Chapter 12
Gastroenterology
The ageing gastrointestinal system
HOW TO . . . Manage weight loss in older patients
HOW TO . . . Insert a fine-bore NG feeding tube
The ethics of clinically assisted feeding
HOW TO . . . Investigate and manage persistent unexplained nausea and vomiting
HOW TO . . . Approach an older patient with abnormal liver function tests
HOW TO . . . Image the older colon
HOW TO . . . Investigate and manage chronic diarrhoea
The ageing gastrointestinal system
Teeth
• Change colour—yellow and less translucent
• Become worn (enamel does not regenerate)
• ↓ vascularity and sensitivity of dentine and pulp
• Caries, periodontitis, and tooth loss are common, but not inevitable in older patients. Being ‘long in the tooth’ refers to gum retraction seen with periodontal disease which ↑ with poor oral hygiene and xerostomia, both common in older people
Mouth
• Mucosa—thinner and more friable, rarely a functional problem
• Salivary glands do not produce less saliva, but causes of xerostomia (see 
‘Xerostomia’, p. 353) are more frequent with ↑ age
• Bone resorption occurs in the mandible alongside osteoporosis. This is accelerated with periodontitis and progresses fast once teeth are lost, leading to a change in facial appearance
• Orofacial muscle tone can diminish with consequent dribbling
Taste
Olfactory function, and hence taste discrimination, ↓ gradually with normal ageing, but an acute change or complete absence of taste should prompt investigations for a cranial tumour.
Oesophagus
• Slight changes in innervation produce clinically insignificant changes in swallow and peristalsis
• The misnamed presbyoesophagus (see ‘Oesophageal motility disorders’, p. 361) is a disorder of oesophageal motility, not a universal age change
• Hiatus hernias and reflux are very common—probably related to anatomical and postural changes
Stomach
• ↑ incidence of atrophic gastritis (with reduced acid production), but in the absence of disease, most older patients maintain normal pH levels
• Reduction in gastric emptying is common
• ↑ mucosal susceptibility to damage
• ↑ Helicobacter pylori carriage, but this is less likely to cause ulceration
Small intestine
• Function well preserved, except for calcium absorption which is ↓
• ↑ incidence of bacterial overgrowth with malnutrition and diarrhoea
Large intestine
• ↓ rectal sensation contributes to high incidence of constipation
Pancreas
• Structural changes including atrophy, but function is well preserved
Liver
• Hepatic weight and volume ↓ by around 25% and there is brown (lipofuscin) pigment build-up, but liver function (and therefore LFTs) is not affected
• Some older patients have a slightly low bilirubin and albumin level, but results still remain within the normal range
Gall bladder
• Incidence of gallstones ↑ (40% ♀ >80), probably related to reduced rate of synthesis and excretion of bile
• Most gallstones are asymptomatic
The elderly mouth
Mouth examination
Use gloves. Be systematic. Important and often not done—serious pathology may be missed. Check:
• Parotid glands (enlarged in parotitis, alcoholism, chronic lymphoid leukaemia)
• Temporomandibular joint (arthritis causes crepitus, subluxation, pain). Dislocation can cause pain and inability to close the mouth
• Soft tissues: tongue and floor of the mouth most common site for oral cancer in smokers/alcoholics. Angular stomatitis
• Salivation: (see ‘Xerostomia’, p. 353)
• Teeth: how many missing, how many restorations, pain/sensitivities. Caries is ↑ by poor brushing and low fluoride exposure, diet of soft sweet foods, xerostomia, poor fitting dentures, and infrequent dentist visits
• Dentures: cleanliness, integrity, and fit
General management
• Nursing help with dental/mouthcare is vital for anyone unable to help themselves
• Referral to a dentist. Dental check-ups should continue every 6 months, regardless of age/disability. This is very difficult to arrange for inpatients, but maxillofacial surgeons (who are also trained as dentists) will sometimes help out in severe/urgent cases
• Consider chlorhexidine mouthwash for patients with poor oral self-care, e.g. stroke, dementia
• Severe periodontal disease may require antibiotics (topical or systemic) and surgical debridement to arrest progress
• Poor oral and dental health contributes to poor appetite and malnutrition—consider nutritional support (see ‘Nutrition’, pp. 354–355)
Facial pain
Consider trigeminal neuralgia, TA, parotitis, temporomandibular joint arthritis, dental caries/abscess, aphthous mouth ulcers, or the idiopathic benign ‘burning mouth syndrome’.
Sore tongue
Can be a side effect of drugs, glossitis (B12, iron, or folate deficiency), candida/thrush, especially after antibiotics or in diabetes. A black tongue may be due to Aspergillus colonization and is treated with nystatin lozenges/mouth rinse.
Parotitis
Acute bacterial parotitis is not uncommon in frail older patients who are not eating. Low salivary flow (dehydration and not eating) and poor oral hygiene predispose to parotid gland infection with mouth flora (staphylococci and anaerobes). Treat with aggressive rehydration, iv flucloxacillin, and chlorhexidine mouth rinses. Response to treatment is usually dramatic—if not, consider abscess formation or MRSA.
Xerostomia
Perception of dry mouth is closely related to salivary flow. Saliva is needed for:
• Taste: dissolves food to present to taste buds
• Swallow: helps form food bolus
• Protection of teeth and mucosa: contains antibacterials, buffers, and mucin. Rapid tooth decay is a risk of xerostomia
Xerostomia is not a normal ageing change and should always be investigated. Causes include:
• Drugs with anticholinergic side effects (e.g. tricyclic antidepressants, levodopa)
• Sjögren’s syndrome (an autoimmune destruction of salivary glands) can be 1° or associated with other autoimmune conditions
• Irradiation, salivary stones, tumours, sialadenitis (viral or bacterial infections)
Treatment depends on cause—stop or ↓ causative drugs, stimulate saliva with grapefruit juice/sugar-free sweets or mints, and promote frequent careful mouthcare. Artificial saliva can provide symptomatic relief for some patients.
Oral candidiasis
May manifest as oral thrush (with removable white plaques on an erythematous base), angular stomatitis (sore cracks in the corner of the mouth), or rarely atrophic forms (e.g. under dentures, may not have creamy plaque). Consider and reverse risk factors such as antibiotics, steroids, hyperglycaemia, and immunosuppression, where possible. Use nystatin 1mL qds, rinsed around the mouth for several minutes. In cases with painful swallowing/dysphagia (i.e. might have oesophageal involvement) and those that cannot comply with rinses, use oral fluconazole 50–100mg od for 7–14 days. Dentures should be kept out where possible and soaked in chlorhexidine during treatment.
Mouth ulcers
Simple aphthous ulcers and ulcers due to poorly fitting dentures should be treated with topical anti-inflammatories (salicylate gel or triamcinolone), hydrocortisone lozenges, or steroids. Ulcers can occur as part of a systemic disease such as inflammatory bowel disease. Any oral lesion persisting >3 weeks merits referral and/or biopsy to exclude cancer, but most mouth cancers are painless.
Oral manifestation of systemic diseases/drugs
A very long list of manifestations, including common and general (e.g. oral candidiasis in immunosuppression), as well as rare and specific (e.g. oral lichen planus). Remember that many drugs also affect the mouth, e.g. xerostomia (see ‘Xerostomia’, p. 353), tardive dyskinesia with antipsychotics, and gum hypertrophy with phenytoin.
Systemic manifestation of dental diseases
Poor oral hygiene with dental or periodontal disease can cause septicaemia or infective endocarditis. Poor teeth can contribute to poor nutrition.
