Approach to diarrhoea Flashcards
What are the main differentials for chronic small intestinal diarrhoea?
Dietary - hypersensitivity/ intolerance (intolerances e.g. lactose/ gluten - v rare!)
Parasitic - whipworm/ hookworm/ giardia (coccidia also possible but very rare unless animal is young or immunocompromised)
Bacteria - antibiotic responsive diarrhoea/ others are rarely the primary cause, can incidentally find campylobacter/ can be salmonella carriers. Some that are important are enteropathogenic e.coli/ enterotoxic clostridia
Viral - FIP, FeLV, FIV, distemper
Extraintestinal - hyperthyroidism, addisons, primary lymphangiectasia, dysautonomia, chronic pancreatitis, hepatic dz, EPI
Inflammatory - lymphoplasmacytic/ eosinophilic/ other IBDs/ chronic partial obstruction
Neoplasia - mostly lymphoma, also adenocarcinoma, leimyomas, MCT
What are the main ddx for large intestine diarrhoea?
Dietary - hypersensitivity/ fibre responsive
Parasitic - whipworms, giardia (both more SI), Tritrichomonas foetus
Bacterial - more SI, e.coli in boxers causes colitis
Viral - FIP
Perineal - hernia/ tumour/ stricture/ other mass effects
Inflammatory - lymphoplasmacytic enteritis/ colitis/ neutrophilic/ histiocytic/ ulcerative/ granulomatous disease
Infiltrative - same as SI
What initial investigations should be done if there are no concerns in the Hx/ PE?
Bloods and UA to assess for more serious disease not clear from PE/ Hx
F+ exam (culture and parasitology) - be aware only 30% of the biome will be assessed, always pool samples
Diet trial
If initial trials and Ix are unrewarding, what bloods should you consider next (based on rest of Hx/ signalment/ PE/ initial bloods?
PLI/ TLI/ folate/ cobalamin TT4 ACTH stim FIP profile Viral testing Infectious disease testing (if has been out of country)
What are the main tests that can be done once initial tx/ tests was unrewarding?
Bloods Imaging (US/ rads/ CT/ endoscopy) Alternative diets Transabdominal sampling Biopsies
What is the difference between Addisons, Atypical hypoadrenocorticism and typical hypoadrenocorticism?
Addisons = typical hypoadrenocorticism (both glucocorticoid and mineralocorticoid deficiency) Atypical = only glucocorticoid deficiency
What is the typical signalment of an animal with hypoadrenocorticism?
Young, although can range from 2m-geriatric
Poodles over represented
Conflicting evidence but possibly more in females
What are possible clinical signs of hypoadrenocorticism?
PUPD V+ D+ bradycardia could be shocky, with hypoglycaemia possible Shivering/ stiffness
What are the bloods signs of animal with low glucocorticoid
Haematology: Regenerative or non regenerative anaemia Eosinophilia (or at lease not 0 in a sick animal) Lymphocytosis No stress leukogram Neutropaenia
Biochem: (due to effects on liver) mild hypoglycaemia
Mild hypocholesterolaemia
Mild hypoalbuminaemia
What are the bloods signs of low mineralocorticoid (aldosterone)
Haematology - no effects Biochem - high K+ low Na+ Low Cl- Pre-renal azotaemia with low USG
When can hypoadrenocorticism cause anaemia?
Steroids are needed for gut integrity - can get ulcers that bleed
How can cushings affect the PCV?
High end normal
How is looking at the Na:K ratio helpful in hypoadrenocorticism?
<23:1 - highly likely has typical hypoadrenocorticism
Atypical will not show abnormality
How many hypoadrenocorticism cases will not have electrolyte changes when bloods are performed?
4-24%
Those with atypical can easily go on to get typical
What is the use of basal cortisol for testing for hypoadrenocorticism?
If levels are <55nmol, or within the equivocal zone, then need to perform ACTH test.
If higher than equivocal zone, can rule it out
Some very sick animals can have low cortisol so does not provide diagnosis, is just a first step
What is the gold standard test for hypoadrenocorticism?
ACTH stimulation test
Do not give IM if any concern animal is dehydrated
All recent steroids except v recent dexamethasone cause interference (within 4 weeks)
Does not differentiate between pituitary/ hypothalamic/ adrenal disease (although most cases have adrenal disease)
What is an endogenous plasma ACTH concentration test for?
