Chronic diarrhoea Flashcards
Small intestinal diarrhoea
Vomiting common
Weight loss common
Polydipsia common
Often appetite increased or reduced
Watery/bulky faeces
Faecal volume increased
Defaecate 1-3 times a day
Faecal fat ± starch may be present
Tenesmus not present
Urgency not present
Mucus not present
If blood present, melaena
Minimal flatulence
Large intestinal diarrhoea
Sometimes vomit (30%)
Usually no weight loss
No polydipsia
Appetite often normal
Faecal type varies
Volume normal or increased
Defaecate > 6 times a day
No faecal fat (unless secondary)
Tenesmus often present
Urgency often present
Mucus often present
If blood present, fresh
Flatulence common
Common dietary causes of chronic SI diarrhoea
Chronic or intermittent scavenging
Chronic dietary intolerance e.g. lactose intolerance, gluten-sensitive enteropathy, other less well-defined food allergies (e.g. as cause of lymphocytic-plasmacytic enteritis)
Common infectious GI causes of chronic SI diarrhoea
e.g. salmonella, campylobacter, trichuris, giardia can particularly become chronic
Common small intestinal disease causes of chronic SI diarrhoea
Chronic inflammatory enteropathy which may be food responsive; antibiotic responsive (“Antibiotic responsive diarrhoea” (ARD)), steroid responsive (idiopathic IBD), or non-responsive/refractory.
SI neoplasia (lymphoma, mast cell tumours, adenocarcinomas)
SI partial obstruction (e.g. FB, intussusceptions - ileo-caeco-colic commonest, then jejuno-jejunal, strictures etc)
Lymphangectasia
Increased permeability due to portal congestion: R-sided CHF, liver disease
Rare brush border enzyme deficits
“Short bowel syndrome” after extensive SI resection (and overgrowth of bacteria particularly if ileocaecocolic valve resected, maldigestion and malabsorption)
Pancreatic causes of chronic SI diarrhoea
exocrine pancreatic insufficiency (EPI); chronic pancreatitis; pancreatic adenocarcinoma
Liver causes of chronic SI diarrhoea
due to portal congestion ± lack of bile salts (-latter actually rare even in cholestatic liver disease)
Renal causes of chrnic SI diarrhoea
due to uraemia ± hypoalbuminaemia/oedema of nephrotic syndrome.
Endocrine causes of chronic SI diarrhoea
hypoadrenocorticism dogs; hyperthyroidism cats
Initial treatment of chronic SI diarrhoea
In many cases, if otherwise bright, hospitalisation for intravenous fluid therapy etc usually not indicated.
Treat any confirmed infections (e.g. giardia, campylobacter, ascarids) and identify/treat extra-GI pathologies (e.g. EPI, pancreatitis etc).
If tests all normal, usually recommend a strict dietary exclusion trial using hypoallergenic or novel protein diet for a minimum of 4 weeks to rule out dietary hypersensitivity/intolerance and/or scavenging (important to prevent scavenging and treats in this time).
You may give a 3-day giardia dose of fenbendazole to rule out intestinal parasitism (as many are intermittently shed and parasitology can therefore be negative) and you may (controversial) elect to give a one month course of metronidazole or tylosin
Otherwise, it is recommended that you do gut biopsies first before a long course of antibiotics.
Radiography for chronic SI diarrhoea
Plain abdominal radiographs for evidence of obstruction (gravel signs, gas-filled loops of bowel), foreign bodies, intussusceptions, abnormalities of other organs.
Plain thoracic radiographs to check for tumour metastases (e.g. pancreatic adenocarcinoma).
Note contrast radiographs (barium follow-through) very limited usefulness in chronic diarrhoea – may be useful for demonstrating partial obstruction (e.g. due to neoplasia or intussusception) but largely replaced by ultrasound.
- Very insensitive to generalised gut wall infiltration.
- Contra-indicated if suspect bowel rupture as barium can cause or exacerbate peritonitis.
Ultrasound for chronic SI diarrhoea
Very useful for evaluating other abdominal viscera, identifying free abdominal fluid, or structural GI pathology (e.g. mass, intusscusceptions etc).
