cats and dogs 14 Flashcards
1
Q
What are the 13 steps in insertion of a oesophagostomy tube
A
- GA
- Right lateral recumbency - oesophagus access on left hand side
- Clip and prep cervical area left side
- Pre-measure tube to apex of heart and mark tube
- Push forceps through mouth and point up and out ½ way down the neck.
- Make a stab incision over the forceps tips
- Enlarge incision so forceps can push through hole
- Grab end of tube
- Pull back towards mouth-expand opening if wish
- Turn the tube around in mouth and push down the oesophagus
- Do a little wiggle/flip and ensure kink is gone and no tube in mouth
- Pull out to predesignated spot, quick skin prep
○ Ensure positioned in the right spot via endoscope (preferred) or radiograph - Secure with pursestring then a chinese-finger trap suture with non-absorbable suture material
2
Q
Gastrostomy (G tubes) what used for, main consideration, biggest risk
A
type of enteral feeding BUT more for referral
- Long-term nutritional support
- Use 16-20 F tubes
- Must stay in place for 7-10 days
- Biggest risk is gastric wall necrosis, peritonitis
3
Q
Gastrostomy (G tube) advantages and disadvantages
A
Advantages
- Long term (months to years) feeding
- Can be fed at home
- Good for oesophageal disease
- Big tubes
Disadvantages
- Need to wait until feed (up to 24 hours????)
- Must be in at least 2 weeks before stoma forms
- If stoma breaks down get septic peritonitis
- Need some specialised equipment
- Gastric wall necrosis possible
4
Q
How to much to feed with nutritional management after abdominal surgery in cats and dogs (equations and illness factor)
A
Dogs
- Only multiply by an illness factor once they are tolerating RER amounts (1.2-1.4 dogs)
- RER = 70 (BW)0.75 or 70 + 30(BW)
Cats
- Only multiply by an illness factor once they are tolerating RER amounts (1.2-1.4 depending on activity)
- RER = 40 x BW (kcal)
5
Q
What are the goals in nutritional management after abdominal surgery how many meals per day, what feed day1-4
A
- The goal is not to get to full RER quickly (or even at all)
○ Divide into 4-6 meals per day
○ Day 1: only feed 25% calculated requirements
○ Day 2: 50%
○ Day 3: 75%
○ Day 4: 100% - Stay at lower levels if not tolerating
6
Q
what are some tips for nutritional management after abdominal surgery
A
- Bolus, intermittent much better
○ Walk around, keep in sternal during feeding
○ Walk around if possible afterward- • - LUKEWARM
- Push food in slowly
- Flush with bolus of water at start and at end
- Reduce IV fluid amount, especially in cat-
- If blocked-Coca Cola or pineapple juice
- First feeds should be < 10 mL/kg
- Don’t stop if one break-through vomit
7
Q
what to feed for nutritional management after abdominal surgery
A
- No evidence one way or the other
- If lipaemic, avoid high fat foods
- Otherwise, completely balanced with reasonable fibre and protein
8
Q
Immunomodulators what do they do, main example what it does and 2 other examples
A
- Added substances to improve gut health:
- Experimental models only
- Glutamine
○ Amino acid used by enterocytes as energy source
○ Reduces villus blunting and bacterial translocation
○ Variable outcomes in human studies, but safe except in renal or hepatic disease
○ Difficult to supplement in enteral formulations - Short chain fatty acids (acetate, butyrate, proportionate)
- Omega-3 fatty acids
9
Q
When use with assisted enteral, partial parenteral, total parenteral, immunodulatory and probiotics
A
- Assisted enteral ○ As soon as possible, virtually all cases - Partial parenteral ○ Only until enteral is tolerated - Total parenteral ○ Only if enteral not tolerated - Immunodulatory ○ Don’t know yet - Prebiotics/Probiotics ○ Don’t know yet but not in pancreatitis or post-op
10
Q
what are the 7 F’s for abdominal distention diagnosis
A
- Fluid
- Fat
- Faeces
- Flatus
- Feel a big mass
- Floppy
- Foetus
11
Q
fluid causing abdominal distention presentation and clinical signs
A
- Fluid wave on ballotment
- Fluid elsewhere in the body
- Other clinical signs
○ Temperature
○ Jugular vein -> distention suggests increase in hydrostatic pressure
○ Body condition
12
Q
fluid causing abdominal distention what is the most important step and types within
A
DETERMINE TYPE OF FLUID
- exudate -blood, chyle, urine, neoplastic, infectious, inflammatory
- ascites - low protein, low cell fluid - MOST COMMON
- modified transudate
- pure transudate
13
Q
exudate what is the most likely causes
A
§ Blood -> a little bit sometimes with bleeding tumours of liver and spleen § Chyle -> can be but rare § Neoplastic -> can be but rare § Infectious -> FIP can cause § Inflammatory -> can but rare
14
Q
ascites fluid what are the 2 types and main causes
A
= low-protein, low-cell count fluid - MOST COMMON
○ Modified transudate
§ Increase vascular permeability OR increase hydrostatic pressure
□ Jugular distention and pleural effusion common clinical signs of increase hydrostatic pressure
□ EG -> portal hypertension, caudal to diaphragm -> abdominal effusion
□ EG -> cardiac or vena cava disease -> abdominal and pleural effusion
○ Pure transudate
§ Decrease in oncotic pressure, albumin <15g/L
□ EG -> hypalbuminaemia -> all cavities +/- dependent oedema
15
Q
Physical exam -> fluid-filled abdomen (not painful), RR 60 breaths/min, HR 140bpm, Temperature 38 degrees, can’t hear lungs sounds ventrally, jugular vein distended, no cyanosis or pallor WHAT DOES THIS SUGGEST, causes and diagnostic plan
A
Ride-sided CHF
- Leads to increase in hydrostatic pressure
- Causes
○ Right atrial mass
○ Tricuspid valve disease
○ Pulmonic stenosis
○ RV cardiomyopathy
○ Pericardial effusion - cannot fill during diastole and increase pressure on right ventricular wall
§ Even after drainage of pleural effusion heart sounds still muffled as still fluid between you and heart
- Diagnostic plan
○ Radiograph - don’t want the animal to die!!!
