Horses 4 Flashcards
1
Q
what are important history things to ask when go out to sick foal
A
- 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
2
Q
Neonatal encephalopathy what is it common causes
A
- 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
3
Q
What are common clinical signs of foals with neonatal encephalopathy
A
- 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
4
Q
What other organs other than the brain that are affected and how for neonatal encephalopathy
A
○ 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
5
Q
what are the other differentials for neonatal encephalopathy and historical problems/risk factors
A
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
6
Q
What are the 8 principles for treatment of hepatic encephalopathy and what is important
A
- 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
7
Q
in terms of treatment for hepatic encephalopathy what is involved in prevention of sepsis and seizures
A
- 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
8
Q
in terms of treatment for hepatic encephalopathy what is involved in supportive care and anti-inflammatories
A
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
9
Q
In terms of treatment for hepatic encephalopathy what is involved with haemodynamic and respiratory support
A
- 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
10
Q
Nutritional support in terms of treatment for hepatic encephalopathy what is needed, how give and what need to consider
A
○ 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
11
Q
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
A
- 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
12
Q
in foals what is their main diet, what are electrolyte levels and therefore what are neonatal kidneys good at
A
- 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
13
Q
Uroabdomen when occurs, prediposed, where on urinary tract and the 2 distinct presentations
A
- 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)
14
Q
Uroabdomen clinical signs
A
○ 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
15
Q
Uroabdomen diagnosis
A
- 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]
16
Q
Once diagnose uroabdomen what need to do, most life threatening thing to correct
A
- 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
17
Q
in terms of treatment for uroabdomen what need to do
A
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
18
Q
What are the 4 main things within the stabilization of foal with uroabdomen
A
1) peritoneal drainage
2) fix hyperkalaemia: if severe (>6mmolL) and/or ECG changes present
3) fix hypovolaemia - careful volume resuscitation
4) fix hyponatraemia
19
Q
peritoneal drainage in uroabdomen what does it do and how done
A
○ 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
20
Q
in the treatment of uroabdomen what are the ways to fix hyperkalaemia
A
○ 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
21
Q
In terms of treating hyperkalaemia in uroabdomen what are 2 other things to consider and why/when
A
○ 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)
22
Q
In terms of treating hyponatraemia for uroabdomen what need to do and why
A
○ 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
23
Q
Uroabdomen what is involved in post-op management and prognosis
A
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
24
Q
define PU/PD in horses
A
- Water intake > 100ml/kg/d
○ 50L for 500Kg horse - Urine output > 50ml/kg/d
○ 25L for 500Kg horse
25
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
26
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
27
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
28
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
29
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
```
30
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
31
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
```
32
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
33
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)
34
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
35
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
36
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
37
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
38
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
39
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
40
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
41
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
42
Water deprivation test what used for and the 2 types, which is best and how performed
To diagnose psychogenic polydipsia
○ 2 types
1) Total water deprivation test - not ideal
□ Chronic PD can result in medullary washout
® Unable to concentrate urine despite dehydration
® Weigh horses every 2 hours (should not lose > 5% BW)
2) Modified protocol
□ Limit water intake to 40mL/kg per day
□ Can be performed over 3-5 days
® Allows for the medullary solute concentrate to return so can concentrate urine
□ Monitor
® Body weight
® USG
® Urea and creatinine - don't want to create pre-renal azotaemia or unmasking kidney disease
43
Water deprivation test for psychogenic polydipsia what results mean what
○ Normal horses should concentrate urine - USG >1.025 - psychogenic
○ Failure to respond to water deprivation test
i. Urine is isosthenuric (USG 1.008 - 1.012)
□ Consider renal failure - recheck urea and creatinine
