Equine Urinary Medicine Flashcards
Define…
1. Pigmenturia.
2. Polydipsia.
3. Polyuria.
4. Pollakuria.
- Coloured urine.
- Excessive volume of drinking.
- Excessive volume of urination.
- Excessive frequency of urination.
Define…
1. Dysuria.
2. Stranguria.
3. Oliguria.
4. Anuria.
- Abnormal urination.
- Straining to urinate.
- Decreased production of urine.
- Stop urinating.
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Define…
1. Pigmenturia.
2. Polyuria.
3. Polydipsia.
4. Pollakuria.
- Coloured urine.
- Excessive volume of urination.
- Excessive volume of drinking.
- Excessive frequency of urination.
Define…
1. Dysuria.
2. Stranguria.
3. Oliguria.
4. Anuria.
- Abnormal urination.
- Straining to urinate.
- Decreased production of urine.
- Stop urinating.
Renal physiology in equine.
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.
Exam of the urinary system - Hx.
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.
Exam of the urinary system - CE.
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.
Exam of the urinary system - blood tests.
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.
Exam of the urinary system - urinalysis.
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).
Urinalysis - USG.
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.
Exam of the urinary system - ultrasonography.
Transrectally/transabdominally.
- uroliths in kidneys and sometimes bladder.
- size and architecture of kidneys.
Exam of urinary system - cystoscopy.
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.
Exam of urinary system - other tests.
Water deprivation and anti-diuretic hormone (ADH) challenge test.
- hyposthenuric polyuria.
- primary (psychogenic) polydipsia vs central or nephrogenic diabetes insipidus).
Renal biopsy.
Developmental malformations.
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.
Acute renal injury (ARI).
- what is it and what causes it?
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).
ARI - clinical signs.
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.
- Diagnosing ARI in horses.
- Treating ARI in horses.
- Azotaemia.
USG.
Casts - show damage.
Rule in/out prerenal and postrenal causes, if not is intrarenal.
If intrarenal, US, ?biopsy. - 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.
Prognosis of ARI.
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.
Chronic renal disease.
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.
CRD causes.
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.
CRD clinical signs.
Present late in disease course.
Uraemic syndrome signs vary and can include:
- lethargy (anaemia).
- anorexia.
- weight loss.
- PUPD.
- dental tartar.
Diagnosing CRD.
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.
Treating CRD.
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.
