Equine Urinary Medicine

Question 1

Define…
1. Pigmenturia.
2. Polydipsia.
3. Polyuria.
4. Pollakuria.

Answer 1

1. Coloured urine.
2. Excessive volume of drinking.
3. Excessive volume of urination.
4. Excessive frequency of urination.

Question 2

Define…
1. Dysuria.
2. Stranguria.
3. Oliguria.
4. Anuria.

Answer 2

1. Abnormal urination.
2. Straining to urinate.
3. Decreased production of urine.
4. Stop urinating.

Question 3

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Question 4

Define…
1. Pigmenturia.
2. Polyuria.
3. Polydipsia.
4. Pollakuria.

Answer 4

1. Coloured urine.
2. Excessive volume of urination.
3. Excessive volume of drinking.
4. Excessive frequency of urination.

Question 5

Define…
1. Dysuria.
2. Stranguria.
3. Oliguria.
4. Anuria.

Answer 5

1. Abnormal urination.
2. Straining to urinate.
3. Decreased production of urine.
4. Stop urinating.

Question 6

Renal physiology in equine.

Answer 6

Elimination of nitrogenous and organic wastes:
- urea metabolism.
- creatinine metabolism.
Control of body water content and ion composition needs…
- renal blood flow.
- glomerular filtration.
- tubular modification of glomerular filtrate.
…to produce the final urine.

Question 7

Exam of the urinary system - Hx.

Answer 7

Standard plus:
- measure water intake over 24h.
- easy for owner to confuse polyuria with pollakuria.
- polydipsia = intake >100ml/kg/d.
– (>50L/500kg horse).
Most common presenting complaints:
- abnormal urination.
- weight loss.

Question 8

Exam of the urinary system - CE.

Answer 8

Standard plus:
- rectal to feel bladder.
– size.
– wall thickness.
– uroliths.
– masses.
–> rectal to feel caudal pole of left kidney.
- examine penis (sedate with alpha-2, butorphanol PLUS ACP.
- pass urine catheter if suspect an obstruction.

Question 9

Exam of the urinary system - blood tests.

Answer 9

Haematology.
- leukocytes.
– think inflammation or infection.
- anaemia.
– chronic disease.
– chronic renal failure (EPO).
Urea/creatinine.
- azotaemia.
- do not increase until >75% nephrons non-functional.
- little use in evaluation of early/ minor changes.
- once elevated, doubling urea/creatinine = 50% decline in remaining function.

Question 10

Exam of the urinary system - urinalysis.

Answer 10

Usually midstream or catheterised.
Most will urinate when in freshly bedded stable.
Don’t even think about doing cystocentesis.
If pigmenturia, note timing and duration of passage of discoloured urine.
USG.
Reagent strip analysis.
Sediment analysis.
(Enzymuria).
(Fractional clearance of electrolytes).

Question 11

Urinalysis - USG.

Answer 11

USG = estimated urine concentration.
Easy to measure horse side with refractometer.
- urine more dilute than serum = hyposthenuric (<1.008).
- urine and serum of similar osmolarity = isosthenuric (1.008-1.014).
- urine more concentrated than serum (>1.014).
– adult normally concentrated, foal dilute.

Question 12

Exam of the urinary system - ultrasonography.

Answer 12

Transrectally/transabdominally.
- uroliths in kidneys and sometimes bladder.
- size and architecture of kidneys.

Question 13

Exam of urinary system - cystoscopy.

Answer 13

Investigate abnormal urination.
Examine urethra (on way out), bladder, watch (can sample) urine coming from ureters (may identify a unilateral renal problem).
Sedation to include ACP if male.

Question 14

Exam of urinary system - other tests.

Answer 14

Water deprivation and anti-diuretic hormone (ADH) challenge test.
- hyposthenuric polyuria.
- primary (psychogenic) polydipsia vs central or nephrogenic diabetes insipidus).
Renal biopsy.

Question 15

Developmental malformations.

Answer 15

Many types, but rare.
Other patent urachus.
- foetus – urine passes from bladder to allantoic cavity via urachus.
- normally, urachus closes at time of parturition.
- congenital patent urachus.
– failure to close at birth (tension during parturition?)
- acquired (usually secondary to umbilical infection).
- drip urine from umbilicus.
- congenital: prophylactic ABX, close with time.
- acquired: US to assess infection, investigate and treat sepsis and failure of passive transfer.
- ? surgical removal.

