Equine Urinary Tract Flashcards
How can you objectively assess if a horse has polydipsia? To answer this question you should find out what the normal water intake for a horse is and what qualifies as Polydipsia in a horse.
In more complex cases water deprivation tests can be performed to differentiate APP (apparent psycogenic polydipsia) from DI (diabetes insipidus)
Resting: 40-60ml/gjk/day – 20-30L for a 500kg horse
Polydipsia if water consumption >70-100ml/kg/day (35-50L/day for a 500kg horse)
Grazing horses get water from grass so water intake should be 10-15ml/kg/day (5-8L) but also may vary of grass quality etc.
Lactating mares have intakes of 80-90ml/kg/day (physiological PU/PD)
Values vary with hotter weather or exercise: water intake may increase, use your judgment and common sense.
In more complex cases water deprivation tests can be performed to differentiate APP (apparent psycogenic polydipsia) from DI (diabetes insipidus)
· What about polyuria ? How can you objectively assess volume of urine produced? How do you define polyuria?
What is normal urine production in the horse?
- Typically 15-30ml/kg/day
- Roughly 7.5 to 15L per day for a 500kg horse
- Faeces are major route of water loss in normal horses
- Environmental temperature and humidity influence also urine output
- Definition of Polyuria
- >50ml/kg/day (5%BWT)
- Difficult to quantify!
- 24h urine collection impractical
You hospitalise a horse to observe his water intake and urine production. After 24 hours you notice that he has drunk some 45L of water. The bedding is also very wet as the owner had described and the horse has been seen urinating frequently large amounts of clear urine.
Does this horse have PUPD?
If you decide to run haematology/biochemistry/urinalysis, what abnormalities would you expect with PUPD?
• Blood tests
– Anaemia
• Often present in CRF (uraemic effects/decreased erythropoietin synthesis)
– Polycythaemia
• Dehydration suggesting PU is the primary problem rather than PD eg. DI
– Neutrophilia
• Glucocorticoid response or inflammatory disease
– CRF
• Severe increase of urea (>15mmol/L) and creatinine (>300mmol/L)
– Dehydration (vs early CRF)
• Moderate increases Urea (8-12mmol/L) and creatinine (180-250mmol/L)
– Hepatic insuficiency or Psychogenic PD+medullary wash-out
- Decreased urea (<4 mmol/L) and creatinine (<75 mmol/L)
- GGT, GLDH and bile acids to rule out liver disease
– PPID
• Persistent hyperglycaemia
– Hypercalcaemia à CRF or paraneoplastic
- total Ca2+ >3.5mmol/L, ionised Ca2+ >1.7mmol/L
- Urinalysis
– Hypothosthenuria
– USG <1.008 - kidney actively excreting water à DI and APP
– Isosthenuria
– USG 1.008-1.014 - kidney neither concentrating or diluting à CRF
– Hypersthenuria
– USG >1.1014 – kidney able to concente à Normal
– Glucosuria
– DM (PPID, primary DM rare, acute stress, α2-agonists)
– Urine creatinine:serum creatinine ratio
– Dehydration shows increased urine and serum creatinine concentrations
– CRF = lower urine creatinine
· PPID is a likely cause in this case because of the previous history of laminitis and the horse’s age. What proportion of horses with PPID present PUPD? How does that compare to other species? How could PPID lead to PUPD?
· What other sings might a horse with PPID present with?
– [MD1]In a review of 17 horses with PPID, PU/PD was found in 13 (76%)
– In other reviews no association was found.
– Osmotic diuresis = when plasma glucose >renal threshold = glucosuria
– Antagonism of ADH action on collecting ducts by cortisol = evidence lacking
– Adenoma growth may impinge on posterior pituitary and hypothalamus = sites of ADH storage and production, Decreased ADH = central DI
Combined mechanisms lead to PU/PD
It is the middle of February in the midlands. An owner calls you to evaluate a week old WB colt, which has been absolutely normal for the first week but appears dull this morning and stands only when assisted. The owners noticed that the foal has produced faeces overnight but has not seen the foal urinating for the past 1-2 days though he seemed to try once standing up. On physical examination the foal appears dull, but responsive, and stands on his own once stimulated appropriately but appears weak and trembling. HR 90bpm, RR 24brpm, RT 38.5°C, MM: pink, slightly moist, CRT:2 sec. GI borgorygmi quiet. Examination of the umbilical stump is within normal limits for a foal of this age. The abdomen appears slightly distended. You suspect this colt has uroperitoneum, why?
– BLADDER RUPTURE
– More common in colts
– Tears usually dorsal bladder
– Urachus
– Clinical signs
– Foal appears normal at birth
– First 24-36h à Stranguria/pollakiuria
– Day 2-4 à Dull demenour + Abdominal distension
– Often can void very small amounts of urine
– Cardiac arrythmias –bradycardia (hyperkaliemia!!!)
– Muscle fasciculations
– Colic
– Sepsis- fever, injected mm, D+, other body system disease
– Can be challenging to establish diagnosis until signs are obvious and foal is sick
You perform haematology and biochemistry as you suspect the foal might have uroperitoneum. What are the findings that would support this diagnosis?
How will you definitely confirm this diagnosis?
– History (=neonate) and clinical signs
– Blood biochemistry
• INCREASED K+,Creatinine & DECREASED Na+, Cl-
– Hyperkalaemiaà bradycardia / cardiac arrest
– Blood gas
• Metabolic acidosis
– Abdominal ultrasound
• Large amounts free fluid in abdomen, collapsed bladder
– Abdominocentesis
• Peritoneal:Serum creatinine >2:1 is diagnostic
– ECG
- Hyperkalaemia = bradycardia
- Increased duration of QRS complex
- Shortened Q-T interval
- Increased P wave duration
- Prolonged P-R interval
- AV conduction disturbances
What is the treatment[MD1] for ruptured bladder in foals?
– [MD1]Ultimately surgical repair of bladder and removal of internal umbilical remnant
– FIRST Stabilise the patient
- IV NaCl 0.45-0.9%±5% glucose solution 1-3 L
- Hyperkalaemia (serum concentration >5.5mEq/L life threatening)
– IV Ca2+ gluconate 1ml/kg over 10 mins
– IV NaHCO3: 1-2mmol/Kg over 15 mins
– 50% dextrose IV 2ml/kg over 5 mins
– Insulin if significant ECG abnormalities or if poor response to initial FT
• Drainage of urine from the abdomen before GA.
– Broad spectrum antibiotic cover
– Consider gastric ulcer prophylaxis
– Care with NSAID use as anti-inflammatory
– ±FPT = plasma
What is the prognosis of a foal ruptured bladder/
– in non-septic foals GOOD
– in those which have concurrent infection or other GI issues 50%
Repeat ruptures can occur
What are the haematological and biochemical parameters in a foal that might be affected by placental disease?
[MD1]Serum creatinine concentration in the newborn foal
– 30-40% higher during day 1-3
Creatinine equilibrates slowly
across the placental membrane
– Do not panic in an otherwise healthy
foal that is urinating normally
– If serum creatinine concentration does
not fall after 3 days investigate
renal causes.
– Premature foals will have higher creatinine
– Could result from placental disease
– Serial measurements useful
