Gastrointestinal and nutritional disorders

12 Gastrointestinal and nutritional disorders

Diseases of the GI tract are a major cause of morbidity and mortality. Approximately 10% of all GP consultations in the UK are for indigestion, and 1 in 14 is for diarrhoea. Infective diarrhoea and malabsorption are responsible for much ill health and many deaths in the developing world.

PRESENTING PROBLEMS

DYSPHAGIA

Dysphagia means difficulty in swallowing, as distinct from globus sensation (a ‘lump’ in the throat without organic cause) and odynophagia (pain during swallowing). Oropharyngeal dysphagia results from neuromuscular dysfunction that affects swallowing, causing choking, nasal regurgitation or tracheal aspiration. Drooling, dysarthria, hoarseness and other neurological signs may be present. Oesophageal causes include benign or malignant strictures and oesophageal dysmotility. Patients complain of food ‘sticking’ after swallowing, although swallowing of liquids is normal until strictures become extreme.

• Endoscopy is preferred to facilitate biopsy and dilatation of strictures.

• Videofluoroscopic barium swallow will detect most motility disorders.

• Oesophageal manometry is occasionally required.

DYSPEPSIA

Dyspepsia (‘indigestion’) may arise from causes within or outside the gut (Box 12.1). Heartburn and other ‘reflux’ symptoms are separate and are considered elsewhere. Although symptoms correlate poorly with diagnosis, careful history may reveal classical symptoms of peptic ulcer, ‘alarm’ features requiring urgent investigation (Box 12.2) or symptoms of other disorders. Dyspepsia affects up to 80% of the population at some time, often with no abnormality on investigation, especially in younger patients.

• Examination may reveal anaemia, weight loss, lymphadenopathy, abdominal masses or liver disease.

• Patients with ‘alarm’ symptoms, and those >55 with new dyspepsia require prompt endoscopy.

• Younger patients should be tested for Helicobacter pylori; if symptoms persist after treatment, these patients should have endoscopy.

12.2 ALARM’ FEATURES IN DYSPEPSIA

• Weight loss

• Haematemesis and/or melaena

• Palpable abdominal mass

CLINICAL EXAMINATION OF THE GASTROINTESTINAL TRACT

GI BLEEDING

ACUTE UPPER GI HAEMORRHAGE

This is the most common GI emergency, accounting for 50–120 hospital admissions per 100 000 each year in the UK.

Haematemesis may be red with clots when bleeding is profuse, or black (‘coffee grounds’) when less severe. Syncope may occur with rapid bleeding. Anaemia suggests chronic bleeding. Melaena is the passage of black, tarry stools containing altered blood. This is usually due to upper GI bleeding, although the ascending colon is occasionally responsible. Severe acute upper GI bleeding occasionally causes maroon or bright red stool. Causes of acute upper GI haemorrhage are shown in Box 12.3.

Management

I.V. access: Should be secured with a large-bore cannula.

Clinical assessment: Should be made for circulatory status (tachycardia, hypotension and oliguria indicating severe bleeding), liver disease (jaundice, cutaneous stigmata, hepatosplenomegaly and ascites) and comorbidity (cardiorespiratory, cerebrovascular or renal disease, which increases the hazards of endoscopy and surgery).

Blood tests: FBC (slow bleeding causes anaemia; haemoglobin may be normal after sudden, major bleeding); cross-matching of at least 2 U of blood; U&Es (shock may cause renal failure; the urea also rises as the luminal blood is digested); LFTs and prothrombin time, if there is clinical suggestion of liver disease or in anticoagulated patients.

Resuscitation: Oxygen should be given to all patients in shock. I.V. crystalloid or colloid infusion restores blood pressure. Normal saline should be avoided in liver disease because it can cause ascites. Blood transfusion should be given if there is shock or the haemoglobin is <100 g/litre. CVP monitoring helps to reveal rebleeding and guide fluid replacement.

Endoscopy: After resuscitation, this will reveal a diagnosis in 80% of cases. Patients with spurting haemorrhage or a visible vessel can be treated by thermal probe, adrenaline (epinephrine) injection or metal clips. This may stop bleeding and, combined with i.v. proton pump inhibitor (PPI) therapy, prevent rebleeding, thus avoiding surgery.

Monitoring: Hourly pulse, BP and urine output.

Surgery: Indicated when endoscopic haemostasis fails to stop the bleeding, or rebleeding occurs once in an elderly or frail patient/twice in younger, fitter patients. Following successful surgery for ulcer bleeding, all patients should be treated with H. pylori eradication therapy if positive and should avoid NSAIDs.

LOWER GI BLEEDING

This may be due to haemorrhage from the small bowel, colon or anal canal.

Severe acute lower GI bleeding

Diverticular disease: The most common cause. Patients present with profuse red or maroon diarrhoea and shock. Bleeding almost always stops spontaneously, but if not, the diseased segment is located by angiography or colonoscopy and resected.

