Disorders of Water Balance Polyuria-Polydipsia and Hypodipsia - PowerPoint Presentation

Disorders of Water BalancePolyuria-Polydipsiaand Hypodipsia Wendy Blount, DVM

PU-PD (PU=>PD & PD=>PU)Diabetes – secretion of a large amount of urine Insipid – tasteless Mellite – pharmaceutical containing honey Polydipsia = >100 ml/kg/day water intake for dogs >50 ml/kg/day water intake for cats Diabetes insipidus (DI) and primary polydipsia (PP) are particularly profound – often >200 ml/kg/day Normal urine production 1-2 ml/kg/hr – 12-45 ml/kg/day Polyuria = >50 ml/kg/day for dogs Urine SG for PU-PD pets Always <1.020, often < 1.012

PU-PD (PU=>PD & PD=>PU) Weight lbs Weight kg PU-PD K9 Water Intake Threshold2.41.24 ounces52.41 cup1151 pint1673 cups21101 quart32141½ quarts4219½ gallon63293 quarts84381 gallon127581½ gallons169772 gallons The average 5 kg cat should not drink more than 8-9 oz. per day

Causes of PU/PDPU => PD Renal Disease – fluid Loss Problem with ADH not produce (central DI) Kidneys don’t respond DrugsPD => PUPrimary PolydipsiaPsychogenic Polydipsia

Causes of PU => PDOsmotic diuresisDiabetes mellitus, Renal glycosuria Osmotic diuresis + medullary washout Chronic renal failure, Polyuric acute renal failure Post-obstructive diuresis, Diuretic therapy Lack of ADH production – central diabetes insipidusLack of response to ADHPrimary nephrogenic diabetes insipidusSecondary nephrogenic diabetes insipidusPyometra, septicemias, pyelonephritisHypercalcemia, liver failure, hyperadrenocorticismHyperaldosteronism, hypokalemia, hyperthyroidismHypoadrenocorticism, acromegaly, polycythemia

Causes of PU => PDDrug TherapyAnticonvulsants Glucocorticoids DOCP – deoxycorticosterone pivalate Diuretics Mannitol ThyroxineAmphotericin BLithiumMethoxyfluraneSodium bicarbonate*Sodium (treats)*Vitamin D toxicity

Causes of PD => PUPrimary PolydipsiaDefect in the thirst center Psychogenic Polydipsia Mental illness in people Learned behavior in response to environment in the dog Not reported in the cat

Confirming PU-PDHave owner collect urine samples2-3 different times in the day For 2-3 days – do not withhold water All <1.012 - confirms PU-PD All 1.012-1.020 - equivocal All >1.020 - PU-PD ruled out If PU-PD is not confirmed with USG despite it being the CC, consider alternative syndromesPollakuria, stranguria, periuriaUrinary incontinenceDehydration and appropriate increased thirst

Work-UpMost common causes of PU-PD in the dog (5) Kidneys disease (CRF, pyelonephritis) Diabetes mellitus Hyperadrenocorticism Liver failure Hypercalcemia Most common causes of PU-PD in the cat (3)Chronic renal failureDiabetes mellitusHyperthyroidism

Work-UpHints on the history & physical examIntact female + vulvar discharge rule out pyometra Lymphadenopathy rule out lymphoma (hypercalcemia)Anal sac massrule out apocrine gland carcinoma (hypercalcemia)Weight loss in the catrule out hyperthyroidism and diabetesEndocrine alopecia Hyperadrenocorticism (dog > cat)diabetes mellitus (both)

Work-UpHints in the urineAll USGs <1.005 Post-obstructive diuresis, aggressive IV fluids Primary polydipsia, central or nephrogenic DI hyperadrenocorticism All USGs 1.005 - 1.008 – many possibilities Liver failure, early CRF and all aboveUSGs 1.008 – 1.015 + proteinuriaRenal disease most likelyMake sure to get a urine cultureIf negative, do urine protein:creatinineUSGs 1.020’s with azotemiaHypoadrenocorticism and pyelonephritis most likelyAny USG >1.020 - diabetes insipidus is ruled out*USG ranges from <1.008 - >1.030**Psychogenic polydipsia most likely