Nutrition
With normal ageing, there are:
• Reduced calorie requirements due to reduced activity and lower resting metabolic rate (↓ muscle mass)
• Reductions in appetite (anorexia of ageing)
• Lower reserves of macro- and micronutrients (vitamins and minerals)
In the presence of disease, older patients quickly become malnourished, which is a powerful predictor of outcome (↑ functional dependency, morbidity, mortality, and use of health-care resources).
Malnutrition is extremely common in the older, frail or institutionalized population, and studies have shown that once in hospital, most patients’ nutritional status actually declines further. Protein–energy undernutrition affects:
• 15% of community-dwelling older patients
• 5–12% of housebound patients with multiple chronic problems
• 35–65% of patients acutely admitted to hospital
• 25–60% of institutionalized older persons
Nutritional assessment
• BMI (weight in kg/(height in m)2) is often impractical, as height cannot be accurately measured in immobile patients or those with abnormal posture (although approximations can be made, e.g. using ulnar length)
• Simple weight is still useful, especially if the patient knows their usual weight—rapid weight loss (>4kg in 6 months) is always worrying, even in obese patients. Mid-arm circumference can be used to approximate
• Nutrition screening tools are often employed by nursing staff to target interventions. The MUST score (see Appendix, ‘Malnutrition universal screening tool (MUST)’, p. 709) is widely used in UK hospitals and is sensitive for detection of protein–energy undernutrition in hospitalized patients
• More complex tools (e.g. Mini Nutritional Assessment) are helpful, but time-consuming, and are rarely used outside research
• Biochemical measures (e.g. hypoalbuminaemia, anaemia, hypocholesterolaemia) develop at a late stage and are confounded by acute illness
Nutritional support
• Identification is key to allow targeted intervention (improves outcome)
• The cause is usually multifactorial and a holistic approach is needed, e.g. medical (immobile, unwell, reflux, constipation, etc.), social (poverty, isolation), psychological (depression, dementia), and age-related (altered hunger recognition)
• Involve a dietician early (especially if anorexia is prominent)
• Record food intake carefully—this highlights deficiencies in intake and helps identify where interventions might help
• Make mealtimes a priority (protected mealtimes) and provide assistance with feeding (care assistants or family)
• Schemes such as using a red tray can highlight those in need of assistance
• Establish food preferences and offer tempting, high-calorie foods (e.g. substitute full-fat milk and yogurt if they are on the lower-fat variety)
• Prescribe dietary supplements according to patient preference (e.g. milky or fruit drinks, soups, puddings, or high-calorie shots)
• Appetite stimulants, e.g. prednisolone, can ↑ weight, but side effects usually outweigh benefits
• Consider the role of enteral feeding
HOW TO . . . Manage weight loss in older patients
Peak body mass is reached at age 40–50, and weight loss can occur after this due to ↓ lean mass, although the proportion of fat is relatively ↑, so overall weight is often remarkably stable.
As a rule of thumb, unintentional weight loss of >2.3kg (5lb)/5% of body weight in a month or 4.5kg (10lb)/10% body weight in 6 months is worrying.
Always try to get recorded weight (rather than relying on patient/carer memory)—a search of old outpatient clinic and 1° care records can help. Record weight regularly while you investigate to look for ongoing trends.
Dramatic weight loss should always prompt a search for remediable pathology. The cause is often multifactorial. It is important to consider:
• Chronic infection/disease, e.g. COPD, heart failure, TB
• Inflammatory conditions, e.g. GCA
• Malabsorption (see ‘Diarrhoea in older patients’, p. 374)
• Mesenteric ischaemia (recurrent postprandial abdominal pain)
• Drug causes, e.g. digoxin, theophyllines, cholinesterase inhibitors
• Metabolic disorders, e.g. hyperthyroidism, uraemia
• Persistent nausea or abdominal pain/reflux
• Social causes, e.g. inability to cook, poverty, social isolation, alcoholism
A careful history (including dietary history and mental state with collateral history where possible), examination, and routine screening tests (see ‘Investigations’, pp. 64–65) will usually give clues of significant underlying pathology. If preliminary investigations are negative, a ‘watch and re-weigh and wait’ plan is reasonable—be reassured if weight is actually stable or rising; re-examine and re-screen if further loss occurs.
Obviously if a remediable cause is found and treated, then weight loss may be halted or reversed. Where no such cause is found, or where it is not reversible, interventions are still possible.
Enteral feeding
Consider enteral feeding early if there is dysphagia (e.g. stroke, MND, Parkinson’s disease) or failure of oral feeding (e.g. severe anorexia syndromes, intensive care unit) with an intact gastrointestinal tract.
There are three common methods:
• Fine-bore NGTs: simple, quick, and inexpensive. The preferred method for short-term feeding. Some patients (usually confused/drowsy) repeatedly pull out NGTs. Interference with the tube ↑ the risk of aspiration. Persistence, supervision, and careful taping can sometimes help, but often a PEG or RIG is required (also described here). There is ↑ experience using NGTs which are held in place via a nasal loop (Bridle™). Trained practitioners can insert these by the bedside, and removal by the patient is very rare
• PEG: the risks of insertion include perforation, bleeding, and infection for a patient who is usually already frail. The patient has to be fit to undergo sedation. Problems obtaining consent from a competent patient and ‘agreement’ from the next of kin for an incompetent one are not uncommon. Once established, this method is discreet and better tolerated than NGTs and is the method of choice for medium/long-term enteral feeding
• RIG: useful if gastroscopy technically difficult (e.g. pharyngeal pouch) and sometimes if small bowel feeding preferred over gastric feeding. Similar complication rate to PEG
Complications for all methods include
• Aspiration pneumonia: there is a common misconception that enteral feeding eliminates aspiration in dysphagic patients. This is not true—reflux of food into the oesophagus is common and this, along with salivary secretions and covert oral intake, may still be aspirated. Always check the position of the tube if the patient becomes unwell, feverish, or breathless. If aspiration is ongoing despite correct tube position, slow the feed, feed the patient sitting upright (i.e. not at night), and add pro-motility drugs, e.g. metoclopramide or erythromycin (pre-meals). A nasojejunal tube or jejunal extension to a PEG tube can also reduce aspiration rates (see ‘Aspiration pneumonia/pneumonitis’, p. 332)
• Re-feeding syndrome: occurs when the patient has been malnourished for a long time. When feeding commences, insulin levels cause minerals (especially phosphorus) to move rapidly into the intracellular space and fluid retention occurs causing hypophosphataemia, hypomagnesaemia, and hypokalaemia. This, in turn, can cause life-threatening heart failure, respiratory failure, arrhythmias, seizures, and coma. Avoid by ‘starting low and going slow’ when introducing feed. It is important to check and correct any abnormal biochemistry before feeding starts and then monitor frequently (check urea and electrolytes, calcium, magnesium, phosphate, and glucose daily for a few days, then weekly). Supplementation of minerals may be done iv or by adding extra to NG feed
• Fluid overload and heart failure: ↓ volume and add diuretics
• Diarrhoea: exclude infection (especially Clostridium difficile). Try slowing the feed rate or changing the feed to one containing more or less fibre
Parenteral feeding
Should be considered when the gut is not functioning. It requires large venous access and should only be undertaken when supervised by an experienced nutrition team. It is usually a temporary measure, e.g. post-gastrointestinal surgery. Complications such as fluid overload, electrolyte disturbance, and iv catheter sepsis are common in older patients.