Angiodysplasia: Characterised by vascular malformations resembling spider naevi in the proximal colon of elderly patients. Bleeding usually stops spontaneously but commonly recurs. Treatment is by colonoscopic thermal ablation, or resection if bleeding continues.

Ischaemia due to inferior mesenteric artery occlusion: Presents with abdominal colic and rectal bleeding. It occurs in elderly patients with atherosclerosis and is diagnosed by colonoscopy. Resection is required only in the presence of peritonitis.

Meckel’s diverticulum: May erode into a major artery and cause profuse lower GI bleeding in children or adolescents. The diagnosis is commonly made only by resection at laparotomy.

Subacute or chronic lower GI bleeding

This is extremely common and is usually due to haemorrhoids or anal fissure. Proctoscopy reveals the diagnosis but if there is altered bowel habit and in all patients presenting at age 40 and over, colonoscopy or barium enema is necessary to exclude colorectal cancer.

OBSCURE MAJOR GI BLEEDING

If upper endoscopy and colonoscopy are inconclusive, mesenteric angiography usually identifies the site and embolisation can be used to stop the bleeding. If angiography is negative, enteroscopy or wireless capsule endoscopy can be used to identify a bleeding source in the small intestine. When all else fails, laparotomy with on-table endoscopy is indicated.

OCCULT GI BLEEDING

Occult bleeding (no visible blood) may reach 200 ml/day, cause iron deficiency anaemia and signify serious disease. The most important cause is colorectal cancer, which may have no GI symptoms. GI investigations should be considered in any patient with unexplained iron deficiency anaemia. A negative faecal occult blood (FOB) test does not exclude important GI disease.

DIARRHOEA

‘Diarrhoea’ most commonly means increased stool frequency and loose or watery stools. Normal bowel frequency ranges from three movements/day to one every third day. Gastroenterologists define diarrhoea as the passage of >200 g of stool daily. In severe cases, urgency of defecation and faecal incontinence occur.

ACUTE DIARRHOEA

Infective diarrhoea is usually due to faecal–oral transmission and is normally short-lived. Diarrhoea lasting >10 days is rarely caused by infection. Drugs including antibiotics, cytotoxics, PPIs and NSAIDs may cause acute diarrhoea.

CHRONIC OR RELAPSING DIARRHOEA

The most common cause is irritable bowel syndrome, in which diarrhoea is most severe before and after breakfast and rarely occurs at night. At other times the patient is constipated. The stool often contains mucus but never blood, and 24-hr stool volume is <200 g. Chronic diarrhoea can also be due to inflammatory or neoplastic disease of the colon or small bowel, or to malabsorption. Negative investigations suggest irritable bowel syndrome.

MALABSORPTION

Diarrhoea and weight loss in patients with a normal diet suggest malabsorption. Bulky, pale and offensive stools which float (steatorrhoea) signify fat malabsorption. Abdominal distension, borborygmi, cramps and undigested food in the stool may be present. Malaise, lethargy, peripheral neuropathy and symptoms related to vitamin or mineral deficiencies may occur.

Malabsorption results from abnormalities of the three components of normal digestion:

• Intraluminal maldigestion due to deficiency of bile or pancreatic enzymes.

• Mucosal malabsorption from small bowel resection or damage to the small intestinal epithelium.

• ‘Post-mucosal’ lymphatic obstruction preventing the uptake of absorbed lipids into lymphatic vessels.

An approach to investigations is shown in Figure 12.1.

Fig. 12.1 Investigation for suspected malabsorption.

WEIGHT LOSS

Unplanned weight loss of >3 kg over 6 mths is significant. Previous weight records may be valuable. Pathological weight loss can be due to psychiatric illness, systemic disease, GI causes or advanced disease of any specific organ system.

History and examination

‘Physiological’ weight loss: Should be obvious from the history but may be more difficult to determine in older patients when nutritional history may be unreliable; a dietitian’s opinion is often valuable.

Psychiatric illness: Features of anorexia nervosa, bulimia and affective disorders may only be apparent after formal psychiatric input. Alcoholic patients lose weight through self-neglect and poor diet.

Systemic diseases: Chronic infections lead to weight loss, and a history of foreign travel, fever, night sweats, rigors, productive cough and dysuria must be sought. Sensitive questions regarding lifestyle (promiscuous sexual activity and drug misuse) may suggest HIV infection. Weight loss is a late feature of disseminated malignancy (carcinoma, lymphoma or other haematological disorders), which may be revealed on examination.

GI disease: Dysphagia and gastric outflow obstruction cause defective intake. Malignancy may cause weight loss by mechanical obstruction, anorexia or systemic effects. Malabsorption from pancreas or small bowel causes profound weight loss and nutritional deficiencies. Crohn’s disease and ulcerative colitis cause anorexia, fear of eating, and loss of protein, blood and nutrients from the gut.

Specific diseases of any major organ system: Endocrine disease, including diabetes mellitus, Addison’s disease and thyrotoxicosis, may cause weight loss. In patients with disabling end-stage respiratory, cardiac or rheumatological diseases, weight loss occurs from a combination of anorexia, physical disability and the systemic effects of their conditions, often compounded by drug effects (e.g. digoxin) which may cause nausea, dyspepsia, constipation or depression.