○ Thoracocentesis - do this first
§ Then drain chest and ultrasound or radiograph
○ ONCE CONFIRM PERICARDIAL EFFUSION -> tap the pericardial sac -> will be bloody but blood WILL NOT CLOT
16
Q
What are the 2 main mechanisms of low protein, disease leading to protein loss and 4 main causes
A
Causes of low protein - Decreased production - liver disease -> WILL ALSO SEE -> low urea, glucose, bile acid stimulation - Increased loss -> skin (can usually tell), urine (only albumin lost, confirm with urine via cystocentesis (urea:creantine protein ratio) , GI tract (albumin and globulin, can also have low lymphocytes or cholesterol) Protein-losing enteropathy 1. Severe IBD 2. Neoplasia 3. Lymphangiectasis 4. Intussusception
17
Q
8 weeks old kitten, Brought in by breeder, distended and fluid filled abdomen, lethargy, dullness, pale mucous membranes
- No signs of pleural fluid and fluid is an exudate
WHAT IS IT, types and how expressed and greatest mortality in
A
Feline infectious peritonitis
- FIP is a virulence biotype of feline enteric coronavirus (FECoV)
- FECoV shed intermittently weeks to months and can be re-infected
- How host responds determines if no clinical signs or wet FIP (completely overwhelmed) or dry FIP (bi-modal, low grade inflammation and may hide in cells until older, present again at 10 years)
- FIP greatest mortality YOUNG cats
18
Q
Feline infectious peritonitis what are the 2 main presentations and clinical signs associated - EXAM
A
FIP - wet
- Most common presentation is abdominal effusion
- Possible conjunctivitis
FIP - dry
- NOT ABDOMINAL DISTENTION - just inflammatory
- Higher involvement of central nervous system and eyes (conjunctivitis)
- Harder to diagnose
19
Q
what are the 4 important diagnostic tools for the diagnoses of feline infectious peritonitis - EXAM
A
- History and signalment
- Haematology
○ Mild-moderate anaemia
○ Stress leukogram - Biochemistry
○ Hyperglobulinaemia
○ Organ-specific changes with dry FIP - Fluid analysis
○ May have green-yellow appearance
○ Often mucinous
○ Rivaltas test in clinic
○ Immunohistochemistry of fluid confirms disease - most common
○ RT-PCR
20
Q
what are some causes of fat or floppy causes for abdominal distention
A
FAT - Hypothyroidism - Hyperadrenocorticism - Obesity FLOPPY - Loss of dorsal muscle mass - Hyperadrenocorticism
21
Q
chronic abdominal pain what are likely causes
A
- More insidious and more likely to be referred pain - pain could be elsewhere in the body
○ Chronic inflammation pancreas, urinary tract
○ Chronic gastric dilation
○ Gastric ulceration
○ Infiltrative neoplasia
○ Functional intestinal spasm
○ Musculoskeletal disease
22
Q
Diagnosis for true chronic abdominal pain and are some differentials
A
1) any -itis - pancreatitis, gastritis etc
2) any ulceration
3) any distention, torison or compression - intestinal spasm main chronic one
4) Non GI -> intervertebral disc, fractured ribs, soft tissue injury, pleural disease
23
Q
what is the approach to animals with chronic abdominal pain
A
- Full and thorough history
- Physical examination
- Radiographs
○ Lateral abdomen (+spine) + thorax - ANALGESIA -> important don’t want for full diagnostics
- Ultrasound if indicated
- Additional testing:
○ Urine analysis/culture
○ Pancreatic lipase
○ Endoscopy
24
Q
Chronic pancreatitis breed, why difficult to diagnose and differentials
A
- Breed predisposition - cocker spaniels
- Difficulties in diagnosis
○ No specific clinical signs
○ No specific clinical pathology changes
○ No reliable change in PLI
○ Intermittent in nature - Differentials
○ Same as vomiting but include IBD
25
Chronic pancreatitis how to get diagnosis and treatment
- Definitive diagnosis - histopathology
○ then?, how?, why? - target treatment, possible effect on diabetes control or development of exocrine pancreatic insufficiency
○ Exploratory laparotomy
- Treatment
○ Treat concurrent disease
○ Rule out (and treat) predisposing causes
§ Hyperlipidaemia
○ Analgesia when needed - gabapentin
○ Anti-inflammatory medication - prednisolone (0.5mg/kg - dog - at anti-inflammatory doses NOT immunosuppressive)
○ Anti-emetics when needed - not chronic
○ No evidence for diet except if hyperlipemia
26
what does the presence of detectable diarrhoea indicate
1. The large intestine cannot cope with excess quantities of fluid entering from the small intestine
2. Large intestinal function is in some way compromised, either by abnormalities of the wall or the contents of faeces
27
What are the 4 pathogenesis of diarrhoea
1) osmotic diarrhoea
2) secretory diarrhoea
3) increased permeability
4) deranged motility
OFTEN COMBINATION
28
what occurs with osmotic dairrhoea
○ Occurs when there are hyperosmolar solutes in the intestinal lumen
○ Water flows in to equal plasma osmolality
○ Sodium follows down the concentration gradient into the lumen (as the intestinal fluid is diluted) and brings more water