Work-UpFirst Tier TestsCBC, panel, lytesHW Test for dogs, FeLV/FIV tests for cats urinalysis Urine culture (cystocentesis) TT4 for cats >5 years old. Second Tier Tests GlobalFAST orthoracic radiographsAbdominal US + radiographsBile acids (pre- and post-prandial)Cortisol:creatinine or ACTH stim (Low Dose Dex)Urine protein:creatinine

Work-UpThird Tier TestsVasopressin challenge Plasma osmolality with free choice water Modified water deprivation test NEVER DO A WATER DEPRIVATION TEST BEFORE RULING OUT ACQUIRED NDI, ESPECIALLY RENAL DISEASE Proceed with caution if * none* of the serial USG are <1.008Isosthenuria + PU-PD is most commonly caused by renal diseaseIsosthenuria + azotemia = renal disease with few exceptions (drugs)Pyelonephritis is one of the two most common causes of PU-PD + USG in the 1.020’s

Leah DrakeKirbyville TX

Work-UpMore pattern recognitionCentral DI or congenital Nephrogenic DI + Neurologic deficits Sodium high normal, as with all PU  PDUSG usually <1.008 if complete DIUSG can be 1.008-1.018 if partial CDIDehydration to 3-5% within a few hours of water deprivation**Psychogenic polydipsia behavioral issuesSodium low normal, as with all PD  PUFluctuating USG 1.005 – 1.030Prolonged time to dehydration with water deprivation**

Central Diabetes Insipidus (CDI)Deficiency of vasopressin from the hypothalamus Vasopressin = ADH = antidiuretic hormone = AVP = arginine vasopressin No ADH to allow kidneys to concentrate urine USG remains below 1.008 (often below 1.005) despite severe dehydration, if complete USG may increase to 1.008-1.015 if partialUSG >1.020 at any time rules it outUsually acquired rather than congenitalIdiopathic (most common)Head trauma or surgery (can be transient)Neoplasia/cystsLP inflammatory destructionParasite migration (*deworm*)

Primary Nephrogenic DI (NDI)Kidneys are unable to respond to ADH at birth Rare disorder in dogs Familial in the Husky Not reported in cats Apparent at 8-12 weeks of age Plasma ADH normal to increasedNo commercially available assay in the US

Primary Polydipsia (PP)Compulsive water consumption PP caused by a hypothalamic lesion to the thirst center has been reported in people, but not in dogs or cats Insufficient ADH secretion in response to hypertonicity has been reported in the dog (Hypodipsic Hypernatremia – HH) Because Psychogenic Polydipsia (PsP) is the only kind of PP reported in the dog, these terms are essentially interchangeable

Primary Polydipsia (PP)Psychogenic Polydipsia (PsP) is idiopathic PP Has not been reported in the cat Affected dogs are usually very active dogs who do not get enough activity attention seeking behavior Often there are changes in the environment at the time of onset Onset at any age, but usually puppy to young adultTemporary psychogenic polydipsia in puppies that seems to resolve at they mature is not uncommonUSG varies widely over time – 1.005 – 1.030ADH response to dehydration or hypertonic saline is appropriate (increased)

Secondary NDIkidneys lose ability to respond to ADH Secondary NDI = acquired NDI Plasma ADH normal to increased Pyometra and Sepsis - Bacterial endotoxins compete with ADH for aquaporin receptors on the renal tubulesHypercalcemiaDecreased response to ADH by the kidneysDecreased Na and Ca in medullary ISFLiver failure – not well understoodImpaired urea production resulting in medullary washoutVasoactive effects – increased renal blood flowHypokalemia, impaired cortisol clearance