CONSTIPATION

Constipation is the infrequent passage of hard stools, often with straining, a sensation of incomplete evacuation and perianal or abdominal discomfort. It may be the end result of many disorders.

In the absence of a history suggesting a specific cause (Box 12.4), it is not necessary to investigate every person with constipation. Most respond to dietary fibre supplementation and the judicious use of laxatives. Middle-aged or elderly patients with a short history or worrying symptoms (rectal bleeding, pain or weight loss) must be investigated promptly, by either barium enema or colonoscopy. Others should be investigated as follows:

• Initially, digital rectal examination, proctoscopy and sigmoidoscopy, routine biochemistry, including serum calcium and thyroid function, and an FBC should be carried out.

• If these are normal, a 1-mth trial of dietary fibre and/or laxatives is justified.

• If symptoms persist, then examination of the colon by barium enema or colonoscopy is indicated to look for structural disease.

ABDOMINAL PAIN

Abdominal pain may be:

• Visceral: usually midline, due to stretching or torsion of a viscus.

• Parietal: usually sharp, lateralised and localised, due to peritoneal irritation.

• Referred: e.g. gallbladder pain referred to the back or shoulder tip.

• Psychogenic: cultural, emotional and psychosocial factors influence the experience of pain. In some patients, no organic cause is found despite investigation.

THE ACUTE ABDOMEN

This accounts for ∼50% of all urgent admissions to general surgical units. It is a consequence of one or more pathological processes:

Inflammation (e.g. appendicitis, pancreatitis, diverticulitis): Diffuse pain develops gradually, over hours. If the parietal peritoneum is involved, pain becomes localised. Movement exacerbates it; rigidity and guarding occur.

Perforation (e.g. peptic ulcer, ovarian cyst, diverticular disease): Pain starts abruptly, is severe and leads to generalised peritonitis.

Obstruction (intestinal, biliary or ureteric): Pain is colicky, with spasms causing the patient to writhe around. If it does not disappear between spasms, this suggests complicating inflammation.

If there are signs of peritonitis (i.e. guarding and rebound tenderness with rigidity), adequate resuscitation is needed. In other circumstances further investigations are required:

• FBC may reveal leucocytosis.

• U&Es reveal dehydration.

• Serum amylase is raised in acute pancreatitis.

• Erect CXR reveals air under the diaphragm and an AXR reveals obstruction.

• USS may help if gallstones, ureteric colic or a soft tissue mass is suspected, and may also reveal free fluid or intra-abdominal abscess.

• Contrast studies, by either mouth or anus, are useful to evaluate obstruction, and essential to distinguish pseudo-obstruction from mechanical large bowel obstruction.

• CT is useful for pancreatitis, retroperitoneal collections or masses, and aortic aneurysm.

• Angiography or multi-slice CT angiography is used in mesenteric ischaemia.

• Diagnostic laparoscopy may be advised if the cause remains obscure.

Management

Perforations are closed, inflammatory conditions are treated with antibiotics or resection, and obstructions are relieved. Most but not all patients require surgery. The speed of intervention and the need for surgery depend on several factors, particularly the presence or absence of peritonitis.

Acute appendicitis: Although conservative treatment can be successful, the risk of perforation or recurrence is high, so surgery is advisable.

Small bowel obstruction: If the suspected cause is adhesions from previous surgery, only patients who do not settle within 48 hrs with i.v. fluids, fasting and nasogastric aspiration, or who develop signs of strangulation (colicky pain becoming constant, peritonitis, tachycardia, fever, leucocytosis) will require surgery.

Large bowel obstruction: Pseudo-obstruction is treated non-operatively. Some patients benefit from colonoscopic decompression, but mechanical obstruction merits surgery. Differentiation between the two is by a water-soluble contrast enema.

Acute cholecystitis: See page 521.

Acute diverticulitis: See page 473.

Perforated peptic ulcer: See page 442.

CHRONIC OR RECURRENT ABDOMINAL PAIN

A detailed history, including associated symptoms, is essential. If abdominal and rectal examination is normal, a careful search should be made for disease affecting other structures, particularly the vertebral column, spinal cord, lungs and cardiovascular system.

The choice of investigations depends on the history and examination (Box 12.5). Persistent symptoms require exclusion of colonic or small bowel disease. A history of psychiatric disturbance, repeated negative investigations or vague symptoms not fitting any particular disease or organ pattern may point to a psychological origin.