HOW TO . . . Insert a fine-bore NG feeding tube
This task is often performed by nursing staff who may be very experienced. Doctors are often asked to help when insertion is proving difficult.
1. Get the patient’s consent—if they refuse, come back later. They may well have just had several uncomfortable failed attempts. It is rarely appropriate to perform against the wishes of the patient
2. Have the patient sitting upright with the chin tucked forward (patients often hyperextend their neck which makes it harder). Draw the curtains (this can be an unpleasant procedure to have done or to watch)
3. Leave the guide wire in the tube and lubricate with lots of jelly
4. Feed the tube down one nostril about 20cm (until it hits the back of the throat). In stroke, start with the inattentive side, as it may be better tolerated
5. If there is a proximal obstruction, try the other nostril
6. If possible, ask the patient to swallow and advance the wire
7. Check the back of the throat carefully—you should be able to see a single wire going vertically down. Start again if there is a loop
8. Secure the tube yourself immediately with tape to both the nose and cheek
Once you believe the tube is in place, you need to check it is in the stomach by one or both of the following methods BEFORE you use the tube.
• Aspiration of gastric contents that are clearly acidic (pH <5)
• CXR is used if there is no aspirate or the pH is equivocal. If you leave the guide wire in, the tube shows more easily. The tip of the tube should be clearly below the diaphragm
The method of blowing air down the tube and listening for bubbles has now been discredited, as a bubbling sound can be generated due to saliva and pulmonary secretions.
The ethics of clinically assisted feeding
Feeding is a highly emotive issue. It is seen by many (especially relatives) as a basic need, and hence failing to provide adequate nutrition is seen as a form of neglect or even euthanasia. In contrast, others feel that artificial enteral feeding is a cruel and futile treatment performed on incompetent patients that only postpones a ‘natural’ death that involves anorexia or dysphagia.
The use of the term ‘clinically assisted nutrition and hydration’ has been suggested by the General Medical Council (UK) to replace the term ‘artificial nutrition and hydration’ underlining the fact that this is a form of treatment.
There are numerous high-profile legal cases regarding feeding (usually withdrawal of), and controversial cases that cannot be resolved locally should always be referred to the courts via the local legal team.
► The key to steering a course through this minefield is communication.
Initiating treatment
• Establish if the patient is competent—even dysphasic patients may understand a little with non-verbal cues, etc.
• If the patient has capacity (see ‘Capacity’, pp. 654–655), ensure they understand the chosen method (and its risks) and projected duration of feeding. Patients with dysphagia must realize that they will be expected to dramatically ↓, or stop, oral feeding
• For patients who lack capacity, ensure you have communicated with all interested carers, family, and the GP. There is sometimes disagreement between interested parties, and these are best detected and ‘thrashed out’ early. A case conference is often helpful
• Establish that everyone accepts the indications for feeding and the aims of treatment, and set a date for review, e.g.:
• 2 weeks of NG feeding in a patient with dysphagia following a stroke, which is hoped will resolve
• PEG insertion in a patient with MND and malnutrition with recurrent aspiration pneumonia, to be reviewed if the patient requests or if enters the terminal phase of the disease
• Do not be afraid of a therapeutic trial (e.g. if you do not know whether the patient’s lethargy/drowsiness/depression is related to malnutrition). Always ensure everyone understands and agrees on review dates and criteria for reassessment. Patients/relatives can be reassured that PEG tubes can be removed if improvement occurs
• Record discussions and plan carefully in the medical records
• If there is still dispute, get a second opinion. As a last resort, legal advice may be needed
Withdrawing treatment
► Withholding treatment is not morally different to withdrawing it.
There are, however, technical and emotional differences, which is why many more ethical problems arise when withdrawing and why some doctors are resistant to trials of treatment.
Artificial feeding can be withdrawn because:
• It is no longer required (rarely controversial)
• A therapeutic trial has failed (see ‘Initiating treatment’, pp. 358–359; this is sometimes controversial)
• Although feeding is successful, the patient’s quality of life is felt to be unacceptable (nearly always controversial)
• A patient with a long-term feed is dying from another condition (sometimes controversial)
When considering withdrawal of long-term feeding for stable conditions (e.g. persistent vegetative state), decisions should be referred to the courts.
Accepting aspiration risk
There is also a group of patients who have dysphagia, weight loss, and recurrent aspiration due to progressive neurological conditions such as dementia, who merit special consideration.
It is not always appropriate to aggressively manage such patients, who are frequently incompetent and derive pleasure from eating normally. It may be appropriate to allow the patient to eat, accepting that there is a risk of aspiration. ‘Feeding at risk’ protocols are becoming more common to document the process and improve interface communication.
Adopting such a palliative policy is impossible, unless everyone, including the whole MDT and relatives, understand and sympathize with the aims of management.
Further reading
General Medical Council. Guidance. 
http://www.gmc-uk.org.
Royal College of Physicians of London (2010). Oral Feeding Difficulties and Dilemmas. London: Royal College of Physicians of London.
Oesophageal disease
Gastro-oesophageal reflux disease
• The symptoms (retrosternal burning, acid regurgitation, belching, atypical chest pain) correlate poorly with the pathology (normal mucosa to severe oesophagitis)
• Sinister features which might suggest malignancy include sudden or recent onset, dysphagia, vomiting, weight loss, and anaemia. They should guide management:
• In the absence of sinister features, a 4-week trial of treatment is given
• If there are sinister features, then a gastroscopy should be arranged
• Oesophageal pH monitoring is rarely necessary
Treatment
Check if the patient is taking prescribed or over-the-counter NSAIDs, steroids, or bisphosphonates, and stop or minimize the dose. PPIs have revolutionalized treatment, making antacids and H2 blockers, such as ranitidine, almost redundant. They are very effective (for symptoms and healing) and generally safe. They are used for prophylaxis with aspirin in high-risk/symptomatic patients—often at lower dose, as well as treatment, and some are licensed for intermittent symptomatic use. Some are available over the counter. Rarely elderly patients can have side effects of diarrhoea or confusion (see ‘Proton pump inhibitors’, p. 144).
Barrett’s/columnar-lined oesophagus
Gastric mucosa replaces the oesophageal squamous cell mucosa. It is associated with an ↑ risk of malignancy and should have endoscopic surveillance based on Prague Criteria, regardless of symptoms.
Hiatus hernia
• Very common in older patients, occurring to a degree in almost all
• Laxity of structures at the gastro-oesophageal junction allows the oesophago-gastric junction or portions of the stomach to move up (permanently or intermittently) into the thorax
• May be asymptomatic but often presents with GORD symptoms and occasionally with dysphagia
• Very large intrathoracic hernias can impair respiratory function and strangulate/perforate
• Diagnosis on CXR (stomach or fluid level behind the heart), at endoscopy, or on contrast radiology
Treatment
To reduce reflux, suggest: lose weight; avoid alcohol and caffeine; eat small meals often; avoid eating before bed; and sleep propped up on pillows or elevate the head of the bed on blocks. PPIs will nearly always relieve symptoms; consider investigations if they do not. Prokinetic agents, e.g. metoclopramide, sometimes help. Younger patients with intractable problems can be assessed for surgery—laparoscopic surgery now available.