Question 16

Acute renal injury (ARI).
- what is it and what causes it?

Answer 16

Is better terminology than Acute Renal Failure (ARF).
Clinical syndrome associated with abrupt reduction in GFR leads to:
- failure of kidneys to excrete nitrogenous wastes causing azotaemia – uraemic syndrome.
- Disturbances in fluid, electrolyte and acid-base homeostasis.
Can result from:
- pre-renal failure.
– decreased renal perfusion without associated cell injury.
– from conditions causing decreased CO/increased renal vascular resistance.
– e.g. D+, endotoxaemia, septic shock, +/- use of NSAIDs in these cases.
- intrarenal failure.
– ischaemic or toxic damage tot he tubules, tubular obstruction (e.g. casts), acute glomerulonephritis, tubulointerstitial inflammation.
- postrenal failure.
– obstruction or disruption of urinary outflow tract (e.g. uroliths).

Question 17

ARI - clinical signs.

Answer 17

In most with haemodynamically mediated (i.e. prerenal, ischaemic) ARI, clinical signs usually from the primary problem.
- ARI may not be suspected / detected unless looked for.
Often oliguria in adults, anuria in foals.
Patients with ARI often treated initially with large volumes of IV fluids for primary disease.
- will become polyuric unless significant renal damage – where stay oliguric and so retain fluid.
–> get oedema, soft faeces.

Question 18

1. Diagnosing ARI in horses.
2. Treating ARI in horses.

Answer 18

1. Azotaemia.
   USG.
   Casts - show damage.
   Rule in/out prerenal and postrenal causes, if not is intrarenal.
   If intrarenal, US, ?biopsy.
2. Reverse underlying cause.
   Correct fluid and electrolyte imbalances.
   If insufficient response dopamine infusion to improve blood flow.
   ?Diuretics.
   Stop aminoglycosides where possible - if not do therapeutic drug monitoring.

Question 19

Prognosis of ARI.

Answer 19

Depends on:
- underlying cause.
- duration.
- response to treatment.
- development of complications like thrombophlebitis, laminitis.
Can live long term:
- but often polyuric.
- must always have access to water.

Question 20

Chronic renal disease.

Answer 20

Better than chronic renal failure.
Renal injury fairly common but failure fairly rare (large reserve capacity).
Disorders leading to CRD may be congenital or acquired.
- glomerulonephritis.
– immune-mediated.
– ischaemia.
– toxic insults.
– infection.

Question 21

CRD causes.

Answer 21

Chronic interstitial nephritis.
- from acute tubular necrosis after ischaemia, endotoxaemia, sepsis, ascending infection, exposure to nephrotoxic compounds.
End-stage kidney disease.
- severe gross and histological changes, can’t determine initiating cause.

Question 22

CRD clinical signs.

Answer 22

Present late in disease course.
Uraemic syndrome signs vary and can include:
- lethargy (anaemia).
- anorexia.
- weight loss.
- PUPD.
- dental tartar.

Question 23

Diagnosing CRD.

Answer 23

Persistent isosthenuria + azotaemia + clinical signs.
Urea:creatinine >10:1.
Often further non-specific abnormalities e.g. anaemia.
If hypercalcaemic, think renal failure.
May see/feel changes on US/rectal.

Question 24

Treating CRD.

Answer 24

Usually presented late and have progressive and irreversible renal disease.
Long term prognosis grave.
Specific corrective treatment for CRD (renal transplantation) not available.
Peritoneal / haemo dialysis only for valuable breeding animals.
Short term px fair.
Palliative efforts to minimise further loss of renal function, monitor closely to PTS before develop uraemic decompensation.
Free access to water,
Palatable diet to encourage appetite and minimise weight loss.
Some others.

Question 25

UTIs in horses.

Answer 25

Not v common.
Primary cystitis not very common, look for a primary problem e.g. urolithiasis.
Dysuria.
Mid-stream urine sample, bacteriology.
Plus, investigate underlying causes.

Question 26

Treating UTIs.

Answer 26

Primary cause:
- systemic abx.
- base on C&S.
- usually TMPS effective (anyway) as get high concentration in urine.
- 1w usually enough.
- 4-6w if recurrent.