12.5 INVESTIGATION OF CHRONIC OR RECURRENT ABDOMINAL PAIN

Symptom	Probable diagnosis	Investigation
Epigastric pain; dyspepsia; relationship to food	Gastroduodenal or biliary disease	Endoscopy and USS
Altered bowel habit; rectal bleeding; features of obstruction	Colonic disease	Barium enema and sigmoidoscopy/colonoscopy
Pain provoked by food in widespread atherosclerosis	Mesenteric ischaemia	Mesenteric angiography
Upper abdominal pain radiating to the back; history of alcohol misuse; weight loss; diarrhoea	Chronic pancreatitis or pancreatic cancer	USS, CT and pancreatic function tests
Recurrent loin or flank pain with urinary symptoms	Renal or ureteric stones	USS and i.v. urography

CONSTANT ABDOMINAL PAIN

Patients with constant abdominal pain usually have features to suggest the underlying diagnosis, e.g. malignancy, chronic pancreatitis or intra-abdominal abscess. Occasionally no cause will be found, leading to the diagnosis of ‘chronic functional abdominal pain’. In these patients a psychological cause is highly likely and treatment is aimed at symptom control, psychological support and minimising disease impact.

DISORDERS OF NUTRITION

MALNUTRITION

STARVATION AND FAMINE

There remain regions of the world, particularly in Africa, where the prevalence of BMI <18.5 in adults remains as high as 20%. In adults, the predominant form of protein–energy malnutrition is undernutrition, i.e. a sustained negative energy (calorie) balance.

Decreased energy intake: Causes include:

• Persistent regurgitation or vomiting.

• Malabsorption (e.g. small intestinal disease).

• Maldigestion (e.g. pancreatic exocrine insufficiency).

Increased energy expenditure: Causes include:

• Increased basal metabolic rate (BMR) (thyrotoxicosis, trauma, fever, cancer cachexia).

• Excessive physical activity (e.g. marathon runners).

• Energy loss (e.g. glycosuria in diabetes).

• Impaired energy storage (e.g. Addison’s disease, phaeochromocytoma).

Clinical features

The severity of malnutrition can be assessed by measurements of BMI, mid-arm circumference and skinfold thickness. The clinical features of severe undernutrition in adults include:

• Loss of weight.

• Thirst, weakness, feeling cold, nocturia, amenorrhoea, impotence.

• Lax, pale, dry skin.

• Hair thinning or loss.

• Cold, cyanosed extremities, pressure sores.

• Muscle-wasting.

• Loss of subcutaneous fat.

• Oedema (even without hypoalbuminaemia).

• Subnormal body temperature, slow pulse, low BP.

• Distended abdomen, with diarrhoea.

• Diminished tendon jerks.

• Apathy, loss of initiative, depression, introversion, aggression if food is nearby.

• Susceptibility to infections.

Undernutrition often leads to vitamin deficiencies, especially of thiamine, folate and vitamin C. Diarrhoea leads to sodium, potassium and magnesium depletion. The high mortality is often due to infections, e.g. typhus or cholera, but the usual signs may not appear. In advanced starvation, patients become completely inactive and may assume a flexed, fetal position; death comes quietly and often quite suddenly.

Management

Patients should be graded according to BMI. Those with moderate starvation need extra feeding, while those who are severely underweight need hospital care. In severe starvation there is atrophy of the intestinal epithelium and the exocrine pancreas.

• Small amounts of food should be given at first; it should be palatable and similar to the usual staple meal, e.g. cereal with some sugar, milk powder and oil.

• Salt should be restricted and micronutrient supplements may be essential (e.g. potassium, magnesium, zinc and multivitamins).

• Between 6.3 and 8.4 MJ/day (1500–2000 kcal/day) will prevent deterioration, but additional calories are required for regain of weight. During refeeding, a gain of 5% body weight per month indicates satisfactory progress.

• Other measures are supportive, and include care for the skin, adequate hydration, treatment of infections, and careful monitoring of body temperature since thermoregulation may be impaired.

MALNUTRITION IN HOSPITAL

One-third of hospital patients in the UK (particularly the elderly) are affected by moderate or severe malnutrition on admission. Once in hospital, many lose weight due to poor appetite, concurrent illness and being kept ‘nil by mouth’ for investigations. Malnutrition leads to impaired immunity and muscle weakness, and to increased morbidity, mortality and length of stay.

Nutritional support of the hospital patient

Normal diet: Inadequate intake may be due to unpalatability of food, cultural and religious factors restricting diet, or simple problems such as difficulty with hand dexterity (arthritis, stroke) or immobility in bed. Patients at risk of malnutrition should have food intake charted.

Dietary supplements: If a patient is unable to achieve sufficient nutritional intake from normal diet alone, then liquid dietary supplements with high energy and protein content should be used.

Enteral tube feeding: Patients who cannot swallow may require artificial nutritional support. The enteral route should be used if possible, as this preserves the integrity of the mucosal barrier, prevents bacteraemia and, in intensive care patients, reduces the risk of multi-organ failure.

• For short-term support, liquid feeds are given by fine-bore nasogastric tube. Tube position should be checked prior to use; gastric aspirate has a pH <4. A CXR can confirm tube position if in doubt.

• A nasojejunal tube can be placed in cases of gastric stasis or outlet obstruction.

• For long-term enteral feeding, a percutaneous endoscopic gastrostomy (PEG) is more comfortable and less likely to become displaced. However, inserting a gastrostomy is an invasive procedure and complications include local infection (30%) and perforation of intra-abdominal organs.