Less useful for evaluating diffuse intestinal disease although can assess gut wall thickness and layering.
May see loss of normal layering with lymphosarcoma whereas this is normally maintained in inflammatory bowel disease, but not invariable.
Endoscopic biopsy for chronic SI diarrhoea
most commonly performed in referral practice
Only duodenum, duodenum, ileum and colon are accessible and samples are generally small and superficial (mucosal/submucosal).
However, multiple biopsies (usually 7-10 from each region) can be taken and under endoscopic guidance so may give a more representative idea of the pathology.
Which part of the instestines cannot be accessed endoscopically?
The jejunum
Laparotomy biopsies for chronic SI diarrhoea
Laparotomy allows visual inspection of other organs including stomach, pancreas, liver and mesenteric lymph nodes and allows full thickness biopsies to be taken from all down gut (although colon usually not biopsied due to risk of dehiscence).
Main disadvantage is the increased invasiveness/morbidity, risk of dehiscence, and often sampling blindly as mucosal lesions not visible externally.
Laparoscopic biopsies for chronic SI diarrhoea
Possible less invasive technique
Pros of endoscopic biopsies
Less invasive
Minimal risk of perforation
Luminal surface can be visualised
Multiple guided biopsies
Inspection/biopsy of stomach, duodenum, oesophagus, colon, ileum possible
Cons of endoscopic biopsies
Technically challenging
Requires expensive equipment
Requires starvation +/- KleanPrep & enema preparation
Partial thickness
More difficult to differentiate IBD and lymphoma
Pros of surgical biopsies
Assessment/biopsy of jejunum and other ogans possible
Full thickness and larger biopsies
More reliable to differentiate IBD and lymphoma
No special equipment needed
Cons of surgical biopsies
More invasive
Increased morbidity and post operative pain
Risk of dehiscence and peritonitis
Fewer samples taken and pathology may not be visible from serosal surface
Oesophagus not accessible and colon not usually biopsied
Chronic inflammatory enteropathis (CIE, IBD)
Small intestine, large intestine, stomach or all three.
Often patchy/focal esp small intestine ± colon.
The aetiology of chronic inflammatory enteropathies in dogs and cats probably represent complex interactions between host genetics mucosal immunity and the intestinal microbiota.
Work in man and lab animals suggests genetic inherent susceptibility to gut immune dysregulation.
Subdivisions of CIE
- Food-responsive enteropathy (FRE)
-ruled out using exclusion hydrolyzed or novel-protein diet >6weeks - Antibiotic-responsive diarrhoea/enteropathy (ARD/ARE)
– ruled out using an appropriate antibiotic trial - Steroid/immunosuppressant-responsive enteropathy (often referred to as idiopathic inflammatory bowel disease, IBD)
- Non-responsive or refractory enteropathy
Food-responsive enteropathies
True food allergy is rare but “food-responsive enteropathy” in general is
common.
SI diarrhoea may improve non-specifically using a low allergy diet because it is very digestible - does not imply there is an allergic basis to the disease.
Most cases of confirmed food allergy in dogs and cats produce pruritic skin diseases rather than GI signs but can (more common in cats).
Which hypersensitivity types are implicated in allergic SI disease?
Types I, III, and IV
Diagnosis of food allergies
generally diagnosed clinically on a good response to an exclusion diet and recurrence on re-challenge
Blood tests and other tests very unreliable.
Antibiotic responsive diarrhoea (ARD)
Defined as cases of diarrhoea with no other cause diagnosed which respond to antibiotic therapy and require long term use to maintain clinical remission.
may have increased numbers of bacteria (whatever that may mean) or may more represent an abnormal host immune response to normal bacteria.
Small intestinal bacterial overgrowth (SIBO)
no longer really described as such.
It was defined on results of duodenal juice culture; defined overgrowth based on standard culture methods.
HOWEVER PCRs now show many more bacteria in small intestine than previously thought (many do not grow in traditional cultures) so it is not really clear what normal bacterial population in dogs and cats is and no real over-lap between dogs with classical SIBO and dogs which respond to antibiotics.
