PUPD Paper

A dalmatian puppy, weighing7 kg, with severe polydipsia andpolyuria. This dog drank up to3.5 litres of water (500 ml/kg)per day in response to itsprimary nephrogenic diabetesinsipidus. The dog is picturedsurrounded by the equivalentof its daily water consumption

Investigation of polyuria andpolydipsia in the dog

Ian Ramseygraduated fromLiverpool Universityin 1990. He iscurrently theWaltham Lecturerin Small AnimalMedicine and ClinicalNutrition at GlasgowUniversity. He holdsa PhD and the RCVSdiploma in smallanimal medicine, andis a diplomate of theEuropean College ofVeterinary InternalMedicine. He is anRCVS Specialist inInternal Medicine.

Yvonne McGrottygraduated fromGlasgow in 1997 andspent two years insmall animal practicein Glasgow. Shereturned to theveterinary school in1999 as a resident insmall animal medicineand was awarded thecertificate in smallanimal medicine in2000. She is currentlyworking as a residentin emergencymedicine and criticalcare at the RoyalVeterinary College.

IAN RAMSEY AND YVONNE McGROTTY

POLYURIA and polydipsia are two common presenting signs in dogs seen in practice. There are a numberof causes and these can be divided into two groups: primary polyuria/secondary polydipsia and primarypolydipsia/secondary polyuria. Some causes may produce clinical signs by more than one mechanism.Compensatory mechanisms that regulate water homeostasis mean that polyuria and polydipsia alwaysoccur together. Careful history taking and hospital monitoring are required to demonstrate polyuria orpolydipsia. This article describes the approach to the investigation of canine polyuria and polydipsia,and discusses some of the procedures which may aid diagnosis.

THE IMPORTANCE OF ALOGICAL APPROACH

As polyuria and polydipsia are such common presentingsigns, it is often tempting to 'spot diagnose' the cause orto treat the signs non-specifically or on a trial basis as ameans of diagnosis. While these approaches may beacceptable for some presenting signs, they are rarelyjustifilble on medical or economic grounds in cases ofpolyuria/polydipsia because:* Some causes of polyurial/polydipsia (eg, hypercalcaemiaand hyperglycaemia) require prompt or even emergencymanagement. It is essential to exclude these causes early inthe investigation of any case of polyuria/polydipsia;* Some causes of polyuria/polydipsia (eg, liver andrenal failure) carry a guarded to poor prognosis. It is

Approach to the investigationof polyuria and polydipsia

* History* Physical examination* Measurement of water consumption* Urinalysis* Biochemistry* Haematology* Adrenocorticotropic hormone (ACTH)stimulation test* Radiography* Ultrasonography* Water deprivation test

Definitions

* POLYDIPSIA is defined as water consumption thatexceeds 100 ml/kg/day. This figure includes waterconsumed with food (typically, a 400 g tin ofcommercial dog food contains 300 ml of water).Some dogs with polydipsia may drink in excess of300 ml/kg/day* POLYURIA is defined as urine production thatexceeds 50 ml/kg/day. The difference betweenwater intake and urine production is due to lossesfrom the respiratory tract and in faeces

NB Abnormally increased thirst and urine produc-tion may occur below the levels indicated above;these should therefore be regarded as guidelinesrather than strict limits

important to exclude these causes early in the investiga-tion to av~oid further (expensive) therapies or tests:

* There are relatively fetv cases of polyuria/polydipsiathat will respond to empirical therapy with antibacterialagents or glucocorticoids. The non-specific use of thesedrugs, while only occasionally contraindicated, oftendelays diagnosis and specific therapy. The cost of theempirical therapy would be better used to identify theuntreatable causes and those that require immediateintervention as outlined above;* Some drugs (eg. mitotane) that ar-e used in the man-

actemnenlt of some causes of polyuria/polydipsia haave a

lowt mar-gin of safety.

