Structure of alimentary tract The small intestine (6m): duodenum, jejunum and ileum & 1) Duodenum (25cm) extends from the pylorus to the duodenojejunal flexture; around the pancreas Superior (5cm) Descending (8cm) Descends diagonally right. Ampulla of Vater lies ½ way down posteriomedical wall Horizontal (10cm) Passes left across posterior abdominal wall then turns up Ascending (3cm) Descends to the duodenojejunal flexture Contains Brunner's glands (secrete alkali) 2) Jejunum Position large intestine (1.5m): caecum, appendix, colon, rectum + anal canal. Rectum (12cm). It is continuous with the sigmoid colon and the anus and lies posteriorly. No mesentry but is partly covered by peritoneum Anus (4cm). Has internal (involuntary control) and external sphincter (voluntary control). Ascending colon (15cm). Fixed to posterior abdominal wall by peritoneum. Ascends from ileocaecal valve to the under surface of the liver where it turns left forming the hepatic flexture. 3) Ileum Duodenojejunal jctn ileocolic jctn –terminal –ileocolic jctn ileum Upper left abdomen Lower right abdomen Extent 40% - 2/5 60% - 3/5 Wall / plicae circularis = circular folds Thick (as many plicae circularis closely packed) Thin Mesenteric fat Less More Peyer's patches Few Many Vascular (arterial) arcades Few – 1/2 Many Vasa rectae Long, closely packed Short, spread out Appearance vascular redder pale Transverse colon (50cm) extends from hepatic flexture to spelnic flexture which lies slightly higher because of the position of the spleen. The spelnic flexture is attached to the diaphragm by the phrenicocolic ligament and to the posterior wall by a mesentry. Descending colon (30cm). Narrowest part of colon. Extends from splenic flexture to pelvic brim (left lateral) where it become the sigmoid colon (40cm). Jejunum and ileum are held to posterior abdominal wall by a mesentry so are v mobile This places the intestines into folds of the mucous membrane = plicae circularis running transversely for about 2/3s of gut circumference. Caecum lies in the right iliac fossa and is a blind ending sac which communicates with the ileum through the ileoceacal sphincter. Appendix (8cm) protrudes from the posteriolateral wall of caecum. Blind ending sac which is covered in peritoneum and has aggregations of lymphoid tissue. Functions of alimentary tract (e.g. motility, fluid and electrolyte balance, absorption, immunity) The small intestine - Secretes digestive enzymes for digestion, and absorbs water 1. Duodenum - Receives bile from the gall bladder (via common bile duct) and pancreatic juice and digestive enzymes are activated here - Its wall contains various glands e.g. Brunner’s glands, that secrete alkaline juice, rich in mucus, that protects the duodenum from the effects of the acidic chime coming from the stomach 2. Jejunum - It contains muscles to help move the food along and aid digestion - Villi and microvilli ↑ SA available to absorb nutrients - It has many large circular folds in its submucosa called plicae circulares to ↑ SA - Across epithelial cells: passive transport of sugar fructose and the active transport of amino acids, small peptides, vitamins, and most glucose. 3. Ileum - Absorption of Vitamin B12, bile salts and remaining products of digestion - Villi + micro villi to ↑ SA for absorption and adsorption (attachment) of enzyme molecules and for the absorption of products of digestion - Villi contain many capillaries: take A.As and glucose to the hepatic portal vein and the liver, and lacteals: small lymph vessels that absorb fatty acid and glycerol - Secretes protease and carbohydrase enzymes (gastrin, secretin, cholecystokinin) responsible for the final stages of protein and carbohydrate digestion. - Layers of circular and longitudinal smooth muscle enable the digested food to be pushed along the ileum by waves of muscle contractions called peristalsis. - Contains payer’s patches: which contain macrophages, dendritic cells, B-lymphocytes, and Tlymphocytes etc Large intestine - Mainly responsible for storing waste, reclaiming water, maintaining the water balance, and absorbing some vitamins, such as vitamin K. 1. Caecum 2. Colon - Some electrolytes like sodium, magnesium, and chloride are left as well as indigestible carbohydrates known as dietary fiber - Most of the remaining water is removed - Chyme is mixed with mucus and bacteria known as gut flora, and becomes faeces - The bacteria break down some of the fiber for their own nourishment and create waste products the cell lining of the colon uses for nourishment - The large intestine produces no digestive enzymes — chemical digestion is completed in the small intestine before the chyme reaches the large intestine. 3. Rectum - A temporary storage facility for feces - When rectal walls expand stretch receptors from the ANS stimulate the desire to defecate. - Intrarectal pressure forces the walls of the anal canal apart allowing the faeces to enter the canal. The rectum shortens and peristaltic waves propel the feces out of the rectum. - The internal and external sphincter allow the feces to be passed by muscles pulling the anus up over the exiting feces. Fluid: Where do fluid volumes come from: – 1200ml ingested per day (along with 800g food) – 7000ml fluid from salivary glands, gastric glands, pancreas, liver and intestinal glands. Water most abundant substance in chyme Approx. 8000ml ingested and secreted water enters the small intestine each day, but only 1500ml passes onto the large intestine. 80% absorbed in the small intestine into the blood – here osmotic potential created by the active absorption of solutes, mostly salts (ions) known as electrolytes. 100ml fluid lost in faeces – represents only 4% of total daily fluid loss. Most lost via the kidneys in urine, and the respiratory system in expiratory air due to the moist lung lining. Electrolytes: Sodium ions account for much absorption because most abundant solute in chime - Active transport occurs using Na+/K+ -ATPase pumps. Other minerals in smaller concentrations include potassium, magnesium, and calcium. Trace elements include iron, zinc and iodide. Na+/K+ -ATPase pump: 1. Transporter protein, with associated ATP molecule, binds 3 sodium ions at high-affinity sites on the intra-cellular protein surface. 2. Phosphorylation of intracellular surface of protein through the action of ATPase catalysing ATP → ADP + phosphorous. 3. Phosphorylation initiates conformational change in protein, releasing sodium ions into the extra cellular fluid. 4. New conformation results in increase affinity of the 2 binding sites for potassium. 5. Potassium binds causing dephosphorylation, returning the protein pump to its original form. 6. Potassium ions released into intracellular fluid, allowing the process to start again. Motility GI smooth muscle is inherently active. The ‘gastric pacemaker’ is on the greater curvature, the interstitial cells of Cajal) - Parasympathetic: Acetylcholine (stimulated by gastrin) - Sympathetic: Adrenaline (inhibited by dopamine / opiates) 3 types of movement: 1) Peristalsis = coordinated action to move food from one portion of the GI tract to another, in the direction of mouth→anus 2) Mass movement = the intense contraction beginning ½ way along the transverse colon that pushes intestinal contents towards the rectum – only occurs a few times a day and is responsible for colonic evacuation 3) Segmentation = alternate contraction and relaxation along the GI tract to mix food, with no forward movement Even without food in the lumen, there is a continuous muscle contraction sequence, the MMC ‘migrating motor complex’, which is initated in the antrum, and has 4 phases. - This removes indigestible particles Prevents bacterial growth Microbiology of alimentary tract Mouth - - 200+ species of oral bacteria: Streptococci, lactobacilli, staphylococci and corynebacteria. Streptococcus salivarius (up to 98%) Eruption of the teeth : colonization by S. mutans and S. sanguis. The onset of puberty : colonization by Bacteroides and spirochetes. Plaque = build-up of material on the teeth, and 60% of this material is microbial e.g. S. mutans and S. sanguis. Gingivitis : caused by increased populations of Actinomyces and other anaerobes Stomach Helicobacter pylori (up to 50%) In the stomach ↑ acidity kills all but the most acid-tolerant (mainly streptococci) Small intestine Lactics, enterics, enterococci, bifidobacteria Microbial populations are much higher in the proximal end of the small intestine than in the stomach, but are still relatively sparse vs the colon Gram-positive bacteria (mainly lactobacilli + Enterococcus faecalis), enteric rods and Bacteroides colonize the small intestine synthesize vitamins K and B complex metabolize some compounds that we cannot can