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
Herniation in foals which location most common, how different to adults and therefore how may present
- Inguinal (common), umbilical
- Most do not strangulate the bowel - resolve spontaneously - not normally colicky
○ This is in contrast to the situation in adult horses - much more open in a foal
Common cause of colic in foal 1) 6 month 2)Up to 2 years old
1) gastroduodenal ulceration - can be life-threatening
2) Intussusception
How does resuscitation therapy occur in terms of volume to be administered and steps afterward
○ For horse requiring rapid fluid resuscitation, concentrate on rapidly correcting hypovolaemia
i. 20mL/kg administered as a relatively rapid bolus (approx. 30-60mins)
□ 1L for a 50kg foal, 10L for a 500kg adult -> over an hour
ii. Patients are assess between boluses
□ Use what we used to determine the deficit
iii. Boluses repeated until resuscitation is complete or the patient has received 60-80mL/kg
iv. After 3-4 boluses the patient is careful re-evaluated
□ If vascular volume is inadequate -> additional boluses administered
□ If vascular volume is adequate but tissue perfusion remains poor - inotrope or vasopressor therapy
what are the standard estimates for maintenance requirements (step 2 in amount of administer)
- Adults: 40-60mL/kg/day
- Foals: 80-100mL/kg/day
Equine neonatal sepsis diagnosis
- suspecision - clinical signs - hypovolaemia
- CBC - leukopaenia with left shift, fibrinogen increase (inflammation at least 24 hours)
- biochemistry - Hypoglycaemic (inadequate nursing, sepsis), Hyperbilirubinaemia (sepsis), decrease in IgG (used to fight infection)
- Blood gas - Metabolic acidosis , Hypoxaemia, Hyperlactatemia (inadequate perfusion)
- blood culture - MAIN DIAGNOSTIC - is the goal bacteriamic (almost always in foals) - most commonly E.coli
What are the 4 main things within the stabilization of foal with uroabdomen
1) peritoneal drainage
2) fix hyperkalaemia: if severe (>6mmolL) and/or ECG changes present
3) fix hypovolaemia - careful volume resuscitation
4) fix hyponatraemia
define PU/PD in horses
- Water intake > 100ml/kg/d
○ 50L for 500Kg horse - Urine output > 50ml/kg/d
○ 25L for 500Kg horse
Pituitary pars intermedia dysfunction (PPID) pathophysiology what occurs
1) Oxidative damage to inhibitory dopaminergic neurons
2) Results in INCREASE IN ACTIVITY OF PARS INTERMEDIA
□ Normal products increase in production -> INCREASE ACTH
® ACTH has it’s own negative feedback on pars distalis (where normally most is produced)
□ Melanotropes are the endocrine cells of the pars intermedia
® Produce long precursor hormone pro-opiomelanocortin (POMC) - 3) INCREASED PRODUCTION of these POMC
◊ Peptide products of POMC have diverse and wide-ranging biological effects
◊ Still poorly understood
Pituitary pars intermedia dysfunction (PPID) how does dexamethasone suppression test work, how to perform and what should occur
□ Commonly used screening test but largely replaced by ACTH
□ Measure cortisol response to exogenous glucocorticoid
- normally -> Inhibition of stimulation of ACTH
PPID - Continue to stimulate cortisol even with dexamethasone - FAILURE OF SUPPRESSION OF ACTH
□ Overnight DST procedure
® Baseline sample late afternoon
® Inject dexamethasone 0.04mg/kg IM (don’t memorise)
® Second sample 19 hours later (next morning)
Pituitary pars intermedia dysfunction (PPID) diagnosis with insulin status why can it be used, what are the 2 main tests, which preferred and how to do
PPDID can be associated with insulin resistance
§ Hyperinsulinemia is a risk factor for laminitis
1) Basal sample - not as good as dynamic test
§ Reference <20mU/L
§ Large number of false negative result
2) In feed oral glucose tolerance test - preferred - dynamic is always better
§ Fast overnight
§ Provide meal with 1g/kg glucose powder
§ Blood sample at 2 hours
§ Reference <87mU/L
PPID treatment and monitoring