Parenteral nutrition: IV feeding is expensive, carries higher risks of complications and should only be used when enteral feeding is impossible. Less than 1wk of parenteral feeding confers little benefit. There are a number of possible routes:

• Peripheral venous cannula: this can only be used for low osmolality solutions due to the risk of thrombophlebitis.

• Peripherally inserted central catheter (PICC): a 60cm cannula is inserted into a vein in the antecubital fossa. The distal end lies in a central vein, allowing hyperosmolar solutions to be used.

• Central line: a single-lumen subclavian catheter in the internal jugular vein is preferred, due to lower infection rates. Hyperosmolar solutions can be used. The main energy source in total parenteral nutrition (TPN) is provided by carbohydrate, usually as glucose. TPN also contains amino acids, lipid emulsion, electrolytes, trace elements and vitamins, mixed as a large bag in a sterile environment. Constituents are adjusted according to the results of regular blood monitoring. Fever indicates a likely line infection.

Refeeding syndrome

When nutritional support is given to a malnourished patient, anabolic hormones are released. Insulin causes cellular uptake of phosphate, potassium and magnesium. Falling levels can lead to serious consequences, such as cardiac arrhythmias. Electrolyte levels should be corrected before refeeding is commenced. Wernicke’s encephalopathy may be precipitated by refeeding with carbohydrates in thiamine deficiency. This can be countered by giving thiamine before feeding.

ANOREXIA NERVOSA

Anorexia nervosa is a well-defined eating disorder, although a much higher prevalence of abnormal eating behaviour in the population does not meet the diagnostic criteria. There is marked weight loss, arising from food avoidance, in combination with bingeing, purging, excessive exercise, or the use of diuretics and laxatives. Despite their emaciation, patients feel overweight due to body image disturbance. Downy hair (lanugo) develops on the back, forearms and cheeks. Extreme starvation is associated with a range of pathophysiological changes, such as cardiac arrhythmias (prolonged QT and ventricular tachycardia), anaemia and osteoporosis. The condition usually emerges in adolescence, and 90% of cases are female.

Diagnostic criteria are:

• Loss of at least 15% of total body weight.

• Avoidance of high-calorie foods.

• Distortion of body image.

• Amenorrhoea for at least 3 mths.

Differential diagnosis includes:

• Depression.

• Inflammatory bowel disease.

• Malabsorption.

• Hypopituitarism.

OBESITY

Obesity is a pandemic with potentially disastrous consequences for health. More than 20% of adults in the UK and more than 30% in USA are obese. The prevalence of obesity is increasing.

The pandemic reflects changes in both energy intake and expenditure. The estimated average global daily supply of food energy per person increased from ∼2350kcal in the 1960s to ∼2800kcal in the 1990s. Portion sizes, particularly of sugary drinks and high-fat snacks, have increased. Corresponding changes in energy expenditure are important; obesity is correlated positively with hours spent watching television, and inversely with physical activity.

Although obese people were ridiculed in the past when they bemoaned their inability to control their weight, it is likely that susceptibility does vary between individuals. Twin studies confirm a genetic pattern of inheritance, suggesting a polygenic disorder. In a few cases, specific causal factors can be identified, such as hypothyroidism, Cushing’s syndrome or insulinoma. Drugs implicated include: tricyclic antidepressants, sulphonylureas, sodium valproate and β-blockers.

Clinical features and investigations

Obesity can be quantified using the body mass index (BMI = weight in kilograms divided by the height in metres squared (kg/m²)):

• Normal 18.5–25.

• Overweight 25–30.

A dietary history may be helpful in guiding dietary advice, but is susceptible to under-reporting of consumption. Alcohol consumption is an important source of energy intake.

• All obese patients should have thyroid function tests performed, and an overnight dexamethasone suppression test or 24-hr urine free cortisol if Cushing’s syndrome is suspected.

• Assessment of other cardiovascular risk factors is important.

• BP should be measured, and type 2 diabetes and dyslipidaemia detected by measuring blood glucose and serum lipids.

• Elevated transaminases suggest non-alcoholic fatty liver disease.

Management

The health risks of obesity are largely reversible. Interventions which reduce weight in studies in obese patients have also been shown to ameliorate cardiovascular risk factors. Lifestyle advice which lowers body weight and increases physical exercise reduces the incidence of type 2 diabetes.

Most patients seeking assistance will have attempted weight loss previously, sometimes repeatedly. An empathetic explanation of energy balance, recognising that some individuals are more susceptible to obesity, is important. Appropriate weight loss goals (e.g. 10% of body weight) should be agreed.

Lifestyle advice: All patients should be advised to maximise their physical activity by incorporating it into the daily routine (e.g. walking rather than driving to work). Changes in eating behaviour (including portion size control, avoidance of snacking, regular meals to encourage satiety, and use of artificial sweeteners) should be discussed.