ii. Urine is hyposthenuric (USG <1.007)
□ Consider rare causes of PU/PD
□ Diabetes inspidus
® Central neurogenic - response to ADH
® Peripheral nephrogenic - no response to exogenous ADH
44
Psychogenic polydipsia management
- Restrict water intake to maintenance requirements
○ Account for level of exercise, ambient temperature
○ Better to overestimate
- Limit boredom in stabled/boxed horses
- Avoid sudden management or feed changes in predisposed animals
45
What are the 3 main common presenting signs of kidney disease
○ PU/PD
○ Oliguria/anuria
§ Despite IVFT
○ Lethargy, inappetance
46
acute renal injury pathophysiology why occur, what occurs and the 2 main mechanisms
- Most AKI due to acute tubular necrosis (ATN)
○ Death and sloughing of tubular epithelial cells
○ Obstruct tubular lumen → no urine output from blocked nephrons
○ 2 mechanisms for acute tubular necrosis
§ ATN caused by toxic insult (including drugs)
□ Different specific toxic actions
□ PCT/cortex most affected (most blood flow)
§ ATN caused by ischaemia
Loop of Henle/medulla most affected (least blood flow
47
Acute renal injury general history
- Administration nephrotoxic drugs
○ Aminoglycosides
○ NSAIDs - common overdose in colitis cases
- Primary disease causing renal hypoperfusion or ischaemia
- COMBINATION OF THESE - most commonly
- Exposure to other renal toxins
48
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
49
How to aminoglycosides lead to acute renal toxicoses
○ Toxicosis almost always due to repeated administration
§ Increase in aminoglycoside cations that destroy renal tubule epithelium
○ High dose vs. frequent dosing
○ Prolonged administration
50
How to NSAIDS lead to acute renal toxicoses
```
○ Excessive doses
○ Hypovolaemic patients
○ Concurrent GI ulceration (RDC, gastric ulceration)
○ Medullary crest necrosis
○ ↓ PGE2, PGI2
○ Loss of vasodilating response
○ Increase in renal vascular resistance
○ Ischaemic ATN (Acute tubular necrosis)
```
51
What is involved in the diagnoses of acute renal injury
- History - exposure to nephrotoxic agent
- Biochemistry
○ Increased creatinine - most common
○ Increased BUN (beware confounding factors)
- Urinalysis
○ USG
○ Dipstick often normal
○ Sediment
§ Casts (often not seen –alkaline pH)
§ Cells
§ Pigments (Hb, Mb)
§ Haematuria
○ How to catch the urine?
§ Cannot do cystocentesis
§ Free catch
□ Saucepan on a stick
□ Urine catcher
52
Acute renal injury treatment
- IV fluids
- Correct electrolyte and acid-base abnormalities
- Determine polyuria/oliguria/anuria
○ Oedema risk if oliguric/anuric
- If oliguric/anuric after 12-24 h IVFT → furosemide
53
what is involved in monitoring acute renal injury patients
- PCV/TP
- Bodyweight
○ no weight gain after initial rehydration
- Urine output (easier said than done...)
- USG - ensure concentrating urine
- BP - blood pressure
- CVP - central venous pressure
- Creatinine +/-BUN
54
Horses with acute renal injury do they recover or progress to chronic disease
- Depends on how bad the effects are on the luminal cells
○ Adaptive repair -> can repair themselves - not back to brand new but close
]○ Maladaptive repair -> develop into chronic kidney disease
55
What is involved in the prevention of acute renal injury in horses
- Close monitoring of patients receiving nephrotoxic medications
○ Creatinine -> change in creatinine relative to ITS normal not the NORMAL
○ GGT:creat ratio - not always useful
○ Therapeutic drug monitoring (aminoglycosides) -> not available in general practices
- Careful use of oxytetin foals
○ Slow administration
○ Administer with IV fluids
○ Don’t administer on consecutive days
- Avoid exposure to toxins
56
Chronic kidney disease what is it, what does it lead to and the 3 common presenting complaints
- Irreversible, progressive decline in GFR
- Glomerularor tubulointerstitial
○ One often leads to the other
- Common presenting complaints/history
1. Weight loss
2. PU/PD (may go unnoticed)
3. Poor performance
57
Chronic kidney disease what are common physical exam biochemistry and urinalysis findings
```
Physical exam
- Non-specific findings
- Dental tartar - canine teeth in males, and possible incisors
- (Mild ventral oedema)
ClinPath
- Plasma
○ Azotaemia
○ Hypercalcaemia
§ Dietary-related
○ +/-Hypermagnesaemia
○ Acid-base normal unless end-stage
- Urine
○ Isosthenuria
○ (Proteinuria–glomerulardisease)
○ (Haematuria, pyuria–pyelonephritis)
○ Urine clear –lack of crystals, mucous - normal products within urine
```
58
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
```
59
What are the 4 things needed for diagnosis of chronic kidney disease
- Biochemistry, urinalysis
- Ultrasound - kidney size and internal architecture
- Biopsy
- Cystoscopy - look at ureters and flow of urine, C&S (pyelonephritis)
60
Chronic kidney disease what treatment for stable, end stage and pyelonephritis
- Acute exacerbation of chronic disease
- Stable CKD
○ Adequate hydration
○ Salt supplementation if needed (NOT if oedema)
○ Diet –good quality, avoid excess protein
○ Monitoring
- End stage
○ Maintain appetite, caloric intake
- Pyelonephritis
○ Antimicrobials –prolonged course
○ Nephrectomy(if unilateral)
61
what are the 5 main causes of gross haematuria
1. Idiopathic renal haematuria
2. Renal calculi
3. Neoplasia
○ Kidneys
○ Bladder
4. Cystic calculi
5. Urethral haemorrhage
62
How to diagnose gross haematuria
```
- Where is the blood coming from?