- pergolide mesylate (dopamine agonist) +/- serotonin antagonist (provides stimulus to pars intermedia)
- repeat endocrine testing 2-4 weeks at start, Generally 1 month, 1 month after that and then make decision about how frequent after that
§ Reassess dose of pergolide
Hair and drinking can take awhile
Psychogenic polydipsia how to diagnose and when wouldn’t you
- Diagnosis of exclusion
○ Evaluate the horse for the other differentials - USG very low <1.006
- Positive response to water deprivation test - those with diabetes will not
○ Do not perform a water deprivation test on an azotaemia horse
§ Minimum clinical data needed
□ Urea, creatinine, USG
Acute renal toxicoses what are the 2 main causes and list some other causes
1) aminoglycosides
2) NSAIDS
- other causes
○ Pigment nephropathy (Hb, Mb (myoglobinuria - exertional rhabdomyolysis)
§ Tubular obstruction
§ Direct toxic effect of pigments
○ Heavy metals
○ Acorn poisoning
○ Other drugs
§ Oxytetracycline
§ Polymyxin B
○ Vasomotor nephropathy
§ Ischaemic ATN
Chronic kidney disease what are the 3 main causes what are they and list 4 others
1) Proliferative glomerulonephritis ○ Type III hypersensitivity ○ Immune complex deposition 2) Chronic interstitial nephritis ○ Sequela to ATN or other kidney disease ○ Fibrosis 3) Pyelonephritis ○ Rare ○ Often concurrent nephroliths/ureteroliths ○ Risk factors ○ Uni-or bilateral Others ○ Amyloidosis ○ Polycystic kidneys ○ Congenital renal dysplasia ○ Neoplasia
Idiopathic renal haematuria how present, breds, both or one, diagnosis, treatment
- Sudden onset gross haematuria
- Haemorrhage may be life-threatening
- Many breeds, Arabians overrepresented
- Often unilateral
- Diagnosis of exclusion, also cystoscopy, U/S
- Signs of blood loss –anaemia, pale membranes
- Usually NOT azotaemic
- Treatment supportive
- Nephrectomy may → IRH in the remaining kidney
Cystic calculi what made of, treatment and prevention
○ Calcium carbonate
Treatment
- Surgical removal
-> Fragmentation and removal (through urethra in mares, perineal urethrostomyin males)
- cannot use dietary management
- Recurrence
Prevention
- Grass hay diet (reduce legumes)
- Urinary acidification (ammonium chloride)?
- Increase water consumption (↑ salt intake)
CASE - what are some differentials - 12 year old warmblood gelding - 2 week history of mild intermittent colic - Unwilling to work/poor performance - Occasional urine dribbling - Frank blood in urine sometimes seen after work hysical examination findings - Bright and alert - Normal TPR - Some blood-stained urine on hindlimbs - No other abnormalities
- Urolithiasis - MOST CONSISTENT
- Neoplasia - possible but not common
- Sabulous urolithiasis - DON’T USUALLY HAVE HAEMTURIA
- Urethral haemorrhage - would expect haematuria at end of urination
- Idiopathic renal haematuria - intermittent, more severe haemorrhage
- Neurologic disease - don’t usually have haematuria
In terms of evaluation of the body within the neurological exam what are the 6 main tests and tests within
1) Bony/muscular asymmetry
2) Focal muscle atrophy - lower motor neuron injury
3) Localised sweating
4) Cutaneous sensation
5) Reflexes
1. Local cervical (cutaneous coli)
2. Cervico-facial (cutaneous faciei)
3. Panniculus (cutaneous trunci
4. Perineal
6) Proprioception tests
how to perform the cervico-facial, panniculus and perineal reflex
□ Pinching down the neck and should see twitch of ear or grimace of the lips
□ Cervical spine lesion
□ Hard to interpret -> need to repeat and compare to the other side
Panniculus (cutaneous trunci)
□ Same in cat or dog but go cranial to caudal (but will get kicked that way)
Perineal
□ Prick around the perineal area and looking for contraction around the anus
what clinical signs are seen with paresis and ataxia
Paresis (weakness): clinical signs include:
○ Low arc of the stride
○ Drag limbs
○ Worm hooves
○ Stumbles and knuckles
Ataxia (incoordination): clinical signs include:
○ Abnormal or inconsistent foot placement