Achalasia
• An idiopathic neurological degeneration causing impaired peristalsis and a lack of lower oesophageal sphincter relaxation, causing a functional obstruction
• Dysphagia for solids and/or liquids is the most frequent presenting complaint
• Onset is insidious and slowly progressive
• CXR may reveal a dilated oesophagus
• Endoscopy is usually performed to exclude malignancy but may be normal
• Barium swallow has characteristic abnormalities (dilated oesophagus terminating in a beak-like narrowing)
• Manometry is the gold standard for diagnosis
• Treatment is aimed at facilitating lower oesophageal sphincter relaxation and can include drugs (calcium channel blockers or nitrates), botulinum toxin injection, endoscopic dilation of the sphincter, or surgical myotomy
Oesophageal motility disorders
• Group of disorders where oesophageal motility is significantly different from normal (excluding achalasia, which is a distinct pathological entity)
• Incorporates those patients previously described as having presbyoesophagus (motility abnormalities ascribed to age, probably incorrectly)
• Presenting features include heartburn, chest pain, and dysphagia
• Syndromes include diffuse oesophageal spasm, nutcracker oesophagus, and hypertensive lower oesophageal sphincter
• Motility disorders can also arise 2° to other diseases (e.g. diabetes, systemic sclerosis, chronic GORD)
• Diagnosis may be made with barium swallow, but manometry is the gold standard
• Treatment is difficult and depends on the condition/dominant symptoms. Try prokinetics or PPIs. Calcium channel blockers or tricyclic antidepressants can relieve chest discomfort. Botulinum toxin and endoscopic dilation are also occasionally used
Oesophageal candidiasis
• Can present with dysphagia or pain
• Consider in frail or immunosuppressed patients, especially if oral candidiasis is present
• Characteristic appearance on endoscopy (biopsy confirms) or barium swallow
• Treat with fluconazole for 2 weeks
Dysphagia
Dysphagia (difficulty in swallowing) is a common symptom in older patients.
History
• Ask what type of food is difficult (solids or liquids) and the level at which food sticks (mouth/throat, retrosternal, or epigastric)
• Distinguish dysphagia from early satiety and regurgitation (when successfully swallowed food returns after seconds/minutes), which usually occurs with gastric outlet obstruction or pharyngeal pouch
• If the swallow ‘tires’ through a meal, consider myasthenia
• Cough, wheeze, or recurrent aspiration pneumonia can be a presentation of swallowing problems which cause aspiration
Signs
Look for weight loss, oral thrush (may be associated with oesophageal candida), supraclavicular lymphadenopathy, and a gastric splash (implies gastric outlet obstruction). Watch the patient swallow some water and food—the diagnosis might be clear.
Causes
These can be divided into two:
• Structural lesions (worse with solids)
• Oesophageal or gastric cancer
• Benign strictures—scarring following, e.g. oesophagitis, scleroderma, polymyositis, radiotherapy
• Oesophageal candida or severe oesophagitis
• Hiatus hernia can produce obstruction symptoms
• External obstruction, e.g. bronchial tumour, aortic aneurysm, or cervical osteophyte
• Functional problems (often worse with fluids)
• Pharynx/throat—the most common neurological cause is stroke but can occur in advanced dementia and MND. Rarer neurological conditions include myasthenia gravis, inclusion body myositis, multiple sclerosis, and parkinsonian syndromes
• Oesophagus—dysmotility problems are relatively common in older patients and include achalasia and diffuse oesophageal spasm
Investigations
Gastroscopy is now the 1° investigation and is well tolerated, even in frail patients. Use a barium swallow first if there is felt to be a high risk of perforation with an endoscope (e.g. suspect pouch), but gastroscopy allows biopsy and therapy, e.g. dilation. Videofluoroscopy provides functional imaging and is useful diagnostically, but the correlation between observed aspiration and clinically significant problems is poor.
Treatment
• An empirical trial of PPI can be used in patients who are deemed unfit for investigation
• If oral thrush is present (suggesting oesophageal infection), try fluconazole for a week
• Oesophageal dilation ± stenting can be very successful for benign or malignant strictures
• For functional problems, always involve a speech therapist. Changing the consistency of food and fluids, and positioning the patient correctly can minimize problems
• Oesophageal dysmotility—try prokinetic/calcium channel blocker
• Gastroparesis causes early satiety and vomiting. It can be very hard to treat—try a prokinetic. Electrical gastric ‘pacing’ or surgery may provide relief (rarely used)
• Nutritional support—elderly patients with dysphagia are usually malnourished to start with and are then put nil by mouth for investigations. Refer to the dietician, and consider dietary supplements and early enteral feeding by NGT or PEG (see ‘Enteral feeding’, p. 356)
Aspiration pneumonitis (see ‘Aspiration pneumonia/pneumonitis’, p. 332) is largely a chemical, rather than infective, insult that may be complicated by infection. It is treated by:
• Preventing/minimizing aspiration (nil by mouth, NG feeding)
• Antibiotics are often given to prevent/treat superinfection
Peptic ulcer disease
This disease is becoming much rarer with the advent of effective medical treatment. It remains predominantly a disease of the elderly population. NSAID use is the most common cause, followed by H. pylori.
H. pylori is a spiral Gram-negative bacterium which colonizes the gastric mucosa causing gastritis. Carriage rates ↑ with age. Infection is usually asymptomatic but is the most common cause of dyspepsia in older patients. H. pylori is strongly associated with duodenal ulcers and may have a link with NSAID-associated ulceration.
Presentation
Acute bleeding, pain (epigastric, retrosternal, or back), indigestion, ‘heartburn’, dysphagia, anorexia, weight loss, perforation (peritonitis), iron deficiency anaemia, or an incidental finding (e.g. on endoscopy). Older patients may present non-specifically (‘off food’ or vague abdominal pains).
Investigations
• Upper GI endoscopy is very safe and well tolerated in older patients. It can often be performed using local anaesthesia in the throat only
• H. pylori can be detected with gastric biopsy and histology or with a test for urease activity (Clo test®). Serological tests remain positive, but titres gradually decline after eradication. Breath tests can detect H. pylori colonization but obviously do not demonstrate pathology
Treatment
Dietary restriction is unnecessary (worth specifically mentioning because older patients can remember harsh or bizarre anti-ulcer diets). Stop any NSAIDs. Stop aspirin if possible, and plan for safe reintroduction depending on risk/benefit of the individual patient. Where there is H. pylori and ulceration/gastritis, treat with one of the many ‘triple therapy’ antibiotic PPI regimens. In the absence of H. pylori, just a PPI will suffice. Arrange a repeat scope at 6 weeks to check healing of all gastric ulcers and malignant-looking duodenal ulcers.
For bleeding
• Effective resuscitation is lifesaving
• Early interventional endoscopy with adrenaline injection (or other modalities, e.g. heater probes or clips) into the bleeding point is suitable for almost all patients—do not delay because of age/comorbidity
• iv PPI reduces the risk of re-bleeding
• Continued bleeding/re-bleeding despite endoscopic treatment is an indication for surgical intervention or radiological embolization
• Scores using clinical, laboratory, and endoscopic features can stratify risk of re-bleeding (e.g. Rockall score)
For perforation
(see ‘The “acute surgical abdomen” ’, p. 378.)
Remember ‘silent’ perforation (without signs of peritonitis) is more common in the elderly population (especially if on steroids or diabetic). Mortality is high due to delayed diagnosis, reluctance to perform surgery, and post-operative complications.
HOW TO . . . Investigate and manage persistent unexplained nausea and vomiting
This group of patients can be very challenging, but you should actively manage them from an early stage because they are often very uncomfortable and bed-bound. There is frequently reversible disease and they are at high risk of dehydration/malnutrition and complications of immobility.