Secondary NDIRenal Failure decreased number of nephrons > increased GFR per nephronincreased tubular flow rate > osmotic diuresisHyperadrenocorticism Glucocorticoids inhibit ADH release (temporary CDI)Increase osmotic thresholdDecreased renal response to ADH (temporary NDI)Rarely, physical disruption by macroadenoma (CDI)Hyperaldosteronism – poorly understoodMineralocorticoids reduce ADH releaseDecreased renal response to ADHPyelonephritis – see renal failure and sepsis

Secondary NDIHypokalemia - Decreased renal response to ADH Hyponatremia - Blunting of the medullary urea gradientHypoadrenocorticism - **ACTH Stim > LDD**Mineralocorticoid deficiency results in sodium wasting and medullary washoutSee hypercalcemia**Look at USG** to distinguish from renal failureHyperthyroidism – poorly understoodIncreased renal perfusion, medullary washoutThyrotoxicosis results in PsPConcurrent renal insufficiency in older cats

Secondary NDIAcromegaly Glucosuria renal insufficiency Polycythemia Hyperviscosity stimulates thirstVery Low Protein DietLack of BUN associated results in loss of renal medullary hypertonicity

DI and PsPHistory and physical examWeight loss is not uncommon Water intake often exceeds 200 ml/kg/day PU-PD often present for 1-6 months prior to seeking veterinary care BAR, not lethargic Unless CDI is secondary to large tumor Inappetance, stuporCerebral signs – pacing, disorientation, pacing, ataxia, seizures, head pressing, getting stuck in cornersHydration normal if water not restrictedNo vomiting, regurgitation, diarrhea, coughingUrinary incontinence not uncommon, especially when sleeping

DI and PsPDiagnosticsCBC – mild polycythemia not uncommon Owners often withhold water to some degree out of desperation Serum panel, electrolytes BUN may be low when free choice water BUN may be high if water withheld May have mildly low Na+ and K+ when free choice waterMay have high Na+ and K+ if water withheldUA – urine osmolality often < 300 mOsm/kgUSG for PP often varies from <1.008 to >1.030USG for CDI and NDI usually <1.008 and always <1.020USG for partial CDI can be 1.008-1.018, if water withheld

DI and PsPConfirm and differentiate CDI, NDI, PP Rule out acquired NDI - 2 tier work-up Tier 3: Response to DDAVPPlasma osmolality with free access to waterModified water deprivation testRule out acquired NDI prior to water deprivation!!Tier 1:CBC, panel, lytes, UA, urine culture and sensitivity (cystocentesis > mid-stream catheter), HW, FeLV/FIVTT4 on the cat > 5 yearsTier 2:Imaging (GlobalFAST or Thoracic rads + Abd US/rads)Urine protein:creatinine, cortisol:creatinine/ACTHstim, bile acidsConsider a trial of antibioticsPU-PD that responds to antibiotics is strong evidence for pyelonephritis, regardless of a negative urine cultureWater deprivation + renal disease = disaster

Plasma OsmolalityOften can distinguish PsP from DI Done with free access to water Normal dog – 280-300 pOsm Complete CDI – 285-340 pOsm - high normal to highNDI – 285-340 pOsm – high normal to highPartial CDI – 280-320 pOsm – normal to highPsP – 275-305 pOsm – low to normal

Response to DDAVPDDAVP = D-Desmopressin Acetate VasoPressin Tablets, injection, nasal drops used as eye drops Oral tablets or drops BID x 7 days (2x dose) Collect urine daily on days 5-7 and test USG Medullary washout will resolve in 1-3 days, allowing you to assess response at 5-7 days Increase in USG by 50% or more, especially >1.030, indicates response to DDAVPCDI – excellent and durable response to DDAVPAcquired NDI – temporary response to DDAVPPsP – mild response to DDAVPPrimary NDI – no or minimal response to DDAVP, unless exceedingly high doses are used