Weight loss diets: In overweight people, the lifestyle advice given above may gradually succeed. In obese patients, more active intervention is usually required. Weight loss diets require a reduction in daily total energy intake of ∼2.5MJ (600kcal) from the patient’s normal consumption. The goal is to lose ∼0.5kg/week. Patient compliance is the major determinant of success. In some patients more rapid weight loss is required, e.g. in preparation for surgery. There is no role for starvation diets, which carry a risk of sudden death from heart disease. Very low calorie diets produce weight loss of 1.5–2.5kg/week, but require the supervision of a physician and nutritionist.

Drugs: Drug therapy is usually reserved for obese patients with a high risk of complications. Patients who continue to take anti-obesity drugs tend to regain weight with time. This has led to the recommendation that anti-obesity drugs are used short-term to maximise the weight loss in patients who are demonstrating their adherence to a low calorie diet by current weight loss.

• Orlistat: inhibits pancreatic and gastric lipases, reducing dietary fat absorption by ∼30%. Side-effects relate to the resultant fat malabsorption: namely, loose stools, oily spotting, faecal urgency, flatus and malabsorption of fat-soluble vitamins.

• Sibutramine: reduces food intake by blocking re-uptake of both noradrenaline and 5-HT in the CNS. Side-effects include dry mouth, constipation, insomnia, tachycardia and hypertension. It is therefore a second choice after orlistat and cannot be used in those with hypertension or cardiovascular disease.

Surgery: Surgery to reduce the size of the stomach is the most effective long-term treatment for obesity. It should be contemplated in patients with a very high risk of developing the complications of obesity, in whom dietary and drug therapy has been ineffective. The mechanism of weight loss may not relate to limiting the stomach capacity per se, but rather in disrupting the release of ghrelin from the stomach, which signals hunger in the hypothalamus. Mortality is low in experienced centres but post-operative complications are common.

DISEASES OF THE MOUTH AND SALIVARY GLANDS

Aphthous ulceration: Common, superficial, painful and idiopathic. In severe cases other causes, such as infection, drug reaction or Behçet’s syndrome, must be considered. Topical triamcinolone in Orabase or choline salicylate gel can aid healing.

Squamous carcinoma of the oral cavity: Common world-wide and increasing in the UK. Mortality is ∼50%, largely as a result of late diagnosis. Poor diet, alcohol excess, smoking or tobacco chewing, or chewing areca nuts wrapped in betel leaves (‘betel nuts’) are the main risk factors. Suspicious lesions should be biopsied if treatment for local trauma or infection fails to produce improvement after 2 wks. Treatment is by resection, radiotherapy or both.

Vincent’s angina: Deep, sloughing gum ulcers, caused by invasion of the mucous membranes by organisms such as Borrelia vincentii. Poor oral hygiene, malnutrition, debility and AIDS predispose. Symptoms include halitosis and fever, and treatment with hydrogen peroxide mouthwashes and broad-spectrum antibiotics is indicated.

Candida albicans: A normal mouth commensal which proliferates to cause thrush in babies, patients receiving corticosteroids, antibiotic or cytotoxic therapy, people with diabetes and the immunosuppressed. White patches are seen on the tongue and buccal mucosa. Dysphagia suggests pharyngeal and oesophageal candidiasis. A clinical diagnosis is sufficient to instigate therapy, using nystatin or amphotericin suspensions or lozenges.

Parotitis: Due to viral or bacterial infection. Mumps causes a self-limiting acute parotitis. Bacterial parotitis usually occurs as a complication of major surgery and can be avoided by good post-operative care. Broad-spectrum antibiotics are required, whilst surgical drainage is necessary if abscesses are present.

DISEASES OF THE OESOPHAGUS

GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)

Gastro-oesophageal reflux resulting in heartburn affects ∼30% of the general population.

GORD develops when the oesophageal mucosa is exposed to gastric contents for prolonged periods, resulting in symptoms and, in a proportion of cases, oesophagitis. Reflux may occur if there is reduced oesophageal sphincter tone or frequent inappropriate sphincter relaxation. Herniation of the stomach through the diaphragm (hiatus hernia) occurs in 30% of the population >50 and is often asymptomatic. It causes reflux because of loss of the oblique angle between the cardia and oesophagus. Almost all patients who develop oesophagitis, Barrett’s oesophagus or peptic strictures have a hiatus hernia. Defective oesophageal peristaltic activity is common in patients with oesophagitis, and persists after oesophagitis has been healed by acid-suppressing drugs.

Gastric acid is the most important oesophageal irritant and there is a close relationship between acid exposure time and symptoms. Gastric emptying is delayed in patients with GORD. Increased intra-abdominal pressure due to pregnancy and obesity may contribute. Weight loss may improve symptoms. Dietary fat, chocolate, alcohol and coffee relax the lower oesophageal sphincter and may provoke symptoms.

Complications

Oesophagitis: Features a range of endoscopic findings, from mild redness to severe, bleeding ulceration with stricture formation, with a poor correlation between symptoms and appearances. A normal endoscopy and normal histology do not exclude significant reflux disease.