○ Large volume, watery diarrhoea generally doesn't persist during fasting
29
what occurs with secretory diarrhoea
○ Characterised by an increase in the active ion transport mechanisms that are normally present
○ Net stimulation of secretion and inhibition of absorption
○ Lesion is biochemical
○ Associated with fluid overload of the large intestine
○ Typically, passage of large volumes of isotonic fluid and persists during fasting
30
what occurs with increased permeability diarrhoea
○ Permeability changes occur with diseases which there is disruption of the gut mucosa and/or an increase in the tissue pressure in lamina propria - generally more chronic
○ In both cases, the changes in permeability cause water and electrolytes to be secreted rather than absorbed
○ Retention of electrolytes then also creates an osmotic gradient
○ May also lose red cells and proteins
31
what occurs with deranged motility
○ Changes in intestinal motility rarely a primary cause of diarrhoea in animals
○ Increased motility contributes to diarrhoea in most diseases in some way
○ Increased motility may actually be protective mechanism
○ Increased intestinal transit time decreases exposure to toxins - if slow gut down can increase exposure to toxin
32
What are 6 systemic diseases that effect small intestinal function
1. Thyroid
2. Exocrine pancreas
3. Adrenal
4. Vasoactive peptides - tumour of pancreas - RARE
5. Increased hydrostatic pressure
6. Liver disease
33
what are the 8 main differentials for diarrhoea
1. Primary lymphangiectasis
2. Dietary indiscretion
3. Dietary sensitivity
4. Lymphoma or other diffuse neoplasia
5. IBD
6. Neoplastic partial obstruction
7. Viral, protozoal, bacterial, fungal, parasitic infection
8. Partial FB obstruction
34
What is important with history for diarrhoea
1) history of diarrhoea - long, changed, continuous
2) SI vs LI
3) melena - indicates gastric or small intestinal bleeding
4) steatorrhea -> undigested fats in faeces (exocrine pancreatitis insufficency)
5) other signs - altered appetite, weight loss, abdominal distention/pain, vomiting, borborygmi (stomach noises)
6) background infor - vaccination, medications, prphylaxis (worming), diet, environemnt, scavenger
35
in terms of diarrhoea history/physical exam what is considered serious and not so serious
```
What is considered serious
- Steatorrhea, polyphagia
- Significant weight loss
- Palpable abnormality
- Geriatric animal (older) or paediatric (more likely infectious)
- Evidence of hypoproteinaemia, anaemia
- Unwell or dehydrated
- When considered serious from owner
When not serious so treat without investigation
- Sick but likely self-limiting cause
- Not sick
- Owner constraints
- When just diarrhoea
```
36
diarrhoea what are the basics of non-specific treatment essential and controvesial
```
- Essential
○ Fluid and electrolyte replacement
○ Diet
○ Fenbendazole - to ensure don't have giardia
- Controversial
○ Motility modifiers
○ Antibiotics
```
37
diarrhoea investigation baseline data what are the main screenign tests
- Haematology
- Biochemistry (including electrolytes)
- Urine analysis
- T4 (Cats)
- Trypsin-like immunoreactivity (TLI) cats and dogs to test exocrine pancreatic function
○ Circulating trypsin
38
Screening tests for diarrhoea what can this tell you and what if you don't find anything
```
What can this tell you
-Low protein
- Anaemia
- Evidence of metabolic disease
- Nothing
If don't find anything
- Animal is well
○ Can elect treatment trail
○ Can start diagnostics (less to more invasive)
- Animal is sick or has lost body weight
○ Need to start diagnostics
○ Can start supportive treatment in meantime
```
39
What are 9 additional diagnostics for further investigations for diarrhoea
1. Serum trypsin-like immunoreactivity (TLI)
2. Serum folate (B9) and cobalamin (B12)
3. Pancreatic lipase - NO DIFFERENCE
4. Faecal analysis
5. Other lab testing
6. Imaging
7. Biopsy
8. Endoscopy
9. Exploratory laparotomy
40
Serum trypsin-like immunoreactivity (TLI) what measures, when reduced, indication and when DON'T USE
○ Reduced in exocrine pancreatic insufficiency
○ Measures circulating trypsin and trypsinogen
○ Indication
§ Breed
§ Clinical signs - skinny, bright and happy, steatorrhoea, polyphagia
§ Previous history pancreatitis
§ Cats: not typical clinical signs as for dogs
○ This is not a test for a sick dog or cat
§ Generally dogs are WELL therefore don't delay other diagnostics in SICK dog while waiting for TLI
41
Serum folate (B9) and cobalamin (B12) where abosrbed and therefore when low, what need to interpret with
○ Folate absorbed by specific carriers in proximal jejunum - produced by bacteria
○ Cobalamin absorbed by receptor-mediated endocytosis in ileum, required intrinsic factor (produced by pancreas)
§ Inherited defects of B12 absorption in giant schnauzers and border collies
○ Cats and dogs with chronic GI diseases often low serum cobalamin
