Transcript Diabetes Inspidus - Wendy Blount, DVM

Disorders of Water
Balance
Polyuria-Polydipsia
and 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
– 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
• Urine SG
– Always <1.020, often < 1.012
Causes of PU/PD
PU => PD
1. Renal Disease – fluid Loss
2. Problem with ADH
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not produce (central DI)
Kidneys don’t respond
3. Drugs
PD => PU
1. Primary Polydipsia
2. Psychogenic Polydipsia
Causes of PU => PD
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Osmotic diuresis
– Diabetes mellitus, Renal glycosuria
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Osmotic diuresis + medullary washout
– Chronic renal failure, Polyuric acute renal failure
– Post-obstructive diuresis, Diuretic therapy
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Lack of ADH production – central diabetes insipidus
Lack of response to ADH
– Primary nephrogenic diabetes insipidus
– Secondary nephrogenic diabetes insipidus
• Pyometra, septicemias, pyelonephritis
• Hypercalcemia, liver failure, hyperadrenocorticism
• Hyperaldosteronism, hypokalemia, hyperthyroidism
• Hypoadrenocorticism, acromegaly, polycythemia
Causes of PU => PD
• Drug Therapy
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Anticonvulsants
Glucocorticoids
DOCP – deoxycorticosterone pivalate
Diuretics
Mannitol
Thyroxine
Amphotericin B
Lithium
Methoxyflurane
Sodium bicarbonate
*Sodium (treats)*
Vitamin D toxicity
Causes of PD => PU
• Primary Polydipsia
– Defect 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-PD
• Have owner collect urine samples
– 2-3 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 syndromes
– Pollakuria, stranguria
– Urinary incontinence
– Dehydration and appropriate increased thirst
Work-Up
• Most common causes of PU-PD in the dog (5)
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Chronic renal failure
Diabetes mellitus
Hyperadrenocorticism
Liver failure
Hypercalcemia
• Most common causes of PU-PD in the cat (3)
– Chronic renal failure
– Diabetes mellitus
– Hyperthyroidism
Work-Up
Hints on the history & physical exam
• Intact female + vulvar discharge
– rule out pyometra
• Lymphadenopathy
– rule out lymphoma (hypercalcemia)
• Anal sac mass
– rule out apocrine gland carcinoma (hypercalcemia)
• Weight loss in the cat
– rule out hyperthyroidism and diabetes
• Endocrine alopecia
– Hyperadrenocorticism (dog > cat)
– Acromegaly (cat >> dog)
– diabetes mellitus (both)
Work-Up
Hints in the urine
• All 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 above
• USGs 1.008 – 1.015 + proteinuria
– Renal disease most likely
– Make sure to get a urine culture
– If negative, do urine protein:creatinine
• USGs 1.020’s with azotemia
– Hypoadrenocorticism and pyelonephritis most likely
Any USG >1.020 - diabetes insipidus is ruled out
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• *USG ranges from <1.008 - >1.030*
– Psychogenic polydipsia most likely
Work-Up
• First Tier Tests
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CBC, panel, lytes
HW Test for dogs, FeLV/FIV tests for cats
urinalysis
Urine culture (cystocentesis)
TT4 for cats >5 years old.