Barrett’s oesophagus (‘columnar lined oesophagus’, CLO): A premalignant condition in which the squamous lining of the lower oesophagus is replaced by columnar mucosa with areas of metaplasia. It occurs in response to chronic reflux and is seen in 10% of endoscopies for reflux. The true prevalence may be up to 20 times greater, as it is often asymptomatic or first discovered when the patient develops oesophageal cancer. CLO carries a lifetime risk of oesophageal adenocarcinoma of ∼10%. The absolute risk is low and >95% of patients with CLO die of causes other than oesophageal cancer. Prevalence is increasing, especially in white men aged >50. It is weakly associated with smoking but not alcohol. Duodenogastro-oesophageal reflux, containing bile, pancreatic enzymes and pepsin in addition to acid, may be important.

Diagnosis requires multiple biopsies to detect intestinal metaplasia and/or dysplasia.

Neither acid suppression nor antireflux surgery stops progression of CLO, and treatment is only indicated for symptoms of reflux or complications such as stricture. Endoscopic ablation or photodynamic therapy can induce regression but islands of glandular mucosa remain and cancer risk is not eliminated. Regular endoscopic surveillance is controversial; it can detect dysplasia and early malignancy but, because most CLO is undetected until cancer develops, will not reduce overall oesophageal cancer mortality.

Oesophagectomy is widely recommended for those with high-grade dysplasia (HGD), as the resected specimen harbours cancer in up to 40%. Close follow-up with biopsies every 3 mths is an alternative for those with HGD.

Iron deficiency anaemia: Occurs as a consequence of chronic blood loss from oesophagitis. Many such patients have bleeding from erosions in a hiatus hernia. Nevertheless, hiatus hernia is very common and other causes of blood loss, particularly colorectal cancer, must be considered even when endoscopy reveals oesophagitis and a hiatus hernia.

Benign oesophageal stricture: Develops as a consequence of longstanding oesophagitis, usually in elderly patients presenting with dysphagia for solids. A history of heartburn is common but not invariable in the elderly. Diagnosis is by endoscopy, when biopsies can be taken to exclude malignancy. Endoscopic balloon dilatation or bouginage is helpful, followed by long-term therapy with a PPI to reduce the risk of recurrence. Dentition should be checked and the patient advised to chew food thoroughly.

Gastric volvulus: Occasionally a massive intrathoracic hiatus hernia twists upon itself (gastric volvulus), causing complete obstruction, severe chest pain, vomiting and dysphagia. The diagnosis is made by CXR and barium swallow. Most resolve spontaneously but recur and surgery is usually advised.

Investigations

Young patients with typical symptoms of GORD can be treated empirically without investigation.

Endoscopy: Advisable if patients present in middle or old age, if symptoms are atypical or if complications are suspected. A normal endoscopy in a patient with typical symptoms should not preclude treatment for reflux.

24-hr pH monitoring: If the diagnosis is unclear after endoscopy or if surgery is considered. Intraluminal pH and symptoms are recorded during normal activities. A pH of <4 for more than 6–7% of the study is diagnostic of reflux.

OTHER CAUSES OF OESOPHAGITIS

Infection: Oesophageal candidiasis is mentioned above (p. 431).

Corrosives: Suicide attempt by bleach or acid causes painful burns of the mouth and pharynx and erosive oesophagitis. Complications include perforation, mediastinitis and stricture. Early treatment is conservative (analgesia and nutritional support); vomiting and endoscopy are avoided to prevent perforation. Later, endoscopic dilatation of strictures is usually necessary, although hazardous.

Drugs: Potassium supplements and NSAIDs may cause oesophageal ulcers if tablets are trapped above a stricture. Bisphosphonates cause oesophageal ulceration and should be used with caution in patients with oesophageal disorders.

MOTILITY DISORDERS

PHARYNGEAL POUCH

Incoordination of swallowing leads to herniation of a pouch through the cricopharyngeus muscle. Most patients are elderly and asymptomatic, but regurgitation, halitosis and dysphagia can occur. A barium swallow demonstrates the pouch and may show pulmonary aspiration. Endoscopy may perforate the pouch. Surgical resection is indicated in symptomatic patients.

ACHALASIA OF THE OESOPHAGUS

Achalasia is characterised by a hypertonic lower oesophageal sphincter which fails to relax during swallowing and failure of propagated oesophageal contraction, with progressive dilatation. The cause is unknown, although failure of the local nerve supply is implicated. Chagas disease (infestation with Trypanosoma cruzi) is endemic in South America and causes an indistinguishable clinical syndrome (p. 112).

Clinical features and investigations

Achalasia is rare, affecting 1 : 100 000 people. It usually develops slowly in middle age with intermittent dysphagia for solids, which is eased by drinking, standing and moving around. Heartburn is absent, but some patients experience severe chest pain due to oesophageal spasm. As dysphagia progresses, nocturnal pulmonary aspiration develops. Achalasia predisposes to squamous carcinoma of the oesophagus.

• CXR shows widening of the mediastinum and features of aspiration.

• Barium swallow (Fig. 12.2) shows tapered narrowing of the lower oesophagus and a dilated, aperistaltic and food-filled oesophageal body.