Modified Water Deprivation TestTo determine if endogenous ADH is released in response to dehydration And whether kidneys respond to the ADH Confirming DI and Differentiating CDI from NDI 3 Steps: Patient Preparation Phase I – water restriction until 3% weight lossNormal response is USG >1.030 in the dog and >1.035 in the catPartial & complete CDI, NDI – inadequate responsePhase II – continue only if inadequate urine concentration in Phase IAssess response to ADH *after* water deprivation

Modified Water Deprivation TestPatient Preparation – progressive water restriction to minimize interference of medullary washout Decrease water intake to 100 ml/kg/day prior to the start of the test Allow unrestricted water intake for 3 days, and measure Decrease water intake by 10% every 1-2 days until intake of 100 ml/kg/day is reached Divide daily water intake into 6-8 aliquots and give some during the night No food for 12 hours prior to starting the testAbort if :animal becomes aggressive for waterEvidence of hypertonic dehydrationChange in mentation or demeanor

Modified Water Deprivation TestPhase I - determines the effect of endogenous ADH on the kidneys Start at the beginning of the work day Observe and evaluate patient frequently End point is 3% weight loss or USG >1.030 or clinically dehydrated or ill Most with CDI or primary NDI will reach the endpoint in 3-10 hours Partial CDI and PP will take 10-24 hours to reach end pointNormal dogs will take 24 hours or more to reach the endpointLeaving a DI patient unattended for several hours can result in severe complications, including deathPhase I may require 24 hours or more

Modified Water Deprivation TestPhase I Time 0 Confirm neurologic status normal Make sure no access to food or water Empty the bladder by walking or catheterization for dogs and indwelling catheter for cats, and weigh Save sample for urine USG and ideally osmolalityTake blood for serum osmolality, BUN, ElectrolytesRepeat every 1-2 hoursEmpty the bladder by walking or catheterization for dogs and indwelling catheter for cats, and weighEvery hour – Weigh and assess for dehydration and change in mentationTake blood sample for BUN and sodium if dehydration, or periodically

Modified Water Deprivation TestPhase I Abort if BUN >30, hypernatremia, severe dehydration or changes in mentation If endpoint not reached in 10 hours Refer for 24 hour testing or repeat Phase I with water withheld after midnight the night before starting Urine concentration plateaus may be seenIndicates maximal renal response to water deprivationThree consecutive urine samples with the same osmolality (+ 5% USG or 30 mOsm/kg)USG is less reliable for detecting plateaus

Modified Water Deprivation TestPhase II - determines the effect of exogenous ADH on the kidneys in the face of dehydration Differentiates CDI from NDI Time 0 (= end point of Phase I) Empty bladder, keep urine for USG/osmolality, weigh Take blood for ADH if available BUN, electrolytes, serum osmolalityAdminister vasopressinaqueous vasopressin (Pitressin®) 0.2-0.4U/kg IM, maximum dose 5UDDAVP® injection 5 mcg SCEmpty bladder, keep urine and weighIf Pitressin® - at 30, 60 and 120 minutes post injectionIf DDAVP® – at 2 and 4 hours post injectionRun USG and ideally osmolality on urine

Modified Water Deprivation TestPhase II Weigh every hour and assess for dehydration and change in mentation Take blood sample for BUN, sodium, plasma osmolality if dehydration, and at end Offer small amounts of water (10-20 ml/kg) over the next 2 hours, to avoid water intoxication Then gradually return to free choice water over several hours Abort if BUN >30 mg/dl, hypernatremia, severe dehydration or changes in mentationLess likely to abort in Phase II than Phase I