○ Haematology, biochemistry
○ Urinalysis - ensure red blood cells not pigment
○ Ultrasound
○ Cystoscopy
```
63
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
64
Neoplasia leading to gross haematuria what are the 2 main ones, types within and prognosis
```
- Kidneys
○ Adenocarcinoma/Renal cell carcinoma
○ (Nephroblastoma)
○ Secondary
§ Adenoma
§ Lymphosarcoma
§ Haemangiosarcoma
§ Melanoma
- Bladder
○ Squamous cell carcinoma
○ Transitional cell carcinoma
- Prognosis usually poor
```
65
Cystic calculi what made of, occurance, presentation and diagnosis
- Usually single, large, spiculatedstones
○ Calcium carbonate
- Bacteria often present but role unclear
- Occurrence rare in horses
- Haematuria after exercise
○ Stranguria, dysuria, pollakiuria, incontinence also occur
Diagnosis
- Palpation per rectum
- Cystoscopy - the best way to confirm
- Ultrasound (per rectum)
66
Cystic calculi treatment and prevention
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)
67
Urethral hemorrhage what sec most common, presentation and which breed overrepresented
- Male horses
- Gross haematuria at end urination, end ejaculation (also haemospermia)
○ Normal voiding of urine
○ “squirts” of frank blood at end
○ Differentiate from pigmenturia
- QH & QHX breeds overrepresented
68
what are the 5 main causes of urinary incontinence
1. Cystic calculi
2. Sabulous urolithiasis
3. Urinary tract infection
4. Neurologic causes
5. Ectopic ureter
69
Sabulous urolithiasis what is it, what lead to and common presentation
- Accumulation sabulous material in the bladder - NOT A UROLITH
○ Which occurred first???
- Bladder paralysis/incomplete emptying
○ Often don’t identify cause
- Urinary incontinence common presentation
70
Sabulous urolithiasis diagnosis, treatment and prognosis
```
Diagnosis
- Palpation per rectum
○ large bladder
- Cystoscopy
- Ultrasound
Treatment
- Bladder catheterisation and lavage -> hard has cannot regain neurological function of bladder
- Prokinetics? (bethanechol)
Prognosis guarded, may regain athletic use
```
71
Urinary tract infection common risk factor, types of pathogens, clinical signs, diagnosis and treatment
- Bladder paralysis most common risk factor
○ Trauma
○ Neurologic disease
- Gram positive and negative pathogens
- Dysuria/stranguria/pollakiuria/incontinence
- TPR and routine haematology usually normal
- Urinalysis:
○ > 20 organisms/HPF and > 10 WBCs/HPF (sediment exam)
○ Positive culture
Treatment - Antimicrobials (C&S
72
Neurologic cause of incontinence what are the 4 common ones, what all can lead to and clinical signs
1) LMN lesions → loss of detrusor function
2) EHV-1 myelitis
3) Cauda equinaneuritis (polyneuritis)
4) EPM (North or South America)
All can → sabulous urolithiasis
- Spinal cord lesions → UMN bladder
○ Usually not a big problem in horses
○ May not be recognised until overflow incontinence occurs
73
```
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
```
1. Urolithiasis - MOST CONSISTENT
2. Neoplasia - possible but not common
3. Sabulous urolithiasis - DON'T USUALLY HAVE HAEMTURIA
4. Urethral haemorrhage - would expect haematuria at end of urination
5. Idiopathic renal haematuria - intermittent, more severe haemorrhage
6. Neurologic disease - don't usually have haematuria
74
After urolith (Cystic calculi ) surgery what are the recommendations for post op management and follow up
Lucerne hay should be limited and he should be rested
- Rested as abdominal surgery, bladder needs healing
§ 1 month in box, 1 month small yard, 1 month paddock then back to work generally
- Lucerne hay has high calcium content - want to reduce calcium intake
§ Switch to a grass hay
Follow-up
- Post-op cystoscopy
- Cystoscopy lavage
- Mucosal healing
75
What are hte 2 main questions in equine neurology
1. Does the horse have neurologic disease
| 2. What is the location of the neurologic lesion
76
In terms of neurological examination what is involved
- Signalment and history
- Evaluate patient from a distance
○ Interaction with environment, mentation
- Start at the front and go around just once -> don't want to move around a possibly unstable horse more than once
- Evaluation of:
○ Head
○ Body
○ Posture and gait
§ Walk up and down
§ Walk up and down with head in the air
§ Etc. -> want to tease out subtle abnormalities
- -> ask the patient to perform tasks of increasing complexity
77
What neurological examination techniques aren't done in horses