○ Legs may weave during the swing phase of the stride
○ Stepping or brushing opposite foot or limb
○ Swaying of the pelvis or trunk
○ Pace rather than walk
What are the 6 main clinical signs of cerebral disease
1) changes in behaviour
2) Seizures
○ Neonates (sepsis, HIE, meningitis)
○ Adults (EPM, parasite migration)
○ Epilepsy
3) Depression and coma
4) Abnormal head posture
○ Head turn/tilt
5) Vision disturbances
6) Facial and nasal Hypalgesia/analgesia
How does the tetanus and botulism toxin work (mechanism of action)
- Cell binding: toxin circulate in bloodstream
○ Both BoNT and TeNT bind receptors on the pre-synaptic membranes of the NMJ
○ Tetanus neurotoxin -> transported to spinal cord -> blocks GABA (inhibitory) -> spastic paralysis
○ Botulinum neurotoxin -> mostly remains at NMJ -> flaccid paralysis - blocks release of acetylcholine - fed round bail hay (Type B)
Tetanus clinical signs and what result in
- Vague stiffness and lameness initially
○ Reflect local effects of the absorbed toxins - Generalised stiffness
○ Hypertonia most evidence in anti-gravity muscles
○ Sawhorse stance
○ Excessive facial muscle tone -> lock jaw
○ Eyeball retracted into orbit with menace -> 3rd eyelid flashes across the cornea
○ Lips retracted -> sardonic grin
○ Ears pulled slightly downward and caudally
○ Tailhead elevated - Tetanic spasm elicited by auditory, visual or tactile stimulation
○ Severely affected animals become recumbent with opisthotonus (totally rigid)
○ Increased muscle activity -> pyrexia (sweating in horse) - Aspiration pneumonia develops in some cases -> contributes to mortality
- Death due to respiratory muscle paralysis and heart failure
Tetanus what are the 6 main things need to do
1) provide muscular relaxation - quiet room, ace
2) ensure good footing - sling
3) elimination of infection - surgical debridement, penicillin
4) neutralise unbound toxin - tetanus anti-toxin
5) maintain hydration adn nutritional status
6) establish active anti-toxic immunity - if unsure on vaccination history - opposite sides of the neck - NOT MIXED
what disease looks like tetanus and horses associated with
□ Hypocalcaemia leads to hyperexcitable nerves - looks like tetanus
associated with:
○ Lactating mares
○ GIT disease
○ Renal disease
○ Prolonged transport with food deprivation
○ Endurance events (esp during hot weather) - sweat a lot which contains a lot of calcium
What are common clinical signs in foals with botulism
- Lie down more often than normal
○ When forced to rise, stands for a few moments, then develops generalised muscle tremors (shaker foal) and drops to the ground - Typically well- nourished, bright and alert
○ Normal heart rate, respiratory rate and rectal temperature - Clinical pathology findings are often normally
- Progressive symmetric myasthenia -> recumbency
Botulism what are the early clinical signs in adults
- Clinical signs are always symmetric and progressive
- Early clinical signs include:
○ Decreased exercise tolerance
○ Dysphagia -> slow to eat, diminished ability to swallow
○ Mild depression
○ Colic -> gastrointestinal ileus and gas accumulation - Decreased tongue, eyelid and tail strength
○ Typically occur before obvious skeletal muscle weakness - Vital signs usually normal initially
What are the 4 main parts of therapy for botulism and prognosis
1) anti-toxin administration - lasts 60d only unbound toxin
2) excercise restriction - don’t want to deplete acetylcholine stores
3) antimicrobial therapy
4) supportive care
Good prognosis with money
Stringhalt treatment
- Treatment
○ Many of the pasture associated cases will resolve eventually with removal
○ Phenyoin - not sure how works
○ Resection of the lateral extensor tendon
Equine metabolic syndrome clinical picture
- Generalised obesity –BCS 7/9 or greater
○ Regional adiposity - neck, ribs, rump - or just generally
○ Crestyneck - Laminitis - multiple founder lines (repeated subclinical)
- Pony breeds, some horse breeds
○ Morgans, paso fino