Nausea and vomiting can be the major presenting feature of illnesses as diverse as pneumonia, MI, intracerebral haemorrhage, Addison’s disease, UTI, and constipation.
• Start with a careful history (especially drug history)
• Thorough examination (including rectal examination and neurological assessment)
• Regular observations of vital signs (looking for intermittent pyrexia, arrhythmia, etc.)
• Screening blood tests (including calcium, thyroid function, CRP, iron studies, liver function, coeliac screen), urinalysis, CXR, and ECG
Drugs
Look very carefully at the drug history—almost any drug can cause nausea and vomiting, but digoxin (even with therapeutic serum levels), opiates, tramadol, antiparkinsonian drugs, antidepressants, NSAIDs, and PPIs are some of the common candidates. New drugs are the most likely, but remember poor compliance with drugs at home which are prescribed in hospital, e.g. co-codamol used occasionally at home may be written as 2 qds in hospital. If there is polypharmacy, try stopping the drugs one at a time, remembering that some drugs can take days to ‘wash out’.
Central causes
Raised intracerebral pressure can occasionally present this way. A CT scan is needed if there is drowsiness, focal neurology, or a past history of intraventricular blood (exclude hydrocephalus). If there is vertigo or tinnitus, consider labyrinthitis or posterior circulation stroke (see Table 21.1).
Gut causes
• Constipation is a very common cause of nausea
• Obstruction should be excluded with an abdominal X-ray (AXR). Consider repeating this if symptoms persist and you remain suspicious. Plain radiology will remain normal in high obstruction, and an oesophagogastroduodenoscopy (OGD) or small bowel follow-through may help
• Severe gastritis/peptic ulceration can present with nausea and vomiting without pain/bleeding
• Gastroparesis is most common in people with diabetes and is very hard to treat—try prokinetics
The liver and gall bladder
Cirrhosis
Chronic liver disease can present for the first time in older people. The presentation is often non-specific. The prognosis is worse than for a younger person with the same degree of liver damage. Common causes include alcohol, hepatitis C, autoimmune hepatitis, and non-alcoholic fatty liver. A proportion are cryptogenic (thought to be ‘burnt-out’ autoimmune hepatitis or non-alcoholic fatty liver disease).
• Hepatitis C may have been transmitted from blood products received before 1991 when screening was introduced. Alcohol consumption is known to ↑ the percentage of those infected with hepatitis C who develop cirrhosis
• Alcohol excess can present with falls, confusion, and heart failure at any age, but older patients are less likely to volunteer (or be asked) their alcohol history. ► Always enquire about alcohol
Investigations
If you suspect cirrhosis, should include: α-1 antitrypsin, autoimmune profile (ANA, smooth muscle antibody (SMA), liver–kidney microsome antibodies (LKM), antimitochondrial antibody, and immunoglobulins), ferritin and iron studies, caeruloplasmin, hepatitis B and C serology, and ultrasound including Doppler of the portal and hepatic vein.
Non-alcoholic fatty liver disease
Is not always a benign condition (half will be progressive and 15% develop cirrhosis; outlook worse with advancing age). Obesity, hyperlipidaemia, and type 2 diabetes are risk factors, so this condition is more common in older patients. If an ultrasound scan reveals fatty liver, advise about weight reduction and alcohol cessation.
Gallstones
• Very common (1:3 elderly ♀) and mostly asymptomatic, although troublesome symptoms often misdiagnosed as GORD or diverticulitis in older age groups
• Management largely as for younger patients, but the risks with endoscopic retrograde cholangiopancreatography (ERCP)/surgical intervention are higher, so conservative/less invasive approaches often adopted
• Acute cholecystitis in older patients may present atypically (e.g. without pain) and is not always associated with gallstones. It has a 10% mortality and should be aggressively treated with iv antibiotics and supportive care. Failure to improve should prompt early surgical review
HOW TO . . . Approach an older patient with abnormal liver function tests
This is not an uncommon finding, and investigation is as for younger patients. However, the following should be considered:
• Drug injury to the liver is common and may occur up to 6 months after exposure (e.g. statins, co-proxamol, penicillins, some over-the-counter medications)
• Liver metastases may present this way (more common in older patients)
• Deranged LFTs may occur as part of a systemic illness, e.g. sepsis (consider gall bladder/biliary infection if the LFTs are very abnormal), cardiac failure (with hepatic congestion), inflammatory conditions (PMR), ischaemic liver damage (after prolonged hypotension), Addison’s disease, and thyroid disease
• The picture is often mixed, with both cholestatic and hepatocellular components
A careful history should be taken, looking for duration of the problem and whether (if old) it has been previously investigated. If new, ask about possible drug or toxin exposure, associated symptoms (e.g. heart failure, sepsis, 1° malignancy), and alcohol use (do not make lifestyle assumptions—alcohol excess is under-recognized in older people).
Clarify that that abnormality is from the liver:
• An isolated elevated ALP is often from a bone source (commonly Paget’s disease), but do not assume this—liver metastases can present this way
• Isoenzymes can be measured, but clinical judgement is usually sufficient to guide investigation
• Muscle disorders can cause transaminase elevation
Persistent elevation should always prompt investigations:
• Bloods including electrolytes, clotting, TFTs, autoimmune screen (serum electrophoresis, ANA, antimitochondrial antibodies, SMA, and LMK), viral serology (hepatitis B and C), iron studies (haemochromatosis), caeruloplasmin (Wilson’s disease), coeliac disease screen, and α-1 antitrypsin
• Liver ultrasound—a good screening test that will usually identify liver metastases, as well as highlighting any biliary duct dilation prompting referral for ERCP
If the liver damage is progressive, or the diagnosis elusive, then refer to a hepatologist for consideration of liver biopsy.
Constipation
The term constipation is used in different ways, indicating one or more of the following:
• The time between bowel evacuations is longer than normal
• The stool is harder than normal
• The total faecal mass present within the abdomen is ↑
The most precise definition may be delayed alimentary tract transit time, but this is hard to measure and is delayed in age, in the institutionalized, and in those eating a Western diet.
There are said to be three types of constipation:
• Hard faeces present in the rectum (often in massive amounts)
• The whole distal large bowel loaded with soft, putty-like faeces that cannot be evacuated
• High (proximal) impaction which may be due to obstructing pathology (e.g. diverticular disease, carcinoma)
Diagnosis
The diagnosis is largely clinical (based on history and examination alone).
► Ask specifically, as some patients are embarrassed to trouble doctors with bowel symptoms.
Constipation may rarely be the 1° cause of delirium but commonly contributes to the presentation of frail older patients with other pathology such as sepsis or renal failure.
Rectal examination may be diagnostic, and sometimes the rectum will barely admit the examining finger. If the rectum is empty, consider high impaction. In a thin patient, high impaction is unlikely if the loaded colon cannot be felt during abdominal examination. In more obese subjects, a plain AXR will be necessary to confirm high impaction but is insensitive in the very obese.
► Do not exclude constipation as the cause of faecal incontinence until there has been an adequate therapeutic trial for high faecal impaction.
Causes
• Reduced motility of the bowel: drugs (e.g. opiates, iron, anticholinergics, antidepressants, antipsychotics, calcium channel blockers, calcium preparations), immobility, constitutional illness, electrolyte disturbances, dehydration, hypothyroidism, lack of dietary fibre, hypercalcaemia
• Failure to evacuate the bowels fully: any painful condition of the rectum or anus, difficulty in access to the toilet, lack of privacy, altered daily routine
• Neuromuscular: Parkinson’s disease, diabetic neuropathy pseudo-obstruction
• Mechanical obstruction of the bowel: carcinoma of the colon, diverticular disease
Prevention and treatment
Precipitating causes, such as dehydration, hypothyroidism, hypercalcaemia, and drugs, should be identified and reversed.