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○ Myotactic and withdrawal reflexes
§ Expect in recumbent animals and foals
§ Subtle
○ Hemi-walking
§ Thoracic limb hopping possible in cooperative horses
○ Wheel-barrowing
```
78
What are the 3 ways evaluation of the head (brain) occurs
1) behaviour and mentation
2) head posture and movement
3) cranial nerve function
CN I - olfactor nerve
CN II - optic nerve
CN III - oculomotor
IV - trochlea
V - trigeminal
VI - abducens
VII - vestibulocochlear nerve
IX - glossopharyngeal
X - vagus
XI - accessory
XII - hypoglossal
79
What looking at with behavior and mentation evaluation for the brain
changes in behaviour or mentation expected with intracranial disease
○ Mania, anxiety
○ Seizures
○ Dull, depressed, obtunded
○ Stupor, coma
○ Head pressing -> forebrain of brain -> typical intra-cranial disease
80
What looking at with head posture and movement for evaluation of the brain
Head posture and movement - asymmetric brain lesions cause deviation of the head and neck from the midline
○ Head turn: usually seen with forebrain disease - less common than head tilt
○ Head tilt: usually indicates vestibular disease, direction in which the top of the head is deviated
81
How to examine cranial nerve 1 function
Olfactory nerve (CN1)
§ Large animals require an intact sense of smell to eat normally
§ -> animals with good appetites likely have an adequate sense of smell
§ HARD TO ASSESS
82
How to examine cranial nerve II function
Optic nerve (CN II)
1) Menace response (response NOT REFLEX, learned behaviour)
□ Newborn animals lack a menace response for at least 10 days
□ Required intact CN VII (motor response)
2) Pupillary light reflex
□ Response is slower in LA species
□ CN III constricts the pupil
□ Swinging light test -> check the direct and indirect response (shine light into one eye check response there and on the other eye)
® Direct stimulus is stronger than indirect
83
How to examine the cranial nerves that are involved with the eyes
Oculocephalic reflex (cranial nerves III (oculomotor), IV (trochlea) and VI (abducens)
§ Rotation of eyes -> Trochlear - dorsal oblique (rotate around axis), abducens lateral rectus (pulls out), oculomotor -> does everything else
§ normal (physiological) nystagmus as the head is moved from side to side
□ Rotation in direct away from moving the head, fast flick in same direction of movement of head
§ When head is elevated, eyeballs tend to maintain horizontal axis and move ventrally within bony orbit
84
How to examine cranial nerve 5, 3 3 branches
Trigeminal nerve (CN V)
§ Sensory of the face
□ Three branches - prick those areas and assess for response
a) Mandibular
b) Maxillary
c) Ophthalmic
□ In stoic animals might have to stimulate the inner ear or nasal septum - may not respond to prick
§ Mandibular branch is motor to the muscles of mastication
□ Atrophy/tone sometimes more easily appreciated by palpation
□ Unilateral damage: typically no dysphagia
□ Bilateral damage: "dropped jaw" and inability to chew
85
How to examine cranial nerve 7 and its 2 components with the 2 types of diseases
1) Cochlear component
□ Hearing loss difficult to detect, especially if unilateral
2) Vestibular component
□ Clinical signs
® Staggering gait, falling, rolling
® Circling (towards lesion)
® Head tilt (toward lesion)
® Spontaneous nystagmus (fast phase away from the side of the lesion)
□ Types
1. Central vestibular disease - generally see other signs like depressed mentation while peripheral vestibular disease generally bright
2. Paradoxical vestibular disease - cerebellum involved
□ Can compensate -> may need to blind fold them to appreciate
86
Cranial nerve IX, X and XI what are they, function, clinical signs of dysfunction and examination
Glossopharyngeal (IX), Vagus (X) and Accessory (XI) nerves
§ Sensory and motor innervation of pharynx and larynx
□ Accessory n. also provides motor input to the superficial neck muscles - injury difficult to evaluate
§ Clinical signs of CN IX and X dysfunction include:
□ Dysphonia (snoring and roaring)
□ Dysphagia ( -> aspiration pneumonia)
□ Regurgitation
§ Endoscopic evaluation of larynx often useful
□ Thoraco-laryngeal response (slap test) -> slap the horse just behind the weathers (feel the contralateral CAD muscle (arytenoids) twitch or use endoscope to find)
87
How to examine cranial nerve XII and what generally results from unilateral and bilateral injury
