Gastroenterology
The ageing gastrointestinal system
Teeth
Change colour—yellow and less translucent
Become worn (enamel does not regenerate)
Decreased 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 increases 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.355) are more frequent with increasing 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 also diminish with consequent dribbling
Taste
Olfactory function, and hence taste discrimination, decreases 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.363) 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
Increased 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
Increased mucosal susceptibility to damage
Increased Helicobacter pylori carriage but this is less likely to cause ulceration
Small intestine
Function well preserved except for calcium absorption which is decreased
Increased incidence of bacterial overgrowth with malnutrition and diarrhoea
Large intestine
Decreased rectal sensation contributes to high incidence of constipation.
Pancreas
Structural changes including atrophy but function is well-preserved.
Liver
Hepatic weight and volume decrease 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
Gallbladder
Incidence of gallstones increases (40% females > 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 mouth
Soft tissues: tongue and floor of mouth commonest site for oral cancer in smokers/alcoholics. Angular stomatitis
Salivation: (see ‘Xerostomia’, p.355)
Teeth: how many missing, how many restorations, pain/sensitivities Caries is increased 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 selfcare, eg 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’, p.356)
Facial pain
Consider trigeminal neuralgia, temporal arteritis, 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 (eg tricyclic antidepressants, levodopa)
Sjögren’s syndrome (an autoimmune destruction of salivary glands) can be primary or associated with other autoimmune conditions
Irradiation, salivary stones, tumours, sialadenitis (viral or bacterial infections)
Treatment depends on cause—stop or decrease 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 erythematous base), angular stomatitis (sore cracks in corner of mouth), or, rarely atrophic forms (eg 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 mouth for several minutes. In cases with painful swallowing/ dysphagia (ie 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 more than 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 including common and general (eg oral candidiasis in immunosuppression) as well as rare and specific (eg oral lichen planus) manifestations. Remember that many drugs also affect the mouth, eg xerostomia (see ‘Xerostomia’, p.355), tardive dyskinesia with antipsychotics, 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 (decreased 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 (increased functional dependency, morbidity, mortality, and use of healthcare resources).
Malnutrition is extremely common in the elderly frail or institutionalised 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, eg 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.695) is widely used in UK hospitals and is sensitive for detection of protein-energy undernutrition in hospitalized patients
More complex tools (eg Mini Nutritional Assessment) are helpful but time-consuming and rarely used outside research
Biochemical measures (eg 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 multidisciplinary approach is needed eg 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 meal times) and provide assistance with feeding (dietetic 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 (eg substitute full fat milk and yogurt if they are on the lower fat variety)
Prescribe dietary supplements according to patient preference (eg milky or fruit drinks, soups, puddings, or high-calorie shots)
Appetite stimulants, eg prednisolone can increase 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 decreased lean mass, although the proportion of fat is relatively increased so overall weight is often remarkably stable.
As a rule of thumb unintentional weight loss of more than 5lb (2.3kg)/5% of body weight in a month or 10lb (4.5kg)/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 primary 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:
Dementia
Depression
Malignancy
Chronic infection/disease, eg COPD, heart failure, TB
Inflammatory conditions, eg giant cell arteritis
Malabsorption (see ‘Diarrhoea in older patients’, p.376)
Mesenteric ischaemia (recurrent postprandial abdominal pain)
Drug causes, eg digoxin, theophyllines, cholinesterase inhibitors
Metabolic disorders, eg hyperthyroidism, uraemia
Swallowing problems
Persistent nausea or abdominal pain/reflux
Social causes, eg 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’, p.66) 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 (eg stroke, motor neurone disease, Parkinson’s disease) or failure of oral feeding (eg severe anorexia syndromes, intensive care unit) with an intact gastrointestinal tract.
There are three common methods:
Fine-bore NG tubes: simple, quick, and inexpensive. The preferred method for short-term feeding. Some patients (usually confused/ drowsy) repeatedly pull out NG tubes. Interference with the tube increases 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 increasing experience using NG tubes 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 next of kin for an incompetent one are not uncommon. Once established, this method is discreet and better tolerated than NG tubes and is the method of choice for medium/longterm enteral feeding
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 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 patient becomes unwell, feverish, or breathless. If aspiration is ongoing despite correct tube position slow the feed, feed with patient sitting upright (ie not at night) and add promotility drugs, eg metoclopramide 10mg tds or erythromycin 250mg tds (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 patient has been malnourished for a long time. When feeding commences, insulin levels cause minerals (especially phosphorus) to move rapidly into 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 U + E, Ca, Mg, phosphate, and glucose daily for a few days, then weekly). Supplementation of minerals may be done intravenously or by adding extra to NG feed
Fluid overload and heart failure: decrease 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 central venous access and should only be undertaken when supervised by an experienced nutrition team. It is usually a temporary measure, eg postgastrointestinal 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.
Get the patients 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
Have the patient sitting upright with 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)
Leave the guide wire in the tube and lubricate with lots of jelly
Feed the tube down one nostril about 20cm (until it hits the back of the throat)
If there is a proximal obstruction try the other nostril
If possible ask the patient to swallow and advance the wire
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
Secure the tube yourself immediately with tape to both 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)
Chest X-ray 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 (often nurses) 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’, p.654) 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 decrease, 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, eg:
2 weeks of NG feeding in a patient with dysphagia following a stroke, which is hoped will resolve
Don’t be afraid of a therapeutic trial (eg if you don’t 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 medical record
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’, p.360— this is sometimes controversial)
Although feeding is successful the patient’s quality of life is felt to be unacceptable (nearly always controversial)
British Medical Association advice is that all cases of withdrawal of longterm feeding should be referred to the courts. This is certainly true if there are any parties who object, but there are non-controversial cases in elderly patients where this is not necessary.
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.
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
Finucane TE, Christmas C, Travis K, et al. (1999). Tube feeding in patients with advanced dementia: a review of the evidence. JAMA 282 (14): 1365-70.
GMC guidance. (2010) Treatment and care towards the end of life: good practice in decision making. Online: 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 (GORD)
The symptoms (retrosternal burning, acid regurgitation, flatulence, 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 ‘blind’ 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. Proton pump inhibitors (PPIs) have revolutionalized treatment, making antacids and H2 blockers such as ranitidine almost redundant. They are very effective (for symptoms and healing) and safe. They are used for prophylaxis with aspirin—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.148).