• Second Tier Tests
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thoracic radiographs
Abdominal US + radiographs
Bile acids (pre- and post-prandial)
ACTH stim
Urine protein:creatinine
Work-Up
• Third Tier Tests
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Vasopressin 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
<1.008
• Isosthenuria + PU-PD is most commonly caused by
renal disease
• Isosthenuria + azotemia = renal disease with few
exceptions
• Pyelonephritis is one of the two most common
causes of PU-PD + USG in the 1.020’s
Work-Up
More pattern recognition
• Central DI or congenital Nephrogenic DI
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+Neurologic deficits
Sodium high normal, as with all PU => PD
USG usually <1.008 if complete DI
USG can be 1.008-1.018 if partial CDI
Dehydration to 3-5% within a few hours of water
deprivation
• Psychogenic polydipsia
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behavioral issues
Sodium low normal
Fluctuating USG 1.005 – 1.030
Prolonged 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 partial
• USG >1.020 at any time rules it out
• Usually acquired rather than congenital
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Idiopathic (most common)
Head trauma or surgery (can be transient)
Neoplasia/cysts
LP inflammatory destruction
Parasite 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 increased
– No 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
adult
– Temporary psychogenic polydipsia in puppies that
seems to resolve at they mature is not uncommon
• USG varies widely over time – 1.005 – 1.030
• ADH response to dehydration or hypertonic saline
is appropriate (increased)
Secondary NDI
kidneys 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 tubules
Hypercalcemia
• Decreased response to ADH by the kidneys
Liver failure – not well understood
• Impaired urea production resulting in medullary washout
• Vasoactive effects – altered renal blood flow
Secondary NDI
Hyperadrenocorticism
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Glucocorticoids inhibit ADH release
Increase osmotic threshold
Decreased renal response to ADH
Rarely, physical disruption by macroadenoma
Hyperaldosteronism – poorly understood
• Mineralocorticoids reduce ADH release
• Decreased renal response to ADH
Pyelonephritis – see renal failure and sepsis
Hypokalemia
• Decreased renal response to ADH
• Blunting of the medullary urea gradient
Secondary NDI
Hypoadrenocorticism - **ACTH Stim > LDD**
• Mineralocorticoid deficiency results in sodium wasting and
medullary washout
• See hypercalcemia
• Look at USG to distinguish from renal failure
Hyperthryoidism – poorly understood
• Increased renal perfusion
• Thyrotoxicosis results in PsP
• Concurrent renal insufficiency in older cats
Acromegaly
• Glucosuria
• renal insufficiency
Polycythemia
• Hyperviscosity stimulates thirst
CDI and PsP
History and physical exam
• Weight 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, stupor
– Cerebral signs – pacing, disorientation, pacing, ataxia,
seizures, head pressing, getting stuck in corners
• Hydration normal if water not restricted
• No vomiting, regurgitation, diarrhea, coughing
• Urinary incontinence not uncommon, especially
when sleeping
CDI and PsP
Diagnostics
• CBC – mild polycythemia not uncommon
– Owners often withhold water to some degree out of
desperation
• Serum panel, electrolytes
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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 water
May have high Na+ and K+ if water withheld
• UA – urine osmolality often < 300 mOsm/kg
– USG for PP often varies from <1.008 to >1.030
– USG for CDI and NDI usually <1.008 and always <1.020
– USG for partial CDI can be 1.008-1.018, if water
withheld
CDI and PsP
Confirm and differentiate CDI, NDI, PP
1. Rule out acquired NDI
2. Response to DDAVP
3. Plasma osmolality with free access to water
4. Modified water deprivation test
Rule out acquired NDI prior to water deprivation!!