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Causes of polyuria and polydipsia

A Griffon Bruxellois which was presented with severepolyuria and polydipsia. The dermatological changes seenare suggestive of hyperadrenocorticism. Although it istempting to proceed directly to a confirmatory test, such asthe ACTH stimulation test, it is important that preliminaryinvestigations are performed first (eg, measurement ofblood glucose) as the results of these may alter thetherapeutic approach and prognosis that is offered

HISTORY

Polyuria/polydipsia is rarely observed in a consultationand identification of this problem requires owner obser-vation. The accuracy of owners' assessments of waterintake and urine output will inevitably vary. In some

Primary polyuria/secondarypolydipsia* Diabetes mellitus* Chronic renal failure* Liver disease* Hyperadrenocorticism* Endotoxaemia (especially pyometra,pyelonephritis and septicaemia)* Neoplasia* Hypercalcaemia* Hypokalaemia* Primary central and nephrogenicdiabetes insipidus* Hypoadrenocorticism

* Hyperthyroidism* Fanconi's syndrome* Polyuric phase of acute renal failure* Post-urethral obstruction diuresis* Primary renal glucosuria* Phaeochromocytoma* Drugs (eg, steroids, diuretics,levothyroxi ne)

Primary polydipsia/secondarypolyuria* Pain, stress, heat, exercise* Hyperthermia* Psychogenic polydipsia

cases, it is useful to hospitalise dogs to accurately mea-sure their water intake. However, it is important not todismiss an owner's report of polyuria/polydipsia whenthe quantities of water being consumed or urine beingproduced seem normal. Changes in thirst are as impor-tant an indicator of disease as an increase above aspecific limit. Although a full history should always beobtained, the following points are particularly important:* Extent of the polyuria/polydipsia;* Time of onset;

Regulation of water balance

Water balance is one of the most fundamental process-es to life. No other substance within the body is moretightly regulated. As little as 15 per cent deficit or sur-plus of total body water is fatal. The organ that is main-ly responsible for water balance is the kidney. However,renal water resorption is regulated by the productionof antidiuretic hormone (ADH) by the hypothalamic-pituitary axis and, in the longer term, by aldosteronefrom the adrenal cortex. ADH acts on the collectingducts of the kidney to increase water uptake, therebyconcentrating the urine. The urine produced may beclassified as follows:* HYPOSTHENURIC (more dilute than plasma), if ADH isabsent;* ISOSTHENURIC (same concentration as plasma), if insuf-ficient renal tubules are functional or the dog has aprimary polydipsia;* HYPERSTHENURIC (more concentrated than plasma), ifADH is present and the renal tubules are functional.

Aldosterone promotes the resorption of sodium inthe distal convoluted tubule and thereby conservesthe osmotic potential of the extracellular fluid. Loss ofbody sodium due to aldosterone deficiency or antago-nism leads to a failure of the concentration gradientwithin the renal medulla. Atrial natriuretic factor(ANF) may influence sodium balance in the short term.It is released by the myocardium in response to volumeoverload and acts to increase sodium excretion, bothby its direct effect on the nephron and by inhibitingthe renin-angiotensin-aldosterone system.

The concentration of urine is most accuratelydefined in terms of its osmolality. Osmolality is a mea-

sure of the number of particles in solution, as opposedto specific gravity which is influenced by both thenumber and size of particles in solution. Osmolalitytherefore provides a better measure of the amountof water in both urine and serum, allowing the twoto be directly compared. Unfortunately, facilities formeasuring osmolality are uncommon in the UK, exceptin human hospitals, and such measurements tend to bequite expensive.

Changes in urineosmolality in variousparts of the nephron.Adapted from Cannon(1977)

H20

H20I

m

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* Rate of progression;* Frequency of urination;* Any loss of toilet training;* Changes in urination habits;* Changes in urine colour or odour;* Signs of other diseases (eg, changes inor skin condition; ocular, vulval or preputialdiarrhoea, vomiting or changes in appetite);* Recent drug administration.