§ Can't interpret accurately in dogs without TLI
□ If normal TLI and decrease cobalamin then have small intestinal disease
§ Exocrine pancreatic insufficiency
□ Cobalamin decrease 74%, folate increase 32%
§ Bacterial overgrowth
□ Increase folate, decrease cobalamin
42
pancreatic lipase measurement what for, how good is it
NO DIFFERENCE
○ Approx 25% people with IBD have concurrent pancreatitis, this worsens prognosis
○ Uncertain if related to prognosis in dogs and cats
○ May be useful addition (not in isolation)
43
Faecal analysis for diarrhoea investigation what are the 5 aspects of the analysis
```
○ Faecal flotation
§ Trichuris (colitis) from poor worming history
○ Rectal smear/scrap
§ May be indicated in endemic areas
§ Occasional diagnostic in lymphoma
○ Faecal enterotoxin assay
§ What is faecal pathogen
○ Faecal culture
§ What is faecal pathogen
○ Faecal PCR
§ SNAP test if suspect parvovirus
```
44
What are some other lab testing for dairrhoea investigation
○ In endemic areas is it important to remember other infectious cases
○ Animal often systemically unwell with significant lymphadenopathy
§ Pythiosis
§ Prototheca
§ Histoplasmosis
○ Diagnosis via demonstration of organisms, culture or possible serology
45
Imaging for diarrhoea investigation what are the 2 modalities used and what good for
```
○ Radiograph seldom useful, except for organomegaly
○ Ultrasound very useful
§ Fluid
§ Intestinal wall layering and thickness
§ Lymph nodes
§ Other abdominal organs
§ Echogenicity of mucosa
○ BUT can be normal in face of severe intestinal disease
§ Cannot give histological diagnosis
Operator and equipment dependent
```
46
Biopsy with diarrhoea investigation when indicated and not indicated and main issues
○ Theoretically gold standard for diagnosis
○ Not usually indicated in acute disease
○ In reality, lots of overlap between conditions
Can be normal even if have severe diseass
47
Endoscopy for diarrhoea investigation wy good, bad, what cannot assess and what need to do if during
```
○ Minimally invasive
○ Expensive
○ Operator experience required
○ Mucosal lesions only
○ Can't assess abdominal viscera
○ Can't always get to ileum
○ Must biopsy even if appears normal
```
48
Exploratory laparotomy what can assess for diarrhoea investigation, issue and what must do during
○ Can assess whole GI tract
○ Can assess sub-mucosal and muscularis lesions
○ Can be potentially curative as well as diagnostic
○ Expensive and invasive
○ Difficult to assess mucosa
○ Must BIOPSY
49
acute diarrhoea what is the definition what do we want to know and the 2 important diseases for small intestinal
- Less than 14 days in duration
What do we want to know?
- Does the animal need in clinic treatment
- Is it likely to be self-limiting?
- Is it infectious?
PARVO AND ACUTE HAEMORRHAGIC DIARRHOEA SYNDROME
50
What 6 indications within history/ohysical exam that would indicate infection - so need to be cautious with diarrhoea
1. Young animal
2. Signs of ill thrift
3. Poor husbandry
4. Supportive vaccination history
5. Bloody diarrhoea or fever - not always
6. Outbreak
51
What are the main groups and organisms within that cause acute small intestinal diarrhoea
```
- Helminths
○ Hookworm
○ Roundworm
○ Cestodes
- Bacterial
○ Campylobacter spp
○ Clostridium perfingens
○ C difficile
○ E. coli, Salmonella
- Protozoal
○ Cryptosporidium
○ Giardia
○ Isospora
○ Trichomonas
- Fungi and algae
- Viral
○ Enteric coronavirus
○ Distemper
○ Parvovirus
```
52
what are the 2 main parasites that cause acute small intestinal diarrhoea transmission, main clinical signs and treatment for each
1. Hookworm
○ Transmammary infection - poor husbandry situations
○ Clinical signs approx 8 days post infection
○ Blood loss +/- diarrhoea (generally not the main sign)
○ Solely responsible for clinical signs only in puppies
Treatment -> fenbendazole or monthly preventative if >6weeks of age
2. Roundworm
○ Can have migrating damage
○ Pot-bellied appearance can have signs of intestinal obstruction
Treatment -> fenbendazole or monthly preventative if >6weeks of age
53
Campylobacter what cause, where found, clinical signs and treatment
- Campylobacter
§ C jejuni up to 49% healthy dogs and 46% healthy cats
○ May invade intestine and cause watery diarrhoea with fever
○ Worse clinical signs with concurrent infection
○ Treatment - erythromycin, clindamycin, quinolones, tetracyclines -> SIDE EFFECTS, DON'T REACH FOR UNLESS SURE (opportunistic how can you be sure?
54
Clostridium perfringes/difficile) what effects, pathogenicity, main cause and treatment
produces enterotoxin A
○ Is a commensal
○ Unproven pathogenicity
○ Only consider for acute LARGE intestinal disease with high likelihood of a nosocomial infection
○ Treatment -> give fibre (treatment of the disbiosis in the gut)
55
E.coli and salmonella are they pathogenic, what cause, treatment and importance
acute small intestinal diarrhoea??
