Clinical features

Risk factors include advancing age, debility with faecal impaction with spurious diarrhoea, perianal or rectal injury from childbirth or radiotherapy, anal surgery, irritable bowel syndrome, chronic constipation (and laxative abuse), neurological disorders and psychiatric disorders.

History will often lead you to the underlying cause. A rectal examination is necessary to assess sphincter tone, and proctoscopy to examine rectal mucosa.

Investigations

• Sigmoidoscopy.

• Patients with advanced incontinence or those resistant to initial treatment should be evaluated by anorectal physiology testing to establish the severity and type of incontinence (e.g. anorectal manometry, nerve conduction studies for suspected neurogenic incontinence).

• Endoanal ultrasound to identify defect in the internal or external sphincter.

• CT scan of pelvic or lumbosacral spine in suspected cases of spinal cord lesion.

• Stool examination for chronic diarrhoea.

Therapeutics

Treatment will be determined by the cause. Try dietary modification and treatment of diarrhoea or constipation.

Proper clinical assessment followed by conservative medical therapy leads to improvement in more than 50% of cases,¹³ including patients with severe symptoms.

Patients with gross sphincter defects should undergo surgical repair. Those who fail to respond to sphincteroplasty and those with no anatomical defects have the option of sacral nerve stimulation or other advanced procedures.

GLOSSODYNIA (PAINFUL TONGUE)

‘Glossodynia’ refers to persistent burning or pain in the mouth, which may be accompanied by dryness, paraesthesia and altered taste or smell. It may be a result of altered oral sensory function but the mechanism is unknown. It is two to three times more common in women and mostly occurs in middle age.

Therapeutics

• Exclude or assess and treat any underlying causes.

• Correct nutritional deficiencies with diet and supplementation.

• Assess and advise on stress management. Psychological assessment and counselling may benefit.

HICCUPS

Hiccups are a reflex muscular contraction causing sudden inspiration against a closed glottis. It usually responds to simple measures. Persistent or intractable hiccups (present for over 24 hours) may come to the attention of a healthcare professional and can be a sign of serious underlying disease.

Persistent hiccup can result from direct stimulation or irritation of the afferent or efferent vagal or phrenic nerve pathways, from lesions in the medulla or be secondary to metabolic disturbances.

Aetiology

Self-limited episodes:

• Gastro-oesophageal reflux disease (GORD) (may be cause or effect)

• Gastric distension

• Sudden temperature change.

Persistent or intractable hiccups:

• Medullary lesion—infarction, tumour, abscess, aneurysm, haematoma, syrinx, demyelination etc

• CNS infection—viral encephalitis, syphilis, HIV encephalopathy, meningitis

• Irritation of neuronal pathway—oesophageal or small bowel obstruction, achalasia, pancreatic or biliary disease, foreign body in external auditory meatus (auricular branch of vagus nerve)

• Mediastinal disease—tumour, thoracic aortic aneurysm, diaphragmatic irritation from subphrenic or hepatic disease, pleural or pericardial effusion, myocardial infarction

• Metabolic/endocrine—diabetes, uraemia, hypocalcaemia, hyponatraemia, Addison’s disease

• Medication side effect—alcohol, general anaesthetic, corticosteroids, benzodiazepines, barbiturates, etoposide

• Idiopathic.

Diagnosis

Investigation of persistent hiccups is directed at identifying an underlying cause.

History should include close questioning about neurological, gastrointestinal, cardiac and respiratory symptoms and drug and alcohol use.

Physical examination should include full neurological assessment, cognitive assessment, cardiopulmonary examination, examination of auditory canals, and abdominal examination.

Investigations will be guided by symptoms and physical findings. Initial investigations will include:

• metabolic screen (serum electrolytes, serum calcium, blood glucose, liver function tests)

• full blood count

• chest X-ray and ECG if a cardiopulmonary cause is suspected

• thoracic CT scan if mediastinal disease is suspected

• upper abdominal ultrasound or CT scan if hepatic or subdiaphragmatic pathology suspected

• endoscopy if oesophageal or gastric cause is suspected

• oesophageal motility studies.

