Always try to get recorded weight (rather than relying on patient/ carer memory) \200\224 a search of old outpatient clinic and primary care records can help. Record weight regularl y while you investigate to look for ongoing trends. Dramatic weight loss should always prompt a search for remediable pathology. The cause is o ften multifactorial. It is important to consider: \200 Dementia \200 Depression \200 Malignancy \200 Chronic infection/disease, eg COPD, heart failure, TB \200 In \202 amm atory conditions, eg giant cell arteritis \200 Malabsorption (see b \200\230Diarrhea in older patients \200\231, p.376) \200 Mesenteric ischaemia (recurrent postprandial abdomin al pain) \200 Drug causes, eg digoxin, theophyllines, cholinesterase inhibitors \200 Me tabolic disorders, eg hyperthyroidism, uraemia \200 Swallowing problems \200 Persistent nausea or abdominal pain/re \202 ux \200 Social causes, eg inability to cook, poverty, social isolation, alcoholism A careful history (including dietary history and mental state with col- lateral history where possible), examination, and routine screening tests (see b \200\230Investigations \200\231, p.66) will usually give clues of signi \201 cant under- lying pathology. If preliminary investigations are negative a \200\230watch and re-weigh a nd wait \200\231 plan is reasonable \200\224 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 reve rsed. Where no such cause is found, or where it is not reversible, interventions are still possible. 358 CHAPTER 12 Gastroenterology Enteral feeding Consider enteral feeding early if there is dysphagia (eg stroke, motor neur on disease, Parkinson \200\231s disease) or failure of oral feeding (eg severe anorexia syn dromes, 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 fe eding. 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 incr easing experience using NG tubes which are held in place via a nasal loop (Bridle \204 ). Trained practitioners can insert these by the bedside and removal by the patient is very r are \200 PEG : the risks of insertion include perforation, bleeding, and infection for a patient who is usually already frail. The patient has to be \201 t to undergo sedation. P roblems obtaining consent from a competent patient and \200\230agreement \200\231 from nex t 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/long- term enter al feeding RIG : useful if gastroscopy technically dif \201 cult (eg pharyngeal pouch) and sometimes if small-bowel feeding preferred over gastric feeding. Similar complication rate to PEG Complications for all methods include \200 Aspiration pneumonia : there is a common misco nception that enteral feeding eliminates aspiration in dysphagic patients. This is not true \200\224 re \202 ux of food into esophagus is common and this along with salivary secretions and covert oral i ntake may still be aspirated. Always check the position of the tube if patient becomes unwe ll, feverish, or breathless. If aspiration is ongoing despite correct tube position slow th e feed, feed with patient sitting upright (ie not at night) and add pro- motility drugs, eg metoclopramide 10mg tds or erythromycin 250mg tds (pre-meals). A nasojejunal tube or jejun al extension to a PEG tube can also reduce aspiration rates (see b \200\230Aspiration pneu monia/ pneumonitis \200\231, p.332) Re-feeding syndrome : occurs when patient has been malnourished for a long time. When feedi ng commences, insulin levels cause minerals (especially phosphorus) to move rapidly into in tracellular space and \202 uid retention occurs causing hypophosphataemia, hypomagnesaemi a, and hypokalaemia. This in turn can cause life-threatening heart failure, respiratory fai lure, arrhythmias, seizures, and coma. Avoid by \200\230starting low and going slow \200 \231 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 gluc ose daily for a few days, then weekly). Supplementation of minerals may be done intravenous ly or by adding extra to NG feed Fluid overload and heart failure : decrease volume and add diuretics \200 Diarrhea : excl ude infection (especially Clostridium dif \201 cile ). Try slowing the feed rate or changi ng the feed to one containing more or less \201 bre ENTERAL FEEDING 359 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 post- gastrointestinal surgery. Complications such as \202 uid ov erload, electro- lyte disturbance, and iv catheter sepsis are common in older patients. HOW TO Insert a \201 ne-bore NG feeding tube This task is often performed by nursing staff who may be very experi- enced. Doctors are of ten asked to help when insertion is proving dif \201 cult. 1. Get the patients consent \200\224 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 chin tucked forward (patients often hyperextend th eir 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) 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 \200\224 you sho uld be able to see a single wire going vertically down. Start again if there is a loop 8. Secure the tube yourse lf 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. \200 Aspiration of gastric contents th at are clearly acidic (pH <5) \200 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 t ube 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. 