Non-pharmacological measures, including regular exercise, improving access to the toilet, adequate dietary fibre, and adequate hydration, are effective.
Laxatives should be used in combination with non-pharmacological measures. Unless there are reversible factors, always prescribe regular laxatives. Waiting for constipation to occur, then using ‘PRN’ doses is far less effective. You will need to titrate the laxative dose with time and changing patient circumstances.
There is little good evidence to guide the choice of laxative, and prescription varies with geography and personal choice. Here are some guiding principles:
• Stimulant laxatives, such as senna or bisacodyl, or stimulant suppositories may be appropriate for those with bulky, soft faecal overloading
• Avoid stimulant laxatives in patients with hard rocks of faeces, as this may produce abdominal pain. Use a stool softening (osmotic) laxative instead such as lactulose or a macrogol
• Long-term use of stimulant laxatives has been said to cause ‘bowel tolerance’/neuronal damage, leading to a dilated, atonic colon that required even more laxatives. There is very little evidence to support this, and stimulant laxatives are now considered safe, in moderate doses, for long-term use
• Sometimes stimulant and osmotic laxatives are used in combination, typically in severe constipation (e.g. opiate-induced) that has been unresponsive to a single drug
• Stool-bulking agents, such as methylcellulose or ispaghula, are useful in prophylaxis but are less effective in treating established constipation; both fibre and other bulking agents will ↑ stool volume and may ↑ problems
• Newer agents with novel mechanisms of action are available as third-line agents (e.g. prucalopride and lubiprostone)
• Costs of laxatives vary enormously, and there is no correlation between cost and patient acceptability. Try cheaper preparations first (fibre, senna)
Faecal retention severe enough to cause incontinence nearly always needs a determined effort to clear the colon (see ‘HOW TO . . . Treat “overflow” faecal incontinence’, p. 547).
Diverticular disease
Narrow-necked pockets of colonic mucosa which occur adjacent to blood vessel penetrations of the muscle bands, like ‘blowouts’ on a tyre. Occur anywhere in the large bowel, but most commonly in the sigmoid.
• Rare in <40 years, ↑ frequency with age and almost universal in >85 years
• Cause: thought to be raised intraluminal pressure due to low-fibre Western diet
• Investigation: colonoscopy/flexible sigmoidoscopy and barium enema are usually diagnostic and rule out other pathology. CT colonography (abdominal CT with oral contrast) is increasingly used as a better tolerated test in older patients
► The majority of cases are asymptomatic the majority of the time. On other occasions, innocent diverticulae are blamed for symptoms that arise from other pathology, e.g. constipation, irritable bowel disease, or gastroenteritis. The previous diagnosis of diverticular disease should not stop the careful evaluation of new bowel symptoms to exclude important diagnoses such as colitis or cancer.
Pain may occur and, especially if associated with constipation, can be improved by a high-fibre diet with or without extra stool-bulking drugs (e.g. ispaghula).
Complications
Diverticulitis
Should be thought of as ‘left-sided appendicitis’. Infection occurs within a pocket and may be due to a faecolith blocking the neck, so avoiding constipation is key to prevention. Abdominal pain and tenderness, diarrhoea, and vomiting occur with fever and raised inflammatory markers. Treat with antibiotics (include anaerobic cover)—mild cases oral antibiotics at home, severe cases may need admission for iv rehydration, antibiotics, and liaison with surgical services.
Haemorrhage
Selective angiography can be used to demonstrate bleeding point.
Diverticular abscess
Ultrasound or CT for diagnosis. Surgical or interventional radiographically guided drainage is required.
Perforation/peritonitis
see ‘The “acute surgical abdomen” ’, p. 378.
Fistula
Most commonly to the bladder, causing urinary infection and bubbles in the urine (pneumaturia). Cystoscopy or CT scan for diagnosis. Surgery is required, but simple defunctioning colostomy is often sufficient.
HOW TO . . . Image the older colon
This requires careful consideration of the risk and discomfort of a test, balanced against the quality of the information obtained. Discussing the pros and cons of each investigation with the patients and/or relatives will often help. It is useful to clarify that a patient is fit for bowel preparation on the request form, if relevant.
• Flexible sigmoidoscopy is safe and generally well tolerated, requiring only an enema in preparation, allowing direct visualization and biopsy of rectal and lower colonic pathology. Sedation is usually not needed
• Colonoscopy allows direct imaging and biopsy of more of the colon, and is the preferred method for general population investigation but carries an ↑ risk of bowel perforation in the over 75s. Full bowel clearance and sedation are required
• CT colonography involves using a CT scanner to produce two- and three-dimensional images of the colon, which are interpreted by a radiologist. This requires full bowel clearance and air insufflation during the procedure, both of which can be difficult to tolerate. It is less invasive than colonoscopy but is equivalent for detection of lesions of a reasonable size. The technique is improving all the time and is the investigation of choice for patients >75 who are able to tolerate full bowel clearance
• Minimal preparation CT colon involves ingestion of a contrast agent 48–72h before the scan, which then tags the faecal matter and removes the need for bowel clearance. It is therefore a better investigation for frailer patients, although it misses smaller lesions
• Plain CT abdomen has reasonable sensitivity for large colonic lesions, may reveal other pathologies, and requires no bowel preparation. It is therefore useful in emergency assessment or where the pathology is not clearly colonic
• Barium enema requires bowel clearance and is less sensitive than CT colonography, so is becoming less frequently used
Inflammatory bowel disease
Ulcerative colitis and Crohn’s disease are chronic, relapsing conditions caused by inflammation of the bowel wall. Inflammatory bowel disease is idiopathic and has an ↑ incidence in the population as a whole. Initial presentation is usually in adolescence, but there is a second peak of incidence in older patients. Diarrhoea and urgency in this age group can be particularly disabling and may result in incontinence and social isolation.
Features
• Diarrhoea (often with blood), malaise, weight loss, and abdominal pain. Delayed presentation may result from embarrassment or fear of cancer. Delayed diagnosis more common in older people because symptoms are ascribed to one of the common differential diagnoses such as diverticular disease, CDAD, colonic carcinoma, and ischaemic colitis
• Associated conditions include arthritis, iritis, sclerosing cholangitis, ankylosing spondylitis, and skin disorders (pyoderma gangrenosum, erythema nodosum)
• Complications include thromboembolism, malabsorption and malnutrition, perforation, stenosis with obstruction, fistula formation, and colonic and biliary malignancy
Investigations
• Exclude infection with stool culture and examination for ova, cysts, and parasites and Clostridium toxin (if in hospital or recent antibiotics)
• ESR and CRP are usually elevated but may be normal in localized disease
• A normochromic normocytic anaemia is common, but if there is excessive bleeding, iron deficiency can develop
• Plain X-rays are usually normal, but contrast studies are often diagnostic
• Sigmoidoscopy/colonoscopy and biopsy have high diagnostic yield
Treatment
Confirmed cases are best managed by gastroenterology teams. Treatment in older patients is not greatly different and is aimed at obtaining and then maintaining remission. Some principles for treating older patients include:
• Exacerbations of distal colitis are usually treated with topical mesalazine and steroids given as enemas—this may be impractical in older patients, unless a carer can help, and oral steroids can be a better option
• Budesonide is a steroid with high topical potency (poor absorption and rapid first-pass metabolism), so equivalent doses cause fewer side effects
• Side effects, drug interactions, and polypharmacy may be more problematic, e.g. always consider bisphosphonates with oral steroids therapy
• Look for, and treat, proximal constipation which can impair the efficacy of treatment of a distal colitis
• Oral 5-aminosalicylic acid preparations (e.g. slow-release mesalazine) are often successful (for exacerbations and maintenance) and well tolerated
• The risk of malignancy is higher the longer the patient has active disease, so theoretically many older patients should be under surveillance by a gastroenterologist. Unfortunately the risk of colonic perforation during colonoscopic screening is higher in the elderly population, so many screening programmes stop at age 75
• For failure of medical management, elective colectomy is well tolerated and may give the best quality of life. In contrast, emergency surgery in older patients has high mortality
Diarrhoea in older patients
Acute
Short-lived bouts of diarrhoea are commonly due to viral gastroenteritis. Supportive management (rehydration, light diet) is usually sufficient for this self-limiting condition. It can spread rapidly in institutions (especially if due to norovirus—responsible for much of the so-called ‘winter vomiting’), and appropriate infection control measures should be put in place. In frail, hospitalized patients, especially with recent antibiotic exposure, consider CDAD earlier rather than later.