1) E. coli
○ Commensal and no associated with clinical signs
○ Pathogenic strains
§ EIEC - enteroinvasive
□ Can only tell by advanced molecular tests
§ Not likely
2) Salmonella
○ 1-30% healthy dogs, 1-18% healthy cats - NOT ALWAYS FOUND
○ Fever, diarrhoea with blood and mucus, may have signs of systemic toxicity
○ Culture in susceptible animals
○ Treatment -> if give antibiotic will shed for longer and not necessarily remove the infection
§ ZOONOTIC RISK (increased if give treatment)
56
What are the 4 main protozoal species that cause diarrhoea, what type of diarrhoea, are they are primary pathogen
1) cryptosporidium - acute small intestinal diarrhoea - no mucous, blood or diarrhoea
2) giardia - not primary pathogen
3) isospora - don't worry about
4) trtrichomonas foetus - only real pathogenic one but large intestinal chronic signs
57
cryptosporidium what are the main species, transmission, in which animals, clinical signs and treatment also how to treat giardia
C. felis and C. canis > C. parvum
○ Contact and grooming -> infected prey
○ Incidental
○ May cause in young or immune compromised animals
○ No mucus, blood and diarrhoea -> SMALL INTESTINE
○ Can sometimes see on faecal, PCR sensitive
Treatment - diet +/- antiprotozoal - but cannot cure
giardia -Treatment - fibre +/- fenbendazole first (before metronidazole - resistant)
58
Enteric coronavirus what are the 2 main types of infection, pathogenicity and treatment
○ Faecal PCR often/always positive in healthy dogs and cats - asymptomatic or not pathogenic
○ If clinical signs < 6 weeks of age
§ +/- vomiting, fever, lethargy, diarrhoea
§ Usually self-limiting
○ New virulent strain in US -> mortality associated - BAD
○ Treatment -> supportive only - NOT FIP
59
Distemper virus when do signs develop, severity depends on, diagnosis, treatment and prognosis
```
○ Signs develop 8-9 days post infection
○ Severity dependent on immune status
§ Usually poor vaccination history
§ Signs of fever and URT infection
○ to diagnose in healthy animal, easier post mortem
§ Need to see viral inclusions to diagnose
○ Treatment -> non-specific
○ Prognosis - OK unless CNS involvement
```
60
Parvovirus what age, shed how long, transmission, main results within GI tract- EXAM
○ Usually puppies, low socio-economic areas
○ Shed 3-14 days post infection
○ Rapid Oronasal spread
○ Fomites important infectious loci
§ Resistant to common detergents
○ Mid-distal small intestine villous destruction
§ Anorexia, vomiting (mild) THEN diarrhoea (severe), dehydration
61
Parvovirus diagnosis and treatment - EXAM
○ Diagnosis -> faecal SNAP test
§ False positives - generally not an issue
§ False negatives - not enough sample or too late - ISSUE WITH CONTAMINATION
○ Treatment
§ IV fluids +/- colloids, plasma
§ Antibiotics and anti-emetics as needed
§ Nutrition - ONLY THING PROVEN TO INCREASE SURVIVAL
§ If survive first 3-4 days likely to be better within the week -> generally in hostpiral for 7 days
□ Monitor for introsusception
□ Isolated and need full PPE, continual monitoring, send to 24 hour care areas - VERY EXPENSIVE ($3-5 thousand)
§ No guaranteed treatment success
§ New treatment trial -> maropitant, convenia, sub-cut administration of fluids 3 times daily
□ At home treatment, much cheaper - may save animals that owners cannot afford, owners house is infected
62
Parvovorus prevention options in clinic, at home and dog itself - EXAM
In clinic:
□ Barrier nursing
□ Disinfectant all surfaces and fomites in contact
□ Disinfect all uniforms
□ Avoid main waiting area if possible
□ Don't put in with cats - demonstrated cross-species transmission, same with ferrets
At home
□ Same as above
Dog
□ If recovered- immune > 20 months -> not immune
□ Treat for giardia -> susceptible to secondary or concurrent infection
□ Should vaccinate other puppies
® Probably too late if other infected
® Virus can survive in environment for months (just in time for next litter)
63
PCR panels for diagnosis of diarrhoea what present on cat and dog one and what useful for
- Feline -> clostridium perfingens enterotoxin A gene, Cryptosporidium spp, feline coronavirus, feline panleukopenia virus, giardia, salmonella, toxoplasma gondii and Tritrichomonas foetus
○ MOST NON-PATHOGENIC
§ except for Tritrichomonas but LARGE INTESTINE
□ Salmonella possibly
- Canine -> canine distemper virus, canine enteric coronavirus, canine parvovirus 2 (ONLY PATHOGENIC ONE), clostridium perfringens enteroxtoxin A gene, cryptosporidium spp, giardia spp, salmonella spp.
Expensive but hard to interpret -> is it actually causing the issue???? - only a few are pathogenic
64
Wha are 4 indications that acute dirrhoea is not infectious
- Relatively well puppy or kitten
- Older animal
- Negative faecal testing for the pathogens that count
- Good vaccination, worming prophylaxis and environmental conditions
65
What are the 3 main causes of non-infectious acute diarrhoea in kittens/puppies
1) osmotic - milk, changes in diet, over-eating
2) dietary indiscretion - common, older, known to be scavenger, supportive treatment
3) acute haemorrhagic diarrhoea syndrome (AHDS)
66
acute haemorrhagic diarrhoea syndrome what caharaterised by, what other things may play a role and main clinical signs - EXAM