In terms of equine metabolic syndrome what are the 6 main tests for diagnostics and what is important
- BCS, crestyneck score, midneck circumference, girth circumference at withers and umbilicus
- Basal plasma insulin concentration
- Oral glucose tolerance test/oral sugar test - most common
- Oral sugar test
- Insulin tolerance test
- Combined glucose-insulin test
- Minimise stress
Hyperlipidaemia and hyperlipaemia define and which can lead to hepatic lipidosis
Hyperlipidaemia and hyperlipaemia define and which can lead to hepatic lipidosis
What are the 4 main ways to diagnose hepatic lipidosis
1) Signalment history
2) Plasma triglyceride concentration
○ Consider treatment when TGs > 1.1 mmol/L (100 mg/dL)
3) Biochemistry
○ GGT, SDH, bile acids, bilirubin, ammonia
§ Not always evidence of hepatic impairment
○ Check for azotaemia
§ Impedes lipid removal from blood (inhibits LPL (lipoprotein lipase))
4) Ultrasound (liver)
Treatment for hyperlipaemia/hepatic lipidosis what are the 2 main things and thing within
1) reduce negative energy balance ○ Nutritional support ○ Termination of pregnancy § Foals usually don’t do well if labour induced/early c-section § Value of fetus vs. mare/jenny ○ Termination of lactation § Alternative milk source for foal 2) Pharmacological treatment - insulin (promotes lipoprotein lipase activity) and heparin (same as above - to increase TG uptake in adipocytes
When are horses mainly at risk for re-feeding syndrome
Horses at risk if:
- BCS of less than 3.5/9 and an unknown dietary history
- Fasted for greater than 5 –10 days regardless of body condition score
- Lost greater than 10% of their body weight over less than a 2 month period
- Hepatic lipidosis
re-feeding protocol in order to prevent re-feeding syndrome in starving horses, what monitoring is needed
- Lucerne hay (high protein, P and Mg)
○ Start at 25-30% of maintenance energy requirements for current bodyweight divided into 6 feeds/day
○ Build up to 100% maintenance energy requirements for current bodyweight over 2-3 days (4-6 feeds/day)
○ Gradually increase to maintenance energy requirements for ideal bodyweight over 7-10 days (4-6 feeds/day)
○ Gradually decrease frequency of feeding and increase amount fed at each feed (2-3 feeds/day)
What is VO2 max and what depends on
Increase VO2 max (volumes of oxygen in mls/minute that can be used for
○ Depends on: pulmonary diffusion capacity, o2 carrying capacity of blood, muscle diffusion capacity, capillary density in muscle, mitochondrial enzymes
○ 4 major components - respiratory, cardiac, blood and muscle
○ HORSE IS TWICE THE HUMAN ATHLETE
what is the main muscle adaptation with training
- VO2max can increase by 25%
○ Improvement of oxidative capacity: on type I and IIA fibres
○ Improvement of anaerobic capacity: type II fibres - Aerobic capacity - can measure VO2max but difficult in the field with very high flow rates in horses, equipment not readily available
VLa4 what is it an indicator of, how measured and what used for
used for fitness testing
Vla4 - an indicator of aerobic capacity
- Blood samples are taken during incremental exercise test, after each speed step
Heat stress what is it, what horses occurs in and clinical signs
- Environmental temperature and humidity important
- Increase risk if recently moved from a cooler climate, local horse not yet adapted to warmer/more humid conditions, dehydrated, larger horses, overweight horses, darker colour, inadequate fitness
Range of signs - can rapidly progress - Know the signs as may be unsafe to take temp - may lash out with hindlegs and become ataxia
- Increase HR (125-150/min 10-15min after exercise) - should be down to 90-120
- Increase RR (panting 120-140/min), flared nostrils - should be down to 60
- Slower than normal recovery mentation normal -> irritable, uncooperative, kicking out, head shaking, gait changes -> incoordination disorientation -> seizure, coma and death