If diarrhoea persists, always send samples for culture, ova, cysts, and parasites, and C. difficile toxin (see ‘Clostridium difficile-associated diarrhoea’, pp. 614–615).
Chronic
There is a group of elderly people who have chronic or recurring episodes of diarrhoea that merit active investigation—untreated, they suffer high morbidity (especially if diarrhoea induces faecal incontinence) and many causes are treatable. see ‘HOW TO . . . Investigate and manage chronic diarrhoea’, p. 375 for a suggested plan of investigation.
Malabsorption
Patients do not always have diarrhoea. Look for low BMI and falling weight despite reasonable oral calorie intake. Biochemical markers of malnutrition, e.g. hypoalbuminaemia, may be present. Anaemia is caused by malabsorption of iron, B12, or folate and is therefore microcytic, macrocytic, or normocytic.
The common causes of malabsorption in older patients often coexist and include:
• Coeliac disease/gluten-sensitive enteropathy:
• Peak incidence at age 50 but can manifest for the first time in old age with weight loss, bone pain (osteoporosis), fatigue (anaemia), and mouth ulcers
• Duodenal biopsy should be performed in all who present with iron deficiency undergoing endoscopy
• Anti-endomysial or tissue transglutaminase antibodies have very high specificity (100%) and reasonable sensitivity (around 85%). False negatives can occur with low immunoglobulin A (IgA), so always check serum immunoglobulins at the same time
• Pancreatic insufficiency can occur without a history of pancreatitis, alcoholism, or gallstones. Request a faecal elastase—a low level supports pancreatic insufficiency
• Bile salt malabsorption. Ileal resection or disease allows bile salts to reach the colon which causes diarrhoea
• Bacterial overgrowth is particularly common in any person with an anatomical abnormality of the gut (e.g. post-gastrectomy, small bowel diverticula) but can also occur with normal gut architecture
HOW TO . . . Investigate and manage chronic diarrhoea
Diagnoses to consider in the elderly population include:
• Constipation with overflow diarrhoea
• Drugs—many drugs can cause diarrhoea; review the list and stop any that may be implicated. Common culprits include laxatives, antibiotics, bisphosphonates, NSAIDs, and PPIs
• Inflammatory bowel disease or microscopic colitis
History
Ask about foreign travel, antibiotic exposure, full drug history, previous gut surgery/pancreatitis, and family history of inflammatory bowel disease. Ask the patient or carer to make a record of stool frequency/texture.
Examination
Abdominal and digital rectal examination. If rectum is loaded, be highly suspicious of overflow diarrhoea.
Investigations
• Stool: culture, C. difficile toxin, ova, cysts, and parasites
• Blood tests: FBC (anaemia), haematinics (iron, B12, folate deficiency), tissue transglutaminase antibodies (and IgA levels), CRP, and ESR
• Radiology: plain AXR is rarely diagnostic (except unexpected, left-sided faecal loading)
• Sigmoidoscopy: biopsy in several places, even if the mucosa looks normal to exclude microscopic colitis (see ‘Other colonic conditions’, pp. 376–377)
• More extensive colonic imaging may be needed (see ‘HOW TO . . . Image the older colon’, p. 371)
• Faecal calprotectin is useful to rule out inflammatory bowel disease
Treatment
Obviously depends on the cause, but in patients in whom diagnosis is not clear and are not fit for, or refuse, more complex investigations, there is a place for trial of empirical treatment. One such strategy is at least 2-week trials of:
• Metronidazole (for overgrowth/diverticular disease)
• Pancreatin, e.g. Creon® (pancreatic disease)
• Bile acid sequestrants, e.g. colestyramine (bile salt malabsorption)
Pick the most likely, or try each in turn for a few weeks.
Other colonic conditions
Irritable bowel syndrome
A chronic, non-inflammatory condition characterized by abdominal pain, altered bowel habit (diarrhoea or constipation), and abdominal bloating, but with no identifiable structural or biochemical disorder.
• New onset is rare in older age, and this diagnosis should not be made ‘de novo’ in older patients without very careful exclusion of structural disease (particularly colonic tumours and diverticulitis)
• Lifelong sufferers may continue with symptoms in later life, but if the symptoms change, the patient should also undergo investigations
• Pain or diarrhoea that wakes a patient at night, blood in stool, weight loss, or fever are NEVER features of irritable bowel syndrome
• Some drugs used to treat irritable bowel syndrome (e.g. tricyclic antidepressants) are less well tolerated in older patients. Mebeverine might be better tolerated for spasm
• Dietary advice should be given (low fibre for bloating or wind, high fibre for diarrhoea or constipation, exclude exacerbating foods)
• Stool-bulking drugs can be useful for constipation
• Loperamide or codeine can be used for disabling diarrhoea
Angiodysplasia
Tiny capillary malformations (like spider naevi) that can occur anywhere in the gut are important only because they bleed.
• Slow blood loss leads to unexplained recurrent iron deficiency anaemia; brisk loss may produce life-threatening haemorrhage
• Unless they are inherited in a syndrome (e.g. hereditary haemorrhagic telangiectasia), they are acquired and therefore have ↑ prevalence with age (most cases aged over 70)
• Asymptomatic angiodysplasia in older patients is common. Diagnosis is often by exclusion of other causes of iron deficiency anaemia. Many patients are reinvestigated for recurrent anaemia, and the absence of sinister features over a period of time with no demonstrated pathology on standard tests may suggest angiodysplasia is the cause
• Sometimes colonoscopy can visualize lesions (which can then be treated by diathermy), but CT does not reveal this pathology
• Selective mesenteric angiography can demonstrate lesions that are actively and rapidly bleeding
• Tranexamic acid, oestrogens, and thalidomide are sometimes successful in controlling chronic blood loss
Microscopic colitis
Also known as collagenous or lymphocytic colitis. An idiopathic condition causing chronic or episodic watery, non-bloody diarrhoea, but with no gross structural changes seen on colonoscopy.
• Biopsy changes are diagnostic with collagenous thickening of the subepithelial layer and infiltration with lymphocytes
• There is no ↑ risk of cancer
• Keep treatment as simple as possible—start with diet and anti-diarrhoeal drugs (e.g. loperamide), then try steroids (e.g. budesonide)
Intestinal ischaemia
There is a variety of presentations. Pain out of proportion to the abdominal examination findings is common in these syndromes and should always make you consider them. An elevated lactate ± acidosis should alert you to the possibility of dead bowel.
