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The Acute Abdomen 123
• An erect chest X-ray may show air under the diaphragm with a perforated viscus, but its absence does not exclude perforation. Plain abdominal X-ray shows dilated loops of bowel and fluid levels in obstruction. Ultrasound examination is useful in the diagnosis of acute cholecystitis, cholangitis, appendicitis and gynaecological conditions such as ruptured ovarian cyst and ectopic pregnancy. Spiral CT scan is the most accurate modality in the investigation of the acute abdomen but is usually reserved for patients with inconclusive or negative ultrasound results.
• Surgical intervention with a laparoscopy or laparotomy may be necessary depending on the diagnosis.

Acute appendicitis

Acute appendicitis occurs when the lumen of the appendix becomes obstructed by a faecolith.
Epidemiology
It affects all age groups but is rare in the very young and very old.
Clinical features
The typical clinical presentation is the onset of central abdominal pain which then becomes localized to the right iliac fossa (RIF), accompanied by anorexia and sometimes vomiting and diarrhoea. The patient is pyrexial, with tender­ness and guarding in the RIF due to localized peritonitis. There may be a tender mass in the presence of an appendix abscess.
Investigations
The white cell count, C-reactive protein and ESR are raised, but these are not specific. Ultrasonography may show an inflamed appendix and can also show an appendix mass. CT is highly sensitive and specific, and has reduced removal of histologically normal appendices by 90%.
Differential diagnosis
Non-specific mesenteric lymphadenitis, terminal ileitis due to Crohn’s dis­ease or Yersinia infection, acute salpingitis in women, inflamed Meckel’s diverticulum and functional bowel disease can all mimic acute appendicitis.
Management
The treatment is surgical, with removal of the appendix either by open sur­gery or laparoscopically. An appendix mass is treated conservatively initially with intravenous fluids and antibiotics and later appendicectomy.
Complications
Complications may arise from gangrene and perforation, leading to localized abscess formation or generalized peritonitis.
124 Gastroenterology and nutrition

Acute peritonitis

Localized peritonitis occurs with all acute inflammatory conditions
of the gastrointestinal tract, and management depends on the underlying condition, e.g. acute appendicitis, acute cholecystitis.
Generalized peritonitis occurs as a result of rupture of an abdominal
viscus, e.g. perforated duodenal ulcer, perforated appendix. There is a sudden onset of abdominal pain which rapidly becomes generalized. The patient is shocked and lies still, as movement exacerbates the pain. A plain abdominal X-ray may show air under the diaphragm; serum amylase must be checked to exclude acute pancreatitis.

Intestinal obstruction

Intestinal obstruction is either mechanical or functional.
Mechanical (see Table 3.17) The bowel above the level of the obstruction is
dilated, with increased secretion of fluid into the lumen. The patient complains of colicky abdominal pain, associated with vomiting (occurs earlier with small bowel than large bowel obstruction) and absolute constipation (occurs earlier with large bowel than small bowel obstruction). On examination there is distension and ‘tinkling’ bowel sounds. Small bowel obstruction may settle with conservative management (i.e. nasogastric suction and intravenous fluids to maintain hydration). Large bowel obstruction is treated surgically.
Functional This occurs with a paralytic ileus, which is often seen in
the post-operative stage of peritonitis or of major abdominal surgery, or in association with opiate treatment (acute colonic pseudo-obstruction, Ogilvie’s syndrome). It also occurs when the nerves or muscles of the intestine are damaged, causing intestinal pseudo-obstruction. Unlike mechanical obstruction, pain is often not present and bowel sounds may be decreased. Gas is seen throughout the bowel on a plain abdominal X-ray. Management is conservative.