MOUTH ULCERS

Oral ulcers are extremely common and usually limited to 5–10 days duration. Serious or recurrent painful ulceration can be an indicator of underlying systemic or gastrointestinal disease requiring further investigation.

Differential diagnosis

• Idiopathic aphthous ulcers

• Trauma (toothbrush, hard foods, biting buccal mucosa, sharp or malaligned dentition or poorly fitting denture)

• Reaction to chemical in mouthwash

• Poor oral hygiene

• Excessive stress

• Crohn’s disease, ulcerative colitis

• Coeliac disease

• Pernicious anaemia

• Iron deficiency

• Herpes simplex (begins as clusters of vesicles and transforms into small punctuate ulcers mainly on the hard palate, gingival and alveolar ridges)

• Oral candidiasis

• Blood dyscrasia

• Autoimmune disease (e.g. lichen planus)

• Erythema multiforme (preceded by vesicles)

• Pemphigus and pemphigoid (preceded by bullae)

• Behçet’s syndrome (oral ulceration occurs in conjunction with ocular and genital ulceration; can also affect skin, joints and gut)

• Neoplasm—biopsy if solitary ulcer not healed in 3 weeks.

Prevention

• Establish or exclude underlying disease

• Regular dental checks

• Maintain oral hygiene

• Stress management.

FIGURE 30.2 Aphthous ulcer

DYSPHAGIA

Dysphagia refers to difficulty swallowing, frequently associated with pain. It can be caused by structural or neuromuscular oesophageal problems in the oropharynx or oesophagus.

Diagnosis

Comprehensive questioning and physical examination are required to identify the nature of any underlying cause.

• Exclude globus sensation, which is usually a painless sensation of a lump in the throat, felt between meals and often relieved by food.

• Progressive dysphagia predominantly for solids indicates a structural disorder. Malignant dysphagia is usually a short history of progressive difficulty with swallowing over weeks or months, and may be associated with weight loss.

• Sudden onset in association with other neurological symptoms may indicate a cerebrovascular cause.

• Intermittent dysphagia for liquids and solids, look for a motility disorder such as oesophageal spasm or pharyngeal cause.

• The patient’s perception of the site of the hold-up of the bolus is notoriously unreliable.

• Associated symptoms such as dry mouth, heartburn, cough, nausea, weight loss or skin changes may provide clues to any underlying cause.

Investigation

• Barium swallow to assess motility and identify structural lesion. Should precede endoscopy.

• Endoscopy required in most cases to detect mucosal disease and obtain biopsies. Enables dilatation where indicated. Cannot diagnose motility disorders or external structural problems.

• Oesophageal manometry—for cases where endoscopy and barium swallow have failed to confirm a diagnosis. Required for definitive diagnosis of achalasia.

• ENT assessment may be necessary to exclude pharyngeo-laryngeal malignancy.

• Nutritional assessment, particularly where diet has become limited by inability to swallow solids.

• Blood tests may be helpful where indicated: CPK, FBC, ESR, ANA, thyroid function tests (TFT).

Therapeutics

• Identify and treat any underlying cause.

• Establish a safe means of nutrition.

INDIGESTION, DYSPEPSIA AND HEARTBURN

A detailed history is needed to find out exactly what a patient means when they complain of ‘indigestion’. Find out if they are referring to regurgitation, epigastric burning or pain, eructation (burping), bloating or something else.

Dyspepsia generally refers to persistent or recurrent pain or discomfort in the upper abdomen, and may include heartburn or acid regurgitation. ‘Discomfort’ may also embrace sensations such as postprandial fullness, early satiety, nausea and upper abdominal bloating.

Heartburn and regurgitation imply oesophageal disease and often occur together.

Heartburn is described as a burning lower retrosternal pain that radiates upwards as far as the neck. It occurs intermittently, often 5 to 30 minutes postprandially or when the patient bends forward or lies flat in bed.

Larger meals can be an exacerbating factor, and certain foods can precipitate an attack. It is usually relieved by antacid medication within several minutes.