metabolize compounds to produce damaging products e.g. carcinogens + are opportunistic pathogens e.g. if damage to the intestinal wall. Colon Bacteroides, lactics, enterics, enterococci, clostridia, methanogens Same sorts of species as rest of GI tract but many more in numbersIncl. enteric rods, streptococci, clostridia and lactobacilli. The predominant species by far are the strictly anaerobic e.g. bacteroides fragilis Intestinal flora facilitate: conjugated bilirubin → urobiligen, + remaining urobiligen → stercobiligen If Pts on a broad spectrum antibiotic commensals are killed allowing gut infections e.g C. Dif Able to perform examination of alimentary system Able to perform rectal examination See clinical examination handbook Able to explain to family issues relating to hygiene (e.g. infant feeding, food preparation) The Foods Standards Agency in the UK has identified the '4 Cs' to help prevent food poisoning, including food poisoning caused by Salmonella: Cleanliness Keep work surfaces and utensils clean. Wash and dry your hands regularly but especially after going to the toilet, before preparing food, after handling raw food, after touching pets, after gardening, and before touching 'ready-to-eat' food. Don't prepare food for others if you have diarrhoea or vomiting. Cover any sores or cuts on your hands with a waterproof plaster before you touch food. Change dishcloths and tea towels regularly. You should also wash your hands after touching pets or animals, after visiting farms and after gardening to help avoid infection. Cooking Make sure that you cook food thoroughly, especially meat. This will kill bacteria. Food should be cooked right through and be piping hot in the middle. If you are reheating food, it needs to be cooked right through and be piping hot in the middle. Don't reheat food more than once. You should also wash raw fruits and vegetables before you eat them. Don't drink water thought to be unsafe (including avoiding drinks containing ice cubes that may have been made from unsafe water). This includes untreated water from rivers, lakes and streams. Drink pasteurised or boiled milk and avoid raw eggs. Chilling Food that needs to be chilled or refrigerated should be. If food is left out of the fridge, bacteria may multiply to levels that can cause food poisoning. Your fridge needs to be kept between 0°C and 5°C. Don't leave the door open. Cool leftover food quickly and then refrigerate. Taking it out of the cooking pot and putting it into a shallow container can speed the cooling process up. Cross-contamination Wash your hands after touching raw foods. Separate raw and cooked or 'ready-to-eat' foods. Keep raw meat in a sealable container at the bottom of the fridge. Don't use the same surface or chopping board for preparing raw and ready-to-eat foods. Make sure that knives and utensils are cleaned after preparing raw foods. In addition to these measures, as reptiles and amphibians including terrapins and tortoises can commonly carry bacteria, you should not keep them in a house where children under the age of one year live, or where someone with a weakened immune system also lives. Able to institute methods to reduce risk of spread of diarrhoea In addition to the above If your baby has diarrhoea, be especially careful to wash your hands after changing nappies and before preparing, serving, or eating food. For older children/adults, whilst they have diarrhoea, the following are recommended: Regularly clean the toilets used with disinfectant. Also, clean the flush handle, toilet seat, sink taps, bathroom surfaces and door handles at least daily with hot water and detergent. Disposable cleaning cloths should be used (or a cloth just for toilet use). If a potty has to be used, wear gloves when you handle it, dispose of the contents into a toilet, then wash the potty with hot water and detergent and leave it to dry. If clothing or bedding is soiled, first remove any faeces into the toilet. Then wash in a separate wash at as high a temperature as possible. Don't share towels and flannels. Don't prepare food for others. Stay off school/nursery, work/college etc, until at least 48 hours after the last episode of diarrhoea or vomiting. Sometimes this time may be longer with certain infections. If the cause of diarrhoea is known to be (or suspected to be) Cryptosporidium, one should not swim in swimming pools for two weeks after the last episode of diarrhoea. Take extra measures when in countries of poor sanitation. E.g. avoid tap water, avoid food washed in unsafe water. Breast-fed babies are less likely to develop infectious diarrhoea compared to bottle-fed babies. Role of carriers of disease A 'carrier' is a person who is well, has no symptoms, but is infected with a bacterium. Carriers are at risk of passing on the infection to others if their personal hygiene is not good. C. difficile lives harmlessly in the gut of many people (~3/100 adults, 7/10 babies) The vast majority of people with a salmonella infection clear the infection and bacteria completely from their body soon after symptoms ease. Rarely, on recovery from a salmonella illness, some people become carriers and continue to pass out salmonella bacteria in their faeces for weeks or months. This is more common in children. A small number of children aged less than five years pass out salmonella bacteria for up to a year. Over the age of five years, salmonella carriers are rare, and the maximum duration of shedding appears to be up to 12 weeks. (Note: this is different to people with typhoid or paratyphoid. A small number of people who recover from these diseases remain carriers for life.) Able to take a focussed history from patient or parent regarding diarrhoea HPC - What does the patient mean by diarrhoea? What is the normal bowel habit Duration and severity of diarrhoea Frequency and timing of bowel movements Presence of blood, mucus Changes in colour or consistency - evidence of steatorrhea Circumstances of onset (including recent travel, food ingested (meat, poultry, dairy, shellfish), source of water) Triggers Does anything relieve it / Have you tried any treatments Associated symptoms - Constipation - Abdominal pain or vomiting - Rectal bleeding - Mouth ulcers - Other upper GI symptoms - Associated changes in weight or appetite - Rectal urgency or tenesmus - Altered size of stools passed - Systemic symptoms – malaise, lethargy, fever, night sweats, weight loss, anorexia - Simultaneous occurrence of diarrhoea in close contacts should be ascertained - Signs of thyrotoxicosis PMH - Recent admittance to hospital Recent surgery to bowel Hyperthyroidism, Diabetes mellitus, Hypoparathyroidism, Addison's disease DH - - Any antibiotics within the previous 3 months - is it C. Dif? – is it an antibiotic reaction e.g. erythromycin? Mg containing drugs, NSAIDs, theophyllines, anti-arrhytmics, anti-neoplastic agents – all can cause diarrhoea On laxatives?! - Are close contacts well? History of coeliacs, inflammatory bowel disease Autoimmune disorders / endocrine disorders - Recent travel abroad High alcohol intake Food additives such as sorbitol and fructose - FH SH Able to take a dietary history Adult / child 1. Have you experienced any change in weight? 2. How many meals and snacks do you eat in at 24 hour period? 3. How many times a week do you eat the following meals away from home? Breakfast ______ Lunch ______ Dinner ______ 4. What types of eating places do you frequently visit? Fast-food ______ Diner/cafeteria ______ Restaurant ______ Other ______ 5. On average, how many pieces of fruit or glasses of juice do you eat or drink each day? Fresh fruit ______ Juice (8 oz cup) ______ 6. On average, how many servings of vegetables do you eat each day? 7. On average, how many times a week do you eat a high-fiber breakfast cereal? 8. How many times a week do you eat red meat (beef, lamb, veal) or pork? 9. How many times a week do you eat chicken or turkey? 10. How many times a week do you eat fish or shellfish? 11. How many hours of television do you watch every day? 12. Do you usually snack while watching television? 13. How often do you usually consume dairy products, and what type? 14. How many times a week do you eat desserts and sweets? 