Anhydrosis what is it, when occur and what can lead to
( dry coat, puffs)
- Partial or total loss of ability to sweat - sweat glands stop working
- Can occur if moved from temperature to hot humid climate or in horse native to hot country
○ Kept in air-conditioned stables in areas like this
- Cause PP and can lead to serious hyperthermia
Anhydrosis signs and diagnosis
- Gradual or sudden onset
- Increase HR and temperature
- Panting and nostril flare at rest
- Patchy dry coat after exercise
- Flakey/scurfy skin (forehead)
- Hair loss (face, chest) over time
Diagnosis - Sweat test - terbutaline intradermal injections - little or no response is abnormal
Anhydrosis management
Move to a cooler climate is the only curative solution
○ Partial remission in winter
○ Full remission possible if remove from climate early
○ Keep valuable athletic horses in air conditioning
- Diet - reduce grain/protein
- No strenuous exercise especially in heat
- Ensure well hydrated
Left sided and right sided murmurs what involved if systolic or diastolic
LEFT systolic - mitral - most common but rare diastolic - aortic/pulmonic RIGHT systolic - tricuspid and VSD (size important)
what is the most common cause of cardiac performance issues and types
arrhythmias NORMAL - high vagal tone, vagally mediated brady arrythmias 1. second degree AV block - most common 2. sinus arrhymia 3. sinoatrial block PATHOLOGIC 1) Atrial fibrillation - IMPORTANT - most common cardiac issue Other arrhythmias (less common) 1. Atrial premature complexes (APCs) 2. Ventricular premature complexes (VPCs) 3. Ventricular tachycardia (VT) 4. AV block ○ 3rd degree
A fib what rhythm, when irreversible and when resolve
○ “Irregularly irregular” rhythm
- Cardiac remodelling occurs if A fib longstanding
○ After 3 months becomes
○ Resolves spontaneously in minutes-hours-days after exercise
○ Exercising ECG can be important to detect in these cases irreversible
Atrial fibrillation what are the 4 important tests for diagnosis and the best one
- ECG
○ Exercising ECG (Certain circumstances) - Echocardiography - ideal
○ Determine presence of underlying heart disease
§ Structural normal heart or not? - changes prognosis - CTnl
- Electrolytes
What are the 2 main options for conversion of atrial fibrillation and how works
1) Quinidine (sulfate)
§ Class 1A antiarrhythmic drug (sodium channel blocker)
§ Prolongs action potentials and lengthens myocardial cell refractory period
- 80-90% success
2) Transvenous electrocardioversion (TVEC)
§ Deliver
§ Whole atria refractory and so sinal node takes over again
§ Reserve for horses that develop complications during quinidine OR those who don’t convert with quinidine
Ventricular premature complexes what associated with, can lead to and when cause for concern
○ Most often associated with other disease
§ May be due to primary cardiac disease
○ Runs VPCs = ventricular tachycardia
○ Isolated VPCs common when HR slowing after exercise
○ VPCs during exercise
§ Cause for concern
§ May occur in normally performing horses
§ Further research needed…
Ventricular premature complexes and ventricular tachycardia when treat, with what and when can go back to work
□ Treatment indicated if: - increased risk of ventricular fibrillation
® HR > 100-120
® Multiform VT - different shapes of QRS - multiple ventricular premature complexes
® R on T
□ Treat with
® Magnesium sulfate(50 mg/kg = 25 g/500 kg horse)
® Lidocaine (1.3 mg/kg bolus followed by 0.05 mg/kg/min CRI)
□ Implications for work?
Another ECG performed before back into work
What are the 3 most common causes of weight loss
- Dental disease - induced maldigestion (NOT reduced appetite or dysphagia)
- Diet inadequate to caloric requirements
- Gastrointestinal parasitism
Multiple concurrent contributing factors
Case - Boris - 12 yo Standardbred gelding - Laceration over upper radius - Dirt present all over laceration - Muscle exposed, some bone - No synovial structures involved Does Boris need antimicrobials?