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CBC, panel, lytes, UA, urine culture and sensitivity
(cystocentesis > mid-stream catheter)
TT4 on the cat > 5 years
Urine protein:creatinine + cortisol:creatinine
In addition to negative urine culture, rule out pyelonephritis
with either:
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Abdominal US *or*
Trial of antibiotics
PU-PD that responds to antibiotics is strong evidence for
pyelonephritis, regardless of a negative urine culture
Water deprivation + renal disease = disaster
Plasma Osmolality
• Can identify PP
• Done with free access to water
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Normal dog – 280-300 pOsm
Complete CDI – 285-340 pOsm - high normal to high
NDI – 285-340 pOsm – high normal to high
Partial CDI – 280-320 pOsm – normal to high
PP – 275-305 pOsm – low to normal, rarely mildly high
Response to DDAVP
DDAVP = D-Desmopressin Acetate VasoPressin
Tablets, injection, nasal drops uses as eye drops
1. Oral tablets or drops BID x 7 days
2. Collect urine daily on days 5-7 and test USG
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Medullary washout will resolve in 1-3 days, allowing
you to assess response at 5-7 days
3. Increase in USG by 50% or more, especially
>1.030, indicates response to DDAVP
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CDI – excellent and durable response to DDAVP
Acquired NDI – temporary response to DDAVP
PP – mild response to DDAVP
Primary NDI – no or minimal response to DDAVP,
unless exceedingly high doses are used
Modified Water Deprivation Test
To determine if endogenous ADH is released in
response to dehydration
And whether kidneys respond to the ADH
3 Steps:
1. Patient Preparation
2. Phase I – water restriction until 3% weight loss
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Normal response is USG >1.030 in the dog and >1.035
in the cat
Partial and complete CDI – inadequate response
3. Phase II – continue only if inadequate response
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Assess response to ADH analog
Modified Water Deprivation Test
Patient Preparation – progressive water restriction
to minimize interference of medullary washout
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Decrease water intake to 100 ml/kg/day prior to the start
of the test
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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 test
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Abort if :
• animal becomes aggressive for water
• Evidence of hypertonic dehydration
– Change in mentation or demeanor
Modified Water Deprivation Test
Phase 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
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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
point
Normal dogs will take 24 hours or more to reach the
endpoint
Leaving a DI patient unattended for several hours can
result in severe complications, including death
Phase I may require 24 hours or more
Modified Water Deprivation Test
Phase I
1. Time 0
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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 osmolality
Take blood for serum osmolality, BUN, Electrolytes
2. Repeat every 1-2 hours
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Empty the bladder by walking or catheterization for
dogs and indwelling catheter for cats, and weigh
3. Every hour – Weigh and assess for dehydration and
change in mentation
4. Take blood sample for BUN and sodium if
dehydration, or periodically
Modified Water Deprivation Test
Phase I
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Abort if BUN >30, hypernatremia, severe
dehydration or changes in mentation
If endpoint not reached in 10 hours
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Refer for 24 hour testing
or repeat Phase I with water withheld after midnight
the night before starting
Urine concentration plateaus may be seen
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Indicates maximal renal response to water deprivation
Three consecutive urine samples with the same
osmolality (+ 5% USG or 30 mOsm/kg)
USG is less reliable for detecting plateaus
Modified Water Deprivation Test
Phase II - determines the effect of exogenous ADH on
the kidneys in the face of dehydration
Differentiates CDI from NDI
1. Time 0 (= end point of Phase I)
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Empty bladder, keep urine for USG/osmolality, weigh
Take blood for ADH if available
BUN, electrolytes, serum osmolality
2. Administer vasopressin
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aqueous vasopressin (Pitressin) 0.2-0.4U/kg IM,
maximum dose 5U
