Horses 2 Flashcards
what are the 7 main differential diagnosis for acute colitis and types common
1) salmonella - type B and C
2) clostridium - type A and C most common
3) antimicrobia-assoacited colitis
4) potomac horse fever
5) viral - coronavirus
6) cyasthostomiasis (parasite)
7) non-pathogenic - grain overload and right dorsal colitis (NSAID toxicosis)
acute colitis how important is the diagnosis
REGARDLESS OF THE CAUSE, CLINICAL APPEARANCE IS THE SAME - smell, haemorrhagic, non-haemorrhagic
YOU CANNOT MAKE A DIAGNOSIS BASED ON CLINICAL SIGNS ALONE
Problem list for acute enteritis cases
- Diarrhoea ○ Infectious (vs. noninfectious) - Hypovolaemia/ haemoconcentration ○ Fluid loss in diarrhoea - Hypoproteinaemia ○ Protein-losing enteropathy - SIRS (“endotoxaemia”) Secondary to GI compromis - Thrombocytopenia ○ Hypercoagulable state - Leukopenia/neutropenia ○ SIRS - Mild azotaemia ○ Pre-renal/renal/post-renal ○ Probably pre-renal - Hyperglycaemia ○ Stress ○ Severe disease
Acute enteritis diagnostic plan what need to submit
- WILL need to start treatment before results back
○ OFTEN don’t get an answer, need to tell the owners - Samples to submit
○ Faeces
§ Clostridial toxins
§ Salmonella PCR/culture (series of 5) -> one negative doesn’t indicate horse is negative
□ Shed in varied quantities, intermittently
§ Parasitology
○ If PHF season/area
§ EDTA blood – PHF PCR
§ Serum – PHF IFAT
+/- Ultrasound - can help assess oedema
What are the 4 main complications of acute colitis and when at risk
- Laminitis - most common - ANY CASE ○ All colitis cases at risk ○ PHF, grain overload big risks - Coagulopathy ○ Thrombophlebitis – consequence of SIRS - Hypertriglyceridaemia - Rectal prolapse - really oedematous rectums straining to pass large amounts of diarrhoea
Acute enteritis describe the supportive/preventative measures needed
○ Reduce risk laminitis
§ Ice boots (how long?) -> a few days after white cell count normalises
○ Anti-diarrhoeals
§ Di-tri-octahedral smectite (Biosponge®)
○ Probiotic?
§ Saccharomyces boulardii
○ Analgesia
§ Control colic pain
□ Usually due to ileus, dysmotility, (colon infarction)
§ NSAIDs (not in right dorsal colitis (RDC)- caused by NSAIDS)
□ Look a lignocaine and opioids
○ Anti-endotoxin treatment??
§ (Hyperimmune plasma) -> 50:50 in literature, risks that have with transfusions
§ Flunixin meglumine (not RDC) -> works on the clinical effects -> WORKS
foal diarrhoea difference to adults, result, treatment and how to balance referral and management on farm
- Easier to diagnose - generally higher identification of the pathogen
- Neonates do become bacteraemia (useful to take blood culture)– consequences
○ Sepsis
○ Septic joints/other synovial structures
○ Omphalitis - umbilical structures - Treatment largely supportive, still expensive
- Referral vs. management on farm
○ Severity of disease (i.e. intensity of required treatment)
○ Ability and knowledge of owners/farm managers
What are the 9 main differentials for neonatal foal diarrhoea
- Salmonellosis
- Clostridiosis – usually perfringens – often haemorrhagic - can be so severe than become anaemic
- Coronavirus
- Rotavirus - 5d - 4w - lactase replacement
- Cryptosporidium - zoonosis - self-limiting
- Enterococcus durans***
○ New discovery in terms of being pathogenic - Nutritional – orphans especially - incorrect milk replacer
- FOAL HEAT - 7-9d, ‘mare foal heat’ - coprophagic - self-limiting
- Parasitic – Strongyloides
What are the 4 main differentials for older foals/weanlings
- Strongyles
- Ascarids
- Rhodococcus equi
- Equine proliferative enteropathy/Lawsonia (weanling age, usually chronic)
Rhodoccus equi what cause in foals and 2 other causes of diarrhoea
- Usually pneumonia (pulmonary abscesses), but many extrapulmonary manifestations ○ Ulcerative colitis 1) Sepsis, neonatal encephalopathy ○ Period of poor perfusion to GI tract ○ Treat primary problem, supportive care 2) Intestinal nematode parasites ○ Older foals/weanlings
In general what are more likely colic causes in young horses (neonates) and immature horses
Young horses
- First manure getting stuck (meconium impaction)
- congenital abnormalities of the gut (atresia coli)
Immature
- Prone to infectious problems
- Enteritis (small intestinal)
- Parasitic
○ Ascarid impactions of the small intestine (foal lecture)
○ Intussusception (association with worms)
Broodmare colic what need to consider and main differentials and when high risk
- Broodmare: pre or post-partum?