15. What types of beverages do you usually drink? How many servings per day? Water ____ Juice ______ Soda ____ Diet soda ____ Sports drinks ______ hot drinks +/- sugar _____ Milk (whole, semi-skimmed, skimmed)______Alcohol (Beer, Wine, spirits) ______ Infant o Is the baby bottle or breast fed? If breast fed o What is the duration of exclusive breast feeding? o Was this a satisfying experience for mother and baby? o How often did she feed? o Was the infant content? Were there any problems? o How did he sleep, feed and gain? o Did she feed on demand or to some sort of schedule? o Was she complementing the breast milk with anything else? If bottle fed o Was he fed on formula or unmodified cow’s milk? o Which formula did he receive? How was it prepared? o What volume did he take each feed and how long did he take over it? o Frequency of feeds? o Total daily intake? Any additives (iron or vitamins) given with milk? o Duration of exclusive milk feeding? Determinants of nutritional status Nutritional status = The condition of health of a person that is influenced by the intake and utilisation of nutrients. Malnutrition covers both the states of undernutrition and overnutrition. Causes Decreased availability of food due to: - Increased in population / Low production / stocks Decreased absorption of foods e.g. coeliacs Poor education Economic conditions Stress conditions (increased nutritional need) Poor personal hygiene and environmental sanitation - Outcome Lowered food intake - Lowered intake of foods / nutrients - Wrong feeding practices Inability to make correct choice of food resulting in over/under-nutrition Lowered purchasing power causing undernutrition Higher purchasing power causing overnutrition Inability to meet the increased nutrient needs during periods of rapid physical growth e.g. in young children, adolescents, pregnant women, lactating mothers Inability to meet increased demands of illness Increased susceptibility to infections and thereby illnesses - - Able to prepare patient for imaging and endoscopic procedures Colonoscopy What is colonoscopy? A colonoscopy is a test where an operator (a doctor or nurse) looks into your colon (large intestine/bowel). A colonoscope is a thin, flexible, telescope. It is about as thick as a little finger. It is passed through the anus and into the colon. The colonoscope contains fibre optic channels which allow light to shine down so the operator can see inside your colon. The colonoscope also has a 'side channel' down which devices can pass. These can be manipulated by the operator. For example, the operator may take a small sample (biopsy) from the inside lining of the colon by using a thin 'grabbing' instrument which is passed down a side channel The procedure Colonoscopy is usually done as an outpatient or day case. You will usually be given a sedative to help you to relax. This is usually given by an injection into a vein in the back of your hand. This makes you drowsy but it is not a general anaesthetic. You will be asked to wear a gown, and lie on your side on a couch. The operator will gently push the colonoscope into your anus and up into the colon. This can be a little uncomfortable. The operator can look down the colonoscope and inspect the lining of the colon. Modern colonoscopes transmit pictures through onto a TV monitor for the operator to look at. Air is passed down a channel in the colonoscope into the colon to make the inside lining easier to see. This may cause you to feel as if you want to go to the toilet. The air may also make you feel bloated, cause some mild 'wind pains', and may cause you to pass wind. This is normal and there is no need to be embarrassed, as the operator will expect this to happen. The operator may take biopsies (small samples) of some parts of the inside lining of the colon. This is painless. It is also possible to remove polyps (small lumps of tissue which hang from the inside lining of the colon.) At the end of the procedure the colonoscope is gently pulled out. A colonoscopy usually takes about 20-30 minutes. However, you should allow at least 2 hours for the whole appointment. What preparation do I need to do? The colon needs to be empty so that the operator can get a clear view. You will be instructed on how to take a special diet for a few days before the test. You will also be given some laxatives to take. You will need somebody to accompany you home, as you will be drowsy with the sedative. Side effects The sedative may cause you to feel tired or sleepy for several hours afterwards. You may pass some blood from your anus if a biopsy was taken, or a polyp removed. Occasionally, the colonoscope may cause damage to the colon. This may cause bleeding, infection and, rarely, perforation. If any of the following occur <48 hours after a colonoscopy, consult a doctor immediately: × Abdominal pain. (In particular if it becomes gradually worse, and is different or more intense to any 'usual' pains that you may have.) × Fever (raised temperature). × Passing a lot of blood from your anus. Sigmoidoscopy What is sigmoidoscopy? The sigmoid colon is the final portion of the bowel that is joined to the rectum. A sigmoidoscope is a small tube with an attached light source about the thickness of your finger. A doctor or nurse inserts the sigmoidoscope into the anus and pushes it slowly into the rectum and sigmoid colon. This allows the doctor or nurse to see the lining of the rectum and sigmoid colon. The procedure is not usually painful but it may be a little uncomfortable. The flexible sigmoidscope allows your doctor to see around bends in the colon and usually makes the examination more comfortable. The rigid sigmoidoscope allows your doctor to look into the rectum and the bottom part of the colon, but it does not reach as far into the colon as the flexible sigmoidoscope. What preparation do I need to do? The colon needs to be empty so that the operator can get a clear view. This is usually by taking powerful laxatives for a day or two, or by using one or two enemas prior to the procedure. A commonly used laxative to clear the bowel is called Picolax. The procedure This test takes just a few minutes. Usually you do not need an anaesthetic or sedation. You wear a hospital gown so that the lower half of your body is exposed. You will be asked to lie on your left side with your knees drawn up toward your chest. First the doctor or nurse will gently insert a gloved and lubricated finger (or fingers) into the rectum to check for blockage and to widen the anus. Then the sigmoidoscope will be inserted and gently pushed further into the rectum and colon. Air is gently pumped through the sigmoidoscope to help viewing. This can cause you to feel bloated and uncomfortable, and give you an urge to defecate ('move your bowels'). As the sigmoidoscope is slowly removed, the lining of the bowel is carefully examined. A small sample (biopsy) of bowel lining may be taken during the procedure. The sample is sent to the laboratory to be looked at under the microscope. It may also be tested for various conditions that can affect the bowel. Side-effects Some people have some crampy pains and excess wind after the procedure. Occasionally, the sigmoidoscope causes some damage to the rectum or colon. This may cause bleeding, infection and, rarely, perforation of the colon. If any of the following occur within 48 hours after a sigmoidoscopy, consult a doctor immediately: × Severe abdominal pain. × Bloody bowel movements or rectal bleeding. × Fever. Barium enema What is a barium enema? A barium enema is used to look for problems in the colon, such as polyps, inflammation (colitis), narrowing of the colon, tumours, diverticula, etc. The gut does not show up very well on ordinary X-ray pictures. However, if a liquid that contains barium is placed in the gut, the outline of the intestines (gut) shows up clearly on Xray pictures. This is because X-rays do not pass through barium. A thick white liquid that contains barium is used as an enema to place in the colon (lower gut) The procedure You will be asked to wear a gown and to lie on a couch on your side or front. A small tube is then put into your anus (back passage) and gently pushed up a few centimetres. Barium liquid is then passed through the tube into your colon. The aim is to get the barium liquid to spread all along the colon as far as the caecum (where the small intestine joins the colon). To help with this, the person doing the test may: Ask you to move into different positions to help with the flow of the barium liquid. Give you an injection of a drug that makes the muscles in the wall of the colon relax. Pass some air down the enema tube into the colon. (This may feel a little uncomfortable like 'trapped wind'.) When the barium has spread throughout the colon, several X-ray pictures are taken with you in different positions. The aim is to have pictures of all parts of the colon. (Low-dose X-rays are used so the total amount of radiation is quite small and thought to be safe.) The tube is then removed and you can go to the toilet. The test takes 15-20 minutes. What preparation do I need to do? The preparation aims to clear out any faeces (stools) from your colon before the test. So, you should be given some strong laxatives. You should also be advised on the kind of