DDAVP injection 5 mcg SC
3. Empty bladder, keep urine and weigh
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If Pitressin - at 30, 60 and 120 minutes post injection
If DDAVP – at 2 and 4 hours post injection
Run USG and ideally osmolality on urine
Modified Water Deprivation Test
Phase II
5. Weigh every hour and assess for dehydration
and change in mentation
6. Take blood sample for BUN, sodium, plasma
osmolality if dehydration, and at end
7. Offer small amounts of water (10-20 ml/kg) over
the next 2 hours, to avoid water intoxication
8. Then gradually return to free choice water over
several hours
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Abort if BUN >30 mg/dl, hypernatremia, severe
dehydration or changes in mentation
Less likely to abort in Phase II than Phase I
Modified Water Deprivation Test
Interpreting 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 (280310 mOsm/kg) in Phase I
• Urine osmolality will increase in Phase II by 50-600%
Hyperadrenocorticism, Partial CDI and some PP
• Urine osmolality increase above 300 mOsm/kg in Phase I
• Further 10-50% increase in Phase II
Modified Water Deprivation Test
Interpreting the Modified Water Deprivation Test
Primary (congenital) and secondary (aquired) NDI
• Urine osmolality will not exceed plasma osmolality (280310 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
Primary Polydipsia
• Given enough time, USG will exceed 1.030 in Phase I
• Could take 24 hours or longer
• Phase II is rarely needed, but if carried out, will produce
little change
Modified Water Deprivation Test
Pitfalls
• 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
– Partial CDI patients can have an enhanced response to
ADH early on due to up regulation of receptors
Modified Water Deprivation Test
The Dehydrated Patient
• 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 >1.030
• If neurologic signs
– Careful fluid therapy – see next slide
– adjust patient preparation to prevent dehydration the
next time around
Modified Water Deprivation Test
Treating the Clinically Dehydrated Patient
• There are three forms of dehydration
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Isotonic – proportional loss of water and electrolytes
• GI loss a common example
• Sodium usually normal
• Clinical signs proportional to hypovolemia
2. Hypotonic – loss of electrolytes > water loss
• Hypoadrenocorticism an example
• Sodium usually low, pre-renal azotemia common
• Clinical signs pronounced relative to hypovolemia
3. Hypertonic - loss of free water > electrolytes
• Water deprivation + PU-PD an example
• Cell dehydration > plasma hypovolemia
• Severe hypernatermia with hyposthenuria
• Weight loss shows dehydration prior to symptoms
Modified Water Deprivation Test
Treating the Clinically Dehydrated Patient
• Signs of hypertonic dehydration
– Neurologic signs – hypertonic brain cell shrivel
• Mild – irritability, weakness, ataxia
• Moderate – stupor
• Severe – coma and seizures
• Treatment goal - Restore hydration slowly, with minimal
brain cell damage & cerebral edema
Modified Water Deprivation Test
Treating the Hypertonic Dehydrated Patient
Correct dehydration with IV 0.9% NaCl + K+ as needed
(potassium chart) over 4-6 hours
– Sodium should decline no more than 1 mEq/L/hr
– If neurologic signs worsen, slow rate and treat for
cerebral edema with hypertonic saline or mannitol
2. Once rehydrated, correct water deficit if still hypernatremic
– 0.45% NaCl + 2.5% dextrose
– or half strength LRS + 2.5% dextrose
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L=(
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current Na+
normal Na+
- 1 ) x (0.6 x weight-kg)2
• oral route preferred, IV if PO not possible
• Replace 50% in the first 24 hours
• Remainder over the next 24-48 hours
If hypernatremia persists after 12-24 hours
• Switch to 5% dextrose IV until sodium normal
Referral – MRI/CT
• Consider neoplasia in the older dog with CDI
– if client would consider radiation therapy
• T1-weighted images 80% diagnostic for CDI in
people
Treatment of CDI
DDAVP Intranasal drops 100 mcg/ml (2.5 ml & 5ml)
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$150-200
Transfer to a sterile eyedropper bottle
1 drop = 1.5-4 mcg DDAVP
Start at 1-2 drops in either eye SID-BID, alternate eyes
DDAVP 0.1mg and 0.2 mg tablets
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bioavailability 5-15% that of nasal drops
0.05 mg PO BID for cats and dogs < 5 kg
0.1 mg PO BID for dogs 5-20 kg
0.2 mg PO BID for dogs > 20 kg
Increase to TID if not effective
If TID not effective, switch to eyedrops
Once symptoms are controlled, wean down to
lowest effective dose
Treatment of CDI
