Horses 4 Flashcards
what are important history things to ask when go out to sick foal
- Mares normal gestation length - gestation length and was it abnormal
- how was the foaling
- Has the mare had any other sick foals
- Has the foal urinated or defecated
- Has the foal suckled, stood
- Have there been other sick foals on the farm this season, abortions
- Any history of trauma
- was the IgG checked, value
- Vaccination program - insight into management of the farm not necessary the foal itself
Neonatal encephalopathy what is it common causes
- Hypoxic-ischaemic encephalopathy (HIE); neonatal maladjustment syndrome, dummy foals
1. Often follows episode or peri-parturient hypoxia or anoxia
○ Dystocia and delivery by cesarean section are risk factors
○ Perinatal asphyxia syndrome (PAS) in human infants
2. NE also seen with in utero exposure to inflammation
○ Occult placentitis
§ Chronic hypoxia
§ Exposure to pro-inflammatory mediators
3. However, in many cases there is no obvious asphyxia
○ Affected foals make a rapid and complete recovery
○ Contrasts human infants with PAS and NE
What are common clinical signs of foals with neonatal encephalopathy
- Some foals abnormal at birth, but clinical signs can develop at any time in the first 72 hours
- Typically related to cerebral dysfunction
○ Loss of or a poorly coordinated suckle reflex
○ Loss of affinity for dam
○ Abnormal suckling behaviour
○ Mentation can range from hyper-responsive to comatose
○ Seizures (focal to generalised)
○ Abnormal respiratory patterns
○ Occasionally unilateral
What other organs other than the brain that are affected and how for neonatal encephalopathy
○ Gastrointestinal tract -> may not tolerate enteral feeding
○ Kidneys -> persistent azotaemia
§ Which doesn’t resolve with fluid therapy - UNLIKE NORMAL FOALS
○ Lungs
○ Immune system
-> clinically difficult to differentiate from sepsis
what are the other differentials for neonatal encephalopathy and historical problems/risk factors
Differentials - Trauma - Bacterial meningitis - Hydrocephalus Historical problems - Dystocia - Prolonged stage II labour - Thickened placenta CAN OCCUR IN THE ABSENCE OF THESE FACTORS Risk factors for sepsis in NE foals: - Might not stand to nurse colostrum - Indiscriminate nursing behaviour - Immune function VERY DIFFICULT TO DEFINITIVELY RULE OUT SEPSIS IN SICK FOALS
What are the 8 principles for treatment of hepatic encephalopathy and what is important
- Early identification is important
1. Prevention of sepsis
2. prevention of seizures
3. supportive care
4. anti-inflammatory/anaglesics
5. haemodynamic support
6. respiratory support
7. nutritional support
8. nursing care - same as neonatal sepsis
in terms of treatment for hepatic encephalopathy what is involved in prevention of sepsis and seizures
- Prevention of sepsis
○ Affected foals are commonly septic OR often become septic
§ FPT
§ Immunocompromised
§ Increased exposure
○ Broad-spectrum antibiotics - Prevention of seizures
○ If don’t manage properly then become more hardwired into the horse - harder to treat later
○ Diazepam/midazolam (CRI) -> short-half life
§ Good to pull out and then monitor to see if still occurring
○ Phenobarbital
in terms of treatment for hepatic encephalopathy what is involved in supportive care and anti-inflammatories
3. Supportive care ○ Monitor GI and renal function ○ Ensure adequate DO2 § Adequate oxygenation (INO2) § Maintain blood pressure ○ Careful glucose management ○ Excellent nursing care and careful, repeated monitoring 4. Anti-inflammatories/analgesics ○ Flunixin meglumine ○ Corticosteroids NOT indicated ○ Treatment to reduce cerebral oedema, support brain function and scavenge free radicals
In terms of treatment for hepatic encephalopathy what is involved with haemodynamic and respiratory support
- Haemodynamic support
○ Judicious fluid therapy
§ Care to avoid over-hydration (brain, kidneys, lungs)
○ Care with sodium load
§ Sodium requirements 3mEq/kg/day
§ Hartmann’s [Na+] = 140mmol/L - Respiratory support
○ Some affected foals will display abnormal respiratory patterns that can lead to hypoxaemia and hypercapnia
§ Intra-nasal O2 insufflation sufficient in most cases
Nutritional support in terms of treatment for hepatic encephalopathy what is needed, how give and what need to consider
○ Meet MER in critically ill foals
§ Approx. 50kcal/kg/day
§ Equates to approx. 10% of bodyweight in mare’s milk/day
