Investigating PUPD Flashcards
What is normal water intake for a horse?
- Resting: 40-60 ml/kg/day
- Roughly 20-30L/day for a 500kg horse
- In grazing horses 10-15ml/kg/day (5-8L/day)
- Affected by environmental temperature and humidity
- Lactating mares, horses working hard, hot environmental conditions 80-90ml/kg/day - physiological PU/PD
- Smaller breeds drink more than larger breeds
How would you define polydipsia in horses?
H20 consumption > 70-100ml/kg/day (>7-10% BWT)
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
How would you define polyuria in the horse?
- > 50ml/kg/day (5%BWT)
- Difficult to quantify!
- 24h urine collection impractical
What are the physiological causes of PUPD?
- Excessive dietary protein
- Excessive salt consumption
- Drug administration
- Glucocorticoids
- Diuretics eg. Furosemide
- α-2 agonists
- High environmental temperature
What are pathological causes of PUPD?
- Apparent Psychogenic polydipsia (APP)
- PPID (Equine Cushings’ disease)
- Chronic renal failure (CRF)
- Hepatic insufficiency
- Sepsis/endotoxaemia
- Renal medullary solute washout
- Any cause of chronic diuresis
- Inappropriate renal tubular Na+ handling
- Diabetes Mellitus (DM)
- Diabetes Insipidus (DI)
- Nephrogenic
- Neurogenic (Central)
What is apparent psychogenic polydipsia? How is it diagnosed? How is it managed?
- Rare, but probably most common cause of PU/PD in adult horses where O has noticed excessive urination
- Good BCS/not azotaemic
- Results in significant PU - often “flooded” stables
- PD Stable vice boredom
- Reflection of change diet, stabling, management, environment, meds
- Excessive salt consumption FENa, salt intake >5-10% DMI before see signs PU/PD
- Diagnosis of exclusion
-
Management
- Restrict salt intake
- Restrict water intake
- Maintenance +work + environmental requirements
- Alleviate boredom – turnout, increase exercise, companion, stall toys etc
- Increase feeding frequency of roughage - more time eating/less drinking
What mechanisms of PPID lead to PUPD?
- 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
What clinical signs are associated with PPID? How is it diagnosed? How is it treated?
Clinical Signs
* PU/PD (76%)
* Long, curly haircoat (55-80%)
* Weight loss/Muscle wastage (88%)
* Quieter demeanour/lethargy/poor performance
* Regional adiposity (supraorbital)
* Potbellied appearance
* Laminitis
* Recurring infections
* Hyperglycaemia
* Hyperhidrosis/anhidrosis
* Neurologic deficits/blindness
* Narcolepsy
* Absent reproductive cycle/infertility
Diagnosis
* Resting ACTH
* TRH stimulation
* Dex Supression Test
* Combined DST-TRH test
* Assess insulin status
* POMC
Treatment
* Pergolide
* Bromocriptine
* Cyproheptadine
* Dietary management
* Management of clinical signs
* Farriery
* Antimicrobials with infections
* Vitex agnus castus - ineffective!
How does diabetes insipidus cause PUPD?
Neurogenic (central)
* Inadequate secretion of ADH
* Hereditary and acquired forms reported
* Fail to concentrate urine in face of water deprivation test
Nephrogenic
* Decreased sensitivity of epithelial cells on collecting ducts to circulating ADH
* Hereditary and acquired forms reported
* Infectious/mechanical/neoplasia/drugs
* Fail to concentrate urine in face of water deprivation test
How does diabetes mellitus cause PUPD?
- State of chronic hyperglycaemia + glucosuria
- Osmotic diuresis
- Type 1: insulin dependant - lack of insulin production
- Type 2: insulin independent - high insulin present but tissues are insensitive to it
- PPID, EMS: increased plasma cortisol antagonises the effects of insulin
How does sepsis/endotaxaemia cause PUPD?
- PU/PD described BUT other signs predominate
- Mechanism unclear ? Endotoxin prostaglandin (PGE2) production
- PGE2 effect
- Potent renal vasodilator - antagonises ADH effects on the collecting ducts
What are iatrogenic causes of PUPD?
- IV fluid therapy
- Diuretics
- Corticosteroid administration
- mechanism not known
- Sedation with α2-agonists
- Xylazine and detomidine -> transient hyperglycaemia + glucosuria, direct effect on collecting duct epithelial cells -> antagonise ADH
- Excess dietary salt
What are the steps to investigating PUPD?
**History **
* Recent disease
* Drug administration
* Fluid therapy
* Change in diet
* Change in water quality/availability
* ?presence of renal disease
Hx helps rule out iatrogenic causes
**Confirm presence of PU/PD **
* Verification and quantification of water intake
* Over 24h period, horse must be stabled
* Might repeat over few days??
* Evaluation of urine out put - impractical
* If water intake >100ml/kg/day PD is confirmed, PU is inevitable
* If water intake <70ml/kg/day PD is not confirmed
* If water intake 70-100ml/kg/day PD is suspected in absence of physiological causes
Blood tests - check for disease
* 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 -> CRF or paraneoplastic - total Ca2+ >3.5mmol/L, ionised Ca2+ >1.7mmol/L
Urinalysis
* Hypothosthenuria
* USG <1.008 - kidney actively excreting water - DI and APP
* Isosthenuria
* USG 1.008-1.014 - kidney neither concentrating or diluting - CRF
* Hypersthenuria
* USG >1.1014 – kidney able to concente - 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
What is the water deprivation test? How is it undertaken?
- Differentiates APP from DI
- DO NOT perform on azotaemic horses with renal compromise
- Purpose of test can horse concentrate urine??
- APP cases can concentrate the urine
- DI cases cannot concentrate the urine
Process
* Weigh horse
* Check serum urea and creatinine are normal (if not DO NOT proceed)
* Take baseline urine sample and measure SG (if >1.008, DO NOT proceed)
* Keep horse stabled and remove water
* Check serum urea and creatinine and USG q 6h and re-weigh
When would you stop a water deprivation test? What results do you expect?
STOP the test if:
* 24h of water deprivation
* 5% reduction in body weight
* Clinical signs of dehydration
* Azotaemia develops
* USG >1.020
Results
* If USG > 1.020 – Normal: can concentrate urine!!
* rule out DI, rules in APP
* If USG <1.020 & horse becomes dehydrated
* DI or medullary washout - perform a modified water deprivation test
* If USG still low after 24h, but horse does not show marked dehydration
* APP + medullary washout or DI
* Perform a modified water deprivation test.
What is the modified water deprivation test? How do you interpret the results? When is it chosen?
- Allow water consumption 40ml/kg/day - offer in several amounts throughout day
- Measure serum urea and creatinine, USG q 6h
- Continue for 2-3 days or until 1 criteria is reached
- USG >1.020
- Confirms APP
- Progressive dehydration
- Inability to concentrate urine (DI)
- USG >1.020
MWDT can be performed instead of standard WDT or started after standard WDT if:
* USG <1.020 after 24h water deprivation
* <5% reduction in body weight
* No azotaemia
* No clinical signs of dehydration
What is the ADH response test?
ADH (vasopressin) response test
* DI and to differentiate central and nephrogenic forms
* Central DI cases -> concentrate urine after exogenous administration of ADH
* Nephrogenic DI -> little or no response
Serum ADH (vasopressin) concentrations
* Normal hydrated horses ADH = 1-2 pg/ml
* In response to 24h WDT increase to 4-8 pg/ml
* Low resting or failure of increase during WDT -> central DI
* APP and nephrogenic DI have normal ADH concentration and response