Modified Water Deprivation TestInterpreting the Modified Water Deprivation Test Normal USG >1.030 for dogs and >1.035 for cats in Phase I Urine osmolality >1100 mcOsm in Phase I Complete CDI Urine osmolality will not exceed plasma osmolality (280-310 mOsm/kg) in Phase IUrine osmolality will increase in Phase II by 50-600%Hyperadrenocorticism, Partial CDI and some PPUrine osmolality increase above 300 mOsm/kg in Phase IFurther 10-50% increase in Phase II

Modified Water Deprivation TestInterpreting the Modified Water Deprivation Test Primary (congenital) and secondary (acquired) NDI Urine osmolality will not exceed plasma osmolality (280-310 mOsm/kg) in Phase I and Phase II Dogs with primary NDI are young and otherwise normal Dogs with secondary NDI usually have significant concurrent disease and should not have water deprivationPrimary PolydipsiaGiven enough time, USG will exceed 1.030 in Phase ICould take 24 hours or longerPhase II is rarely needed, but if carried out, will produce little change

Modified Water Deprivation TestPitfalls Easily differentiates complete CDI from primary NDI, but may not differentiate partial CDI from PP, Cushing’s Disease or many other causes of secondary NDI Confounding variables Chronic polyuria results in medullary washout, which in turn reduces maximal urine concentration Patient preparation is key!!Partial CDI patients can have an enhanced response to ADH early on due to up regulation of receptors – can take longer to reach end of phase I

Robert MeansMcKinney TX

Modified Water Deprivation TestThe Dehydrated Patient at Phase I Time 0 The most common cause of dehydration in the PU-PD patient is owner withholding water If no neurologic signs proceed with Phase I if BUN <30, sodium normal and USG <1.030 Proceed with Phase II if USG < 1.030If USG >1.030, DI and PsP have been ruled outDouble check for HAC and other causes of secondary NDIIf neurologic signsAbort the water deprivation testCareful fluid therapy – see next slideadjust patient preparation to prevent dehydration the next time around

Modified Water Deprivation TestTreating the Clinically Dehydrated Patient There are three forms of dehydration Isotonic – proportional loss of water and electrolytes GI loss a common example Sodium usually normal Clinical signs proportional to hypovolemiaHypotonic – loss of electrolytes > water lossHypoadrenocorticism an exampleSodium usually low, pre-renal azotemia commonClinical signs pronounced relative to hypovolemiaHypertonic - loss of free water > electrolytesWater deprivation + PU-PD an exampleOr heat strokeCell dehydration > plasma hypovolemiaSevere hypernatremia with hyposthenuriaWeight loss shows dehydration prior to symptoms

Modified Water Deprivation TestTreating the Clinically Dehydrated Patient Signs of hypertonic dehydration Neurologic signs – hypertonic brain cell shrivel Mild – irritability, weakness, ataxia Moderate – stupor Severe – coma and seizuresTreatment goal - Restore hydration slowly, with minimal brain cell damage & cerebral edema

Modified Water Deprivation TestTreating the Hypertonic Dehydrated Patient Correct dehydration with IV 0.9% NaCl + K + as needed ( potassium chart ) over 4-6 hoursSodium should decline no more than 1 mEq/L/hrIf neurologic signs worsen, slow rate and treat for cerebral edema with hypertonic saline or mannitol2. Once rehydrated, correct water deficit if still hypernatremic0.45% NaCl + 2.5% dextroseor half strength LRS + 2.5% dextrosecurrent Na+normal Na+ ()- 1x (0.6 x weight-kg)2oral route preferred, IV if PO not possibleReplace 50% in the first 24 hoursRemainder over the next 24-48 hoursIf hypernatremia persists after 12-24 hoursSwitch to 5% dextrose IV until sodium normalL =

Referral – MRI/CTConsider neoplasia in the older dog with CDIif client would consider radiation therapy T1-weighted images 80% diagnostic for CDI in people