§ Feeding tube if unable to nurse to drink from a bottle/bucket
○ Start with very small meals initially
§ Normal foal: 20% BW/day -> approx 850mL q 2hours
§ NE foal: 50-100ml q 2hours (approx 2% BW/day) initially
§ Gradually increase if enteral nutrition is tolerated
○ Consider early institution of TPN in foals that do not tolerate enteral feeding
§ Monitor [glucose], [triglycerides] and [electrolytes]
§ Nutrition for enterocytes
renal function what diet do horses have and therefore kidneys need to and urine has what concentration of electrolytes and what is the normal plasma levels
- Horses have a low salt (NaCl), high potassium diet
- Kidneys actively
○ Conserve Na+
○ Excrete K+ - As a consequence, urine has*
○ Very low [Na+] (low FE)
○ High [K+]
○ (high creatinine concentration) - Remember plasma [Na+] = 133-145mmol/L and [K+] = 3-5mmol/L
in foals what is their main diet, what are electrolyte levels and therefore what are neonatal kidneys good at
- Milk diet
- Relative to plasma, milk is:
○ Low in Na+ (9-15mEq/L)
○ High in K+ (approx 21mEg/L)
○ High in water - Neonatal kidneys are therefore especially good at:
○ Holding on to sodium
○ Excreting potassium
○ Excreting water
Uroabdomen when occurs, prediposed, where on urinary tract and the 2 distinct presentations
- Can occur during birth, or after
○ Colts more predisposed - longer, narrower urethra? - Urinary tract can be disrupted anywhere any its length
○ Bladder rupture most common
○ Dorsal bladder wall most common site of rupture - Two (somewhat) distinct presentations
○ Otherwise healthy foal (clinical signs at 3-5 days)
○ Sick foal (usually recumbent)
Uroabdomen clinical signs
○ Dull, lethargic ○ Stranguira and /or pollakiuria § Some affected foals will pass a fairly normal urine stream ○ Loss of interest in nursing ○ Abdominal distention ○ Some foals may be found dead
Uroabdomen diagnosis
- Signalment - colts more predisposed
- Clinical signs
- Characteristic clin path changes
○ Post-renal azotaemia
○ Electrolytes - HYPONATRAEMIA, HYPERKALAEMIA - Ultrasonographic finding - large volume of free peritoneal fluid
- Analysis of fluid collected via abdominocentesis - Peritoneal fluid [creatinine] ≥2x plasma [creatinine]
Once diagnose uroabdomen what need to do, most life threatening thing to correct
- Stabilise the foal with IV fluids and peritoneal drainage, then go to surgery
- Hyperkalaemia: Can have serious (fatal) effects on myocardial electrical activity! - MAIN ISSUE
○ Bradyarrhythmia
○ Loss of P waves –atrial standstill
§ Peaked T waves (can be hard to appreciate in equine ECGs)
§ Widened QRS complexes -can lead to ventricular fibrillation
in terms of treatment for uroabdomen what need to do
1) stabilisation
1. Correct electrolyte abnormalities
○ Especially hyperkalaemia
○ Care with sodium
2. Address cardiovascular compromise (hypovolaemia)
3. Address underlying disease (e.g., sepsis)
2) surgical repair of the rupture
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
peritoneal drainage in uroabdomen what does it do and how done
○ Removes source of K+
○ Removes excess water
○ Reduces pressure on diaphragm when foal in dorsal recumbency
○ Teat cannula or small chest drain -> may need to be within for a few days before surgery - or sometimes quite quick
§ Blocked by omentum
○ Urinary catheter passed into abdomen via urethra
in the treatment of uroabdomen what are the ways to fix hyperkalaemia
○ IV fluids - MOST IMPORTANT
§ dilution
○ IV Glucose (Dextrose) - if not very high
§ Stimulates endogenous insulin response
§ Stimulates intracellular K+ movement
○ Exogenous insulin
§ 0.1-0.2 IU/kg SC or IV + dextrose infusion
○ Sodium Bicarbonate
§ Alkalosis stimulates intracellular K+ movement as K+ moves in while H+ moves out
In terms of treating hyperkalaemia in uroabdomen what are 2 other things to consider and why/when
○ Calcium borogluconate(23% solution)
§ Helps restore normal differential between resting membrane potential and firing threshold
○ IV fluids with low [K+] or no K+ often recommended
§ Probably unnecessary in most cases
§ 0.9% NaClhigh in Na+(poor for slow correction of Na+if hyponatraemic), and acidifying (will → K+into ECF)
In terms of treating hyponatraemia for uroabdomen what need to do and why
○ Care with longstanding (> 24-48 hours) hyponatraemia (< 120 mmol/L)
§ If you don’t know how long it’s been going on, assume longstanding.