360 CHAPTER 12 Gastroenterology 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 t hat arti \201 cial enteral feeding is a cruel and futile treatment performed on incompeten t patients that only postpones a \200\230natural \200\231 death that involves anorexia or dysphagia. The use of the term \200\230clinically assisted nutrition and hydration \200\231 has been suggested by the General Medical Council (UK) to replace the term \200\230arti \201 cial nutrition and hydration \200\231 underlining the fact that this is a form of treatment. There are numerous high-pro \201 le legal cases regarding feeding (usually withdrawal of), and controversial cases that cannot be resolved locally should always be referred to the c ourts via the local legal team. 2The key to steering a course through this mine \201 eld i s communication. Initiating treatment \200 Establish if the patient is competent \200\224 even dysphasic patients may understand a little with non-verbal cues, etc If the patient has capacity (see b \200\230Capacity \200\231, p.654) ensure they understand the chosen method (and its risks) and projected duration of feeding. Patients wi th dysphagia must realize that they will be expected to dramatically decrease, or stop, ora l feeding For patients who lack capacity, ensure you have communicated with all interested carers, fa mily, and the GP. There is sometimes disagreement between interested parties and these are best detected and \200\230thrashed out \200\231 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: \200 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 patient requests or if enters terminal ph ase of disease Don \200\231t be afraid of a therapeutic trial (eg if you don \200\231t know whether the pa tient \200\231s lethargy/drowsiness/depression is related to malnutrition). Always ensure e veryone understands and agrees on review dates and criteria for reassessment. Patients/rela tives can be reassured that PEG tubes can be removed if improvement occurs Record discussions and plan carefully in medical record \200 If there is still dispute ge t a second opinion. As a last resort legal advice may be needed THE ETHICS OF CLINICALLY ASSISTED FEEDING 361 Withdrawing treatment 2Withholding treatment is not morally different to withdrawing it. Th ere are however, technical and emotional differences, which is why many more ethical proble ms arise when withdrawing and why some doctors are resistant to trials of treatment. Arti \201 cial feeding can be withdrawn because: \200 It is no longer required (rarely c ontroversial) \200 A therapeutic trial has failed (see b \200\230Initiating treatment \200\231, p.360 \200\224 this is sometimes controversial) Although feeding is successful the patient \200\231s quality of life is felt to be unacceptable (nearly always controversial) British Medical Association advice is that all cases of withdrawal of long- term feeding sh ould 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 incom petent 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 an d relatives, understand and sympathize with the aims of management. Further reading Finucane TE , Christmas C , Travis K , et al . ( 1999 ). Tube feeding in pa tients with advanced dementia: a review of the evidence . JAMA 282 ( 14 ): 1365 \200\223 70 . GMC guidance . ( 2010 ) Treatment and care towards the end of life: good practice in decisi on making . Online: M www.gmc-uk.org . Royal College of Physicians of London . ( 2010 ). Oral Feeding Dif \201 culties and Dilemm as . London : Royal College of Physicians of London . 