food to eat for a day or so before the test. You will usually be advised to carry on with your normal medication, except iron tablets. You will need to arrange travel home as you may not be able to drive safely* Are there any side-effects or risks from a barium enema? The barium does not get absorbed into the body! Some people feel a little sickly or have stomach cramps for a few hours afterwards. The barium may make you constipated. So, to help prevent constipation: o Have lots to drink for a day or so to flush the barium out of your gut. o Eat plenty of fruit for a day or so. o See your doctor if you haven't passed any faeces (stools) after three or four days. The barium will make your faeces white or pale until it has all passed out from your colon (after a day or so). If you had an injection to relax the muscles in your colon, it may cause some blurring of your vision for an hour or so. If this happens it is best not to drive until this passes* Rarely it can cause perforation of the colon (making a small hole in the wall of the colon). This is generally only a risk if you have a badly inflamed colon. Rarely a person may have a reaction to the injection of muscle relaxant mentioned above. DIARRHOEA = Diarrhoea means 'loose or watery stools (faeces), usually at least three times in 24 hours' – can be defined as the passage of more than 300 g of stool per day. Often there is an increase in the frequency of defaecation and a loosening of the consistency. Global impact on infant mortality Diarrhoeal disease is the second leading cause of death (16%) in children under five years old. It is both preventable and treatable. Diarrhoeal disease kills 1.5 million children every year. Globally, there are about two billion cases of diarrhoeal disease every year. >50% of these are in Africa and South Asia Diarrhoeal disease mainly affects children under two years old. Diarrhoea is a leading cause of malnutrition in children under five years old. Able to detect features of dehydration in infancy and childhood Feature Consciousness Cap refill Alert 2 sec Moderate (610%) Lethargic 2-4 sec Mucous membranes Tears Normal Dry Normal ↓ Passing little urine Sunken eyes Weakness Being irritable or lethargic Tachycardia Mild (<5%) Severe (>10%) Obtunded >4 seconds + cool limbs Parched, cracked Absent Hypotension Fast (but often shallow) breathing Pale or mottled skin Altered skin turgor Cold hands or feet Able to maintain fluid balance change (e.g. in children with acute diarrhoea) Able to commence and monitor rehydration therapy particularly in children When to start a fluid chart 1) Actual or potential dehydration o Nil by mouth 5) Actual or potential acute illness o Diarrhoea o Risk of level 2 or 3 care o Excessive vomiting o Sepsis o Excessive surgical loss o EWS triggered/patient unstable o Excessive wound exudate 2) Commencing IV fluid 3) Routine post op management 4) Doubt over fluid status 6) Fluid restriction o Unstable cardiac failure o Liver failure o Acute renal failure Daily maintenance 0-10 kg : 100ml/kg 10-20kg : 50ml/kg 20+kg : 20ml/kg → divide by 24 to get mls/hr Estimate of weight (Age + 4) x 2 = kg Rehydration for deficit Kg x est % deficit x 10 = ml Which fluids? Need: Na, K, dextrose <6 months – 10% dextrose + electrolytes Other children – 5% d.extrose + electrolytes MATINTENANCE = 0.45% NaCl + 10% dextrose BOLUS = 0.9% NaCl (normal saline) Able to explain use of oral rehydration therapy Oral rehydration therapy o Principally this involves giving the dehydrated individual glucose and sodium (salt). 1) WHO ORS (sodium chloride 3.5g, sodium citrate 2.9g, potassium chloride 1.5g and glucose in one litre). 2) Dioralyte Ingredients: Na+, K+, Cl-, citrate and glucose Dose: 200-400ml solution after every loose motion - Infant: 1-1 1/2 times usual feed volume - Child: 200ml after every loose motion Instructions: Sachets: make up one sachet with 200 ml of water, freshly boiled and cooled for infants Effervescent tablets: 2 tablets in 200 ml of water, only for adults and for children over 1 year Fluids to prevent dehydration Encourage plenty of fluids. Breast or bottle feeds should be encouraged as normal. ADULTS - As a rough guide, drink at least an extra 200 mls after each bout of diarrhoea (after each watery stool). Rehydration drinks are recommended for people who are frail, or over the age of 60, or who have underlying health problems: salts, sugar and water Do not use home-made salt/sugar drinks, as the quantity of salt and sugar has to be exact. Avoid fruit juices or fizzy drinks as these can make diarrhoea worse. In conditions where the sterility of bottles and teats is in question, the fluid should be given via a cup and spoon. Sometimes a child may need to be admitted to hospital for treatment if they are dehydrated: Treatment in hospital usually involves rehydration solution via a special tube called a 'nasogastric tube'. This tube passes through the nose, down the throat and into the stomach. An alternative treatment is with intravenous fluids (fluids given directly into a vein). Eat as normally as possible once any dehydration has been treated + keep drinking Do not 'starve' a child with diarrhoea this is now known to be wrong. Breast-fed babies should continue to be breast-fed if they will take it. This will usually be in addition to extra rehydration drinks. Bottle-fed babies should be fed with their normal full-strength feeds if they will take it. Again, this will usually be in addition to extra rehydration drinks. Older children/adults – small light meals when ready If you do feel like eating, avoid fatty, spicy or heavy food at first. Plain foods such as wholemeal bread and rice are good foods to try eating first. Medication (usually needed) You should not give medicines to stop diarrhoea to children under 12 years old. You can give paracetamol or ibuprofen to ease a high temperature or headache. ADULTS may take loperamide to decrease number of diarrhoeal episodes for up to 5 days Initiates appropriate investigations (e.g. stool exam and culture; imaging; endoscopy; serum electrolytes; tests for malabsorption) Able to interpret basic investigations Key Investigations to consider include: ● digital rectal examination, to exclude overflow diarrhoea due to constipation and a low rectal carcinoma ● blood tests include: o full blood count, ESR o creatinine and electrolytes, glucose o C reactive protein o clotting screen o B12 and folate o TIBC o thyroxine o immunoglobulins o fasting gut hormones - if other tests negative ● Radiology: o especially important when the abdomen is distended or tender o a plain abdominal film may reveal fluid levels, gas- filled loops or loss of gas in parts where the loops are inflamed o barium enema ● sigmoidoscopy +/- biopsy ● colonoscopy +/- biopsy ● stool microbiology, including microscopy, culture and antibiotic sensitivity determination ● stool for faecal fat estimation to exclude steatorrhoea Disorders of fluid/ electrolyte balance Condition Definition Hyponatraemia Serum Na < 136 mEq/L caused by an excess of water relative to solute. Aetiology Common causes include diuretic use, diarrhea, heart failure, and renal disease. Clinical features Primarily neurologic (due to an osmotic shift of water into brain cells causing oedema): headache, confusion, seizures and coma. Serum Na. Serum and urine electrolytes and osmolality help determine the cause. Restricting water Controlled water intake and promoting replacement. If poor its loss, replacing any response, testing (e.g. Na deficit, and monitored water treating the cause. deprivation or vasopressin) to detect other causes Tests Treatment Hypernatremia Hypokalaemia Hypernatraemia is Serum K < 3.5 mEq/L serum Na > 145 mEq/L. (deficit in total body K stores or abnormal movement of K into cells) It implies a deficit of Excess losses from total body water kidneys or GI tract e.g. relative to total body chornic diarrhoea, Na, caused by water vomiting, protracted intake being less than gastric suction, clay water losses. (bentonite) ingestion (binds to K), villous adenoma of the colon Thirst; neurologic (due Muscle weakness and to an osmotic shift of polyuria; cardiac water out of brain hyperexcitability may cells): confusion, occur with severe seizures, coma neuro- hypokalemia. muscular excitability Serum K measurement. Giving K and managing the cause. Hyperkalaemia Serum K > 5.5 mEq/L (excess total body K stores or abnormal movement of K out of cells) Increased K intake, drugs that impair renal K excretion, and acute or chronic kidney disease. It can also occur in metabolic acidosis as in diabetic ketoacidosis. Neuromuscular: muscle weakness and cardiac toxicity Hypocalcaemia Hypocalcemia is total serum Ca < 8.8 mg/dL & normal plasma protein conc.s OR serum ionized