THE PERITONEUM

The peritoneal cavity is a closed sac lined by mesothelium. It contains a little fluid to allow the abdominal contents to move freely. Conditions which affect the peritoneum include:
• Infective (peritonitis)
• Secondary to gut disease, e.g. appendicitis, perforation
• Chronic peritoneal dialysis
• Spontaneous (associated with cirrhotic ascites)
• Tuberculous
• Neoplasia
• Secondary deposits, e.g. from ovary
• Primary mesothelioma
• Vasculitis: connective tissue disease.
Nutrition 125
Table 3.18 Protein, energy and water requirement of normal and hypercatabolic adults
Metabolic state Nutritional
Protein (g/kg)
Nitrogen (g/kg)
Energy (kcal/kg)
Water (mL/kg)
requirements Normal
1
0.17
25–30
30–35
Hypercatabolic
2–3
0.3–0.45
35–50
30–35

NUTRITION

Dietary requirements

Food is necessary to provide the body with energy. The average daily require­ment (Table 3.18) of a 55-year-old female in the UK is 8100 kJ (1940 kcal), and a 55-year-old man is 10 600 kJ (2550 kcal). This is at present made up of about 50% carbohydrate, 35% fat, 15% protein ± 5% alcohol. In developing countries, however, carbohydrate may be >75% of the total energy input, and fat <15% of the total energy input. Energy requirements increase during periods of rapid growth, such as adolescence, pregnancy and lactation and with sepsis.
Body weight is maintained at a ‘set point’ by a precise balance of energy intake and total energy expenditure (the sum of the resting or basal metabolic rate, physical activity, and the thermic effect of food eaten). Weight gain is almost always due solely to an increase in energy intake which exceeds total energy expenditure. Occasionally weight gain is due to a decrease in energy expenditure, e.g. hypothyroidism, or fluid retention, e.g. heart failure or ascites. On the other hand, weight loss associated with cancer and chronic diseases is due to a reduction in energy intake secondary to a loss of appetite (anorexia). In a few conditions, such as sepsis and severe trauma, there is an increase in energy requirements (hypercatabolic or hypermetabolic) which will result in a negative energy balance if there is no compensatory increase in energy intake.
A balanced diet also requires sufficient amounts of minerals and vitamins. In the developed world vitamin deficiency is rare except in specific groups, e.g. alcohol dependent and patients with small bowel disease, and patients with liver and biliary tract disease, who are susceptible to deficiency of the fat-soluble vitamins (A, D, E, K). Deficiencies of the B vitamins riboflavin and biotin are rare in all patient groups. Dietary deficiency of vitamin B6 (pyridoxine, pyridoxal and pyridoxamine) is also extremely rare, but drugs
126 Gastroenterology and nutrition
(e.g. isoniazid and penicillamine) that interact with pyridoxal phosphate may cause deficiency and a polyneuropathy.

NUTRITIONAL SUPPORT

Patients should be screened for nutritional status on admission to hospital and during their stay:
• Patients should be asked about recent weight loss, their usual weight and whether they have been eating less than usual.
• Their weight and height should be recorded and body mass index (BMI) calculated (weight [kg]/height [m]2). The acceptable range of BMI is 20–25 kg/m2 for men and 19–24 kg/m2 for women.
Nutritional supplementation is required in those patients who cannot eat, should not eat, will not eat or cannot eat enough. It is necessary to provide nutritional support for:
• All severely malnourished patients (indicated by a BMI less than 15 kg/m2)
on admission to hospital
• Moderately malnourished patients (BMI 15–19 kg/m2) who, because of
their physical illness, are not expected to eat for 3–5 days
• Normally nourished patients not expected to eat for 7–10 days.
Enteral nutrition is cheaper, more physiological and has fewer complications than parenteral (intravenous) nutrition, and should be used if the gastrointestinal tract is functioning normally. With both enteral and parenteral nutrition a complete feeding regimen consisting of fat, carbohydrates, protein, vitamins, minerals and trace elements can provide the nutritional requirements of the individual (see Table 3.18). Ideally a multidisciplinary nutrition support team should supervise the provision of artificial nutritional support.

Enteral nutrition

Foods can be given by:
• Mouth
• Fine-bore nasogastric tube for short-term enteral nutrition
• Percutaneous endoscopic gastrostomy (PEG): this is useful for patients
who need feeding for longer than 2 weeks
• Percutaneous jejunostomy where a tube is inserted directly into the
jejunum either endoscopically or at laparotomy.
A polymeric diet with whole protein, carbohydrate and fat is usually used; an elemental diet composed of amino acids, glucose and fatty acids may be used for patients with CD.