Treatment of CDIDDAVP Intranasal drops 100 mcg/ml (2.5 ml & 5ml)$150-200 Transfer to a sterile eyedropper bottle 1 drop = 2-5 mcg DDAVP Start at 1-2 drops in either eye SID-TID, alternate eyes Increase up to 4 drops per eye PRN DDAVP 0.1mg and 0.2 mg tablets (more affordable)bioavailability 5-15% that of nasal drops0.025-0.05 mg PO BID for cats and dogs < 5 kg0.1 mg PO BID for dogs 5-20 kg0.2 mg PO BID for dogs > 20 kg0.3 mg PO BID for dogs >40 kgIncrease to TID & dose by 0.05 mg per week if not effectiveIf TID not effective, switch to eye dropsOnce symptoms are controlled, wean down to lowest effective dose

Treatment of CDIDDAVP injection 4 mcg/ml (2 ml)5-20x as potent as nasal drops in people Start at 0.2-0.25ml SC SID in dogs Start at 0.5-1 mcg/cat (0.1-0.25ml) SC SID Increase dose & frequency as needed to control symptomsHyponatremia a possible side effectOnset within 2 hrs, regardless of route of administrationDuration of action 6-18 hoursHigher doses prolong duration of actionExpense is often the limiting factorAdministration in the evening can allow the family to get proper sleep

Treatment of CDIOther oral treatments Thiazide diuretics - along with low sodium diet Chlorothiazide 20-40 mg/kg PO BID Hydrochlorothiazide 2.5-5 mg/kg PO BID dogs (1-2mg/kg cats)CDI and *NDI* – reduces urine output by 30-50% in peopleInhibits renal sodium resorption in Loop of Henle > contracts ECF > increases salt and water absorption in the proximal renal tubule > reduces osmotic diuresisOccasional hypokalemia can be a side effectCheck electrolyte panel every 3 monthsLow salt dietMay be helpful for CDI and NDI< 1g Na/Mcal - Hill’s H/DCommercial diets up to 4g/Mcal No salty treats!!!

Treatment of CDIOther oral treatments Chlorpropamide (oral hypoglycemic) Reduces urine output 30-70% in people with CDI Seems to be more effective for partial CDI in dogs and cats 10-40 mg/kg/dayHypoglycemia can be a side effect, managed by offering multiple small meals

Prognosis of CDIPrognosis is good if medication given dailyEye irritation is an infrequent side effect of eye drops Not uncommon for CDI to be part of a polyendocrine syndrome Look especially for hyperadrenocorticism if PU-PD recurs Progressive neurologic signs may indicate a macroadenoma that carries a grave prognosis without surgery or radiation therapy CDI persists even if tumor shrinkage is achieved, because PU-PD develops when 90% of magnocellular neurons are gone Chemo with BCNU can be tried, but has variable outcome

Prognosis of NDIExtremely high doses of injectable DDAVP (0.33 U/kg IM TID) can sometimes control primary NDIBut therapy is very, very expensive Thiazide diuretics are sometimes the only viable option for treatment Long term prognosis generally poor

Prognosis of Untreated DIDogs with CDI and NDI can do fine if they have unlimited access to water, and live in and environment where multiple urinations per hour are not a problem In most cases, untreated animals are outdoor animals Many discontinue treatment after a few months due to expense Some will administer medications periodically when needed, or only at night time. Lack of access to water of illness that causes adipsia or vomiting can be life threatening within hours – guarded prognosis Large water receptacles are neededMean survival about 2 years

Treatment of PsPWater RestrictionMeasure free choice water intake Gradually restrict water intake by 10% per week until 60-80 ml/kg/day is reached Divide into several aliquots and give the last at bedtime Rapid water restriction can result in anxiety and/or dehydration NaCl 1 g/30kg BID or NaHCO 3 0.6g/30kg PO BID x 3-5 days to help resolve medullary washout, if needed

Treatment of PsPBehavior ModificationDaily exercise Con-specific play, if the patient likes it Environmental enrichment with interactive toys Increased contact with people during the day The dog needs a job!!! Prognosis PsP – generally excellent, though relapse can occur