Ca < 4.7 mg/dL Causes include hypoparathyroidism, vitamin D deficiency, and renal disease. Serum K, and ECG. Serum Ca with adjustment for serum albumin. Treatment is administration of Ca, sometimes with vitamin D. Decreasing K intake, adjusting drugs, giving a cation exchange resin and, in emergencies, Ca gluconate, insulin, and dialysis. Manifestations include paresthesias, tetany, and, when severe, seizures, encephalopathy, and heart failure. Condition Definition Aetiology Clinical features Tests Treatment Hypercalcaemia Hypercalcemia is total serum Ca concentration > 10.4 mg/dL or ionized serum Ca > 5.2 mg/dL. Hyperparathyroidism, vitamin D toxicity, and cancer. Hypophosphatemia Serum phosphate (PO4) < 2.5 mg/dL Alcoholism, starvation, diuretic use. Hyperphosphatemia Hypomagnesemia Serum phosphate (PO4) Serum Mg < 1.4 > 4.5 mg/dL mEq/L (< 0.70 mmol/L). burns, Chronic renal failure, and hypoparathyroidism, and metabolic or respiratory acidosis. Hypermagnesemia Serum Mg > 2.1 mEq/L (> 1.05 mmol/L). Inadequate Mg intake The major cause is renal and absorption or failure. increased excretion due to hypercalcemia or drugs such as furosemide. Polyuria, constipation, Muscle weakness, Features may be due to Features due to Symptoms include muscle weakness, respiratory failure, accompanying accompanying hypotension, respiratory confusion, and coma. and heart failure; hypocalcemia e.g. hypokalemia and depression, and cardiac seizures and coma can tetany. hypocalcemia: arrest. occur. lethargy, tremor, tetany, seizures, and arrhythmias. Serum ionized Ca and Serum PO4 concentration. Diagnosis is by serum Mg concentration. parathyroid hormone. Increase Ca excretion PO supplementation. Restriction of PO Mg replacement. IV administration of Ca 4 4 and reduce bone gluconate and possibly intake and resorption of Ca administration of PO4furosemide; hemodialysis involves saline, Na binding antacids, such can be helpful in severe diuresis, and drugs as Ca carbonate. cases. such as pamidronate. Able to classify type of diarrhoea Anatomically Colonic: o Diverticular disease o Colonic neoplasia o o Ischaemic colitis Overflow diarrhea secondary to constipatoin Ulcerative colitis and Crohn's colitis o Infective colitis Small bowel: o Coeliac disease o Crohn's disease o Terminal ileitis e.g. TB o Other small bowel enteropathies (e.g. Whipple's disease, tropical sprue, amyloid, intestinal lymphangiectasia) o Bile acid malabsorption o Disaccharidase deficiency o Small bowel bacterial overgrowth o Mesenteric ischaemia o Radiation enteritis o Lymphoma Pancreatic: o Chronic pancreatitis o Pancreatic carcinoma o Cystic fibrosis o By aetiology Viral e.g. rotavirus, adenovirus Bacterial food poisoningCampylobacter, Salmonella and Escherichia coli. o Recent antibiotic therapy and Clostridium difficile infection. Previous surgery: o Extensive resections of the ileum and right colon lead to diarrhoea o Bacterial overgrowth, particularly in bypass operations such as in gastric surgery and jejunoileal bypass procedures for morbid obesity o Shorter resections of the terminal ileum can lead to bile acid diarrhoea that typically occurs after meals and usually responds to fasting and cholestyramine o Chronic diarrhoea may also occur in up to 10% patients after cholecystectomy Drugs: o Up to 4% of cases o Particularly magnesiumcontaining products, antihypertensive and nonsteroidal anti-inflammatory drugs, theophyllines, antibiotics, anti-arrhythmics, and anti-neoplastic agents o Also food additives such as sorbitol and fructose Other non-infective o Alcohol: diarrhoea is common in alcohol abuse. o Anxiety o Immunodeficiency. o Autonomic neuropathy. o Factitious diarrhoea o Irritable bowel syndrome. o o Endocrine: o Hyperthyroidism o Diabetes mellitus o Hypoparathyroidism o Addison's disease o Hormone secreting tumours (VIPoma, gastrinoma, carcinoid) Infective o Chronic infection, e.g. amoebiasis, giardiasis, hookworm. Acute diarrhoea can be categorised into (a) osmotic; (b) secretory; (c) inflammatory and (d) dysmotility. Clinico-pathological features of index conditions / Able to provide advice to travellers about prevention and management of diarrhoeal illness / Epidemiology of infective diseases in UK/overseas / Prevention of traveller’s diarrhoea / Pharmacology of treatments for diarrhoeal disease / Role of surgery in index conditions / Able to initiate appropriate drug therapy and monitor its effectiveness…. To follow: Infective diarrhoeas – incl Microbiology of infective diarrhoea - - - Infection of the gut – gastroenteritis A virus is the common cause of infective diarrhoea in the UK. Various viruses are easily spread from person-to-person by close contact, or when an infected person prepares food for others. Infection with rotavirus is the most common cause of diarrhoea in children in the UK. Almost every child in the UK has a rotavirus infection before they are five years old. Adenovirus is another common cause. Food poisoning causes some cases of diarrhoea. Food poisoning is usually caused by a bacterial infection. Common examples are bacteria called Campylobacter, Salmonella and Escherichia coli. Toxins (poisons) produced by bacteria can also cause food poisoning. Parasites can also be a cause of food poisoning. Water contaminated by bacteria or other germs is another common cause of infective diarrhoea, particularly in countries with poor sanitation. Symptoms of infective diarrhoea Can range from a mild stomach upset for a day or two with slight diarrhoea, to severe watery diarrhoea for several days or longer. Blood or mucus can appear in the stools with some infections. Crampy pains in the abdomen (tummy) are common. Pains may ease each time some diarrhoea is passed. Vomiting High temperature (fever), aching limbs and headache may also develop. Diarrhoea often lasts for 3-5 days, sometimes longer. It often continues for a few days after any vomiting stops. Slightly loose stools (loose faeces) may persist for a week or so further before a normal pattern returns. Causes Parasites: Cryptosporidium parvum, Giardia lamblia, Entamoeba histolytica etc Bacteria : Campylobacter, Clostridium dificile, Escherichia coli, Listeria monocytogenes, salmonella enteritidis, Shigella Viral : HIV, rotavirus, Hepatitis A and E SHIGELLA Source – contaminated foods Diarrhoea (bloody) Fever Abdominal cramps SHIGELLA = Gram –ve, bacilli, aerobic, simple growth requirements, non-lactose fermenting, oxidase -ve ESCHERICHIA COLI Source – raw meat and unpasteurised milk E. COLI = Gram –ve, bacilli, aerobic, simple growth requirements, lactose fermenting Severe diarrhoea (bloody) Abdominal cramps Usually no fever E. coli 0157:H7 = very serious, kills the elderly and the very young ! Can cause haemolytic uraemic syndrome: haemolytic anaemia, acute renal failure, thrombocytopenia Listeria Source – unpasteurised milk, hot dogs, deli meats, raw meats (poultry), raw vegetables Diarrhoea Fever and muscle ache Nausea Can cause headaches, confusion, fits Can lead to listeria meningitis LISTERIA= Gram +ve, bacilli, aerobic E.g. L. monocytogenes SALMONELLA Aetiology Transmission Salmonella typhi can cause typhoid fever (more severe) Salmonella paratyphi (types A,B,C), can cause paratyphoid fever. Symptoms / signs Salmonella can contaminate meat, poultry, eggs, milk and other dairy Sometimes, other foods such as fruit and vegetables can become contaminated via contact with manure / Shellfish may be contaminated if in contact with infected sewage in the water. Adequate cooking of meat and poultry usually kills salmonella bacteria. Dogs, cats and rodents can sometimes become infected with salmonella and tortoises and terrapins are also common salmonella carriers. Diarrhoea +/- blood Stomach cramps Nausea and vomiting Fever Onset within 12-72 hours of eating the contaminated food / being in contact with the infected animal or person = 'incubation period' Symptoms are usually relatively mild and improve within 4-7 days If severe, dehydration can occur Typhoid fever Symptoms Malaise High fever Headache CNS: coma, delirium, meningism Pea soup diarrhoea (+/- constipation in 1st week) Signs High fever with bradycardia Hepatosplenomegaly Abdominal distension Rose spots: pink blanching papules found on the trunk (40% of patients) Tachypnoea (3rd week) Parathyroid fever – is a similar illness to typhoid fever but symptoms are generally milder. Investigations Often remains undiagnosed, if patients do not seek medical help. Temperature, pulse, BP Abdominal exam Stool culture – diagnosis of salmonella Bloods: LFTS ↑, WCC↓, anaemia SALMONELLA = Gram – Typhoid / paratyphoid fever Blood culture (1st 10 days) Bone marrow culture (idea) Urine / stool culture ve, bacilli, aerobic, simple growth requirements, non-lactose fermenting , oxidase –ve Management Most do not need specific treatment – see info on general tx for diarrhoea Babies <6 months old - seek medical advice if they develop gastroenteritis. An antibiotic (usually ciprofloxacin) is givien to: - Children <6 months with salmonella - Adults >50 years - Malnourished or immunocompromised - Patients with heart valve problems - For thyphoid/parathyphoid fever Loperamide for adults Probiotics are not generally recommended Prevention Vaccine for: Travellers o endemic areas (e.g. South Asia and Africa) Laboratory workers at risk of contact with S. typhi Prognosis Parathyroid/Typhoid fever: Untreated 20% die, commonly in 2-4 weeks due to: Toxaemia, Encephalopathy, GI perforation and haemorrhage, Peritonitis, Toxic myocarditis CLOSTRIDIUM DIFFICILE Epidemiology / incidence Most cases occur in people who are in hospital (or care homes), or who have recently been in hospital because: a) bacteria and spores more likely to be found b) people in hospital are more likely to have been given antibiotics. 