- Pre-partum -> Pregnant causes
a. Foal movement can result in low gr colic
b. foaling/ate term abortion
c. uterus can twist: uterine torsion (last 2 months)
Post-partum
a. rupture of uterine artery - most common
b. foal can damage uterus during foaling
c. can also damage GI tract - peritonitis/endotoxaemia - euthanse
Foaled within 3 months - HIGH RISK - most common large colon volvulus (this until proven otherwise) - surgical emergency - CV compromise
Rupture of uterine artery leading to colic in recently foaled broodmare what is the treatment options
□ NSAIDs, careful sedation to calm -> don’t want to drop blood pressure too dramatically
® Detomidine and top up if needed
□ Tranexamic acid: antifibrinolytic (10mg/kg in 1L IV) - stabilises the clot
□ +/- blood transfusion (indications below)
® Decided by: lactate>4, HR 80, Hb<8g/dL, PCV<15% (unreliable in acute stage)
® Can lose approx 11L without need to transfuse
® (1/3 of blood volume: b.vol = 8% body weight)
What are the 4 main causes of colic based on geographical location
1) sandy soil - sand impactions - SA,WA, VIC
2) enteroliths - WA,NSW,QLD (NOT VIC)
3) infectious agents - QLD, northern NSW
4) swim colic - racehorse swum for excercise within 30mins - most respond to pain relief (95%)
Febrile colic what is generally the cause types of pathogen within large intestine, small intestine and abdominal cavity
- Febrile suggests infectious (most commonly)
○ Bacterial
§ Large intestine= Colitis (Salmonella/Clostridia)
§ Small intestine= Anterior Enteritis (Clostridia)
§ Abdominal cavity=
□ Peritonitis (Actinobacillus equuli)
□ Peritonitis due to GI catastrophe
○ Viral
§ Hendra
Analyse situation and give diagnosis - General history ○ 8yo TB, Quiet /lying down approx 12 hrs ○ Little manure passed today No drugs given so far - Physical exam ○ Occasional flank watching/dull ○ HR 48 ○ Mmbs salmon pink ○ Hasn’t passed much manure ○ Temp 39.0 ○ NGTube: no reflux ○ Abdominocentesis: Turbid, yellow WCC 210x109 cells/L TP 30 g/dL Lactate <2 mmol/L
No drugs - know that pain is the actual level
PE
- Low grade abdominal pain consistent with MMbs salmon pink
- hasn’t passed much manure -> § Reduced LI motility? - Large colon impaction - know if rectal
FEVER NARROWS DOWN
§ Narrows ddx down: SI / LI / peritoneal cavity - no longer routine LC impaction
□ Ddx Colitis, Anterior Enteritis, Peritonitis
- no reflex - NOT ANTERIOR ENTERITIS
- abdominocentesis - peritonitis
What are the 6 main differentials diagnosis for chronic diarrhoea in horses
a. Right dorsal colitis (NSAID toxicity)
b. Sand enteropathy
c. Cyathostomiasis
d. Inflammatory bowel diseases
e. Alimentary lymphosarcoma
f. Equine proliferative enteropathy (Lawsonia intracellularis)
Right dorsal colitis treatment and prevention
- Treatment
○ NO NSAIDs – use alternative analgesics to control colic pain
○ Supportive, esp. colloids
○ +/- misoprostol (Prostaglandin replacement)
§ No good evidence surrounding use
§ Need to wear gloves -> nothing that is pregnant
○ Omeprazole, sucralfate for concurrent gastric ulceration
○ Low roughage diet - finely chopped chaff, off hay
○ Surgical resection in severe cases - Prevention
○ Monitor TP in cases receiving prolonged NSAID treatment
Cyathostomiasis which causes issues, what are those issues and diagnosis
- Encysted larval stages – L3
- Commonly causes chronic diarrhoea, assoc. with ill thrift
- Acute severe diarrhoea associated with mass emergence of encysted larvae
- Diagnosis
○ FEC – but won’t tell you about encysted larvae
§ Useful for herd management but not individual management
○ Hypoalbuminaemia
○ Response to treatment
○ Rectal mucosal biopsy - generally not done -> lucky to get piece of tissue with encysted larvae
Cyathostomiasis treatment and prevention
- Treatment ○ Anthelmintics - larvicidal § Fenbendazole – 10 mg/kg PO SID for 5 days □ Resistance problems § Moxidectin – 0.4 mg/kg PO once (usual dose) ○ Supportive - Prevention ○ Good de-worming protocol
Inflammatory bowel disease what are the 4 recognized types how common in what age group, main presentation and prognosis
1) Granulomatous enteritis (GE)
○ Young horses, idiopathic, low % have diarrhoea
2) Lymphocytic-plasmacytic enterocolitis (LPE)
○ Rare, no specific identifying features
3) Eosinophilic enterocolitis (EE)
○ Colic primary sign, not weight loss; better prognosis
4) Multisystemic eosinophilic epitheliotropic disorder (MEED)
○ Young horses, skin lesions, other organs affected (liver, spleen)
Inflammatory bowel disease diagnosis
○ Glucose absorption test
§ Prior fasting, feed withheld during test (water OK)
§ 1 g/kg glucose (as 20% solution) administered via NGT
§ Blood glucose measurements taken at baseline, then q 30 min for 3-4 hours, then q 60 min for another 2-3 hours (total 6 hours)
§ Glucose should peak (>85% of baseline value) by 120 minutes.