362 CHAPTER 12 Gastroenterology Oesophageal disease Gastro-oesophageal re \202 ux disease (GORD) \200 The symptoms (retr osternal burning, acid regurgitation, \202 atulence, atypical chest pain) correlate poorl y with the pathology (normal mucosa to severe oesophagitis) Sinister features which might suggest malignancy include sudden or recent onset, dysphagia, vomiting, weight loss, and anemia. They should guide management: \200 In the absence of sinister features a \200\230blind \200\231 trial of treatment is given \200 If there are sinister features then a gastroscopy should be arranged Oesophageal pH monitoring is rarely necessary Treatment Check if the patient is taking pres cribed or over-the-counter NSAIDs, steroids, or bisphosphonates, and stop or minimize the d ose. Proton pump inhibitors (PPIs) have revolutionalized treatment, making antacids and H2 blockers such as ranitidine almost redundant. They are very effec- tive (for symptoms and h ealing) and safe. They are used for prophylaxis with aspirin \200\224 often at lower dose, as well as treatment and some are licensed for intermittent symptomatic use. Some are avai lable over the counter. Rarely elderly patients can have side effects of diarrhea or con- f usion (see b \200\230Proton pump inhibitors \200\231, p.148). Barrett \200\231s/columnar-lined esophagus Gastric mucosa replaces the oesophageal squamous cell mucosa. It is associated with an increased risk of malignancy and should have regular endoscopic surveillance regardless of symptoms. Hiatus hernia \200 Very common in older patients, occurring to a degree in almost all \200 Laxity of structures at the gastro-oesophageal junction allows oesophago-gastric junc tion or portions of 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 \202 uid level behind heart), at endoscopy, or on contrast r adiology. Treatment: To reduce re \202 ux, suggest: lose weight, avoid alcohol and caffeine, eat sma ll meals often, avoid eating before bed, and sleep propped up on pillows or elevate head of bed on blocks. PPIs will nearly always relieve symptoms, consider investigations if they d on \200\231t. Prokinetic agents, eg metoclopramide 10mg tds sometimes help. Younger patient s with intractable problems can be assessed for surgery \200\224 laparoscopic surgery now available. OESOPHAGEAL DISEASE 363 Achalasia \200 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 \200 CXR may reveal a dilated esophagus \200 Endoscopy is usually performed to exclude malignancy, but may be normal Barium swallow has characteristic abnormalities (dilated esophagus terminating in a beak-like narrowing) Manometry is the gold standard for diagnosis \200 Treatment is aimed at facilitating lowe r oesophageal sphincter relaxation, and can include drugs (calcium channel blockers or nitrates), botulinum toxin i njection, endoscopic dilation of the sphincter, or surgical myotomy Oesophageal motility disorders \200 Group of disorders where oesophageal motility is sign i \201 cantly 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 \200 Syndromes include d iffuse oesophageal spasm, nutcracker esophagus, and hypertensive lower oesophageal sphincter Motility disorders can also arise secondary to other diseases (eg diabetes, systemic sclerosis, chronic GORD) Diagnosis may be made with barium swallow, but manometry is the gold standard Treatment with calcium channel blockers or tricyclic antidepressants has some evidence base although other drugs, botulinum toxin, and endoscopic dilation are also occasionally used Oesophageal candidiasis \200 Can present with dysphagia or pain \200 Consider in frail or immunosuppressed patients, especially if oral candidiasis is present Characteristic appearance on endoscopy (biopsy con \201 rms) or barium swallow Treat with \202 uconazole 50 \200\223100mg od for 2 weeks 364 CHAPTER 12 Gastroenterology Dysphagia Dysphagia (dif \201 culty in swallowing) is a common symptom in older patients. History \200 Ask what type of food is dif \201 cult (solids or liquids) and the level at which food sticks (mouth/throat, retrosternal, or epigastric) \200 Distinguish dysphagia from early satiety and regurgitation (when successfully swallowed food returns after seconds/minutes), which usually occurs with gastr ic outlet obstruction If the swallow \200\230tires \200\231 through a meal consider myasthenia \200 Cough, whe eze, or recurrent aspiration pneumonia can be a presentation of swallowing problems which c ause aspiration Signs Look for weight loss, oral thrush (may be associated with oesophageal candida), supra clavicular lymphadenopathy, and a gastric splash (implies gastric outlet obstruction). Watc h the patient swallow some water and food \200\224 the diagnosis might be clear. Causes These can be divided into two: \200 Structural lesions (worse with solids) \200 Oesophageal or gastric cancer \200 Benign strictures \200\224 scarring following, eg oes ophagitis, scleroderma, polymyositis, radiotherapy Pharyngeal pouch \200 Oesophageal candida or severe oesophagitis \200 Hiatus hernia can produce obstruction symptoms \200 External obstruction, eg bronchial tumor, aortic aneur ysm, or cervical osteophyte Foreign bodies (eg hair balls) are commoner in patients with dementia Functional problems (often worse with \202 uids) Pharynx/throat \200\224 commonest neurological cause is stroke but can occur in advanced d ementia and MND. Rarer neurological conditions include myasthenia gravis, inclusion body my ositis, multiple sclerosis, and parkinsonian syndromes Esophagus \200\224 dysmotility problems are relatively common in older patients and include achalasia and diffuse oesophageal spasm Investigations Gastroscopy is now the primary investigation and is well tolerated even in f rail elderly patients. Use a barium swallow \201 rst if there is felt to be a high risk o f perforation with an endoscope (eg suspect pouch), but gastros- copy allows biopsy and the rapy, eg dilation. Video \202 uoroscopy provides functional imaging and is useful diagnost ically, but the correlation between observed aspiration and clinically signi \201 cant pro blems is poor. DYSPHAGIA 365 Treatment of dysphagia \200 An empirical trial of PPI can be used in the very frail and t hose who are deemed un \201 t for investigation If oral thrush is present try \202 uconazole 50 \200\223100mg od for a week \200 Oesoph ageal 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 \202 uids, and positioning patient correctly can minimize pro blems Oesophageal dysmotility \200\224 try PPI and a calcium channel blocker or a nitrate Gastroparesis causes early satiety and vomiting. It can be very hard to treat \200\224 try metoclopramide 10mg tds or erythromycin 250mg tds, with domperidone 30mg pr tds if oral ro ute not viable. Electrical gastric \200\230pacing \200\231 or surgery may provide relief ( rarely used) Nutritional support \200\224 elderly patients with dysphagia are usually malnourished to s tart with and are then put nil by mouth for investigations. Refer to the dietician and cons ider dietary supplements and early enteral feeding by NG tube or PEG (see b \200\230Entera l feeding \200\231, p.358) Aspiration pneumonitis (see b \200\230Aspiration pneumonia/pneumonitis \200\231, p.332) is largely a chemical rather than infective insult that may be complicated by infection. It i s treated by: \200 Preventing/minimizing aspiration (nil by mouth, NG feeding) \200 Oxy gen therapy \200 Chest physiotherapy \200 Iv antibiotics are given to prevent/treat sup erinfection 366 CHAPTER 12 Gastroenterology Peptic ulcer disease This disease is becoming much rarer with the advent of effective medic al treatment. It remains predominantly a disease of the elderly population. NSAID use is th e most common cause, followed by H. pylori . H. pylori is a spiral Gram-negative bacterium which colonizes the gastric mucosa causing ga stritis. Carriage rates increase with age \200\224 40 % at age 50, 75 % at age 70. Infecti on is usually asymptomatic but is the commonest cause of dyspepsia in older patients. H. py lori is strongly associated with duodenal ulcers and may have a link with NSAID-associated ulceration. Presentation Acute bleeding, pain (epigastric, retrosternal, or back), indigestion, \200 \230heart- burn \200\231, dysphagia, anorexia, weight loss, perforation (peritonitis), iron de \201 - ciency anemia, or an incidental \201 nding (eg on endoscopy). Older patients may present non-speci \201 cally ( \200\230off food \200\231 or vague abdominal pains). Investigation \200 Upper GI endoscopy is very safe and well-tolerated in older patients. It can often be performed using local anesthesia in the throat only \200 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 gradu ally decline after eradication. Breath tests can detect H. pylori colonization but obviousl y do not demonstrate pathology Treatment Dietary restriction is unnecessary (worth speci \201 cally mentioning because ol der patients can remember harsh or bizarre anti-ulcer diets). Stop any NSAIDs. Stop aspirin if possible, and plan for safe reintroduction depending on risk/bene \201 t of individual patient. Where there is H. pylori and ulceration/gastritis treat with one of the many \200\230triple therapy \200\231 antibi- otic PPI regimens. In the absence of H. pylori just a PPI will suf \201 ce. Arrange a repeat scope at 6 weeks to check healing of all gastric ulcers and malig- nant-looking duodenal ulcers. For bleeding \200 Resuscitation with blood product is life saving \200 Early interventi onal endoscopy with adrenaline injection (or other modalities, eg heater probes or clips) into bleeding point is suitable for almost all patie nts \200\224 don \200\231t delay because of age/comorbidity Iv proton pump inhibitor reduces the risk of re-bleeding \200 Continued bleeding/re-bleed ing despite endoscopic treatment is an indication for surgical intervention. These patients have a high mortality but overall do b ene \201 t from operative