‘Waterbrash’ is a symptom describing the appearance of a volume of salty-tasting or tasteless fluid in the mouth. It is the result of salivary gland stimulation in response to gastro-oesophageal reflux or peptic ulcer disease.

Regurgitation of acid or stomach contents can be associated with dry cough, vocal hoarseness (chemical laryngitis), asthma, halitosis, choking attacks, glossodynia, dental caries and nasal aspiration. Patients may wake in the night with a choking sensation.

Symptoms of dyspepsia and GORD often overlap.

Causes of dyspepsia/indigestion

The causes of dyspepsia are many and varied, so precise elicitation of symptoms is important. Differential diagnosis includes:

• chronic peptic ulcer—duodenal ulcer pain is localised, worst at night and relieved by food; gastric ulcer pain is aggravated by food

• non-ulcer dyspepsia

• oesophagitis (pain on swallowing hot or cold liquids)

• H. pylori gastritis

• hepatobiliary—hepatitis, biliary dyskinesia, cholelithiasis

• chronic pancreatitis

• Crohn’s disease

• upper GI malignancy

• mesenteric vascular insufficiency—diarrhoea 30 minutes after a meal

• metabolic—renal failure, hypercalcaemia, gastroparesis or gastric hypomotility

• irritable bowel sndrome

• psychosocial factors (stress, anxiety, depression)

• myocardial ischaemia

• referred back pain

• drug side effect (especially non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, antidepressants, digoxin, potassium, iron, zinc)

• alcohol-related.

Investigation

The aim of investigation is to identify any underlying treatable cause for the heartburn, indigestion or dyspepsia. Detailed history and physical examination will direct the choice of investigations.

• Test for H. pylori with serology (blood test) and C14 breath test.

• In the absence of associated ‘red flag’ symptoms, a trial of treatment such as lifestyle modification and antacid therapy may provide relief (see GORD).

• Upper gastrointestinal endoscopy is indicated if symptoms do not resolve after 8 weeks. The aim is to exclude peptic ulcer, significant reflux oesophagitis and malignancy.

• Epigastric or retrosternal pain, especially if precipitated by exercise, needs to be investigated for coronary ischaemia.

GASTRO-OESOPHAGEAL REFLUX DISEASE

A typical history of heartburn or acid regurgitation is usually sufficient to satisfy a diagnosis of gastro-oesophageal reflux disease (GORD). There are no specific signs on physical examination to support the clinical diagnosis.

Barrett’s oesophagus

A complication of gastro-oesophageal reflux, Barrett’s oesophagus is a metaplastic transformation (intestinal metaplasia) of the stratified squamous epithelium in the lower oesophagus. It is a precursor to malignant adenocarcinoma of the distal oesophagus. Patients with high-risk dysplasia need to be monitored with surveillance endoscopy and biopsy every 2 years.

Guidelines

• No dysplasia: 3-yearly

• Low-grade dysplasia: yearly

• High-grade dyaplasia: repeat ∼ 1 month (definitive treatment).

Investigation of symptoms suggesting GORD

• Trial of therapeutics.

• Upper gastrointestinal endoscopy if symptoms do not resolve after 8 weeks. The aim is to exclude peptic ulcer, significant reflux oesophagitis and malignancy.

Therapeutics

First-line

Aims of treatment are to reduce regurgitation, reduce stomach acid content, improve stomach emptying, and protect the lining of the oesophagus.

• Weight loss, if overweight

• Small light meals, avoiding eating close to bedtime

• Elevate the head of the bed with a house brick

• Avoid cigarettes, caffeine, alcohol and carbonated drinks

• Avoid foods that trigger symptoms

• Avoid carbonated drinks

• Reduce or exclude coffee, tea and chocolate

• Remove or replace medications or supplements possibly responsible for symptoms

• Relaxation and stress management including exercise, yoga, t’ai chi and meditation

• Deglycyrrhizinated licorice (DGL) (Glycyrrhiza glabra) has anti-inflammatory, mucoprotective and anti-ulcer effects. Approved by Commission E for treatment of gastric and duodenal ulcers.