SIADHSyndrome of Inappropriate ADHSustained release of ADH Etiology Functional neoplasia – CNS or paraneoplastic Especially bronchogenic adenocarcinomas CNS disease - Head trauma, demyelinating disease, infection/inflammation Porphyria Endocrine disease – hypoadrenocorticism, pituitary dwarf, profound hypothyroidismPulmonary disease – acute respiratory failure, aspergillosis, pneumonia, tuberculosisDrugs

SIADHDrugs that cause SIADHACE inhibitors Chlorpropamide Cyclophosphamide, vincristine Omeprazole SSRIs Thiazides

SIADHClinical Presentation – water intoxicationHyponatremia <130 for 48 hours or longer Lethargy, weakness, muscle fasciculation anorexia, vomiting Obtundation, disorientation, seizures, coma (Na <120) Diagnosis Hyponatremia with plasma osmolality <275 pOsmInappropriately high urine osmolalityNormal renal and adrenal functionCorrection by water restrictionPlasma ADH normal to high (if available)

SIADHTreatment of the hypotonic dehydrated patient Increase sodium to 125 mEq/L IV 0.9% NaCl or hypertonic (3-5%) saline, start at 0.5-1 ml/lb/hr Increase Na + no more than 0.5-1.0 mEq/L per hourWhen sodium >125mEq/L, Further correction by water restrictionIdentify the daily water intake that maintains sodium at low end of normal rangeDivide into 6-8 aliquots per dayNever allow free access to waterCan’t go swimming or have access to ponds or swimming pools or rainDiscontinue any drugs that may be causing SIADHSome have tried tolvaptan 3 mg/kg PO BID (ADH receptor antagonist)

Hypodipsic HypernatremiaNeurologic disorder causing decreased thirst and diminished ADH release in response to hyperosmolalityHH = chronic hypernatremia & hyperosmolality due to decreased water intake Normal kidney function, but inappropriately dilute urine for the hypernatremia Most common in Miniature Schnauzers Causes in dogs:Neoplasiahydrocephalus and other degenerative CNS diseasescongenital hypothalamic dysplasiainflammatory CNS disease

Hypodipsic HypernatremiaTreatment:If possible, treat underlying disease Treat hypernatremia per previous instructions for hypertonic dehydration Increase water intake Add water/broth to food Offer flavored broths multiple times daily SC fluids at homeSome dogs do well only with increased water intake after correction of hypernatremia, and some are still hypernatremic with euvolemiaChlorpropamide (33 mg/kg/day) has been tried with inconsistent results

SummaryPowerPoint: .pptx 1 slide per page 6 slides per pageVet HandoutsIV K+ supplementation ChartDiagnostic Algorithm – PU-PDProtocol – Water Deprivation Test

SummaryClient Handout Diabetes Insipidus PU-PD Drug Handouts DesmopressinThiazide diureticsHidden SlidesChlorpropamide treatment for DIMRI/CT imaging for DI

Acknowledgements Nelson Richard. Canine & Feline Endocrinology, 4 th Edition. Ch 1 – Water Metabolism and Diabetes Insipidus.Brett Wasik DVM, DACVIM (Small Animal). Veterinary Information Network (VIN) – Feline Associate – Central Diabetes InsipidusLinda Shell DVM, DACVIM (Neurology). Veterinary Information Network (VIN) – Canine Associate – Central Diabetes Insipidus

Acknowledgements Kari Rothrock and Linda Shell DVM, DACVIM (Neurology). Veterinary Information Network (VIN) – Canine Associate – Nephrogenic Diabetes Insipidus, Polyuria/Polydipsia; Feline Associate – Polyuria/polydipsiaKari Rothrock DVM. Veterinary Information Network (VIN) – Feline Associate – Nephrogenic Diabetes Insipidus