○ Need to correct Na+ slowly
§ Avoid fluid shifts
§ Avoid osmotic demyelination syndrome
Uroabdomen what is involved in post-op management and prognosis
POST-OP management
- Indwelling urinary catheter
○ Give bladder chance to heal, don’t want bladder to distend for a few days
- Close monitoring of urination following removal
- Monitor nursing, general demeanour of foal
PROGNOSIS
- Prognosis excellent in otherwise healthy foals,
- Prognosis in sick foals depends on primary disease
define PU/PD in horses
- Water intake > 100ml/kg/d
○ 50L for 500Kg horse - Urine output > 50ml/kg/d
○ 25L for 500Kg horse
What are the 4 common differential diagnosis for PU/PD and the 2 rare causes
- Common causes
○ Renal failure
○ Pituitary pars intermedia dysfunction (PPID)
○ Psychogenic polydipsia - drink more due to neurological dysfunction
○ Iatrogenic (drug administration, fluid therapy) - Rare causes
○ Diabetes mellitus
○ Diabetes insipidus
Pituitary pars intermedia dysfunction (PPID) how common, why important and what bred
- Most common endocrinopathy of equids
○ Approx. 20% of horses aged >15 years in Australia - Important due to its associated with laminitis
○ Crippling lameness may necessitate euthanasia
○ Not all cases develop laminitis - More common in pony breeds
Pituitary pars intermedia dysfunction (PPID) what is it and what occurs normally
- Chronic neurodegenerative condition
○ Progressive spectrum of disease - Normally
○ Pars intermedia is autonomously active -> ALWAYS ON
Regulation of hormone production is via inhibitory effect of dopamine
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) clinical signs in early and advances stages
Early - Laminitis (seasonal) - Change in attitude - Delayed hair shedding - Regional hypertrichosis - Abnormal fat distribution Advanced - Laminitis (year-round) - Lethargy - Generalised hypertrichosis/hirsutism - Abnormal fat distribution - Hyperhydrosis - PU/PD - Hyperglycaemia - Recurrent infections - Infertility - Neurological abnormalities
Pituitary pars intermedia dysfunction (PPID) what are the main ways to diagnose
1) visual examination - clinical signs - poor coat (Commonly diagnosed in paddock)
2) endocrine tests
1. endogenous ACTH assay
2. dexamethasone suppression test
3. other tests (TRH stimulation test)
3) insulin status
Pituitary pars intermedia dysfunction (PPID) what is the goal of the endocrine tests for diagnosis
○ Establish baseline § Decide whether treatment is warranted § Monitor disease progression § Monitor response to treatment ○ Normalisation of endocrine status before improvement in most clinical signs and vice versa
Pituitary pars intermedia dysfunction (PPID) how does the endogenous ACTH assay work, how to perform and what need to be aware of
□ Preferred screening test
□ Expect to be produced in larger amount in PPID
□ Single blood sample
□ Seasonal variation (Autumnal hyperactivity)
® Expect much larger increase through autumn -> autumn reference <47pg/mL
® BETTER SENSTIVITY AND SPECIFICITY DURING AUTUMN
□ Careful sample handling required
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) what are the 3 main limitations of using dexamethasone suppression test
1) Seasonality
- High rate of false positive results in autumn
- > Won’t suppress in autumn
2) 2 visits required
- Owner to give dexamethasone injection
3) Risk of inducing laminitis - not really a factor
Pituitary pars intermedia dysfunction (PPID) in terms of endocrine tests what is the main other useful test, 2 potentially useful and 2 not useful
□ Useful
® TRH stimulation test (measuring ACTH)
◊ Difficult to source TRH - gold standard in research
◊ Normal mild increase, PPID large increase in ACTH
□ Potentially useful
® Domperidone stimulation test
® Measurement of alpha-MSH, CLIP, beta-endorphin
□ Not useful
® Basal cortisol or assessment of diurnal rhythm
® Urinary creatine: cortisol ratio
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
Pituitary pars intermedia dysfunction (PPID) what is the treatment and what does it do
- Pergolide mesylate
○ Dopamine agonist (activation of inhibitory dopaminergic neurons - decrease ACTH and the other factors)
○ Start at 2ug/kg PO SID (1mg for a 500kg horse)
○ Increase dose in 0.5mg graduations
Compounded formulation vs commercial preparation
Pituitary pars intermedia dysfunction (PPID) monitoring what are we monitoring and when to monitor
○ What do we monitor
§ Clinical signs
□ Can take months/years for some signs to improve
§ Endocrine function
□ ACTH, DST
○ When to monitor
§ Repeat endocrine testing 2-4 weeks after starting treatment
§ Generally 1 month, 1 month after that and then make decision about how frequent after that
§ Reassess dose of pergolide
Pituitary pars intermedia dysfunction (PPID) what if pergolide isn’t working as a treatment
○ What are we waiting for
§ Do we worry if ACTH improves by hair hasn’t fallen out yet
□ If summer can also clip long hair, main issue is laminitis cases
○ Wait longer?
○ COMBINATION THERAPY
§ Serotonin antagonist
□ Serotonin provides stimulation to pars intermedia
® Remove some of additional stimulation -> only a small contribution though
§ Not useful as monotherapy
Pituitary pars intermedia dysfunction (PPID) in additional to treatment what is some further management
a. Dental care
b. Hoof care
§ Regular hoof care important
§ Radiographs useful to assess progress
c. Parasite control
d. Nutrition - low GI diet if insulin resistance
e. Clipping long hair
f. Aggressive treatment of infections