○ Characterised by sudden onset of vomiting followed by profuse and bloody diarrhoea (strawberry jam) and severe haemoconcentration
§ Due to massive fluid loss into gut
ROLE
○ Clostridial toxins
§ Not inflammatory - probably functional - DON'T KNOW YET
§ Functional defect (secretion or permeability)
○ All ages, toys and miniature breeds - not infectious
○ Vomiting precedes diarrhoea by few hours
§ Depression and shock quickly develops
67
Acute haemorrhagic diarrhoea syndrome (AHDS) diagnosis, treatment and mortality rate and recurrence - EXAM
○ Diagnosis -> bloods
§ WCC, biochemistry and imaging usually normal
§ Marked elevation PCV (60-70) with normal skin turgor - WHAT WE USE (and look of diarrhoea)
○ Treatment
§ Prompt and aggressive IV fluid therapy -> shock rate crystalloids until PCV <50 then PRN
□ Plasma/colloid if hypoproteinaemia
§ No need for antibiotics -> unless have sepsis
§ Anti-emetics if concurrent vomiting
□ Care with maropitant in young puppies, off label for cats
§ NO FEED for first 24 hours then feed
□ Nutritional support - high fibre, low fat and easily digestible for outpatient and inpatient
® NO FIBRE IN BOILED RICE AND CHICKEN - use brown rice + vegetable (carrot, parrot)
§ Must treat adequately otherwise high mortality rate
§ May recur (uncommon)
68
the use of antibiotics in acute diarrhoea when do and don't use and what use
- Not really necessary in acute cases unless
○ Known compromised gut mucosa
○ Pyrexia AND neutropenia/neutrophilia with left shift
○ Signs of sepsis
○ Aspiration pneumonia
- If use -> metronidazole, ampicillin or amoxycillin-clavulanate
- NO INDICATION if treating as outpatient (except for parvovirus protocol)
69
What are some additional things can use to treat acute diarrhoea when use
1) pre/probiotic
- Prebiotic -> feeds the bacteria that you want to grow
- Probiotic -> adds bacteria to the system
Don't use for acute unless shelter situation
2) What about drugs to stop diarrhoea
- Locally acting drugs (absorbents)
○ Kaolin (improves consistency only)
○ Bismuth subsalicylate effective with enterotoxigenic bacteria
○ Unlikely to coat entire
○ Scourban -> DON'T USE
○ Most contain anti-cholinergic as well
- BUT - any treatment that slows gut transit time may result in firmer stool but may actually exacerbate the problem by allowing for translocation of bacteria or continued absorption of toxins
- don't use
70
chronic small intestinal diarrhoea define, which species more common in and main causes (cat or dog or both) and hungry or not
- Greater than 14 days duration
- More common presentation in dogs than cats (cats generally chronic vomiting)
Differential diagnosis
- Exocrine pancreatic insufficiency - dog
○ HUNGRY
- Food responsive diarrhoea - dog, cat
○ HUNGRY
- Antibiotic responsive diarrhoea
○ HUNGRY
- Inflammatory bowel disease (IBD) - dog, cat
○ Diminished appetite
- Liver disease
- Hypoadrenocorticism - dog
- Hyperthyroidism - cat
- Neoplasia (GI or extra GI) - dog, cat (very common)
○ Diminished appetite
71
what is small and large intestinal signs what are the 4 main differentials
- Food responsive
- Antibiotic responsive
- IBD
- Diffuse neoplasia (lymphoma) if severe signs
72
What are the 3 main initla options after history and physical exam for chronic SI diarrhoea examination and when use which
1. Treatment trail - majority of cases should investigate
2. Investigate a little
○ No response to treatment trail
○ Weight loss - significant disease is present - INVESTIGATION - rule out metabolic disease
○ Concurrent vomiting or other clinical signs
○ Owner concerned, but dog is OK
3. Investigate a lot
73
What is involved with investigating a little for chronic SI diarrhoea and what may diagnose at this step
1. Routine haematology, biochemistry and UA (urinalysis) -> in most cases better for exclusion than diagnosis
2. Serum thyroxine in cats
3. Serum TLI in dogs particularly if appetite increased
○ Other signs in cats
4. +/- cobalamin/folate
What may diagnose?
- Exocrine pancreatic insufficiency (EPI)
74
Exocrine pancreatic insufficiency how common, main presentation and 3 common causes with age of onset
```
- Uncommon in dogs, rare in cats
○ Young, weight loss, happy, hungry, German shepherd -> THINK THIS
- Aetiology:
1.. Pancreatic acinar atrophy
§ Rough collie, GSD inherited disease
§ Age of onset 6months - 2 years
§ Due to lymphocytic pancreatitis
2.. Pancreatic hypoplasia (fail to develop pancreas) generally co-current diabetes
§ Rare, signs at very young age
3.. Chronic pancreatitis
§ Any age of onset
§ +/- endocrine deficits
```
75
what are some exocrine pancreatic functions
○ Secretion of digestive enzymes (trypsin, co-lipase) to help break down lipids, proteins and polysaccharides in the proximal duodenum
○ Secretion of bicarbonate to neutralise gastric acid
○ Secretion of anti-bacterial factors
○ Secretion of cofactors to enhance cobalamin and zinc absorption
○ Protection against auto-digestion
76
Exocrine pancreatic insufficiency when result and what occurs as a result
- absence of sufficient exocrine function (>90%)
○ Maldigestion
○ Osmotic diarrhoea
○ Intestinal bacterial overgrowth - DYSBIOSIS - regulation to control bacteria population in stomach is no longer occurring
○ Micronutrient deficiency
○ Ongoing pancreatic destruction
77