Total parenteral nutrition (TPN)

Parenteral nutrition may be administered via a feeding catheter placed in a peripheral vein or a silicone catheter placed in the subclavian vein.
Nutritional Support 127
Table 3.19 Complications of total parenteral nutrition
Catheter related: sepsis, thrombosis, embolism and pneumothorax Metabolic, e.g. hyperglycaemia, hypercalcaemia Electrolyte disturbances Liver dysfunction
Central catheters must only be placed by experienced clinicians under strict aseptic conditions in a sterile environment. These catheters should only be used for feeding purposes, and not the administration of drugs or blood to reduce the risk of introducing infection. Complications of TPN are given in Table 3.19.

Monitoring of artificial nutrition

Patients receiving nutritional support should be weighed twice weekly, and they require regular clinical examination to check for fluid overload or deple­tion. Patients receiving nutritional support in hospital initially require daily measurements of urea and electrolytes and blood glucose. More frequent measurement of blood glucose is indicated in patients beginning TPN. Liver biochemistry, calcium and phosphate are measured twice weekly. Serum magnesium, zinc and nitrogen balance (see below) are measured weekly. The frequency of biochemical monitoring is adjusted according to the patient’s clinical and metabolic status.
It is necessary to give 40–50 g of protein per 24 hours to maintain nitrogen balance, which represents the balance between protein breakdown and synthesis. The aim of any regimen is to achieve a positive nitrogen balance, which can usually be obtained by giving 3–5 g of nitrogen in excess of output. The amount of protein required to maintain nitrogen balance in a particular individual can be calculated from the amount of urinary nitrogen loss, using the formula:
N2 loss (g/24 h) = Urinary urea (mmol/24 h) × 0.028 + 2
Urinary nitrogen × 6.25 = grams of protein required
(most proteins contain about 16% nitrogen)
Most patients require about 12 g of nitrogen per 24 hours, but hypercatabolic patients require about 15 g/day.

Refeeding syndrome

The refeeding syndrome occurs within the first few days of refeeding by the oral, enteral or parenteral route. It is underrecognized and can be fatal. It involves a shift from the use of fat as an energy source during starvation
128 Gastroenterology and nutrition
to the use of carbohydrate as an energy source during refeeding. With the introduction of artificial nutrition and carbohydrate by any source, insulin release is augmented and there is rapid intracellular passage of phosphate, magnesium and potassium resulting in hypophosphataemia, hypomagnesae­mia, and hypokalaemia. Phosphate is an integral part of cellular machinery. Deficiency results in widespread organ dysfunction (muscle weakness, rhabdomyolysis, cardiac failure, immune suppression, haemolytic anaemia, thrombocytopenia, coma, hallucinations, fits). Thiamine deficiency can be precipitated. Patients at risk of refeeding are underweight (e.g. anorexia nervosa, alcohol-dependent syndrome) or those with recent rapid weight loss (5% within preceding month), including patients after treatment for morbid obesity. These at-risk patients should receive high-dose vitamin B and C, e.g. Pabrinex® beginning before feeding, and begin feeding at 25%–50% of estimated calorie requirements, increasing by 100 calories per day. Serum phosphate, magnesium, calcium, potassium, urea and creatinine, body weight and evidence of fluid overload should be checked daily for the first week, and electrolyte deficiencies corrected as necessary.

DISORDERS OF BODY WEIGHT

Obesity

Obesity, defined as an excess of body fat contributing to comorbidity, is an increasingly common problem in developed and developing countries. It is defined as a BMI of 30 kg/m2 or greater. Overweight is defined as a BMI of 25–30 kg/m2 and may be associated with a mildly increased risk of complica­tions that have been identified in obese patients. In almost all obese individuals weight gain is a result of increased energy intake and energy expenditure is normal or indeed increased. In a few conditions, e.g. hypothyroidism, weight gain is due at least in part to reduced energy expenditure. Obese patients are at risk of a premature death, mainly from diabetes, ischaemic heart disease, and cerebrovascular disease. Obesity is also associated with an increased risk of hypertension, hyperlipidaemia, obstructive sleep apnoea, osteoarthritis of the knees and hips, fatty liver disease, gallstones and an increased cancer risk. Weight reduction can be achieved with a reduction in calorie intake and an increase in physical activity, although this is often difficult to achieve. A 10% loss of body weight (i.e. 10 kg in a 100 kg person) is associated with a fall in blood pressure and a reduced risk of diabetes and overall mortality. Drug treatment such as orlistat, an inhibitor of pancreatic lipase and hence fat digestion, may be used in the severely obese patient. Bariatric surgery is increasingly performed in patients with morbid obesity (BMI >40 kg/m2) or patients with a BMI >35 kg/m2 and obesity-related complications, after con­ventional medical treatment has failed. The techniques used are restrictive, such as gastric banding (which restricts the ability to eat) or intestinal bypass (which reduces the ability to absorb nutrients) or a combination (Roux-en-Y).
Therapeutics 129