- No? - different between infection and contamination - ensure clean out properly
○ If synovial structure involved then YES
what situations should certain antimicrobials be avoided or are contraindicated
- Organ system disease
○ Liver –rifampin, consider effects of elimination of drugs metabolised by the liver
○ Kidney –aminoglycosides, oxytetracycline
○ Neuromuscular disease –aminoglycosides - Age of patient
○ Macrolides in adult horses (antimicrobial-associated colitis) - NO
○ Enrofloxacinin foals - NO - Physiologic state e.g. pregnancy
○ TMS in early pregnancy? - worry - Previous hypersensitivity reaction
PE findings
HR - 28-40
RR - 8-16
Temp - 37-38.4
paralumbar fossa - 30-60s
trans-tracheal wash what used for, what sedative, how performed and with what
- Used for pleuropneumonia as get all parts of the lungs
- Add butorphanol with sedation as anti-tussive - will still cough though
- Inject 50ml and then aspirate generally 1/2 to 1/3rd back
- Can use expensive set or 10g catheter + dog tubing/urinary catheter
AAEP lameness scale
0: lameness not perceptible
1: lameness is difficult to observe and not consistently apparent
2: lameness difficult to observe at a walk or when trotting in a straight line but consistently apparent (circling, hard-surface)
3: lameness consistently observable at a trot under all circumstances
4: lameness obvious at a walk
5: lameness produces minimal weight bearing in motion and/or at rest or complete inability to move
suspensory ligament injury surgical treatment and prognosis
- Fasciotomy and neurectomy treatment
○ Cut the fascia (fibrous tissue) surrounding he ligament
§ To stop compartment syndrome that occurs with swelling and pressure/pain
○ Neurectomy of the deep branch of the lateral plantar nerve (palmar if forelimb)
§ Supplies proximal portion of the suspensory ligament
§ Helps with pain post-surgery and recovery so can properly load the limb and regrow strength
○ Prognosis
§ 80-85% of cases return to soundness and majority of those to athletic activity
osteomyelitis when see evidence via radiographs
- Osteomyelitis - will see signs 14days post infection injection
Primary Peritonitis (Actinobacillus equuli) physical exams, diagnosis, treatment and monitoring
- FEBRILE (reduce list for febrile colic), low grade colic signs, anorexia, reduced gut sounds
- Confirm with abdominocentesis
- Antibiotics -> Penicillin + gentamycin and if low grade colic - NSAID, enteral fluids if dehydrated and little manure passing
- Expect normal physical exam within hours and can re-evaluate in 5 days
tetanus prophylaxis how works with wounds
○ If in the past year then don’t need
○ Past 3 years - booster tetanus toxoid vaccination
○ Unvaccinated or not in the past 3 years then tetanus antitoxin + tetanus toxoid vaccination
§ Booster required in 4 weeks for future protection
normal volumes for 500kg horse and doses 1) xylazine 2) butorphanol 3) detomodine 4) bute 5) flunixin 6) penicillin 7) gentamicin 8) TMS
1) for mild sedation 0.1-0.5mg/kg - 1.5-2ml IV per 500kg
§ For pre-GA give 5ml xylazine IV
2) +/- butorphanol 0.01-0.04mg/kg - 0.4-2ml IV
3) Detomodine (dormosedan) - 0.5-1ml IV for 500kg horses, lasts 40mins (0.1-0.8ml per 100kg)
4) Phenylbutazone 2.2-4.4mg/kg
§ Oral past 5ml for adult SID OR BID, IV 10-20ml per 500kg
5) Flunixin - 1.1mg/kg - 10ml IV for 500kg horse
6) Procaine penicillin - 15mg/kg BID IM - average 25ml BID
7) Gentamicin - 6.6mg/kg IV SID or IM - 30ml
8) TMS - 15-20mg/kg IV q12 hours or 30mg/kg PO q12 hours
§ Oral form comes as paste 25ml paste BID or as a powder - 2.5 large scoops BID mixed in damp feed
Hendra and herpes virus vaccination protocol
Hendra
○ From 4 months, or 6 months if mare was vaccinated
○ 2 shots IM 3-6 weeks apart, then one 6 months later and then every 12 months
Herpes virus - EHV 1 AND 4 (Duvaxyn)
○ Vaccinate young horses against viral respiratory disease or pregnant mares to help prevent herpes virus abortion
○ For pregnant mares you vaccinate 5,7,9 months gestation
Horse field anaesthesia induction and top-up doses and time given
○ Induction
§ Diazepam + ketamine (1:2) = 500kg horse 5ml (diazepam) + 10ml (ketamine)
§ Will give about 15mins of anaesthesia
§ Generally works well in terms of breathing even when dorsally dependent
○ Top up
§ Ketamine (1/2 induction dose) + xylazine (1/2 induction dose)
§ Give to effect - can give after about the first 12mins
§ Will give another 15mins of anaesthesia
Euthanasia what catheter, sedation, how much, time takes and how to confirm
- 14G catheter (16G minimum)
- SEDATE first as horse going to fall so want to be pretty sedate before hand - control falling as with anaesthesia
○ Sedate with like 1mg/kg xylazine - 100-120ml of lethabarb for 500kg horse
○ Takes 30seconds to drop and about 1-2mins for heart to stop beating (if in atrial fibrillation still need to wait a bit until death) - Confirm death
○ No respiration, no heart beat
○ No corneal reflex with fixed dilated pupil