Exocrine pancreatic insufficiency cinical signs and diagnosis
- Clinical signs
○ Maldigestion
§ Large volume foul-smelling greasy faeces (=steatorrhoea)
§ Weight loss
§ Systemically well
§ Polyphagia/coprophagic, poor coat (zinc deficiency - micronutrient)
§ Occasionally vomit if concurrent pancreatitis
○ In cats -> Diarrhoea, weight loss and polyphagia
- Diagnosis
○ Serum trypsin-like immunoreactivity (TLI) - measure pancreas FUNCTION
§ Only test you need
§ Fasting sample
□ <2.5 ug/L diagnostic
□ 2.5-5ug/L suspicious
® Re-test or perform stimulation test
May be increased intermittently if due to pancreatitis
78
Exocrine pancreatic insufficiency treatment what is the main issue and things can give
○ Expensive and lifelong (pancreas doesn't regenerate)
§ Uncoated pancreatic extract best
□ Only enteric coated capsules in australia
□ With every meal
□ No need to pre-incubate
§ Fresh frozen pig pancreas alternative
§ Highly digestible diet with MODERATE fat restriction and good quality protein
□ Don't change unless poor quality until stabilised
§ Vitamin supplementation - cobalamin
79
Exocrine pancreatic insufficiency prognosis and approach to poor responders
- Prognosis
○ Good if appropriate treatment expect weight 'gain' but remain polyphagia)
○ Causes of failure to respond:
§ Incorrect diagnosis
□ Many disease respond to enzyme supplementation
§ Poor owner compliance
§ Inadequate enzyme supplementation
§ Secondary bacterial growth +/- concurrent IBD
- Approach to poor responders
○ Ensure adequate enzyme supplementation (dosage and formulation)
○ Treat bacterial overgrowth
○ Treat concurrent IBD if present
○ Change diet
80
Chronic SI diarrhoea what suggests you need to investigate a lot
- Melena
- Anaemia
- Old animal
- Ascites (<15) or signs of hypoproteinaemia (albumin <20) -> protein losing enteropathy
○ Poor prognostic indicator -> accelerate this investigation
- Debilitated
- Substantial weight loss
- Palpable abnormality
- Poor response to treatment
81
Protein-losing enteropathy (PLE) what is it, results from, main causes and clinical signs
```
not a diagnosis just description
- Loss of albumin and globulin (and RBCs) when increased intestinal permeability
- Cause
○ Severe IBD
○ Neoplasia
○ Lymphangiectasia
○ Chronic intussusception
○ GI haemorrhage/ulceration
○ Severe parasitic or viral infections
- Clinical signs - effusion when serum albumin < 15g/L
- Often GI signs are not very obvious
```
82
GI lymphoma in dogs leading to protein-losing enteropathy how common, diagnosis, treatment and prognosis
```
○ Less common than in cats
○ Nasty tumour in dogs
○ Often need full-thickness biopsies to diagnose
○ Required multi-agent chemotherapy
○ Risk of perforation
○ Prognosis guarded
```
83
Adenocarcinoma in dogs leading to protein-losing enteropathy how common, clinical signs, diagnosis and prognosis
```
○ Most common in dogs
○ Often profound weight loss, anaemia, hypoproteinaemia
○ Full thickness biopsies
○ Predilection site: rectum, duodenum
○ Prognosis generally poor
```
84
Intestinal lymphangiectasia leading to protein-losing enteropathy what occurs, cause, breed, clinical signs, treatment
○ Where the lymph vessels supplying the lining of small intestine are blocked -> malabsorption
○ Usually secondary to other disease rather than primary
§ Dilated intestinal lacteals
§ Secondary to other diseases as for IBD
○ Yorkies pre-disposed
○ Lose protein, lymphocytes and chylomicrons into gut lumen -> LYMPH CONTENTS
○ Usually resolves if treat underlying condition
○ If idiopathic
§ Prednisolone - assuming inflammatory nodules block
§ Low-fat diet
85
How to diagnose protein-losing enteropathy cause and what if cannot diagnose
BIOPSY
IF CANNOT DIAGNOSE AS CANNOT DO BIOPSY JUST TREAT FOR INTESTINAL LYMPHANGIECTASIA AS ONLY ONE CAN TREAT
- See if gets better, lymphoma case may get better for a few weeks as well but then decline
86
Treatment trial for chronic small intesinal diarrhoea when to do, what differential
- Well, good appetite, no abnormalities on exam, association with food or concurrent pruritis
Top differential is chronic enteropathy (IBD)
87
Chronic enteropathy (IBD) cause, clinical signs and what contributes
- Has no identifiable underlying cause - NO KNOWN TRIGGER
- Can affect any part of the gastrointestinal tract
- Clinical signs can be intermittent
- Can overlap with many other different disease
- Is probably a spectrum of different disease
- Aetiology
○ Persistent specific - infection
○ Dysbiosis (abnormal ratio of beneficial and detrimental commensal microbial agents)
○ Defective mucosal barrier function
○ Defective microbial clearance
Aberrant immunoregulation
88
Chronic enteropathy (IBD) what are the 4 things that is needed to occur and what results
- What is needed
a. Luminal microbial antigens and adjuvants
b. Genetic susceptibility
c. Environmental triggers
d. Immune response
- What occurs
○ Trigger
○ Acute inflammation -> loss of villous surface area, mucous, dysbiosis
○ Gram negative proliferation
○ AHC invasion
89
Chronic enteropathy (IBD) what are the 3 clinical classifications and what does this mean
1/ Dietary responsive enteropathy
2/ Antibiotic responsive enteropathy
3/ True inflammatory bowel disease (IBD) that requires immune suppression
○ WHAT DOES THIS MEAN?