Many dogs that present with polyuria/polalso have nocturia (a voluntary desire to urinmThis must be distinguished from incontinenccof soiled bedding and/or hair coat. Howeveimals with severe polyuria/polydipsia may durinary incontinence. Polyuria/polydipsia sifore be properly excluded before investigatincases that present with urinary incontinence.

CLINICAL EXAMINATION

All dogs that are presented with polyurishould be examined thoroughly, with particufocused on:

* The peripheral lymph nodes;* Dermatological chanLes;* Vulval discharges;* The abdomen;* The rectum.

PERIPHERAL LYMPH NODESCareful palpation of the peripheral lymph noed to identity any changes in texture or sizenodes that are normally palpable in the(submandibular, prescapular and popliteal)checked first. Neoplastic infiltration of lymoften sariable and so it is important that alare examined. The retropharyngeal, inguinallymph nodes are less frequently enlargedpalpable in the normal animal. Any enlargerprompt further investigation. In particular, aaspirate should be performed (see Dunn I

1 998a,b for further details).

DERMATOLOGICAL EXAMINATIONHyperadrenocorticism often produces derchanges. These may range from mild selsevere alopecia. Other changes that may be r

condition include skin thinning, comedo fornwound healing, hirsutism and changes in

pH Protein Blood Ketones

6 5 + ...

Urinalysis should be performed immediately on all dogs that are presented withof polyuria and polydipsia. In this case, the finding of glucosuria and ketonuria 5

the diagnosis of diabetic ketoacidosis (which requires prompt therapy to prevenprogression to a life-threatening condition). Furthermore, the presence of proteihaemoglobinuria suggests a urinary tract infection and this may be an underlyinin the development of the ketotic state. Although further diagnostic tests such a

biochemistry are advisable, the findings of the urinalysis are more useful and inThe pH is normal (ie, acidic) in this case which is atypical of urinary tract infectioconsistent with diabetic ketoacidosis

Changes are more obvious on the ventrum in many casesof hyperadrenocorticism; it is therefore worthwhile turn-ing dogs over or lifting them by their forelimbs to ensureadequate examination of the ventral area.

VULVAL DISCHARGESEntire female dogs that are presented with a historyof polyuria/polydipsia should be carefully checkedfor pyometra. While other pyogenic foci can producepolyuria/polydipsia, pyometra is the most common.

ABDOMINAL PALPATIONNeoplasia in any organ can lead to polyuria/polydipsiaand careful palpation of the liver, intestines, bladder, kid-neys and sublumbar area is essential. Pyometra can oftenbe identified by palpation but cannot be excluded by thistechnique. Other non-neoplastic conditions may producehepatomegaly or renomegaly. Mesenteric lymphadeno-pathy may also be present and must be distinguishedfrom faecal material in the colon by its shape and lack ofcompressibility.

RECTAL EXAMINATIONFemale dogs that are presented with a history ofpolyuria/polydipsia should be carefully examined foranal gland masses. Adenocarcinomas of these glands areassociated with a very high incidence of paraneoplastichypercalcaemia. The tumours may be very small and notvisible on external examination of the anus.

Prostatic abscessation is a potential cause of polyuria/polydipsia in the entire male dog but other signs usuallypredominate.

LABORATORY TESTS

URINALYSISUrinalysis is the quickest and most economical means oflaboratory investigation of a case of polyuria/polydipsia.It should be performed on the first occasion that anydog is presented with a history that is suggestive ofpolyuria/polydipsia.

Dipstick analysisDipsticks are cheap and reliable for the assessment

rmatological of urinary glucose, ketones, pH, protein, bilirubin andborrhoea to haemoglobin. The presence of small amounts of bili-noted in this rubin (+) may be normal in the dog. The dipstick testsnation, poor for urobilinogen, nitrates, leucocytes and specific gravitycoat colour. are best ignored. Dipsticks deteriorate with prolonged

storage and out-of-date stock should be discarded. The

Glucose test is best performed on freshly obtained urine as stor-age influences the results. Care should be taken to readthe individual tests at the appropriate times.