§ D-xylose absorption test alternative
○ Abdominal ultrasound
○ Rectal biopsy
○ Intestinal biopsy (if colic surgery)
○ Abdominocentesis
○ Can be elusive
Inflammatory bowel disease treatment and prognosis
○ Often palliative
§ EE may gain long-term success
○ Often ongoing
○ Corticosteroids – tapering until find lowest dose that controls clinical signs
§ Some horses may have periods of not needing corticosteroids at all
- Prognosis generally poor
Alimentary lymphosarcoma diagnosis, treatment and prevention
- Diagnosis as for IBD ○ Partial to complete malabsorption - glucose absorption test ○ Abdominal ultrasound ○ Rectal exam ○ Abdominocentesis ○ +/- Rectal biopsy ○ Can be elusive - Treatment as for IBD - Prognosis generally poor
Equine proliferative enteropathy what caused by, age, presentation adn diagnosis
- Lawsonia intracellularis (bacteria)
- Weanling age foals - 5 months old
- Proliferative enteropathy
- Presentation
○ Signs: lethargy, weight loss, colic, diarrhoea, severe hypoproteinaemia, oedema
○ Usually not febrile - Diagnosis
○ Faecal PCR
○ Serology – Serum IPMA (immunoperoxidase monolayer assay)
○ Ultrasound
Equine proliferative enteropathy treatment and prognosis
- Treatment
1) Supportive
§ May require colloids
2) Antimicrobials: choice does not affect survival.
§ Oxytetracycline - needs to penetrate
§ Macrolide + rifampin - can use macrolides in foals NOT ADULTS
§ (Chloramphenicol – NOT in VIC)
Prognosis generally good with prompt Tx
○ Sell for less as yearlings
Cestodes main issue, where mainly found and diagnosis
- No acquired immunity develops
- Attach at ileocaecal valve - can do this in large numbers - can lead to intussusception -> colic
- Diagnosis difficult - proglottids intermediately shed - may not be present and can break down
Saturated sugar float is the easiest way but not always present
What to do after first selective deworming
○ Repeat FECs just after ERP (egg reappearance period) of anthelmintic used
§ Dosing interval determined by ERP (varies between anthelmintics
§ Egg reappearance periods
□ Vary between anthelmintics
® Moxidectin: 12 weeks (now what we have) (16-22 weeks - when first came on the market)
◊ Becomes less and less effective on the luminal larval (late L4) so ERP gets shorter -> this can indicate early resistance
® Ivermectin: 4-8 weeks (9-13 weeks)
® Oxfendazole: 4 weeks (6 weeks)
® Fenbendazole: 4 weeks (6 weeks)
® Pyrantel: 4 weeks (5-6 weeks)
Ascarids how pathogenic in foals, what results in and the worse presentation with prognosis
- Migratory larvae – liver, lungs - why adults have good immunity (6months of age)
○ Larvae in lungs can cause respiratory signs - Large burdens – failure to thrive
○ Small intestinal impactions - Ascarid impactions
○ Recent history of deworming
○ Prognosis guarded if surgical
○ Risk of SI rupture - doesn’t need to have a large burden for this to occur
○ Adult numbers not correlated with rupture
○ Whole worms in faeces, reflux
○ FEC
Deworming foals what is the main objective and current recommendations
- Main objectives:
○ Remove adults
○ Reduce eggs in environment - Traditional recommendations likely overkill
○ Increase in resistance - Current recommendations:
○ Deworm ALL foals at 2 and 5 months and then at weaning as stressful event
○ Then use selective deworming targeted at cyathostomin control at 6 months
○ Don’t deworm before 2 months
§ Larval and juvenile adult population
Volume of transfusion can you replace entire deificit, how done and how much can take from donor horse
○ In neonates it is possible to replace entire deficit - care with volume overload
○ In adults usually impractical to replace entire deficit
§ Given to effect
§ Replacing 20-40% of the calculated deficit is usually sufficient
- Donor horse
○ Normal blood volume is 8% of body weight
§ Should not take more than 20-25% of blood volume
□ Can take 8-10L from a 500g animal every 30 days