DDAVP injection 4 mcg/ml (2 ml)
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5-20x as potent as nasal drops in people
Start at 0.2-0.25ml SC SID
Increase dose & frequently as needed to control symptoms
Hyponatremia a possible side effect
• Onset within 2 hrs, regardless of route of
administration
• Duration of action 6-18 hours
– Higher doses prolong duration of action
• Expense is often the limiting factor
• Administration in the evening can allow the
family to get proper sleep
Treatment of CDI
Other oral treatments
Chlorpropamide (oral hypoglycemic)
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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/day
Hypoglycemia can be a side effect, managed by offering
multiple small meals
Thiazide diuretics – 20-40 mg/kg PO BID along with
low sodium diet
• CDI and *NDI* – reduces urine output by 30-50% in people
• Inhibits renal sodium resorption > contracts ECF > increases
salt and water absorption in the renal tubule > reduces
osmotic diuresis
• Occasional hypokalemia can be a side effect
• Check electrolyte panel every 3 months
Treatment of CDI
Other oral treatments
Low salt diet
• May be helpful for CDI and NDI
• < 1g Na/Mcal
• Hill’s H/D
Prognosis of CDI
• Prognosis is good for if medication given daily
• Eye 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
macrodenoma 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 NDI
• Extremely high doses of injectable DDAVP (0.33
U/kg IM TID) can sometimes control primary NDI
• But therapy is very, very expensive
• Thiazide diuretics are sometimes the only viable
option for treatment
• Long term prognosis generally poor
Prognosis of Untreated DI
• Dogs 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 needed
• Mean survival about 2 years
Treatment of PsP
Water Restriction
• Measure 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 NaHCO3 0.6g/30kg PO BID x
3-5 days to help resolve medullary washout, if
needed
Treatment of PsP
Behavior Modification
• Daily exercise
• Con-specific play, if the patient likes it
• Environmental enrichment with interactive toys
• Increased contact with people during the day
Prognosis PsP – generally excellent, though relapse
can occur
SIADH
Syndrome of Inappropriate ADH
• Sustained release of ADH
Etiology
• Functional neoplasia – CNS or paraneoplastic
– Especially bronchogenic adenocracinomas
• CNS disease - Head trauma, demyelinating
disease, infection/inflammation
• Porphyria
• Endocrine disease – hypoadrenocorticism,
pituitary dwarf, profound hypothyroidism
• Pulmonary disease – acute respiratory failure,
aspergillosis, pneumonia, tuberculosis
• Drugs
SIADH
Drugs that cause SIADH
• ACE inhibitors
• Chlorpropamide
• Cyclophosphamide, vincristine
• Omeprazole
• SSRIs
• Thiazides
SIADH
Clinical Presentation – water intoxication
• Hyponatremia <130 for 48 hours or longer
– Lethargy, weakness, muscle fasciculation
– anorexia, vomiting
– Obtundation, disorientation, seizures, coma (Na <120)
• Plasma osmolality < 275 pOsm
• Urine osmolality inappopriately high
Diagnosis
• Hyponatremia with plasma osmolality >275 pOsm
• Inappropriately high urine osmolality
• Normal renal and adrenal function
• No hypovolemia
• Correction by water restriction
• Plasma ADH normal to high
SIADH
Treatment of the hypotonic dehydrated patient
1. 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 hour
2. When sodium >125mEq/L, Further correction by
water restriction
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Identify the daily water intake that maintains sodium at
low end of normal range
Divide into 6-8 aliquots per day
Never allow free access to water
Can’t go swimming or have access to ponds or swimming
pools or rain
• Discontinue any drugs that may be causing SIADH
• Some have tried tolvaptan 3 mg/kg PO BID (ADH
receptor antagonist)
Hypodipsic Hypernatremia
• Neurologic disorder causing decreased thirst and
diminished ADH release in response to
hyperosmolality
• HH = chronic hypernatremia & hyperosmolality
due to decreased water intake, and even when
euvolemic due to abnormal ADH secretion
• Normal kidney function, but inappropriately
dilute urine for the hypernatremia
• Most common in Miniature Schnauzers
• Causes in dogs:
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Neoplasia
hydrocephalus and other degenerative CNS diseases
congenital hypothalamic dysplasia
inflammatory CNS disease
Hypodipsic Hypernatremia
Treatment:
• 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 home
• Some dogs do well only with increased water
intake after correction of hypernatremia, and
some are still hypernatremic with euvolemia
– Chlorpropamide (33 mg/kg/day) has been tried with
inconsistent results