Anorexia nervosa

Anorexia nervosa is a psychological illness, predominantly affecting young females and characterized by marked weight loss (BMI <17.5 kg/m2), intense fear of gaining weight, a distorted body image and amenorrhoea. Patients with anorexia nervosa control their body weight by a process of semi-starva­tion and/or self-induced vomiting (bulimia) and may develop consequences of undernutrition. Treatment is complex and should be undertaken in a specialist eating disorders unit.

THERAPEUTICS

Drugs for dyspepsia and peptic ulceration

Antacids
Mechanism of action
Main effect is to neutralize gastric acid. Alginate-containing antacids (e.g. Gaviscon®, Mucogel®) form a ‘raft’ that floats on the surface of the stomach contents to reduce reflux and protect the gastro-oesophageal mucosa.
Indications
Symptomatic relief in dyspepsia, gastro-oesophageal reflux and peptic ulcer­ation. Healing of peptic ulcers is much less than with antisecretory drugs (see below) and antacids should not be used for this indication.
Side effects
Magnesium-containing antacids tend to be laxative, whereas aluminium­containing antacids may be constipating; antacids containing both aluminium and magnesium may reduce these colonic side effects.
Cautions/contraindications
Antacids may interfere with the absorption of other drugs and in general other drugs should be given at least 1 hour before or after each dose of antacid. The sodium content of some preparations, e.g. magnesium trisilicate mixture (6.3 mmol/10 mL) and Gaviscon® Advance (4.6 mmol/10 mL; 2.25 mmol/ tablet) should be taken into account in patients on a ‘no added’ salt diet (cardiac, renal or hepatic disease). Aluminium hydroxide is contraindicated in hypophosphataemia. Constipating antacids (i.e. those containing aluminium) should be avoided in liver disease.
H2-receptor antagonists
Mechanism of action
Reduce gastric acid secretion as a result of histamine H2-receptor blockade (e.g. ranitidine, cimetidine).
130 Gastroenterology and nutrition
Indications
GORD, healing of benign gastric and duodenal ulcers, prevention of gas­troduodenal damage in patients requiring intensive care, prevention of NSAID-induced DUs, and in high doses prevention of GUs. However, for all indications, PPIs are more effective and more commonly used in clinical practice.
Side effects
Diarrhoea, altered liver biochemistry, headache, dizziness, rash. Rarely, other side effects (see National Formulary).
Cautions/contraindications
Cimetidine retards oxidative hepatic drug metabolism by binding to micro­somal cytochrome P450. It should be avoided in patients stabilized on warfarin, phenytoin and theophylline (or aminophylline) but other interactions (see National Formulary) may be of less clinical relevance.
Proton pump inhibitors
Mechanism of action
Inhibit gastric acid secretion by blocking the hydrogen/potassium–adenosine triphosphate enzyme system (the ‘proton pump’) of the gastric parietal cell. Examples include omeprazole, esomeprazole, lansoprazole.
Indications
GORD; healing of peptic ulcers; prevention of NSAID-induced peptic ulcers; in combination with antibacterials for eradication of H. pylori; intravenously and after endoscopic therapy to reduce re-bleeding rates in patients with bleeding peptic ulcers; inhibition of gastric acid in pathological hypersecretory conditions, e.g. gastrinoma; prevention of peptic ulcers in critically ill patients; prophylaxis of acid aspiration during general anaesthesia; dyspepsia.
Side effects
Gastrointestinal disturbance (diarrhoea, nausea, vomiting), liver dysfunction, hypersensitivity reactions, headache, skin reactions, increased risk of gastrointestinal infections (due to reduced gastric acidity). Rarely, acute kidney injury, deficiency of vitamin B12, calcium (leading to hip fracture) and magnesium due to reduced intestinal absorption.
Cautions/contraindications
Omeprazole and esomeprazole competitively inhibit the CYP2C19 isoenzyme (which metabolises clopidogrel to its active metabolite) and may reduce the ability of clopidogrel to inhibit platelet aggregation. Omeprazole may decrease the effect of warfarin, phenytoin and diazepam. Lansoprazole may increase
Therapeutics 131
the effect of warfarin, phenytoin and theophylline. Reduce dose in severe liver disease. Proton pump inhibitors are also associated with an increased risk of C. difficile infection as a result of altered pH of intestinal flora and therefore should be discontinued if any concern about C. difficile infection.