Differentiating adrenal v pituitary/hypothalamic disease
Needs v careful/ intricate handling!
Can be affected by steroid
ACTH would be high in adrenal disease, low in the others
Outline the aldosterone test
Can be run on the ACTH response test (post sample)
If aldosterone is poorly stimulated on a post sample, then the patient is likely to progress to typical disease if not already
What would a normal aldosterone test suggest?
Either atypical hypoadrenocorticism or pituitary disease causing glucocorticoid deficiency
What causes hypoadrenocorticism in cats?
N.B just never do IM ACTH in cats
Still mostly immune like dogs, however:
Adrenal - haemorrhage, lymphoma, infectious disease
Pituitary/ hypothalamic - neoplasia
What causes granulomatous colitis and who is suscpetible
Mostly boxers under 4
has been seen in Frenchies/ a cat
What are the signs of granulomatous colitis?
LI signs, but with very severe haematochezia
In some can progress to cachexia, but PE normally fairly unremarkable
How do you investigate granulomatous colitis?
Have to follow the normal investigation profile to rue out other causes. If these are unrewarding, proceed to final step of colonic biopsies (minimum 10 samples)
What do you need to assess on colonic biopsies for granulomatous colitis?
PAS staining
FISH analysis (fluorescent staining of bacteria in mucosa)
Culture and sensitivity
Can get false positives and negatives, but negative more likely
Why is C and S so important with granulomatous colitis?
As up to 50% of cases are now resistant to the standard treatment of 6-8 weeks enrofloxacin with 2 weeks given beyond clinical cure
If you get a negative result but suspect it is a false negative, trial treatment anyway
Describe Tritrichomonas foetus
Small single celled protozoa
Likes warm moist O2 deprived areas (cat colon)
Who tends to be infected with tritrichomonas?
<1 year old purebreed cats in multicat households
Around 12% co-infected with giardia
often more than one cat infected, they are normally fairly well except for their terribe LI d+
How can you increase your chances of getting a positive sample with tritrichomonas?
MUST BE FRESH
No prior treatment
Must be a d+ sample
Cannot be contaminated with cat litter etc
What methods of tritrichomonas diagnosis are there?
All faecal analysis:
Light microscopy of direct smear - low sensitivity/ specificity as hard to always see and can be confused with giardia
Protozoal culture - must be done in house, still only approx 55% sensitive
PCR - most sensitive but still relies on it having been present in the faecal sample to being with
If not treated, what happens to tritrichomonas infected cats?
Most become tolerant with 6m to 2 yrs
50% may shed still though
How do you treat tritrichomonas?
Ronidazole Can get neurotoxicity Can get treatment failure in 1/3 Also need to ensure Tx of co-infections Need to ensure household management as very contagious
Describe parvovirus
Only been around 40 yrs
Small non enveloped DNA virus
Three different types - A, B, C, have emerged with time, seemingly becoming more pathogenic
Who tends to get infected with parvo?
Unvax/ newly vaccinated Black and tan breeds possibly increased risk Normally those 4-12 weeks of age Adult mortality - 1-2% Young mortalitiy - 70%
How does parvo spread? How does it behave?
Oronasal transmission
Incubation 3-7d, no signs during this
Viraemia within 1-5d of infection - fever anorexia, lethargy
Once virus within the mucosa of the SI, causes necrosis of the crypts - V+/D+/Abdo pain
From there can get dehyration, hypovolaemia, bacterial translocation, hypovolaemic or septic shock
What are possible complications of parvo?
Intussusception
Aspiration or parvo pneumonia
Sepsis
How can you diagnose parvo?
SNAP test - bedside ELISA - detects antigen in the faeces
Can get false negatives if low numbers of antigen in the gut or lots of AB present
Can get false positives if has been vax with a modifeid live vax within 1-3 weeks
PCR - tests for viral DNA
Increased sensitivity and specificity than SNAP
Useful in kennels with d+ outbreaks and you’re checking for low shedding carriers
N.B would need virus characterisation to differentiate field and vaccine strain.
What does chronic enteropathy mean?
Animal with chronic GI signs
Can be used for animal where GI inflammation is suspected but not definitely documented
Does not infer the treatment needed
What does inflammatory bowel disease mean?