intervention Scores using clinical, laboratory and endoscopic features can stratify risk of re-bleeding (eg Rockall score) For perforation (see b \200\230The \200\234acute surgical abdomen \200\235 \200\231, p.3 80) Remember \200\230silent \200\231 perforation (without signs of peritonitis) is more co mmon in the elderly population (especially if on steroids or diabetic). Mortality is high d ue to delayed diagnosis, reluctance to perform surgery, and postoperative complications. PEPTIC ULCER DISEASE 367 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 uncom- fortable and bedbound. There is frequently r eversible disease and they are at high risk of dehydration/malnutrition and complications o f immobility. Nausea and vomiting (N + V) can be the major presenting feature of illnesses as diverse as pneumonia, MI, intracerebral hemorrhage, Addison \200\231s disease, UTI, and constipation. \200 Start with a careful history (especially drug history) \200 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), urinalysis, CXR, and ECG Drugs Look very carefully at drug history \200\224 almost any drug can cause N + V but dig oxin (even with therapeutic serum levels), opiates, tramadol, anti- parkinsonian drugs, ant idepressants, NSAIDs, and PPIs are some of the common candidates. New drugs are the most li kely, but remember poor compliance with drugs at home which are prescribed in hospital, eg co-codamol used occasionally at home may be written as 2 qds in hospital. If there is polyp harmacy try stopping the drugs one at a time, remembering that some drugs can take days to \200\230wash out \200\231. Central causes Raised intracerebral pressure can occasionally present this way. A CT scan i s needed if there is drowsiness, focal neurology, or a past history of intraventricular blo od (exclude hydrocephalus). If there is vertigo or tinnitus consider labyrinthitis or poste rior circulation stroke, see Table 21.1. Gut causes Constipation is a very common cause of nausea even without obstruc- tion. An abd ominal X-ray (AXR) should be done early on to exclude obstruction . 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 N + V without pain/bleeding. Gastropa resis is most common in people with diabetes and is very hard to treat \200\224 try metocl opramide, domperidone, or erythromycin. 368 CHAPTER 12 Gastroenterology The liver and gallbladder Cirrhosis Chronic liver disease can present for the \201 rst ti me in elderly people. The presentation is often non-speci \201 c. The prognosis is worse t han for a younger person with the same degree of liver damage. Common causes include alcoho l, hepatitis C, autoimmune hepatitis, and non-alcoholic fatty liver. A proportion are crypt ogenic (thought to be \200\230burnt out \200\231 autoim- mune hepatitis or non-alcoholic f atty liver disease). \200 Hepatitis C may have been transmitted from blood products recei ved before 1991 when screening was introduced. Alcohol consumption is known to increase the percentage of those infected with hepatis C who develop cirrhosis Alcohol excess can present with falls, confusion and heart failure at any age but older pat ients are less likely to volunteer (or be asked) their alcohol history. 2Always enquire abo ut alcohol Investigations If you suspect cirrhosis should include: A -1-antitrypsin, autoimmune pro \201 le (antinuclear antibody (ANA), smooth muscle antibody (SMA), liver-kidney microsome a ntibodies (LKM), antimitochondrial antibody, and immunoglobulins), ferritin and iron studie s, ceruloplasmin, hepatitis B and C serology, and ultrasound including Doppler of portal an d hepatic vein. Non-alcoholic fatty liver disease Is not always a benign condition (half will be progressiv e and 15 % develop cirrhosis). Obesity, hyperlipidaemia, and type 2 diabetes are risk facto rs so this condition is more common in older patients. If an ultrasound scan reveals fatty liver, advise about weight reduction and alcohol cessation. Gallstones \200 Very common (1:3 elderly females) and mostly asymptomatic although troubl esome symptoms often misdiagnosed as GORD or diverticulitis in older age groups Management largely as for younger patients but the risks of surgical intervention are higher so conservative/less invasive approaches often adopted Acute cholecystitis in older patients may present atypically (eg without pain) and is not a lways associated with gallstones. It has a 10 % mortality and should be aggressively treate d with iv antibiotics and supportive care. Failure to improve should prompt early surgical review THE LIVER AND GALLBLADDER 369 HOW TO Approach an older patient with abnormal liver function tests This is not an uncommon \201 nding, and investigation is as