The presence of glucose in the urine is not diagnosticof diabetes mellitus but should prompt further investiga-tion of this condition. Primary renal glucosuria and othertubular defects (such as Fanconi's syndrome) will also

+++ produce severe glucosuria, which must be distinguishedfrom diabetes mellitus. Ketonuria is invariably associat-

suggests ed with glucosuria in the dog and is a reliable indicatorit of ketosis. Ketosis causes polyuria due to an osmoticinuria and

effect. In the vast majority of cases, ketonuria is associ-ig factoras routine ated with diabetic ketosis. Ketonuria and glucosuria mayiportant.

occur in the absence of hyperglycaemia (for example,ins butin Fanconi's syndrome), but this is rare. Proteinuria,

In Practice 0 SEPTEMBER 2002436




haematuria and haemoglobinuria do not cause polyuriabut some conditions that cause these changes may leadto polyuria by other mechanisms.

Specific gravity by refractometerThe specific gravity of a canine urine sample should notbe assessed using human dipsticks, as these are unreliablefor this purpose. A refractometer should be used and itscalibration should be checked regularly using distilledwater. The ranges of urine specific gravity shown in thetable on the right are used to define urine concentration.

The specific gravity of dogs with polyurialpolydipsiawill be below 1 035 except in a very few cases of diabetesmellitus. All causes of polyuria/polydipsia that result inADH resistance can lower the urine specific gravity tohyposthenuric values. Therefore, a urine specific gravityof less than 1 008 is not necessarily indicative of primarydiabetes insipidus. In particular, a significant proportionof dogs with hyperadrenocorticism have hyposthenuricurine. As hyperadrenocorticism is far more common thanprimary diabetes insipidus, a dog with hyposthenuricurine is more likely to have hyperadrenocorticism thanprimary diabetes insipidus.

Sediment examinationSediment examination is of less benefit than specificgravity in the investigation of polyuria/polydipsia butshould still be performed to identify any renal casts asso-ciated with pyelonephritis. Urinary crystals, bacteria andinflammatory cells may be seen and the technique is use-ful for distinguishing haemoglobinuria from haematuria.

SERUM BIOCHEMISTRYSerum biochemistry (including electrolytes) is invalu-able in identifying or excluding causes of polyuria. Likeurinalysis, it should be performed as soon as possible onall cases that are presented with a history that is sugges-tive of polyuria/polydipsia. In particular, hypercalcaemiaand hyperglycaemia need to be identified at an earlystage to prevent patient deterioration.

Hypercalcaemia is seen in a number of neoplasticconditions (particularly lymphoma), hypoadrenocorti-cism, hyperparathyroidism and some forms of chronicrenal failure (especially those associated with juvenilenephropathies).

Severe hyperglycaemia (more than 12 mmol/litre) isseen in diabetes mellitus. The measurement of fructos-amine in the dog is not required to confirm the diagnosis.Mild hyperglycaemia may be seen in a number of dis-eases associated with metabolic stress, the most commonof which is hyperadrenocorticism.

Other useful changes include:* Increases in urea, creatinine and phosphate with nor-mal electrolytes. These are suggestive of renal azotaemiain a dog with a history of polyuria/polydipsia and a urinespecific gravity of less than 1025. Some of these casesmay be mildly hypokalaemic;* Increases in urea, creatinine and phosphate with highpotassium and/or low sodium. These are suggestive ofhypoadrenocorticism. Urine specific gravity may be aslow as 1-008 due to the sodium wasting caused bythe lack of mineralocorticoids. Such cases may alsobe mildly hypercalcaemic, hypoglycaemic and hypo-albuminaemic;M Increases in liver enzymes (particularly alkalinephosphatase) and cholesterol. These are suggestive of