1/5 people with diarrhoea post-antiobiotics have C. difficile C. difficile infection is more common in older people. Over 8 in 10 cases occur in people over the age of 65 because a) older people are more commonly in hospital b) older people more prone to this infection. Risk factors include: - Age - Time spent in hospital - Immunosuppression / comorbidities - Takeing PPIs (proton pump inhibitors) e.g. omeprazole, lansoprazole - Previous C. difficile infection (1 in 4-5 chance of re-infection) C. difficile lives harmlessly in the gut of many (~3/100 adults, 7/10 babies) C. difficile produces spores (like 'seeds') which are resistant to ↑ temps. C. difficile bacteria make toxins that damage the colon. Strain 027 produces more toxins than most other strains and is more likely to cause severe illness. Aetiology Transmission Spores are passed out with the faeces of those with C. difficile in their gut – they can persist (on clothes, bedding, surfaces, etc) for several months/yrs The spores can also be spread through the air They may get on to food, and into the mouth and gut of some people. Symptoms / signs Many cases are mild Mild or moderate watery diarrhoea. Crampy abdominal pains Nausea Fever Symptoms may last from a few days to several weeks. In mild cases, symptoms often clear away without any specific treatment. Pseudomembranous colitis This occurs in some cases and is more serious. Colitis = colon inflammation Pseudomembranous = membrane-like patches on the inside lining of the colon. This can cause: Bloody diarrhoea Abdominal pain A distended colon and abdomen Fever In some cases it becomes severe and life-threatening ('fulminant colitis'). The colon may perforate causing serious infection +/- death. Investigations Management Suspected in: C. DIF = Gram Anyone who develops diarrhoea who has had antibiotics within the previous 2 months ..and/or… +ve, bacilli, When diarrhoea develops during (or within few weeks) aerobic of a hospital stay Stool sample – confirms diagnosis by detecting the C. difficile toxin Blood tests, an abdominal X-ray or a CT scan may be indicated if severe Prevention - not prescribing unnecessary antiobiotics No treatment for carriers If mild symptoms: treat at home, If severe: admission Note: remain off work / school until free from diarrhoea for 48 hrs. Stop any antibiotics Allows normal bacteria to thrive again The ‘overgrowth’ of C. difficile should reduce Start vancomycin / metronidazole These antiobiotics kill C. difficile Symptoms then improve in 2-3 days (in severe cases, may prevent perforation) Ensure plenty of fluids to avoid dehydration (see earlier notes) Surgery in rare cases In cases of fulminant colitis, especially if the colon perforates Avoid anti-diarrhoeals e.g. loperamide – they may slow rate of clearance Probiotics (‘good’ bacteria and yeasts) are not recommended Prognosis Most patients recover, some without treatment Death and perforation of the colon can occur in fulminant colitis CAMPLYLOBACTER Epidemiology The most common bacteria causing food poisoning in the UK. More common in certain groups of people: Children under the age of five and adults over the age of 60. People who travel to developing countries where sanitation and food hygiene may be less strict. People working with farm animals. People who work in the meat industry. Transmission Camplylobacter bacteria are commonly found in raw meat, esp poultry. Adequate cooking of meat thoroughly kills salmonella bacteria. Camplylobacter may also be found in unpasteurised milk or untreated water (including ice cubes made from untreated water). Occasionally mushrooms and shellfish can contain campylobacter Pets (incl cats and dogs) and other animals can also pass on campylobacter to you (without any symptoms themselves!) Symptoms / signs Investigations Management Diarrhoea Nausea +/- vomiting Stomach cramps Fever Onset within 2-5 days of eating the food / being in contact with the contaminated animal… but sometimes the incubation period can be as long as 10 days In most, symptoms are mild and improve within 2-3 days About 9/10 recover in a week If severe, dehydration can occur Often remains unconfirmed, if patients do not seek medical help. Signs of dehydration Temperature, pulse, BP Abdominal exam Stool sample – diagnosis of campylobacter CAMPYLOBACTER = Gram +ve, bacilli, aerobic, fastidious growth requirements Most patients do not need specific treatment. Occasionally, admission to hospital is needed if symptoms are severe, or if complications develop. Antibiotics may then be given. Ensure plenty of fluids to avoid dehydration (see oral rehydration therapy notes for adults/children) Babies under six months old are at increased risk of dehydration. You should seek medical advice if they develop gastroenteritis. Paracetamol / ibuprofen to ease a high temperature or abdominal pain Loperamide for adults Probiotics are not generally recommended Anti-diarrhoeals not indicated for children <12 CHOLERA Epidemiology Endemic in portions of Asia, the Middle East, Africa, South and Central America, and the Gulf Coast of the US – here incidence is highest in children, and tends to decrease with age due to acquired immunity In non-endemic areas: cholera prevalence is not age dependent - this reflects that most of the population have no immunity Aetiology Cholera is caused by infection with the bacterium Vibrio cholera = Over 100 serotypes of V. cholerae exist but only two cause disease: V. cholerae 01 (two biotypes - classic and El Tor) and O139. There are other types of species of V. cholerae which also cause infection in humans including V. parahaemolyticus, V. mimicus, V. damsela and V. hollisae and they also cause diarrhoea. Transmission is usually from contaminated water and direct person-toperson transmission is rare. It is not endemic to UK. Most patients are free of V. cholerae within 2 wk after cessation of diarrhea; chronic biliary tract carriers are rare. Pathophysiology Symptoms Vibrio cholerae colonises the small intestine and produces a potent endotoxin which binds the GMI-ganglioside receptor on cell membrane The active subunits of the endotoxin enters the cell and activates the adenyl cyclise – causing accumulation of cyclic AMP This stimulates active secretion of ionic sodium, chloride, potassium and HCO3 into the lumen, and with it water = diarrhoea The incubation period is 6 to 72 hours. 1) Most people infected do not become ill although they may be excreting the organism for 7 to 14 days. 2) A number of people develop diarrhoea that is undistinguishable from other forms of gastroenteritis. 3) ~10% develop severe illness (3 stages) Evacuation phase - abrupt onset of profuse, watery diarrhoea (rice water stools - because mucus flecks may be seen floating in the watery stools) +/- vomiting Collapse phase - features of circulatory shock, and dehydration. Often apathetic but not usually delirious. +/- severe muscle cramps +/- renal failure. A child may present with convulsions due to hypoglycaemia. Recovery phase - if the patient survives the collapse phase then there is a gradual return to clinical and biochemical normality over 1-3 days Signs Circulatory collapse e.g. tachycardia, cold clammy skin, peripheral cyanosis, hypotension. Dehydration Investigations ● ● ● ● ● ● CHOLERA = Gram –ve, Stool specimen to identify organism. curved bacilli, aerobic, U&E, as likely to be significantly dehydrated, and to simple growth monitor IV fluid replacement. Creatinine may rise if requirements, nonkidneys fail with prolonged hypovolaemia (via renal lactose fermenting, tubular necrosis). Severe metabolic acidosis with K+ depletion (but oxidase +ve normal serum Na+ concentration) occur. FBC will show a high Hb with haemoconcentration. WCC (raised, but will not aid diagnosis or management) A good way of estimating net fluid loss or gain if changes are large is to weigh the patient daily. 