• Endoscopy is essential to rule out carcinoma.

• Manometry confirms the non-relaxing lower oesophageal sphincter and poor contractility of the oesophageal body.

Fig. 12.2 Achalasia. X-ray showing a dilated, barium-filled oesophagus (O) with fluid level and distal tapering, and a closed lower oesophageal sphincter (LOS). (D = diaphragm).

Management

Endoscopic dilatation: Dilatation of the oesophageal sphincter using a fluoroscopically positioned balloon improves symptoms in 80% of patients. Some require repeat dilatation but frequent recurrence is best treated surgically. Endoscopic injection of botulinum toxin into the sphincter induces remission, but relapse is common.

Surgical myotomy: Performed either as an open operation or laparoscopically, this is extremely effective. Both dilatation and myotomy may be complicated by gastro-oesophageal reflux, and for this reason myotomy is often augmented by an anti-reflux procedure and a PPI is given.

OTHER OESOPHAGEAL MOTILITY DISORDERS

Oesophageal spasm or abnormally forceful peristaltic activity: May lead to episodic chest pain mimicking angina. Oral or sublingual nitrates or nifedipine may relieve attacks of pain.

Systemic sclerosis: The oesophageal muscle is replaced by fibrous tissue, leading to heartburn, dysphagia, oesophagitis and benign strictures. Such patients require long-term therapy with PPIs. Dermatomyositis, rheumatoid arthritis and myasthenia gravis may also cause dysphagia.

Rings of submucosal fibrosis at the oesophago-gastric junction: Cause intermittent dysphagia, often in middle age.

Post-cricoid web: A rare complication of iron deficiency anaemia, which may predispose to squamous carcinoma. Benign strictures are treated by endoscopic balloon dilatation.

TUMOURS OF THE OESOPHAGUS

CARCINOMA OF THE OESOPHAGUS

Almost all are adenocarcinoma or squamous cancers. Small-cell cancer is a rare third type.

Squamous cancer: Rare in the West (approx. 4 : 100 000) but common in Iran, parts of Africa and China (200 : 100 000). Squamous cancer can arise anywhere in the oesophagus but almost all tumours above the lower third of the oesophagus are squamous.

Adenocarcinoma: Arises in the lower third of the oesophagus from Barrett’s oesophagus or from the cardia of the stomach. Incidence is increasing in the UK (approx. 5 : 100 000).

Management and prognosis

Approximately 70% of patients have extensive disease at presentation. In these, treatment is palliative and based upon relief of dysphagia and pain. Endoscopic laser ablation or stenting may improve swallowing, while palliative radiotherapy may shrink both squamous cancers and adenocarcinomas.

Despite treatment, the 5-yr survival of patients with oesophageal cancer is 6–9%. Tumours which have breached the oesophageal wall and involve lymph nodes (T3, N1) have a 5-yr survival of ∼10% after surgery. This figure improves significantly for less extensive disease. Five-yr survival following ‘potentially curative’ surgery (all visible tumour removed) is 30%, and may be improved further by pre-operative chemotherapy. Although squamous carcinomas are radiosensitive, radiotherapy alone is associated with a 5-yr survival of only 5%.

PERFORATION OF THE OESOPHAGUS

The most common cause is endoscopic perforation complicating dilatation or intubation. A perforated peptic stricture is usually managed conservatively using broad-spectrum antibiotics and parenteral nutrition; most heal within days. Malignant, caustic and radiotherapy stricture perforations require surgery.

Spontaneous oesophageal perforation results from forceful vomiting. Patients present with severe chest pain, shock, subcutaneous emphysema, pleural effusions and pneumothorax. The diagnosis is made using a water-soluble contrast swallow. Treatment is surgical and mortality is high.

DISEASES OF THE STOMACH AND DUODENUM

GASTRITIS

Acute gastritis: Most commonly results from alcohol, aspirin or NSAID ingestion. It is often asymptomatic and self-limiting, but may cause dyspepsia, anorexia, nausea, vomiting, haematemesis or melaena. In persistent cases, endoscopy is necessary to exclude peptic ulcer or cancer. Treatment involves avoiding the cause; symptomatic therapy with antacids, and acid suppression using PPIs or antiemetics may also be necessary.

Chronic gastritis: The most common cause of chronic gastritis is H. pylori infection. Correlation between symptoms and endoscopic and pathological findings is poor. Most patients are asymptomatic and do not require treatment but patients with dyspepsia may benefit from H. pylori eradication.

Autoimmune chronic gastritis: Usually asymptomatic and results from autoimmune activity against parietal cells in the body of the stomach. Circulating parietal cell and intrinsic factor antibodies may be present. In some patients gastric atrophy leads to loss of intrinsic factor secretion and pernicious anaemia. Other autoimmune conditions, particularly thyroid disease, may be present. There is a fourfold increase in gastric cancer.

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Tags: Davidsons Essentials of Medicine

Apr 3, 2017 | Posted by admin in GENERAL & FAMILY MEDICINE | Comments Off

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