Probably not total numbers which are important but host response and types of bacteria there: some gut bacteria can cause disease, some are protective and some are neutral so absolute numbers probably not important.
Reasons for ARD
Commonest form is “primary” in young, large breed dogs especially GSDs.
- Probably result of aberrant host immune response – defects in innate immunity have been demonstrated in GSDs.
- Defective immune response probably predisposes/progresses to inflammatory bowel disease.
Deranged SI/gastric motility e.g.” gastric dumping”, SI ileus
Increase in unabsorbed nutrients e.g. in EPI, chronic inflammatory enteropathies
Reflux of bacteria from colon if ileocaecocolic valve has been surgically removed – these cases may need long term antibiotics to prevent diarrhoea.
Reduced gastric acid secretion – rare in small animals unless they are on omeprazole
Clinical signs of ARD
chronic diarrhoea (classically steatorrhoea with some largeintestinal character due to fat maldigestion), weight loss and may also be vomiting and reactive increase in hepatocellular enzymes in some.
Mild changes on histology of SI - normal in 60%.
30% show partial villus atrophy and mild lymphocytic-plasmacytic infiltrate
How does ARD cause clinical signs?
Bacterial deconjugation of bile salts reducing fat emulsification so digestion. It is particularly bacteroides species which do this in man (anaerobes) and they also bind B12. Deconjugated bile salts cause colonic irritation and secretory diarrhoea.
Bacterial breakdown of fat to hydroxy fatty acids which also cause secretory diarrhoea in colon (and smell!).
Interference with brush border enzymes and enterocyte function.
Potential for certain bacterial antigens to cause aberrant immune responses which may predispose to inflammatory bowel disease?
Diagnosis of ARD
Best diagnostic tests are to rule out everything else (including endoscopic gut biopsies) + trial of antibiotics (ARD).
N.B. Faecal cultures no help as only give colonic flora!
Treatment of ARD
Antibiotics: 4-8 weeks or longer of metronidazole 10 mg/kg bid or tylosin 10 mg/kg tid or oxytetracycline 10-20 mg/kg bid.
Low fat diet recommended - fat not an essential dietary component except need a small amount as vehicle for fat soluble vitamins and to provide EFAs.
Easily digestible diet important - to reduce undigested nutrients left in lumen for bacteria to work on ± dietary fructo-oligosaccharides may encourage normal flora.
Usually rapid resolution of diarrhoea with treatment but may need to treat for months/years if no obvious precipitating factor e.g. GSD.
Often try to discontinue due to concerns over responsible anti-biotic use but can relapse and require long-term treatment.
Steroid responsive enteropathies
Chronic (>3 weeks) persistent or recurrent GI signs
Histopathological evidence of mucosal inflammation
Exclusion of other causes of the inflammation (such as infectious or food allergic)
Inadequate response to dietary, antibiotic and anthelmintic therapies alone
Clinical response to anti-inflammatory or immunosuppressive agents
Types of IBD found on biopsy
Lymphocytic-plasmacytic enteritis (+/- gastritis +/- colitis)
Eosinophilic enteritis (+/- gastritis +/- colitis)
Lymphocytic-plasmacytic enteritis (± gastritis ± colitis)
commonest form of
inflammatory bowel disease in dogs and cats
However, L-P infiltrate may also occur secondary to other conditions e.g. ARD, giardia, and possible confusion between severe L-P enteritis and lymphosarcoma on biopsy so beware!
Severe cases show protein-losing enteropathy.
Some breed-associated L-P enteritis
Eosinophilic enteritis (± gastritis ± colitis)
usually more severe condition than L-P enteritis ± protein-losing enteropathy.
Need to rule out intestinal parasitism and will produce eosinophilic infiltrate.
Note cats may suffer eosinophilic enteritis as part of more generalised hyper-eosinophilic syndrome involving liver, spleen, mesenteric lymph nodes, kidneys, adrenals ± lungs, skin and other organs - these need life long high doses of steroids and prognosis poor.