1 kg of weight represents 1 litre of fluid. Treatment ► ! notifiable disease ► Resuscitation Replacement of fluid lost. To replace K+ losses, KCl can be added to the IV solution (esp important for children) Oral glucose-electrolyte solution is effective in replacing stool losses ► Antibiotics However, if fluid loss is profuse, antibiotics may help. Tetracycline, erythromycin, doxycycline, norfloxacin, ciprofloxacin and furazolidone may be used - reduce the rate of stool output (minimises fluid loss, stops excretion of vibrio) ► Feeding Feeding during and after cholera is emphasised. × Antidiarrhoeals and antisecretory drugs Prevention Avoid drinking untreated water or eating poorly cooked seafood in endemic areas. An oral cholera vaccine is now available in the UK - not required by most but may be suitable for aid workers assisting in disaster relief or refugee camps, and more adventurous backpackers who do not have access to medical care. Inflammatory bowel disease Crohn’s Ulcerative Colitis Epidemiology ● ● ● ● Peak onset: 20-40 Slight F>M Slightly ↑ smokers than expected Common in whites / jews ● Peak onset: 20-40 ● Slight F>M ● Slightly ↓ smokers than expected ● Common in whites / jews Symptoms Diarrhoea Abdominal cramps (on eating) Weight loss & Anorexia Fever & malaise Vomiting & nausea Diarrhoea Lower abdominal pain Weight loss & Anorexia PR bleeding +/- mucus Urgency and tenesmus May be: relapsing + remitting, continuous, or single episode Signs Pyrexia Abdominal tenderness Perianal lesions Anaemia Mouth ulcers Clubbing Pyrexia, tachycardia, tender distended abdo (severe) Clubbing Investigations Bloods ● FBC, U+E, LFTs, CRP/ESR ● ANCA (Anti-Neutrophil Cytoplasmic Antibody): Raised in UC, not Crohn’s ● ESR and CRP: ↑ in active Crohn’s, ESR ↑ also in UC PR / stool ● Rectal exam ● Stool sample- exclude infectious causes Imaging ● Sigmoidoscopy and biopsy ● Capsule endoscopy for small bowel in Crohn’s ● Barium study- cobblestoning in Crohn’s Pathology Crohns Anywhere mouth → anus may also be inflammation in regional lymph nodes. UC Large bowel only, spreads from rectum proximally Skip lesions Continuous (from rectum) Transmural / deep ulcers Superficial / shallow ulcers Non-caseating granulomas Goblet cell mucus depletion, crypt abscesses, haemorrhagic + adenocarcinoma risk +++ adenocarcinoma risk Management Anti-diarrhoeals: Loperamide Supplements: vitamin and nutrient Anti-inflammatory: Prednisolone , Hydrocortisone if severe. Immunosuppressive: Ciclosporin / Azathioprine For fistulae: Infliximab Complications Malabsorption Small bowel syndrome Fistulae Obstruction ( by strictures) Perforation +/- peritonitis Haemorrhage Anal fissures, fistulas and skin tags (rarely) Systemic amyloidosis Acute - Prednisolone Maintaining remission- 5Aminosaliculic acid (Mesalazine) Curative surgery: pancolectomy, with ileoanal anastomosis/ileostomy Colon - haemorrhage, toxic megacolon (>6cm), adenocarcinma Joints - ankylosing spondylitis, arthritis Eyes - iritis, uveitis, episcleritis Skin – pigmentation, erythema nodosum, pyoderma gangrenosum Liver - fatty change, chronic pericholangitis, sclersosing Cholangitis, cirrhosis, hepatitis Systemic: anaemia, venous thrombosis, electrolyte disturbances Extraintestinal: pyoderma gangrenosum, erythema nodosum, primary sclerosing cholangitis, fatty liver/abscesses, iritis / episcleritis, arthiritis, spondylitis. GI malignancy Colorectal adenocarcinoma Risk factors × Age >50 years × IBD (UC > Chron’s disease) × Hereditary non-polyposis colorectal cancer (can do prophylactic colectomies) × Familial adenomatous polyposis Symptoms PR Bleeding / mucus Altered bowel habit Tenesmus Fatigue / weight loss / pallor (systemic/anaemia) IF bowel obstruction: pain, bloating, vomiting Jaundice (if liver mets) × × × × × × × PMH/FH: colorectal or breast cancer Alcohol abuse Smoking Low-fibre diet? ↑ animal fat/red meat diet? Pre-menopause M > F After menopause F > M Signs Rectal or abdominal mass Weight loss Anaemia Hepatomegaly (if liver mets) Cancers arising in the caecum and right colon are often asymptomatic and present as irondeficiency anaemia Left – sided colonic cancers typically present with looser and more frequent stools +/- abdominal pain Rectal and sigmoid cancers commonly bleed, causing blood in stools, mixed in, as well as tenesmus and ↓ stool diameter Investigations ● Colonoscopy = gold standard. Allows imaging of whole colon and biopsy. Can’t do it in clinic. ● Sigmoidoscopy = accurate for rectal / sigmoid tumours. Only images the last 1/3 of colon. Can be done in clinic. Detects smaller adenomatous polyps than barium enema ● Double contrast barium enema = can visualise colonic tumours ● Endo anal US / pelvic MRI = staging rectal cancers ● CT / PET = assessment of metastases ● FBC – microcytic anaemia ● Faecal occult blood = screening for ages 60-69 ● CEA (carcino-embryonic antigen) – may be used to monitor effectiveness of treatment ● If polyposis in family, refer for DNA testing once a patient is >15 years DUKES A STAGING 5 year prognosis B C D Intramucosal Invaded bowel wall Transmural + lymph nodes Distant metastases 95% 75% 30% <5% Treatment ● Stenting – can give significant palliation, or be used pre-surgery to allow elective resection ● Radiotherapy ● Chemotherapy · Fluorouracil +/- agents such as folinic acid, lavamisole, is used in Dukes stage C · Newer agents include: irinotecan, oxaliplatin ● Surgery Tumour location Surgical procedure Caecal, ascending or proximal transverse colon tumours Right hemicolectomy Tumours in the distal transverse or descending colon Left hemicolectomy Sigmoid colon tumours Sigmoid colectomy Low sigmoid or high rectal tumours Anterior resection – anastomosis / colostomy Low rectal tumours (<8cm from anal canal) Abdomino-perineal (A-P resection) – permenant colostomy and removal of rectum and anus Patients with single-lobe hapatic metastases and no extrahepatic spread May be suitable for curatice surgery with liver reserction Cause / epidemiology × × × × GASTRIC CANCER Strong link with Helicobacter pylori and gastritis Smoking ↑s risk Pernicious anaemia has a small ↑ in risk Veg + fruits, ↓ salt – protect from gastric cancer × Peaks 50-70 years × M>F Symptoms Epigastric pain – relieved by food and antacids (indistinguishable from peptic ulcer) Dyspepsia o > 1 month o Aged 55 and over Vomiting (severe if ca is at pylorus) Weight loss Dysphagia (if ca invades fundus) Anaemia (gross haematemesis is rare) Signs Tender epigastric mass (50%) Weight loss Hepatomegaly, jaundice, ascites (mets) Troisier’s sign = Enlarged left supraclavicular node (Virchow’s node) Gastric cancer is the cancer most commonly associated with dermatomyositis and achanthosis nigricans Investigations ● FBC, LFTs ● Gastroscopy + ulcer edge biopsies ● Staging CT Management Surgical · Endoscopic mucosal resection (early) · Partial or total gastrectomy Chemotherapy Palliative for obstruction/ pain/ haemorrhage Malabsorption syndromes Defective intraluminal digestion Pancreatic insufficiency – pancreatitis – cystic fibrosis defective bile secretion (lack of fat solubilisation) – biliary obstruction – ileal resection – decreased bile salt uptake bacterial overgrowth Insufficient absorptive area – Coeliac’s disease (gluten sensitive enteropathy) – Chron’s – extensive surface parasitisation – small intestinal resection or bypass (procedure for morbid obesity / Crohn’s disease / infarcted small bowel) Lack of digestive enzymes disaccharidase deficiency (lactose intolerance) bacterial overgrowth – brush border damage Defective epithelial transport abetalipoproteinaemia primary bile acid malabsorption – mutations in bile acid transporter protein Lymphatic obstruction lymphoma tuberculosis Vitamin E deficiency low birth weight haemolytic anaemia of mother Vitamin D deficiency Osteomalacia / rickets Vitamin K deficiency Haemorrhage Vitamin A Deficiency Eye changes begin with night blindness. If it is not treated, it leads to complete blindness. Drying of the white portion of the eye. Increased rate of infections especially of the respiratory system. Anaemia General body weakness. The person complains of tiredness and breathlessness. Loss of appetite. Paleness of tongue, white portion of eye (conjunctival pallor) and nail beds. Feeling of being pricked with pins and needles on the fingers and toes. Brittle and spoon shaped nails (koilonychia) The capacity of a person to work decreases considerably. Iodine Deficiency Iodine is an important component of thyroxine. Iodine deficiency is most commonly seen as goitre in adults and cretinism in young children. In adults