Constipation

Treatment of constipation is initially with lifestyle changes and drugs are reserved for use as second-line treatment. It may be necessary to use a com­bination of two different types of laxative, e.g. stimulant plus faecal softener. All laxatives are contraindicated in intestinal obstruction or perforation, para­lytic ileus, and severe inflammatory conditions of the gut such as CD and UC.
Bulk-forming laxatives
Mechanism of action
Agents such as ispaghula husk act to absorb water and increase faecal mass, which stimulates peristalsis.
Indications
Treatment of slow-transit constipation and bulking of stool in patients with a colostomy, diverticular disease and irritable bowel syndrome.
Preparations and dose
Unprocessed wheat bran is one of the most effective fibre laxatives, and patients can add it to meals, e.g. cereal (2–6 tablespoons per day).
Side effects
Flatulence, abdominal distension.
Cautions/contraindications
Maintain adequate fluid intake to prevent faecal impaction; contraindications (see above).
Stimulant laxatives
Mechanism of action
Stimulant laxatives (e.g. bisacodyl, senna, glycerin suppositories) act to increase colonic motor activity.
Indications
Short-term treatment of constipation.
Side effects
Abdominal cramps, diarrhoea and hypokalaemia.
132 Gastroenterology and nutrition
Cautions/contraindications
Contraindications (see above).
Osmotic laxatives
Mechanism of action
Osmotic laxatives (e.g. lactulose, macrogols [polyethylene glycol], phosphate enema) attract or retain water in the intestinal lumen, leading to softer stools and improved propulsion.
Indications
Treatment of constipation. Lactulose is used in the treatment of hepatic encephalopathy. Phosphate enemas are used to evacuate the bowel before radiological procedures, flexible sigmoidoscopy and surgery.
Side effects
Abdominal distension, colic, nausea, local irritation after phosphate enema.
Cautions/contraindications
Contraindications (see above). May also cause electrolyte disturbance. Use with caution in hepatic and renal impairment. Although magnesium ions are absorbed poorly, similar to all osmotic ions some absorption does occur, which can cause problems in patients with abnormal renal function.
Bowel-cleansing solutions
Indications
Bowel cleansing solutions (e.g. Fleet Phospho-soda®, Klean-Prep®, Moviprep®, Picolax®) are used before colonic surgery, colonoscopy or radiological examina­tion to ensure the bowel is free of solid contents. They are not treatments for constipation. Bowel-cleansing agents are coupled with a low residue diet for at least 3 days before the procedure, copious intake of water or other clear fluids and cessation of all solid foods on the day before the procedure. All are contra­indicated in bowel obstruction, perforated bowel or severe colitis and Moviprep® is contraindicated in glucose-6-phosphate dehydrogenase deficiency.
Side effects
Nausea, vomiting, abdominal cramps. Occasionally dehydration and hypoten­sion, electrolyte disturbance.

Diarrhoea

Most cases of acute diarrhoea are infective and will settle without treatment. Oral rehydration salts (Dioralyte®), 1 sachet after every loose motion, are often used especially in the elderly and children. Antidiarrhoeal agents (e.g. loper­amide) relieve symptoms of acute diarrhoea but are not recommended routinely.