Typically means diet and AB trials have failed
Biopsies have been done
Immunosuppresant will be needed
What are the categories of chronic enteropathy?
Food responsive
Antibiotic responsive
Immunosuppressive responsive
Non responsive
Does histology differentiate between the types of chronic enteropathy?
No - this is why in stable patients, definitely worth doing diet and AB trials before endoscopy
What are negative prognostic indicators for chronic enteropathies?
Hypoalbuminaemia
Hypocobalaminaemia
High Canine IBD indexx
Hypovitaminosis D
How may food responsive and immunosuppresant responsive enteropathies differ?
Food tend to be younger, and more frequently are large intestinal
Is there a difference between easily digestible and hydrolysed diet trials?
Yes - hydrolysed much more effective
Is there a difference between novel protein and hydrolysed diet responses?
Not proven
How long do food responsive patients take to improve?
Normally 7 days, up to 14d.
N.B many dogs can have their diet changed again after 12 weeks but this is trial and error.
How can food changes affect the intestines?
Within 6 weeks there are ultrasonic improvements
What are the main histological changes in dogs with PLEs?
Lymphangiectasia
Inflammation
Neoplasia
Crypt abscess
Should you do diet trial alone for dogs with PLE?
Not really recommended
Can trial in happy healthy dogs for up to a week.
If no improvment/ deteriorating during this time then proceed to further Ix/ Tx
What antibiotics can be used to assess response and when should you try them?
After diet trial has failed/ only partial response
Metronidazole/ oxytet/ tylosin
Which dogs are more likely to respond to ABs for CE?
if there is no response within 2 weeks, re-check and re-evaluate
young dogs
GSDs/ other large breeds
How effecting is AB treatment for CE dogs?
For those that respond, there is a very high relapse rate
Often recommend a 6-8 week course initially. Still get relapses extremely frequently within 6-12m
What is the most common histological diagnosis for CE dogs?
Lymphoplasmacytic
What modality can be used to assess for bacteria in tissue?
FISH - Fluorescence in situ hybridisation
Compare treatment styles in PLE dogs cf healthy CE dogs
PLE - step down (immunosuppresant, diet, +/- ABs, drop as response seen)
Healthy - step up (diet, then AB, then drugs)
How effective is cyclosporin for CE?
Sometimes effective
can be useful as a rescue drug is steroids not effective
May still see relapses
How effective is steroid for CE?
Often effective but can get no response and can get relapses
What is the prognosis for PLE dogs with different underlying disease processes?
Large cell lymphoma the worst (<100d)
Small cell lymphoma better (<500d)
CE or lymphangiectasia had the best (>1000d)
Why can it be hard to diagnosis small cell lymphoma in dogs?
A positive test for clonality (PARR +ve) is suggestive of neoplasia
However, clonality can sometimes just be present in inflammatory disease
Some cases very suggestive will be PARR -ve
PARR sensitivity depends on the methodology used
What is the drug of choice for cats with small cell lymphoma?
Chlorambucil
How many dogs with CE are non responsive
Between 15-40%, long term responsive pets tend to be only the food related ones
What are possible future areas of treatment
motility issues are likely under diagnosed
Some promise with the use of pre and probiotics and
Faecal transplants
mesenchymal stem cells
Vitamin D deficiency treatment
What are known risk factors for feline GI lymphoma?
FIV FeLV
Smoking household
Possibly helicobacter?
Compare treatment for lymphocytic lymphoma and lymphoblastic lymphoma
Lymphocytic - pred and chlorambucil, normally live for >2 years
Lymphoblastic - Injectable chemotherapy, COP/ CHOP, MST 6-7m
When is BM aspiration appropriate?
FeLV associated disease
Cytopaenia
Circulating malignant lymphocytes
How does US appearance differ with lymphcytic lymphoma and lymphoblastic?
Lymphocytic - same as IBD - normal or increased intestinal walk thickening with preservation of wall layers, although more likely to be lymphoma than IBD if the muscularis layer is thickened
Lymphoblastic - disrption of normal wall layering, reduced wall echogenicity, localised hypomotility, abdominal lymphadenomegaly, mass lesions
How useful is FNAing mesenteric LNs that are enlarged for comfirmation of lymphocytic lymphoma?