Specific gravity Notes

Reference range 1 015-1 045 Possible range: 1.001-1 065+

Hyposthenuria 1.001-1 007 Reasons for low urine specific gravity include:- Loss of concentration gradient (diuresis, hypoadrenocorticism)- Loss of ADH or its receptors (primary diabetes insipidus)- Antagonism of ADH (hyperadrenocorticism)- Excessive water consumption

Isosthenuria 1 008-1-012 Specific gravity of glomerular filtrate. Indicates that the kidneyshave not concentrated the urine - this may be due to a loss ofnephrons (renal failure) but can be normal

Minimallyconcentratedurine

1 013-1 030 Most normal dogs have a urine specific gravity in this range butso do many dogs with polyuria/polydipsia

Hypersthenuria 1031-1 065+ High urine specific gravity is produced by decreased renalperfusion

hyperadrenocorticism in dogs with polyuria/polydipsia.Hyperphosphataemia, mild hyperglycaemia and slightlyincreased or decreased urea may also be seen in suchcases;* Increases in serum glucose above the renal threshold(10 mmol/litre). These are seen in diabetes mellitus.Such dogs usually have increased liver enzymes and cho-lesterol as well. Diabetic ketoacidosis is very often asso-ciated with an azotaemia. It may also cause decreasedconcentrations of phosphate and potassium but moreoften these are normal at first presentation. Mild hyper-kalaemia can occasionally be seen in these cases;* Decreased urea and albumin and increased liverenzymes. This may be seen in dogs with liver disease.Measurement of serum bile acids does not need to beperformed routinely in animals with polyuria/polydipsiabut should be performed in cases with polyuria/polydip-sia together with signs suggestive of liver disease. Notethat similar changes are common in dogs with hyper-adrenocorticism and that such animals may have mildlyincreased serum bile acids (up to 60 tmol/litre in labora-tories with a reference range of 0 to 10 tmol/litre).

HAEMATOLOGYHaematology is of less use than urinalysis and serumbiochemistry in the investigation of polyuria/polydipsia.Changes in white blood cell counts are common but arefrequently non-specific. Neutrophilia is seen in hyper-adrenocorticism, some inflammatory diseases and manychronically ill (ie, stressed) dogs. A left shift (degenerateor non-degenerate) is suggestive of a pyogenic focus.

Lymphopenia is seen in many of those conditionsthat cause mature neutrophilia. A variety of non-specificchanges may be seen in some neoplastic processes.Occasionally, bizarre forms of lymphocytes may be seenin lymphoproliferative diseases. The extreme example ofthis is overt leukaemia.

Canine urine sample witha specific gravity of 1.010.This is not consistent with adiagnosis of either primarycentral or nephrogenicdiabetes insipidus. A waterdeprivation test is notindicated in this case. Somedogs with partial secondarydiabetes insipidus (forexample, animals withhyperadrenocorticism)may produce a similar urinespecific gravity but otherdiagnostic tests are requiredto identify these conditions.This dog had chronic renalfailure

OTHER INVESTIGATIONS

If the cause of the polyuria/polydipsia is not readilyapparent after performing a thorough physical exam-ination, urinalysis, serum biochemistry and haematologythen further investigations are indicated. The order inwhich these are discussed below represents the authors'usual approach to such cases, but other approaches maybe more suitable in some circumstances.





ACTH STIMULATION TESTHx peradieniocorticismil is olle of thc mOSt ComImIllOnI CaIuseSof- polyuia-iC.pcolydlipsial if 110 ChallICes aIre secCI Oll routi0lcbiochemistrxy. Pol'LIria/polxNdlipsia 111maV OCCuIIr inI theatbseuice ot otherl- SI01S (such as allopecia) thait are1orlally alssoci ated xith hypcriadreiuocoilticism. For these I-casois, all ACTH stilliLlItioll tCst is iudCicatcdI eail1V in thiemv1xcstigatioll of polxuLia/polVdipsil. The test r-elics oIIStim-ilatiOll of aldrllal OLltuIt by syltiletic ACTH aluldl isless likely to gic t'alse positive IesIlts tila tthe los dIoSedexalllcthlasolle SLIpprCSSioll test.