§ No difference in clinical signs except when severe
§ No difference in histology
- difference in trigger therefore treatment
90
Chronic enteropathy (IBD) general presentation and clinical signs
- General presentation
○ Any breed, older than 1 year, exacerbated by stress, if pure bred
○ concurrent pruritis or young more likely to be food responsive
- Clinical signs
○ Vomiting (cats >>dogs)
○ Diarrhoea
○ 4 weeks
○ +/- borborygmus, weight loss
○ Intermittent
▪ Often cyclical and triggered by stress
▪ Differential - atypical hypoadrenocorticism (dogs)
91
Chronic enteropathy (IBD) if diagnose what should do next (next 3 steps)
a. Treatment
§ Fenbendazole (50mg/kg sid 3 days)
□ Treats whipworm
□ Potentially giardia as well
b. Should get a semi-objective score on how severe they are
§ Use as a baseline to ensure the treatment trail is working
§ Canine chronic enteropathy activity index (CCEAI)
□ Attitude/activity, appetite, vomiting, faecal consistency/frequency, serum albumin, weight loss, ascites/peripheral oedema, pruritus
c. BEGIN THE TREATMENT TRIAL
92
Treatment trail what are the 3 main options
1) dietary modification
2) microbiome modification
3) downstream modification - modify the immune response
93
Dietary modification in treatment trial for chronic enteropathy what is the ideal diet and possible benefits of the diet that could help
```
§ IDEAL DIET
□ High amounts of soluble fibre
□ Hypoallergenic or hydrolysed protein
□ Moderate fat content
BENEFITS
□ Decreased allergenic stimulation AND
□ Fibre promotes colonic transit time via stimulation segmental contractions
□ Fibre alters bacterial population
□ Fibre increases production of SCFA
□ Fibre absorbs large amounts of faecal water
```
94
Dietary modification in treatment trial for chronic enteropathy what order of diets should try and if work what should see
§ Order of diet
1) Hydrolysed diet
2) Commercial limited antigen diet
3) Commercial therapeutic GI diet
4) Limited ingredient, novel protein, balanced home cooked diet
® Full dietary history
® Get diet formulated by veterinary nutritional service
® Don't feed longer than 12 weeks without nutritional advice/supplementation
® Show owners previous recipes
§ What should see
Should see >75% reduction in CCEAI within 1-2 weeks
95
Dietary modification in treatment trial for chronic enteropathy when considering changes to next diet and what important to do if see reduction
□ Consider changing to next diet if 50% reduction but some improvement and dog is still WELL
§ REMEMBER
□ Need to withdraw (get responsive)
□ Rechallenge (get recurrence)
□ Over 75% food-responsive GI disease do not recur with re-challenge
96
Microbiome modification in treatment trial for chronic enterpathy list the 4 main options and what should the end result be
1) prebiotics
2) probiotics
3) antibiotics
4) faecal microbial transplantation (FMT)
§ END RESULT
□ Should get >75% reduction in clinical signs within 2 weeks
□ Taper and stop antibiotics if using them
® If unable to taper, or needs repeat antibiotics consider alternative treatment options (try FMT)
97
Probiotic and antibiotics in micrbiome modification for chronic enteropathy when use, examples
Probiotic
® EXAMPLES -> Bifidobacterium, lactobacillus, enterococcus faecium, saccharomyces boulardii
® PROBLEM -> not classified as medication -> products variable in quality control and purity
◊ You want the right probiotic with the right function (genetic coding) that is able to work in an individual gut with a disease causing a specific dysbiosis that is most receptive to change via the probiotic
NO EVIDENCE TO SUPPORT THEIR USE IN CHRONIC ENTEROPATHY
Antibiotics
® Oxytetracycline, metronidazole, tylosin
® All have pros and cons, all are likely to have metabolic effects on host and the microbiome
98
Faecal microbial transplantation for microbiome modification of chronic enteropathy what is important selection criterias for donors
◊ Not obese (there is an obese microbiome CAN TRANSFER, no skin disease
◊ Vaccinated and wormed
◊ No history of GI disease (vomiting/diarrhoea/abdominal pain)
◊ Fed a regular commercial diet without additives consistently
◊ No antibiotics or proton pump inhibitors within 3 months
◊ No long term drugs (immune suppressive)
◊ Screening
} Dysbiosis index
} Faecal examination
} Clinical examination
99
Faecal microbial transplantation for microbiome modification of chronic enteropathy what is the process
1. Collect 50g of faeces from the donor dogs within 4 hours of planned administration
} Do not refrigerate faeces
2. Dilute faeces 1:4 with saline and blend until liquid
3. Remove large particulate matter by passing blended faeces through the sieve
4. Recipient preparation
} Gast dog overnight
} Sedate/anaesthetise pending treatment, attempt to coincide with other procedures such as ultrasound
5. FMT administration
100
FMIT administration for chronic enteropathy what are the steps and what is the main problem
} Administer slowly (5-10minutes) via a large-bore (12-14G) catheter introduced at least in the transverse colon (via rectum)
} Give 10ml.kg transplant up to a maximum of 300-400ml
} Tilt the back end about 30% up to reduce leakage of the transplant
} Keep the dog sedated for 45-60 minutes post-transplant and consider changing position as well ever 10-15mintues (dorsal, lateral R, ventral, lateral)
Problems - the unknown
◊ DON'T KNOW why effective, how frequent (TO EFFECT AT THE MOMENT), colon vs duodenum, volume
101
downstream modification for chronic enteropathy what need to do before commence, when cannot do it and how to do
○ Before doing this need histological confirmation (biopsy)
§ SHOULD NOT DO BIOPSY FOR THE FOLLOWING
□ Melena, anaemia, old animal, ascites or signs of hypoproteinaemia (albumin <20), debilitated, substantial weight loss, palpable abnormality - SAME AS SEVERE NEEDS INVESTIGATION
§ How to biopsy
1. Ex lap
® Risk of poor wound healing
® Full thickness of ileum, duodenum, stomach
® NOT colon
® Look at other organs
2. Endoscopy
® Lower morbidity and expense
® Can biopsy colon and ileum
102
downstream modification for chronic enteropathy what is the main drug to use, what cannot have with and what can add
§ Prednisolone - 1-2mg/kg/d, taper dosage every 2 weeks, consider lower dose in large breed dogs, maximum 60mg/d
□ CANNOT HAVE RAW MEAT WHILE IMMUNOSUPPRESSED
§ Can add ONE additional immune suppressive drug if unable to taper or side effects too severe
□ ADD -> azathioprine or chlorambucil
103
downstream modification for chronic enteropathy what are 3 additional immune suppressive drugs can use and why
1. Azathioprine - preference for monitoring on this than prednisolone
□ In severe cases start at time of prednisolone
□ Alternatively prednisolone-sparing when tapering the dose
□ Takes 1-2 weeks to reach therapeutic effects
□ Side effects include pancreatitis and leukopenia
□ Monitor white cell count regularly
2. Cyclosporine - don't like to use
□ Theoretically beneficial due to T cell suppression
□ Can cause GI side effects - THIS OR THE DISEASE
3. Chlorambucil
□ Recent abstract suggests better than azathioprine in treating protein-losing enteropathy