Questionable - proceed with caution
Histologically, where is cellular infiltrate in IBD and lymphoma?
IBD - mucosa
Lymphoma - starts in mucosa, often irregularly distributed, freqent progression to submucosal and transmural infiltration
N.B lyphoma is not associated with the oedema and mucosal inflammation associated with IBD
What is epitheliotrophic lymphoma?
Subset of lymphocytic lymphoma
Characterised by the infiltration of malignant T cells into the mucosal epithelium
How is immunohistochemistry useful?
Lymphoma cases should have a monoclonal population of B or T lymphocytes
How can chlorambucil be given?
Either EOD or large dose once every 3 weeks
What can be used as a rescue therapy for lymphocytic lymphoma after pred + chlorambucil has failed?
Cyclophosphamide, although many cats do not relapse.
What are the most consistent prognostic indicators for lymphoblastic lymphoma?
- Those with complete remission have much longer survival times
Others: stage 1 (single lymph site) or 2 (regional lymphadenopathy or resectable GI mass) better than other stages
FeLV = poorer prognosis
How should you consider diet for GI lymphoma cases?
Highly digestible and palatable
hydrolysed if concurrent IBD
supplement cobalamin if any concern
What may trigger IBD?
Overly aggressive T cell responses
Genetic defects in regulating microbial killing, mucosal barrier function, or immune responses
Environmental factors
Disbalances in expression of innate immunity receptors (toll-like receptors)
Which cats are more likely to get IBD
Normally middle aged to older
Breed predispositions - asian breeds
What should be considered if there are moderate to large amounts of eosinophils in intestinal biopsies?
Possible parasite involvement or dietary intolerance
What is lymphoplasmacytic enteritis?
The most common histological form of feline IBD
HOWEVER can be associated with parasites, dietary sensitivity, hyperthyroidism
What is eosinophilic enterocolitis?
Marked mucosal infiltration with eosinophils in lamina propria
May be assocaition with hypereosinophilic syndrome in cats
What types of neutrophilic enteropathies are there?
Primarily seen with erosive mucosal lesions
Suppurative IBD can occur in young cats but very rare - normally LI signs
May be associated with enteropathogenic bacteria incl clostridium and campy
Where is the most commonly affected GI place for lesions?
Ileum
Why are cats at more risk of pancreatitis/ cholangitis?
Pancreatic duct enters the common bile duct before it opens into the proximal duodenum
This allows for reflux of GI bacteria (mostly e.coli) or intestinal contents into the pancreatic and biliary system
Small intestinal inflammation (i.e. IBD) may also ascend in the same way
What is the most successful treatment for cats with IBD?
Diet trial (50% response)
What are good adjunctive therapies for IBD?
Cobalamin supplementation
Soluble fibre if colitis present. e.g. psyllium
Probioitcs
Why is fibre good in cats with colitis?
Soluble fibre acts as a prebiotic substrate for the production of beneficial short chain fatty acids which promote colonic healing
What do prebiotics do in cats with GI disorders?
Stimulate growth of protective bacteria
Enhance production of short chain fatty acids
Improve intestinal barrier function
Decrease pro inflammatory cytokines
What do probiotics do in cats with GI disorders?
Alter the intestinal flora to suppress the pathogenic bacteria
Improve intestinal barrier function
Stimulate production of antimicrobial peptides
Decrease pro-inflammatory cytokines
What is the meaning of low albumin in a patient with diarrhoea?
negative prognostic indicator
Agressive early treatment is important as this may potentially decrease mortality rates in severely ill animals.
Increases in albumin can show treatment success, even when d+ still happening - measure every 2-3 weeks
PLE is not really a syndrome seen in cats, but there is some evidence to show cats with IBD and low albumin likely also have pancreatitis
How is cobalamin absorbed?
N.B dogs with low cobalamin have a higher risk of euthanasia, which can be reversed if cobalamin is supplemented
Receptor mediated in the ileum
Also involves intrinsic factor, which is mostly produced in the pancreas - therefore pets with EPI normally need cobalamin
How is cPLi concentration associated with prognosis for IBD dogs?
IBD dogs with high cPLi were often older and had a worse prognosis. There is a suggestion that there is a subset of patients with IBD may also have immune mediated pancreatitis, and treatment should be aimed in a way that can target both (e.g. cyclosporine)
What is faecal a-1 proteinase inhibitor?