for younger patients. However , the following should be considered: \200 Drug injury to the liver is common, and may oc cur up to 6 months after exposure (eg statins, co-proxamol, penicillins, some over-the-coun ter medications) Liver metastases may present this way (more common in older patients) Deranged LFTs may occur as part of a systemic illness, eg sepsis (consider gallbladder/biliary infection if the LFTs are very abnormal), cardiac failure (wi th hepatic congestion), in \202 ammatory conditions (polymyalgia rheumatica), ischaemic li ver damage (after prolonged hypotension), Addison \200\231s 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, as sociated symptoms (eg heart failure, sepsis, primary malignancy) and alcohol use (do not ma ke lifestyle assumptions \200\224 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 \200\231s disease) but don \200\231t assume this \200\224 liver metastases can prese nt this way Isoenzymes can be measured, but clinical judgment is usually suf \201 cient to guide investigation Muscle disorders can cause transaminase elevation Persistent elevation should always prompt investigations: \200 Bloods including electrolytes, clotting, TFTs, autoimmune screen (s erum electrophoresis, ANA, antimitochondrial antibodies, SMA and LMK), viral serology (hepa titis B and C), iron studies (haemochromatosis), ceruloplasmin (Wilson \200\231s disease), endomysial antibodies (coeliac disease) and A -1-antitrypsin Liver ultrasound \200\224 a good screening test that will usually identify liver metastase s as well as highlighting any biliary duct dilation prompting referral for endoscopic retro grade cholangiopancreatography (ERCP) If the liver damage is progressive, or the diagnosis elusive then refer to a hepatologist f or consideration of liver biopsy. 370 CHAPTER 12 Gastroenterology Constipation The term constipation is used in different ways, indicating one or more of the following: \200 The time between bowel evacuations is longer than normal \200 The stoo l is harder than normal \200 The total fecal mass present within the abdomen is increased The most precise de \201 nition 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 Wes tern diet. There are said to be three types of constipation: Hard feces present in the rectum (often in massive amounts) \200 The whole distal large b owel loaded with soft, putty-like feces that cannot be evacuated High (proximal) impaction which may be due to obstructing pathology (eg diverticular disease, carcinoma) Diagnosis The diagnosis is largely clinical (based on history and examination alone). 2Ask speci \201 cally as some patients are embarrassed to trouble doctors with bowel symptoms. Constipation may, rarely, be the primary cause of delirium but commonly contributes to the presentation of the frail elderly with other pathology such as sepsis or renal failure. Rectal examination may be diagnostic, and sometimes the rectum will barely admit the examin ing \201 nger. If the rectum is empty, consider high impaction. In a thin patient, high i mpaction is unlikely if the loaded colon cannot be felt during abdominal examination. In mo re obese subjects a plain abdominal X-ray will be necessary to con \201 rm high impaction, but is insensitive in the very obese. 2Do not exclude constipation as the cause of fecal i ncontinence until there has been an adequate therapeutic trial for high fecal impaction. Causes \200 Reduced motility of the bowel : drugs (eg opiates, iron, anticholinergics, an tidepressants, antipsychotics, calcium channel blockers, calcium preparations), immobility, constitutional illness, electrolyte disturbances, dehydration, hypothyroidism, lack of die tary \201 bre, hypercalcaemia Failure to evacuate the bowels fully : any painful condition of the rectum or anus, dif \201 culty in access to the toilet, lack of privacy, altered daily routine Neuromuscular : Parkinson \200\231s disease, diabetic neuropathy pseudo- obstruction Mechanical obstruction of the bowel: carcinoma of the colon, diverticular disease CONSTIPATION 371 Prevention and treatment Precipitating causes such as dehydration, hypothyroidism, hypercal caemia, and drugs should be identi \201 ed and reversed. Non-pharmacological measures including regular exercise, improving access to the toilet, ad equate dietary \201 bre, 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 \200\230prn \200\231 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: \200 Stimulant laxative s such as senna (1 \200\2234 tablets/day) or bisacodyl (5 \200\22320mg/day), or stimulant suppositories, may be appropriate for those with bulky, soft fecal overloading Avoid stimulant laxatives in patients with hard rocks of feces