Question 27

UTIs - pyelonephritis.

Answer 27

Rare.
Dx - Look for underlying cause.
US.
Urine and ureteral sample.
Tx - Prolonged course appropriate ABX.
Even unilateral nephrectomy.

Question 28

Urolithiasis.
Signalments.

Answer 28

Less common in horses.
Males more affected as easier for mares to pass small calculi due to shorter, wider urethra.
Adults (mean age 10).
Bladder more commonly than kidneys more commonly than ureters more commonly than urethra.

Question 29

Urolithiasis - pathophysiology.

Answer 29

2 steps for formation:
- Nucleation of urine crystals.
– supersaturation of urine.
– prolonged urine retention.
– genetic variation in ion excretion rates.
- Crystal growth.
– once started to grow around a nidus, equine urine very alkaline, favouring crystallisation.

Question 30

Types of uroliths in horses.

Answer 30

All are calcium carbonate:
- type 1 = >90%, yellow, spiculated, easily fragment.
- type 2 = grey, smooth.

Question 31

Nephrolithiasis and ureterolithiasis.

Answer 31

Usually asymptomatic until bilateral obstructive disease leads to ARF / CRF.
When clinical signs are present, they are non-specific associated with uraemia rather than obstructive disease.
Most are in CRF by diagnosis so few amenable to tx.
Unilateral - nephrectomy.
?Lithotripsy.

Question 32

Cystic calculi.
Signs.
Diagnostics.
Treatment.

Answer 32

Signs: Dysuria.
- haematuria.
- stranguria.
- incontinence.
- especially at/after exercise.
Dx: Rectal, endoscopy, US (may empty the bladder).
Tx: Laparocystotomy.
- recovery as for colic surgery.
- low long term complications.
Perineal urethrotomy.
- small stones or need to break up.
- standing.
- but actually more complication.

Question 33

Urethral calculi…
Signalment.
Main cause.
Signs.
Risks.
Treatment.

Answer 33

Usually in males.
Usually small cystoliths that have passed into urethra.
Dysuria.
If blocked…
- colic.
- ARF (postrenal).
- risk rupture.
Repeated temporary blockage, CRF (postrenal).
Perineal urethrotomy.
Lowish recurrence rate.
Cannot acidify urine.
Avoid predisposing factors:
- no supplementary electrolytes.
- no alfalfa/lucerne.
- check for UTI.

Question 34

Pigmenturia.

Answer 34

Urine may contain oxidising agent that can cause it to turn red/brown after exposure to shavings/snow.
Blood, haemoglobin, myoglobin.
See red cells under microscope.
Dipstick can’t differentiate Hb and Mb, there’s a complex test but can tell from Hx/muscle enzymes.
Myoglobin:
- myopathy.
Haemoglobin:
- haemolysis.
Haematuria:
- throughout urination.
– haemorrhage from kidneys, ureters or bladder.
- beginning of urination.
– distal urethra.
- end of urination.
– proximal urethra.
–> rent.
—> haemospermia / haematuria.
—> endoscopy.
—> heal with time.
—» if > 1m / anaemia, temproary perineal urethrotomy.

Question 35

PU/PD.

Answer 35

> 100ml/kg/d.
50L water/day/500kg horse.
- renal failure.
- PPID.
- primary/psychogenic PD.
- (central/nephrogenic diabetes insipidus).
- (DM).
Look for RF - isosthenuria + azotaemia.
Older horses, investigate for PPID.
Lastly, water deprivation test.

Question 36

Neoplasia of the equine urinary tract.

Answer 36

Uncommon other than penile.
- Can have melanoma, sarcoid, papilloma.
- Usually SCC.
– usually older geldings.
– malodorous / swollen sheath.
– haematuria if distal urethra involved.
– early on, no signs.
– urinary tract obstruction uncommon unless tumours large.

Question 37

Urinary incontinence in horses.

Answer 37

Uncommon.
Signs exacerbated by coughing/exercise.
Similar signs to urolithiasis, which is more common so investigate for that.
Upper motor neuron (incl. EHV myeloencephalitis), lower motor neuron or myogenic disorders.
Sabulous urolithiasis (bladder full of sediment).