• Intestinal angina results from chronic arterial obstruction of the coeliac axis or superior mesenteric artery. Epigastric pain occurs after eating. Diagnosis is tricky, as the pain is similar to peptic ulcer pain, but angiography is diagnostic. Treat with antiplatelet agents. Angioplasty or stenting may be useful
• Small bowel ischaemia results from mesenteric artery occlusion, often by an embolus (more common in AF). There is acute colic with rectal bleeding, followed by circulatory collapse. Laparotomy is required, but outcome is poor
• Ischaemic colitis is an under-diagnosed cause of acute diarrhoea ± blood in dehydrated, hypotensive elderly patients with vascular disease. Often self-limiting if volume depletion corrected and the bowel is rested. May result in colonic stricture
• Colonic gangrene occurs after profound hypotension typically in older ITU patients with heart failure and sepsis. Laparotomy and colectomy are required, but fatality is high
The ‘acute surgical abdomen’
► Peritonitis/perforation often presents in a non-specific way. Patients often present to medicine, rather than surgery. The diagnosis is easily missed, so always have a high index of suspicion and examine the abdomen carefully and repeatedly in sick elderly patients without a diagnosis.
Common causes in older patients include:
• Complications of diverticular disease
• First presentation of a tumour (gut, pancreatic)
• Ischaemic bowel (emboli in patients with AF)
• Strangulated hernias (always remember groin examination)
• Ruptured abdominal aortic aneurysm
• Duodenal ulcer perforation (becoming less common)
• Biliary stones/sepsis (stones) and pancreatitis
Signs
Peritonitis/perforation may not have guarding or rigidity, particularly in the very old, those on steroids, or people with diabetes. Lack of bowel sounds can be helpful. Signs may develop with time, so repeated assessments are mandatory.
Investigations
Erect CXR can reveal air under the diaphragm (this is sometimes the only indication of a ‘silent’ perforation). Ultrasound or CT imaging will often reveal the cause.
Management
Always involve the surgical team, even where the patient is unsuitable for operation, as they can advise on conservative management and occasionally an ‘interval’ procedure is appropriate (e.g. gallstone surgery once cholecystitis has settled).
► Ensure that surgical decisions are made on the basis of frailty assessment and comorbidity, not just age alone. Aim to achieve a senior medical, surgical, and anaesthetic consensus about treatment, and then discuss with the patient (or their advocate).
Medical management involves:
• Broad-spectrum iv antibiotics
• Resting the bowel (nil by mouth, NGT if vomiting)
• Careful monitoring of fluid balance—heart failure from fluid overload or renal failure from dehydration are often the mechanisms of death. A urinary catheter and central venous pressure monitoring are sometimes necessary
• Prophylactic low-molecular-weight heparin
It is surprising how often patients survive with conservative measures, so continue to monitor the patient and adjust treatment carefully. Once the signs/symptoms recede, try to get the patient eating, on oral antibiotics, and mobilizing as soon as possible to avoid the complications of malnutrition, pressure sores, VTE, and C. difficile colitis which may be more lethal than the initial peritonitis.
Obstructed bowel in older patients
As with peritonitis, this often presents in a non-specific or non-dramatic way. Common causes in older patients include:
• Strangulated hernias (remember to examine the groins)
• Adhesions (look for old abdominal scars)
• Complications of diverticular disease (abscess, localized perforation, stricture)
Signs
Consider excluding obstruction (with plain X-ray) in any patient with persistent vomiting and/or abdominal bloating (ask the patient if their tummy is a normal size for them). Pain/colic, absence of defecation, tinkling bowel sounds, and gastric splash are helpful when present (but are often absent). Always examine the groins in both sexes for obstructed herniae.
Investigations
Plain AXR shows dilated bowel—standing AXRs have fluid levels but are often impractical in older patients and rarely add diagnostic information to a supine film. CT imaging may localize a cause. Contrast radiology and gastroscopy are sometimes useful.
Management
Always involve the surgical team who can advise on diagnosis and conservative management, e.g. insertion of a flatus tube for sigmoid volvulus.
General management usually involves:
• Resting the bowel (nil by mouth and wide-bore NGT)
• Careful monitoring of fluid balance—heart failure from fluid overload or renal failure from dehydration are often the mechanisms of death
• Therapeutic oral Gastrografin® (hyperosmolar ‘lubricating’ agent and can relieve small bowel obstruction due to adhesions)
• Consider broad-spectrum antibiotics if there is fever or features of coexistent perforation
• Prophylactic low-molecular-weight heparin
Where conservative management fails and an operation is necessary, less invasive/palliative procedures are often more appropriate (e.g. defunctioning colostomy, rather than anterior resection).
Pseudo-obstruction presents with vomiting and dilated bowel on X-ray but is due to an atonic bowel, so bowel sounds are absent or ↓, rather than ↑. Frail, older, immobile, debilitated patients are more at risk. Can occur with electrolyte abnormality (especially low potassium), post-surgery, with drugs (e.g. opiates, anticholinergics), in neurological disease (e.g. Parkinson’s or Alzheimer’s), or any severe illness (e.g. septicaemia). Supportive care with hydration and bowel rest is needed, along with correction of the underlying abnormality. Often resolves with this approach, but decompression or surgery is occasionally needed.
Obesity in older people
In developed countries, there is a general ↑ in body weight and BMI until about 60 years of age, after which both tend to decline. The body composition also changes, with an ↑ proportion of intra-abdominal fat.
Weight gain in older people usually relates to a reduction in activity and falling basal metabolic rate, rather than an alteration in calorie intake (which actually tends to get lower with age).
The ideal body mass for an older person has not been established, although it is probably higher than that for a younger person.
Impact of obesity
The relationship between mortality and obesity in older people has not been established. The following should be considered:
• Weight loss has been reported to ↑ mortality—but all the studies have methodological problems, and weight loss is a marker of underlying disease which may be occult
• Those with chronic disabilities and diseases will reduce activity more than fit older people, and so may gain weight more easily
• In care home residents, only severe obesity (BMI >40) is clearly associated with an ↑ in mortality. Care homes may need special equipment (e.g. wider frames, wheelchairs) to allow for their care
• Obesity will ↑ morbidity from conditions such as arthritis and diabetes and ↑ cardiovascular risk
• Obese older people are more likely to have mobility problems, and their quadriceps strength-to-weight ratio is key to standing ability
• Obesity does not exclude frailty
Treatment
The goal of treating obesity in older people is to reduce weight without losing lean mass or contributing to frailty—excessive weight loss in older people is associated with an ↑ in mortality.
In the very old, there is little to be gained from altering a lifelong dietary and exercise habit where there are few complications from obesity, but younger patients (60s and 70s) with diabetes or vascular disease may benefit greatly from healthier eating habits.
• ↑ physical activity is the mainstay of treatment. This may ↑ energy expenditure and promote weight loss, improve muscle strength and stamina, reduce intra-abdominal fat, and promote a feeling of well-being
• Calorie restriction should be undertaken with caution and include at least 800kcal/day with good fluid intake
• Dietary supplements can be used in patients who have a high BMI during acute illness but should not be continued indefinitely
• Drugs to enhance weight loss are rarely useful (risk > benefit), although inhibitors of fat absorption (e.g. orlistat) may be useful in people with diabetes
• Gastric surgery is higher risk in older obese people and not frequently undertaken