Method* Obtalil a1 hepaIriulisecd blooct salmilc ( 2 111)* Adliililstci 0(25 111m tett-acostactidle (Syumacthctl- Alli'uilcC)liltraxm,cllousiN prefera-bly ) 01' lIltI atlllLuscuLlarlyN* Obtaulll a seccoid bloodl slalillc altei- 3() to 9(1 tilillutes (itUiVCx 1e ilttrax ellO-ISIxV) o (1(0 to 120) Illilluteiut illtralluulrlx ).

Interpretation* Ini orillal dos. po1st-ACTH cortisol couiceltiratlollsshow a tsso- to tilreccfold ilclielase huit rei-Cill less tilal450)1110ol/liti-e;

1600

1400

1200E

o 1000,

a 800

0

600

400

200

0

Normal

IF-- -tthA r

Pre-ACTH Post-ACTH

Interpretation of the ACTH stimulation test. The cortisolconcentration of most dogs with hyperadrenocorticism (HAC)will increase dramatically following the administration ofACTH. In contrast, dogs with hypoadrenocorticism (hAC) or

idiopathic hyperadrenocorticism (iHAC) will show little or

no increase. The dashed lines represent mean concentrations

* In dogs with hlperaleli-ciocorticisIll, post-ACTH coi-ti-sol collcelltratIoIs uSuLall exceed 55(0 n110ol/litre:* False plosit!'VCs oCCLiI 'i Cdo^s x itl 'stlCesst'lil' 11luCesSCs(c,. ullstaIble dibihetes IllellitLsI;* The test is ot' 1o usc ill deteCllillilg tilc ullde-lx ilg,caiuse .

The lo\s closC dleCXltllatlMsoluc suIppr-essioll test

(Heri-t'age 1998) is al alcccptable alternative to tileACTH stiMilkitioll tcst. The dClVIlttgle of LISilg tIlc foi-illCI is its inclclased seilsiti ity: tile dlisadivsaitagl-es atIC tilelengtllh o( tlile tile test taikcs to lerform alud tilhe highernulimber of' ta'tlsc positixc results. IIl additiou. tti lossCIOSC dCXaIIlletila(SOI1C sLIPPlrCssion tcst is aftected IllO-C

hN CXOeiC1LS t'factoLsCt IcS lS asIstCIesaiSldS pool ill jcctioltecilIliclueC.

RADIOGRAPHYSUrx rIidaiograIplps oft tile thlol anla(hclconcil areC LISC

l'iil to iclenltify ncoplastic illaIsses. chililocs ill kiclicy aiclixve sic. lar-oc pyogenlic foci (clg py oillctra. piostalticabscessCs) anlc cillatrgeClelilt of solle 11loll-palpablc lillpllhilocles. The hicc_r the lo(7 the 1o10c illlpolttallt it is to

Cr1rV OLut ahbdomiinal racliOlgraphlx as thie selsitivity ot'alhdcic11.11 p|alpaitiol 10 cletcctillez abilor)lillalitie tails Collsideraixh ill drs xxithl laroer cilrtls.

Idcali v. racligrLapllx aIidLlltrasolSogI(-I(raptl|)0N Sl()Lilcl hc

pciformllecd in alIl paticlnts. Howccver, it siloulcd be ilotecitilat tile seInsiti i tv of racloircgapllx ill cletectiil ablhorillal-ities is increasec ill obese clogs ClIC to tilC ta]ct tilat flatilcl-craScs radio-raphic coiltrast. Coilx esceiv fa'At impilirsUltraS)ilOgrIIplliCeCeatillinltiOIl aCilCi SO tllis illagiiilloc11Moal-It Is1illc)re sclisutsvC In tiltll diliillials.