Used as a test for PLE when albumin not yet low, not widely available
How can PARR be useful in investigating intestinal disease?
= polymerase chain reaction for antigen receptor rearrangements
Used to detect the presence of a clonally expanded population of lymphocytes
What are pANCA?
Perinuclear antineutrophilic cytoplasmic antibodies
Serum autoantibodies, similar to ANA, but more specific for intestinal disease.
Can also be high in pets with other auto-immune diseases
What are the most common causes of acute colitis?
Dietary indiscretion
Whipworm infestation (trichuris vulpis)
Clostridium difficile or perfringens infection
What are the two types of chronic idiopathic large bow diarrhoea in dogs?
Fibre responsive
Stress associated
What are the diagnostic criteria for chronic idiopathic large bow diarrhoea in dogs?
Chronic or chronic recurring d+ more than 3-4 weeks LI d+ No abnormal findings on PE or bloods No or minimal changes on colonoscopy Unremarkable histopathology (no identifiable cause)
What are the following breeds predisposed to for intestinal disease? Irish Setter GSD Basenji Boxer/ Frenchie
Irish Setter - gluten sensitive enteropathy
GSD - ARD
Basenji - immunoproliferative small intestinal disease
Boxer/ Frenchie - granulmatous colitis
What are the following breeds predisposed to for intestinal disease? Lundehund Rotties Soft-coated wheaten terrier Sharpei
Lundehund - PLE, lymphangiectasia, crypt lesions, adenocarcinoma, atrophic gastritis
Rotties - PLE, lymphangiectasia, crypt lesions
Soft-coated wheaten terrier - PLE, PLN
Sharpei - cobalamin deficiency
How can lymphatic abnormalities look grossly?
small white granules on the intestinal mesentry
This is due to lipogranulomatous infammation
Apart from protein, what else is lost with lymphangiectasia?
Malabsorption of long chain fatty acids
What is the mainstay of Tx for lymphangiectasia?
Supplement medium chain tryglycerides (e.g. coconut oil)
Pred - try to avoid immunosuppression as there is a higher risk of sepsis in these patients, therefore 1mg/kg
Consider AB trial at the same imes to prevent bacterial translocation
Can consider antithrombotic
What are the main things lost with PLE?
Albumin
Globulin
Fibrinogen
Antithrombotics
What are the possible causes of PLE?
Inflammation (IBD) ---lymphocytic. plasmacytic/ eosinophilic/ granulomatous enteritis Neoplasia ---lymphosarcoma, adenocarcinoma Infection ---Parvo, salmonella, pythium, histoplasma Lymphangiectasia ---Primary or secondary Endoparasites ---Giardia, ancyclostoma, uncinaria (pups!) Anatomical ---intussuscpetion, chronic obstruction
What can cause lymphangiectasia?
infiltration or inflammation of the lymphatic system either by
Obstruction of the thoracic duct
RHS CHF
lymphoma
When is it not a panhypoproteinaemia with PLE?
Basenjis - have a proliferative disease that leads to excess immunoglobulin production
Can be a rise in globulin with lymphoma (would have a monoclonal spike if protein electrophoresis is performed
How are cholesterol levels different in PLE and PLN
low in PLE, not really in PLN
What other biochemical abnormalities are there normally with PLE?
Low Mg
low Ca
outline the use of faecal analysis with PLN
if campylobacter found, not always pathogenic/ the cause, but should be treated as it may be, and it may be zoonotic
Really important with pups to do faecal analysis as uncinaria can cause gut damage which leads to PLE
Outline general treatment for PLE
Consider the use of colloids
Use of prophylactic antithrombotic medication
Movement of recumbent patients
use of a diurectic -spironolactone drug of choice as it is K+ sparing and slower acting reducing the chance of dehydration
Ensure nutrition - and consider Vit D and E supplementation
In which animals do you and do you not see ARD?
Do - Young large breeds dogs esp GSD
Don’t - cats, doesn’t really start in older dogs, small dogs
What is the appetite normally like in ARD dogs?
normally polyphagic/ coprophagic
Outline treatment regimes for ARD?
Normally a 4-6 week course of ABs, should see a response within 2 weeks
many relapse days to months after treatment, many can be maintained long term on a much lower dose than the original