Dose: standardised extract, 250–500 mg three times daily, chewed either 1 hour before or 2 hours after meals

• Ginger—approved by Commission E for treatment of dyspepsia

• Slippery elm bark powder—half teaspoon in one cup of hot water three times a day

• Chamomile—widely used as a tea for treatment of dyspepsia

• Lemon balm—has antispasmodic activity and is approved by Commission E for functional gastrointestinal conditions

• Globe artichoke leaf extract—reduces symptoms of non-ulcer dyspepsia.¹⁴

Second-line

• Antacids as required for symptomatic relief, e.g. liquid alginate/antacid mixture

• Prokinetic agents such as metoclopramide

• Regular proton pump inhibitors if symptoms are persistent or frequent.

Prevention

• Maintain healthy body weight and waist circumference

• Do not smoke or drink alcohol excessively

• Small, regular meals

• Manage stress.

NAUSEA AND VOMITING

Precise definition of terms is important in establishing the nature and cause of symptoms, as patients will often adopt a common-language term to describe a symptom, rather than the correct descriptor.

• Nausea is a sensation of wanting to vomit and is painless but unpleasant.

• Vomiting is the forceful expulsion of stomach or intestinal contents through the mouth. It may be preceded by autonomic symptoms of various intensity, including salivation, bradycardia, sweating, pallor and hypotension.

• Retching is the repetitive contraction of stomach muscles associated with vomiting, but without the expulsion of stomach contents.

• Regurgitation is the effortless appearance of stomach contents in the mouth without nausea or diaphragmatic contractions.

• Haematemesis is vomiting of blood.

The history should include questions about duration, frequency and intensity of nausea and vomiting and any relationship to eating, and the nature of the vomitus. A comprehensive medical history including any medications or supplements is essential.

Causes

Intestinal obstruction:

• Small bowel obstruction—vomitus is usually bile-stained if the obstruction is below the level of the duodenal ampulla. Faecal vomiting would indicate distal small bowel obstruction. Malignant obstruction is usually associated with anorexia and weight loss.

• Gastric outlet obstruction—vomiting of partially digested gastric contents without the presence of bile.

• Pyloric stenosis—neonate, sudden onset of projectile vomiting week 3–6, failure to thrive, metabolic alkalosis sodium usually under 130 mol/L, more often male (5:1). Clinically may feel a pyloric tumour, or require ultrasound to confirm.

• Gastroparesis—may be associated with long-standing diabetes, often intense nausea, anorexia, postprandial fullness and early satiety. May be associated with peripheral or autonomic neuropathy.

• Chronic intestinal pseudo-obstruction.

• Food poisoning

• Viral or bacterial gastroenteritis—acute onset, usually associated with headache, fever, myalgia and diarrhoea, and tends to settle within 5 days

• Acute viral hepatitis

• Urinary tract infection in children.

Central nervous system disorders:

• Raised intracranial pressure—vomiting, sometimes projectile, on waking in the morning. Likely other neurological signs present. Space-occupying lesions may cause vomiting without nausea.

• Ménière’s disease—associated tinnitus and vertigo

• Motion sickness.

Metabolic and endocrine disorders:

• Renal failure

• Diabetic ketoacidosis

• Hypercalcaemia

• Addison’s disease—characteristic pigmentation

• Hyperthyroidism.

• Theophylline

• Morphine and opiate derivatives

• Chemotherapy

• Oral contraceptive pill

• Peritonitis

• Cholecystitis

• Pancreatitis.

Emotional disorders:

• Anorexia or bulimia nervosa—repeated bouts of vomiting (self-induced) soon after meals with associated features which may include impaired body image, vigorous exercise, and laxative and diuretic abuse, amenorrhoea, binge eating.

• Panic attacks.

• Common in the first trimester of pregnancy but can persist throughout the gestation period. Pregnancy should be excluded in every female patient of childbearing age presenting with nausea and/or vomiting.

Cyclical vomiting syndrome:

• Asymptomatic periods between bouts of nausea and vomiting; often associated history of migraine. Can be associated with significant cannabis use (cannabinoid hyperemesis).

Functional vomiting:

• Conditioned reflexes to offensive sights or smells

• Acute myocardial infarction.