Hypoglossal nerve (CN XII)
§ Motor to tongue - assess from both sides
§ Normal animals strongly resistance pulling on the tongue
§ Unilateral injury: weak retraction but tongue does not protrude from the mouth
§ Bilateral injury: difficulty prehending and swallowing, tongue usually protrudes from the mouth
88
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
89
how to perform the cervico-facial, panniculus and perineal reflex
Cervico-facial (cutaneous faciei)
□ 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
90
What is involved in proprioception tests
○ "knucking" generally unreliable in large animals
○ "placement reaction"
§ Responses to abduction or crossing of the limbs
§ Cautious with interpretation -> asymmetric response might be noteworthy
91
In terms of evaluation of gait within the neurological examination what are you looking for
- Neurologic gait abnormalities typically involve degrees of:
○ Paresis (weakness)
○ Ataxia (incoordination)
- Weakness and incoordination can be difficult to differentiate
○ Many patients have components of both
92
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
93
In terms of evaluation of gait how to evaluate and other ways to detect more subtle abnormalities
```
- Evaluate via:
○ Slow walk on firm, level ground
○ Trot: watch out for changes in gait as the animal warms up
○ Backing: normal horse 'trot' backwards
○ Circling: want outside front leg across inside front leg, take inside back leg across front of outside and step nice and cleanly
○ Tail pull: might help with distinction between LMN and UMP lesions
○ Hopping
- To detect more subtle abnormalities
○ Elevate the head
○ Serpentine manoeuvres
○ Walking the animal on a slope
○ Blind folding
○ Walking across obstacles (curbs)
```
94
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
95
Give examples of changes in behavior from cerebral disease
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○ Yawning -> hepatoencephalopathy
○ Asymmetric lesions -> drift toward one side
○ Lack of recognition of familiar objects
○ Compulsive walking
○ Circling (walk asymmetric disease)
○ Head pressing
○ Biting at inanimate objects
○ Leaving food in the mouth
○ Adopting bizarre postures
```
96
What are the 3 main clinical signs of brainstem disease
1) Severe depression
2) Cranial nerve deficits
3) Vestibular dysfunction
○ Peripheral vestibular disease
○ Central vestibular disease
97
Peripheral vestibular disease what clinical signs are involved
§ Head tilt toward affected side
§ Horizontal or rotatory nystagmus with the fast phase away from the affected side
□ Nystagmus does not change direction with changes in head position
§ Usually staggering, dysmetric gait
□ -> tendency to lean or circle toward the affected side
98
Central vestibular disease what clinical signs are seen
§ Pronounced gait deficits
§ Nystagmus may be variable horizontal, vertical or rotatory
□ Fast phase can be away from to toward the side of the lesion
□ May change direction with changes in head position
□ Head tilt may be toward or away from the side of the lesion
§ Frequently involved adjacent brainstem structures:
□ Depression (reticular activating system)
□ Paresis (motor tracts)
□ Ataxia (proprioception tracts)
□ Other cranial nerve deficits
99
With spinal cord disease what should be normal and what is important to differentiate
- Mentation should be NORMAL - bright and aware of surrounding
Differentiate
Weakness
Ataxia
100
Localising lesions within the spinal cord what are the 2 areas of spinal cord, what present and what does damage lead to
1) Grey matter contains the cell bodies of the motor neurons
○ Damage -> LMN deficits at the lesion site
○ Weakness (paresis/paralysis), hypotonia (decreased muscle tone), hyporeflexia (decrease in reflexes) - hard to assess in LA
2) White matter contains the neural tracts conveying information to the brain and back to the body:
○ Lose the fine control, unsure where the limb is in space
○ Damage -> UMN deficits caudal to the lesion
○ Ataxia, hypermetria (increased steps), hypertonia (increased muscle tone), hyper-reflexia (increase reflexes)
101
what is used to localise lesions and what are the intumescences
- Combination of UMN and LMN neurologic signs used to localise lesions within the spinal cord
- Cell bodies of the limbs are concentrated within the "intumescences"
○ Thoracic limb: C6 to T2
○ Pelvic limb: L3 to S2