What are the 4 main laboratory indicators of hepatic disease and which useful in horses
1) indicators of hepatocellular injury - GLDH, SDH (good), AST (CK), LDH (limited), ALT (not horses)
2) indications of biliary tract obstruction - GGT (good), ALP (intestinal and bone)
3) indicators of hepatic function - bilirubin concentration, serum bile acids - don’t need to stop eating as no gall bladder, ammonia (not great), PT
4) non-specific indicators - hypoalbimaenia (chronic), increase PCV, low urea
Icterus in a foal what are some likely differentials
- Neonatal isoerythrolysis - intravascular haemolysis
○ DISCOLOURED URINE - Liver disease - infectious causes - clostridia
- Sepsis - liver hypoxia
- Haemorrhage (rib or long bone fractures - generally lame though
- Anorexia (generally low level icterus)
- EHV-1 (abortion, weak, new born foals)
Neonatal isoerthrylosis how occurs and what are the 2 main things that may result
- The situation needed
○ Mare Aa negative - no antigens and Stallion Aa positive - does have antigens
○ Foal -> Aa positive - has antigens that mare does not - AT some point mare is exposed to antigens and becomes SENSITISED
○ Breeding trauma, during foaling, transfusions - UNSURE - Udder concentrates the antibodies against foals RBC antigens
- When foal drinks, gets antibodies, lyses of RBC
Antibodies coat erythrocytes and may act as either
a. Haemolysins (intravascular haemolysis)
b. Agglutinins (extravascular haemolysis)
Neonatal isoerthrylosis treatment plan
- Prevent nursing from the mare
○ Feed safe milk or milk replacer via a NGT
○ Gut “closes” at approx 18-24 hours - ensure enough colostrum - Intravenous fluids
○ Correct dehydration
○ Prophylaxis against pigment nephropathy - Prophylactic broad-spectrum antimicrobials
- MONITOR - very important
○ PCV, HR, RR, Lactate and blood gas
○ Urine, creatinine and bilirubin - if PCV gets worse - NEED BLOOD TRANSFUSION (around 15%) - NOT STALLION - mares but needs to be washed
in terms of foal behaviour what is normal times for important things as well as urination
○ Sternal within 5 mins ○ Suckle reflex within 20min § Often present at birth ○ Standing within 1 hour ○ Nursing within 2 hours § Some normal foals take longer ○ Meconium § Passes within 24 hours ○ Urination § May not urinate for 12 + hours § First urine will be quite concentrated § After that -> 1.005 or less generally - due to fluid diet
Foal cardiovascular, respiratory
HR - 60-140 (if touched), arrthymias should resolve, respiratory - 30-40/min
Flexor laxity vs contraction treatment
laxity - resolves as gain strength, heel extensions, no bandage
contraction - bandaging/splinting/heel elevations, oxytetracycline
foal fluid requirements, drink/day, kg gain/day
§ Maintenance = 80mL/kg/day
§ Drink 20-25% of their bodyweight in mare’s milk/day
§ Gain approx. 1kg/day in bodyweight
6-24 hours old foals what are the 3 common causes of colic and the most common
1) meconium impactions - most common
2) Congenital atresias - colon, rectum, anus
3) Paint foals: primarily white and with (frame) overo dam AND sire: risk of ileocecal aganglionosis (lethal white foal)
Meconium impaction what are the 4 main treatment options
1) Commercial enemas just inject into rectum - a lot of time this is already done by the farm hands -> you are doing the next one
2) Retention enema -> warm water or acetylcysteine retention (most aggressive) enemas generally effective
3) Analgesia
4) Minority -> may require surgery - generally at this point prognosis is not good
2-5 day old foals what are the 4 main causes of colic and 2 others that look like colic but aren’t
- Enteritis
- Intussusceptions
- Gastroduodenal ulceration (bruxism/sick)
- Small intestinal
BOTTOM TO -> generally may think is colic but won’t be - Ruptured bladder - will also generally have abdominal distention, dull
- Inguinal hernias - generally not colicking