Examination

Thorough physical examination is necessary to identify underlying causes for nausea and vomiting and to assess clinical consequences of vomiting, such as dehydration and malnutrition.

• Examine for dental caries.

• Careful neurological examination is required, including examination of the fundi for signs of raised intracranial pressure.

• If fever is present, examine for focus of infection, including urinalysis and middle ear.

• Note any scars from previous surgery.

Therapeutics

• Identify and treat any underlying cause.

• Identify and correct dehydration and electrolyte disturbances.

• Nutritional support.

• IV fluids or nasogastric tube if indicated.

• Acupuncture and acupressure.

• Psychotherapy—hypnotherapy, relaxation exercises and other psychotherapies can be useful adjuncts, particularly where psychological or emotional factors are contributing to the presentation or when a patient is having to cope with an unpleasant symptom like chronic nausea and vomiting.

Motion sickness:

• Ginger; or scopolamine transdermal patch; or promethazine 25 mg p.o. 1 hour before travel and repeated 4–6 hourly during trip

• Prokinetic agents (where delayed gastric emptying is a feature):

• metoclopramide (5–20 mg q.i.d.) may cause tardive dyskinesia

• erythromycin (accelerates gastric emptying)—high doses induce nausea. Will need to include a probiotic.

• domperidone (Motilium®) 10 mg t.d.s.

HALITOSIS

Halitosis is an unpleasant odour on the breath that may be physiological or pathological (Box 30.1). Physiological causes may include ingestion of particular foods or medications. It is most commonly caused by action of microflora on oral debris around the teeth and gums. Gram-negative organisms cause putrefaction and release of chemicals, particularly sulfide compounds, in the alkaline oral environment.

BOX 30.1 Differential diagnosis of halitosis

• Foods—garlic, onion, peppers, broccoli, radish, leek, salami, strong cheeses

• Drugs—isosorbide dinitrate, disulfiram, dimethyl sulfoxide, alcohol, tobacco

• Poor oral hygiene

• Dental decay

• Oral inflammation—gingivitis, periodontal disease, ulceration, candidiasis, dehydration

• Tumour or infection in the nasopharynx, tonsils, sinuses or respiratory tract

• Nasal foreign body

• Inhaled steroids for asthma causing candidiasis

• Lower respiratory tract—bronchitis, bronchiectasis, lung abscess, pneumonia, lung cancer, tuberculosis

• Pharyngeal pouch (stagnation and regurgitation of food)

• Oesophageal or gastric neoplasm

• Systemic—diabetic ketoacidosis, uraemia, hepatic failure, starvation, inborn errors of metabolism (aminoacidurias)

The odour can vary depending on diet, time of day, time of menstrual cycle and state of hunger.

Treatment

• Identify and treat underlying cause, if identified.

• Dental referral for treatment of gingival or periodontal disease. Severe cases may require metronidazole for 5–10 days.

• Treat oral candidiasis with topical antifungal (nystatin) or oral fluconazole 150 mg stat.

• Improve dental hygiene, reduce tongue biofilm by brushing off tongue coating.

• Eliminate offending foods from diet.

Prevention

• Eat regularly, low-fat diet high in fruit and vegetables

• Increase fluid intake

• Reduce alcohol and eliminate smoking

• Brush after every meal, and floss between teeth daily

• Mouthwash containing chlorhexidine

• Regular dental checks

• Eliminate or substitute drugs likely to cause xerostomia, e.g. antihistamines, antidepressants, anticholinergics, anorexiants, antihypertensives, antipsychotics, antiparkinsonian agents, diuretics and sedatives. Other drug classes that commonly cause xerostomia include antiemetics, antianxiety agents, decongestants, analgesics, antidiarrhoeals, bronchodilators and skeletal muscle relaxants.

PERIANAL PAIN

Consider severity, duration, timing, relationship to defecation, rectal bleeding or prolapse. Examination needs to be focused on the perianal region but include abdominal and general examination.

Causes to consider are described below.

Anal fissure

Pain with defecation and bright red bleeding are common. Usually associated with intense spasm of internal anal sphincter muscle and initially produced by splitting from passage of a hard stool. Internal sphincter spasm results in ischaemia in anal mucosa. Avoid digital rectal examination because of pain.