as this may produce abdomina l pain. Use a stool softening (osmotic) laxative instead such as lactulose (10 \200\22340mL /day) or a macrogol Long-term use of stimulant laxatives has been said to cause \200\230bowel tolerance \200 \231/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 s afe, in moderate doses, for long-term use 1 Sometimes stimulant and osmotic laxatives are used in combination, typically in severe cons tipation (eg opiate-induced) that has been unresponsive to a single drug Stool bulking agents such as methylcellulose or ispaghula are useful in prophylaxis, but ar e less effective in treating established constipation; both \201 bre and other bulking ag ents will increase stool volume and may increase problems Costs of laxatives vary enormously, and there is no correlation between cost and patient acceptability. Try cheaper preparations \201 rst ( \201 bre, se nna) Fecal retention severe enough to cause incontinence nearly always needs a determined effort to clear the colon (see b \200\230HOW TO Treat \200\234over- \202 ow \200\235 fe cal incontinence \200\231, p.545). 1 Muller-Lissuer SA, Kamm MA, Scarpignato C et al . (2005). Myths and misconceptions about chronic constipation. Am J Gastroenterol 100: 232 \200\22342. 372 CHAPTER 12 Gastroenterology Diverticular disease Narrow-necked pockets of colonic mucosa which occur adjacent to blood vessel penetrations of the muscle bands, like \200\230blow outs \200\231 on a tire. Occur anywhere in large bowel but most commonly in the sigmoid. \200 Rare in <40 years, increa sing frequency with age and almost universal > 85 years Cause : thought to be raised intraluminal pressure due to low \201 bre Western diet Investigation : colonoscopy/ \202 exible sigmoidoscopy and barium enema are usually diagno stic and rule out other pathology. CT colography (abdominal CT with oral contrast) is incre asingly used as a better tolerated test in the frail elderly 2The majority of cases are asymptomatic the majority of the time. On other occasions innoce nt diverticulae are blamed for symptoms that arise from other pathology, eg constipation, i rritable bowel disease, or gastro- enteritis. The previous diagnosis of diverticular diseas e should not stop the careful evaluation of new bowel symptoms to exclude important diag- n oses such as colitis or cancer. Pain may occur, and especially if associated with constipation, can be improved by a high \201 bre diet with or without extra stool bulking drugs (eg ispaghula 1 sachet/day). Complications Diverticulitis Should be thought of as \200\230left-sided appendicitis \200 \231. Infection occurs within a pocket and may be due to a faecolith blocking the neck so a voiding con- stipation is key to prevention. Abdominal pain and tenderness, diarrhea, and v omiting occur with fever and raised in \202 ammatory markers. Treat with antibiotics (incl ude anaerobic cover) \200\224 mild cases oral antibiotics at home, severe cases may need a dmission for iv rehydration, antibiotics, and liaison with surgical services. Hemorrhage Selective angiography can be used to demonstrate bleeding point. Diverticular abscess Ultrasound or CT for diagnosis and radiographically guided drainage un der local anesthesia. Perforation/peritonitis See b \200\230The \200\234acute surgical abdomen \200\235 \200 \231, p.380. Fistula Most commonly to bladder causing urinary infection and bubbles in urin e (pneumaturia). Cystoscopy or CT scan for diagnosis. Surgery is required but simple defunc tioning colostomy is often suf \201 cient. DIVERTICULAR DISEASE 373 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 \201 t for bowel preparation on the request form if relevant. \200 Flexible sigmoid oscopy 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 met hod for general population investigation, but carries an increased risk of bowel perforatio n 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 insuf \202 ation during the procedure, both of which can be dif \201 cult for frailer old people. It is less invasive than colonoscopy and equivalent for detection of lesions o f a reasonable size. The technique is improving all the time, and is the investigation of c hoice for patients > 75 who are able to tolerate full bowel clearance Minimal preparation CT colon involves ingestion of a contrast agent 48 \200\22372hr before the scan, which then tags the fecal 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 pat hologies, 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 Further reading Fenlon HM , Nunes DP , Schroy III PC , et al . ( 1999 ). A comparison of vi rtual and conventional colonoscopy for the detection of colorectal polyps . N Engl J Med 341 : 1496 \200\223 503 .