ULTRASONOGRAPHYU ltrasolilc)grapilic examinlIlation of abdomillnal v iscira is

cly1 UCset'Lil ill tile 11VeCstigattioll of poILulria/polydipsiaf'or xhich 10 Ca.LuseClas hecci suLccsted by the clinicaltests discussccd abox e. Ultrasonlogrlaphll (ofteCl couliecdxith guidled t'illC ieecdle biopsies Or aspirates) is, how -

CxVCe. 1\15 aluable ill tile fi-thllr assessCiSeilt of susipectecihi perlleAcrenlocorticism. liver disease xpyo(geilic tfoci andchdolmlinlal milasses.

Ill particular., ult-alsolic)graphly shoull he uIsedC toasscss p.aricilchmatoLis organs (lix er, spleel anlc klid-nlcys) fcor chailages ill tiei- ecilogenicity alid the pr-eseice

Survey abdominal radiograph of a rottweiler with polyuria/polydipsiathat had no significant abnormalities on routine urine, biochemical andhaematological investigations. A soft tissue mass is seen depressing thecolon ventrally. Cytological evaluation of the mass demonstrated that thiswas a soft tissue sarcoma. Neoplasia may cause polyuria/polydipsia byseveral different mechanisms and some cases may only be detected byradiography

Ultrasonography can be invaluable in the investigation of polyuria/polydipsia.This ultrasonogram shows an adrenal tumour in a dog with polyuria/polydipsiathat was originally suspected as being due to hyperadrenocorticism; however,ACTH stimulation and low dose dexamethasone suppression tests had notbeen diagnostic of the condition. This ultrasound finding encouraged therepetition of these tests

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of focal lesions. Any lesions identified on ultrasono-graphy should be biopsied or a fine needle aspirateobtained to distinguish between benign, malignant andnon-neoplastic lesions.

WATER DEPRIVATION TESTThe water deprivation test is probably overused in someveterinary practices. If carried out properly, it is a time-consuming and expensive test that poses little risk tothe patient. If performed incorrectly, it may pose a sig-nificant risk to the patient and is a waste of time andmoney.

The test should only be performed once the followingconditions have been excluded:* Renal disease, by measuring urea, creatinine and urinespecific gravity;* Diabetes mellitus, by measuring blood glucose;* Hypercalcaemia, by measuring blood calcium;* Hyperadrenocorticism, by carrying out an ACTHstimulation test or a low dose dexamethasone suppres-sion test;* Liver disease, by measuring liver enzymes.

The water deprivation test is therefore principallyof use in distinguishing between psychogenic polydipsiaand central and nephrogenic forms of primary diabetesinsipidus (ie, primary deficiencies of ADH or itsreceptors).

MethodPHASE 1. WATER RESTRICTIONIn cases with very severe polyuria/polydipsia, it maybe worth restricting water intake to twice maintenancefor a couple of days to reduce the effects of medullarywashout, if present. However, it is unclear if the waterrestriction phase is necessary in all cases as medullarywashout is difficult to reproduce experimentally and maynot be a common phenomenon.

PHASE 2. WATER DEPRIVATION* Empty the bladder by catheterisation and check theurine specific gravity;* Weigh the dog;* Deprive the dog of food and water;* Every two hours:

- Empty the bladder completely (by catheterisation)- Check the urine specific gravity- Weigh the dog- Check the levels of urea and creatinine;

* Stop water deprivation when:- The urine specific gravity is greater than 1-025, or- There has been 5 per cent loss in bodyweight, or- The dog becomes azotaemic, or- The dog appears depressed.This phase requires hospitalisation and can be dan-

gerous as dehydration can develop quickly. If diabetesinsipidus is present then azotaemia may develop in threehours.

PHASE 3. DESMOPRESSIN RESPONSE* Inject 2 to 4 mg of desmopressin (DDAVP; Ferring)slowly intravenously or intramuscularly (the latter routeis more painful);* Monitor the urine specific gravity for two to fourhours;* Gradually reintroduce water to avoid cerebraloedema.