Secondary fissures may be due to Crohn’s disease, ulcerative colitis or immunosuppression. Assess for HIV or syphilis testing if indicated.

Treatment

• Topical 0.2% glyceryl trinitrate ointment.

• Treat constipation with a bulking agent and adequate fluid intake.

• Surgery if fissure fails to heal and remains painful.

Haemorrhoids

The main symptom is rectal bleeding. Uncomplicated haemorrhoids may be painless, cause itch or cause discomfort with defecation. Thrombosed or prolapsed haemorrhoids cause acute severe pain. With internal haemorrhoids, bleeding may be a more prominent symptom than pain. Bleeding is bright red and may be seen on toilet paper or in the bowl.

Treatment

• Initial treatment: topical.

• Acute thrombosis can be relieved by surgical incision.

• May require injection, rubber band ligation or surgical excision.

• Treatment includes dietary modification to ensure adequate fibre and fluid intake. Prolonged sitting on toilet or straining should be discouraged.

Anal abscess

An extremely tender perianal lump will be evident. There may be fever if the abscess is large. In most cases an anal abscess develops from a primary infection in an anal gland and may progress to perianal abscess, ischiorectal abscess or supralevator abscess.

May be secondary to Crohn’s disease or ulcerative colitis. Patients should be checked for immune deficiency, immunosuppression and diabetes. Look for evidence of a fistula. Rectal carcinoma should be excluded.

Treatment

Anal abscess requires surgical referral for exploration and drainage. Underlying pathology needs to be identified and treated.

Anal fistula

Mild, dull, localised pain. Look for a sinus opening.

Pruritis ani

Anal itch, usually worse at night, in hot weather and after exercise. Causes include dermatitis, psoriasis, fungal infection (tinea or Candida albicans), haemorrhoids, anal fissure, anal warts, skin tags, anal carcinoma.

In children, threadworm infestation is a possible cause. Consider sensitivity to washing powders, soaps or bubble bath.

Proctalgia fugax

Presents as a history of severe pain in anal canal lasting 5–30 minutes. May wake patient from sleep. Can occur day or night. Affects adults, males more often than females. Thought to be due to spasm of levator ani muscles.

Treatment

• May respond to inhaled salbutamol (2 puffs stat).

• Difficult cases may respond to excision of prolapsing rectal mucosa.

RECTAL BLEEDING

Severity of bleeding varies from a small amount of blood on the toilet paper to heavy bleeding. History should include amount and colour of blood, whether it is on toilet paper only (suggesting local anal pathology) or mixed with stool, associated perianal pain, pattern of bowel habit, diet and family history of colorectal cancer.

Gastrointestinal bleeding should be considered in any patient aged over 40 years with iron deficiency anaemia. Menstrual bleeding and dietary deficiency in young women are common causes of iron deficiency.

Melaena

The passage of dark altered blood is a sign of bleeding in the upper gastrointestinal tract (usually peptic ulceration but may be a result of portal hypertension or portal enteropathy). It has a strong odour. It is an indication for urgent referral for hospital admission.

Black motions can also be the result of ingestion of liquorice or oral iron supplementation.

Bright bleeding

Causes include haemorrhoids, anal fissure, inflammatory bowel disease (proctitis), rectal polyps, infective colitis, Meckel’s diverticulum, intussusception, colorectal cancer, diverticular disease, ischaemic colitis.

Investigation

Examination should include anal, rectal and abdominal examination as well as proctoscopy or sigmoidoscopy.

A bleeding source may be clearly identified (e.g. bleeding haemorrhoids or fissure).

Do not assume that haemorrhoids are the cause of bleeding, especially in an elderly patient. Persistent or recurrent bleeding or any uncertainty regarding the cause warrants a colonoscopy.

Positive faecal occult blood test (FOBT)—population testing for faecal occult blood yields some positive results. The test will detect 40–80% of asymptomatic colorectal cancers and 30–40% of large colorectal adenomas. A positive FOBT is a trigger for colonoscopy.

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