Goitre. Weight gain The person feels tired and is unable to work properly. Dry skin Constipation In young children Growth retardation Mental retardation Speech and hearing defects Disorders of nerves and muscles causing inability to control movements of limbs. CARBOHYDRATE INTOLERANCE Is the inability to digest certain carbohydrates due to a lack of one+ intestinal enzymes. Symptoms include diarrhea, abdominal distention, and flatulence. ● Diagnosis is clinical and by an H2 breath test. Treatment is removal of the causative disaccharide from the diet. GLUTEN MALABSORPTION = COELIAC DISEASE Pathophysiology Coeliac disease is a state of heightened immunological response to ingested gluten in genetically susceptible people. Aetiology achlorhydria: Symptoms Can be diagnosed in any age, presents in children and adults May be asymptomatic Chronic or intermittent diarrhoea Failure to thrive in children Sudden or unexpected weight loss Persistent or unexplained GI symptoms e.g. - nausea and vomiting - Recurrent or abdominal pain - Cramping - Abdominal distension Prolonged fatigue Unexplained faints Unexplained anaemia Investigations May be asymptomatic, therefore, serological testing should also be offered in children and adults with first degree relatives with: × Coeliac’s disease × Autoimmune thyroid disease × Dermatitis hepetiformis × Irritable bowel syndrome × Type 1 diabetes Or other conditions: http://www.nice.org.uk/nicemedia/pdf/CG86FullGuideline.pdf 1) 2) 3) 4) IgA tissue transglutaminase (tTGA) If unequivocal: IgA endomysial antibodies(EMA) testing If either above are –ve: IgA deficiency testing If IgA deficient: IgG tTGA or EMA ● If any of the results are positive, refer for biopsy to exclude or confirm Coeliac disease: Marsh classification Marsh stage 0: normal mucosa Marsh stage 1: increased number of intra-epithelial lymphocytes Marsh stage 2: proliferation of the crypts of Lieberkuhn Marsh stage 3: partial or complete villous atrophy Marsh stage 4: hypoplasia of the small bowel architecture Treatment Only current treatment is a life-long gluten free diet Dietician input is generally requested LACTOSE INTOLERANCE Lactose intolerance is a result of lactase deficiency and is a form of carbohydrate malabsorption. Lactose is hydrolyzed by lactase in the intestinal mucosa. Lactase is one of many betagalactosidases seen in the small bowel and is most active in the jejunum. The byproducts of lactose hydrolysis are the monosaccharides: 1) glucose 2) galactose When lactase is absent or deficient, hydrolysis of the sugar lactose is incomplete because it is osmotically active, the undigested sugar will pull fluid into the intestine. Hydrogen and lactic acid, in addition to other organic acids, are produced when colonic bacteria act on the undigested sugar The combined osmotic effect of the undigested sugar and organic acids results in the passage of acidic diarrheal stools. These stools can produce significant skin irritation and breakdown Infants with lactose intolerance may also present with abdominal distension and vomiting In its most severe forms lactose intolerance can lead to dehydration, electrolyte abnormalities, and failure to thrive. Lactase deficiency has been described as primary, secondary, or congenital a) congenital lactase deficiency A rare hereditary disorder in which lactase activity is absent b) primary lactase deficiency The normal gradual reduction in lactase production seen as an individual matures from infancy into adulthood and is expressed variably across populations c) secondary lactase deficiency Lactase deficiency may also be a secondary occurrence because of gastroenteritis, bowel surgery, cystic fibrosis, or immune disorders. (or transiently in infants exposed to phototherapy and antibiotic therapy) Blind loop syndrome Pathophysiology In blind loop syndrome a portion of the small intestine becomes bypassed and thus cut off from the normal flow of food. The digestion of food becomes slow or stops leading to the growth of bacteria and malabsorption A total aerobic plus anaerobic count of more than 100,000 is diagnostic of bacterial overgrowth. Aetiology Radiation enteritis duodeno-jejunal diverticulae surgery e.g. Polya gastrectomy, Billroth's operation II, Roux-enY procedure, gastric bypass for obesity2 secondary to obstruction: o Crohn's disease o tumour o radiation stricture o pseudo-obstruction fistulae: o especially small bowel to colon fistulae hypogammaglobulinaemia Symptoms Loss of appetite and early satiety Dyspepsia Diarrhoea and steatorrhoea Bloating, flatulence Weight loss Nausea Signs Cachexia abdominal distension evidence of vitamin and mineral deficiencies Investigations ● Bloods may reveal: Macrocytic anaemia (due to vitamin B12 deficiency) Hypocalcaemia Iron deficiency Raised INR (due to vitamin K deficiency) Abdominal imaging including: o Abdominal X-ray o Abdominal CT scan o Barium studies (may reveal diverticulae or strictures) o o o o ● tropical sprue systemic sclerosis / scleroderma autonomic neuropathy: o diabetes mellitus achlorhydria: o vagotomy o drugs o autoimmune o old age ● ● ● Treatment Hydrogen breath test to detect bacterial overgrowth Specialised investigations looking at small intestine function: o D-xylose breath test o Faecal fat test o Bile acid breath test Small intestine aspirate with fluid culture - invasive and difficult ► Broad spectrum antibiotics - E. coli is the most common organism and is sensitive to ampicillin, or tetracyclines (e.g. oxytetracycline) ► Nutritional supplements: Vitamin B12 injections. Oral iron supplements. Oral calcium and vitamin D supplements; other vitamin supplements. Medium chain triglycerides (are more readily digested) ► Surgical correction of the affected small bowel segment Motility disorders Reduced contact time/surface area: Rapid intestinal transit and diminished surface area impair fluid absorption and cause diarrhoea. × Small-bowel or large-bowel resection or bypass × Gastric resection × Inflammatory bowel disease × Microscopic colitis (collagenous or lymphocytic colitis) × Coeliac disease × Stimulation of intestinal smooth muscle by drugs (eg, Mg-containing antacids, laxatives, cholinesterase inhibitors, SSRIs) or humoral agents (eg, prostaglandins, serotonin) also can speed transit. Factitious diarrahoea PAtiet acts as if he or she has an illness by deliberately producing, feigning, or exaggerating symptoms. (aka Münchausen syndrome) The primary aim is to obtain sympathy, nurturance, and attention accompanying the sick role. This is in contrast to malingering, in which the patient wishes to obtain external gains such as disability payments or to avoid an unpleasant situation, such as military duty Epidemiological methods for investigating food poisoning outbreak Food poisoning is one of a number of notifiable diseases. Doctors in Wales and England have a statutory duty to notify a 'Proper Officer' of the Local Authority of suspected cases of food poisoning based on clinical symptoms – under the Public Health (Control of Disease) Act 1984 These data are compiled into a weekly Statutory Notifications of Infectious Diseases (NOIDs) report by the Health Protection Agency (HPA) Centre for Infections in Colindale, North London. Laboratory testing of specimens submitted by patients may undergo laboratory testing to establish the organism responsible for illness Aware of disease notification requirements in relation to diarrhoeal diseases NOTIFIABLE DISEASES RELATED TO DIARRHOEA Food poisoning Cholera Haemolytic uraemic Enteric fever (typhoid or syndrome (HUS) paratyphoid fever) Infectious bloody diarrhoea Who to contact: Notify a 'proper officer' of the Local Authority of suspected cases of certain infectious diseases"; usually the consultant in communicable disease control (CCDC). The GP should fill out a notification certificate immediately on diagnosis without waiting for laboratory confirmation - and ensure it gets to the officer within 3 days (phone if urgent). Books of certificates are available, and there is also a template notification document on the Health Protection Agency website (Centre for Infections). Include the following information: Patient's name, date of birth, sex, and home address with postcode. Patient's NHS number. Ethnicity (used to monitor health equalities). Occupation, and/or place of work or educational establishment if relevant. Current residence (if it is not the home address). Contact telephone number. Contact details of a parent (for children). The disease or infection, or nature of poisoning/contamination being reported. Date of onset of symptoms and date of diagnosis. Any relevant overseas travel history. If in hospital, also: o Hospital address. o Day admitted. o Whether the disease was contracted in hospital.