1 035

1-030

1-025

>1O20)m 1 020v

a)a 1 015

1*010

1-005

1 000

CDI

NDI

0 2 4 6 8 10

DesmopressinTime (hours)

Interpretation of the water deprivation test. The urine specific gravity of normal dogsshould rise when they are dehydrated. This does not happen in dogs with primarynephrogenic diabetes insipidus (NDI). Once dehydrated, desmopressin (DDAVP) isadministered to these dogs. Only dogs with primary central diabetes insipidus (CDI)will respond. This test relies on the exclusion of other, more common, causes ofpolyuria/polydipsia for accurate interpretation

InterpretationIn normal dogs, the urine will be concentrated to a spe-cific gravity of more than 1-025. Dogs with primary dia-betes insipidus will be unable to concentrate their urineto more than 1 008. Dogs with primary central diabetesinsipidus will respond to desmopressin whereas thosewith primary nephrogenic diabetes insipidus will not.

If a dog with hyperadrenocorticism undergoes a waterdeprivation test then its response may mimic that of a nor-mal dog or one with any form of diabetes insipidus. Manydogs with hyperadrenocorticism will be able to concen-trate their urine to a specific gravity of more than 1-008.However, they may not be able to concentrate their urineto a specific gravity of more than 1 025 until desmo-pressin is given. It is therefore important to exclude hyper-adrenocorticism before attempting a water deprivation testto avoid false positive diagnoses of total or partial, centralor nephrogenic, primary diabetes insipidus.

Some authors recommend the measurement of serumand urine osmolality during water deprivation tests. Ifsuch facilities are available then they can prove useful,but they tend to be expensive.

FURTHER INVESTIGATIONSIf a water deprivation test has demonstrated primarycentral diabetes insipidus, the next logical step is to carryout some form of advanced diagnostic imaging of thebrain and pituitary. Magnetic resonance imaging isusually superior to computed tomography in this respectbut the availability of facilities locally is more likelyto determine which technique is ultimately selected. Inmost instances, this will require referral.

If primary nephrogenic diabetes insipidus is diag-nosed, renal ultrasonography is indicated. Renal biopsiesare unlikely to alter the therapeutic options in such casesand are usually unnecessary.

ReferencesCANNON, P. J. (1977) The kidney and heart failure. New EnglandJournal of Medicine 296, 26DUNN, J. K. & VILLIERS, E. (1998a) Collection and preparation ofsmears for cytological examination. In Practice 20, 370-377DUNN, J. K. & VILLIERS, E. (1998b) General principles of cytologicalinterpretation. In Practice 20, 429-437HERRTAGE, M. E. (1998) Canine hyperadrenocorticism. In Manual ofSmall Animal Endocrinology. Eds A. G. Torrance and C. T. Mooney.Cheltenham, BSAVA Publications. pp 55-74

Further readingBARSANTI, J. A., DIBARTOLA,S. P. & FINCO, D. F. (2000)Diagnostic approach to polyuriaand polydipsia. In Kirk's CurrentVeterinary Therapy Xil.Ed J. D. Bonagura. Philadelphia,W. B. Saunders. pp 831-835BRUYETTE, D. S. & NELSON,R. W. (1986) How to approachthe problems of polyuria andpolydipsia. Veterinary Medicine81, 112-128DUNN, J. K. (1998) The dogwith polydipsia and polyuria.In Manual of Small AnimalEndocrinology. Eds A. G.Torrance and C. T. Mooney.Cheltenham, BSAVAPublications. pp 3-10DUNN, J. K. (1998) Disordersof water and sodium balance.In Manual of Small AnimalEndocrinology. Eds A. G.Torrance and C. T. Mooney.Cheltenham, BSAVAPublications. pp 151-162





doi: 10.1136/inpract.24.8.434 2002 24: 434-441In Practice

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