Central Diabetes Insipidus in a

Dog

Brian Caserto
Cornell College of Veterinary Medicine
Class of 2007
May 9, 2007

Advisor: Dr Ken Simpson

Signalment
 Princess, a 12 year old FS mixed breed dog
– 2 month history of PU/PD and right side nasal
discharge, lethargy.
– Hypercalcemia, hyperproteinemia, and
hyperglobulinemia (from referring vet)
– Baseline T4 mild low (1.43 mcg/dL)
– Cortisol slightly elevated (9.24 mcg/dL)
– History of dehydration
Physical Exam

 QAR normal TPR

 Significant findings
– Right side mucopurulent nasal discharge
– Purulent discharge OD
  Purulent ocular discharge (right eye)
 Right side mucopurulent nasal
discharge
Problem List  PU/PD
Problem List continued

 Hypercalcemia
 Hyperproteinemia
 Hyperglobulinemia
 Hypothyroid
 Hyperadrenocorticism
PROBLEMS
Differential Diagnosis

 Purulent ocular
discharge (right
eye)
 Right side
mucopurulent
nasal discharge
 PU/PD
Differential Diagnosis

 Purulent ocular  Keratoconjunctivitis

discharge (right sicca
eye)  Keratitis

 Right side  Conjunctivitis

mucopurulent  Neoplasia
nasal discharge
 PU/PD
Differential Diagnosis

 Purulent ocular
discharge (right
eye)  Keratoconjunctivitis

 Right side  Bacterialrhinitis

mucopurulent  Fungal rhinitis

nasal discharge  Neoplasia

 PU/PD
Differential Diagnosis

 Purulent ocular
 Hypercalcemia
discharge (right
eye)  Diabetes Mellitus
 Right side  Hyperadrenocorticism

mucopurulent  Pyelonephritis
nasal discharge  Liver disease
 PU/PD  Renal disease
PROBLEMS

ocular
discharge
Lethargy PU/PD

KCS

Nasal
Discharge
Diagnostic Plan
 Schirmer tear test Ophthalmology consult
 CBC
 Serum chemistry
 Ionized calcium
 Urinalysis
 Abdominal ultrasound
 Thoracic radiographs
Results
 Below normal tear production OU
– Ophthalmology consult
 Bilateral KCS
 Neutrophilia 10.5 thou/uL Mild/ stress related
 Hyperproteinemia 8.1 g/dL Mild/ hydration)
 Hypernatremia 154 mEq/L (142-151)
 Hyperchloremia 119 mEq/L (107-117)
 Hypercalcemia (iCa) 1.38 mmol/l Mild/hydration
 Elevated Alk Phos 123 U/L Mild/hydration/stress
 Hyposthenuria (1.003)
 Normal chest radiographs
Results
 Below normal tear production OU
– Ophthalmology consult
 Bilateral KCS
 Neutrophilia 10.5 thou/uL
 Hyperproteinemia 8.1 g/dL
 Hypernatremia 154 mEq/L (142-151)
 Hyperchloremia 119 mEq/L (107-117)
 Hypercalcemia 1.38 mmol/l
 Elevated Alk Phos 123 U/L
 Hyposthenuria (1.003)
 Normal chest radiographs
US

 Liver
– Hypoechoic nodule
(right)
 Spleen
– Nodule deforming
the capsule
Conclusions from Lab Work

 Hyposthenuria (1.003)
 No evidence of systemic infection
 Mild Hypercalcemia
 Mild Hypernatremia
Additional Problem List

 Hyposthenuria
 Hypercalcemia
 Hypernatremia
 KCS
Additional DDX List

 Hyposthenuria  Central Diabetes

 Hypercalcemia Insipidus
 Hypernatremia  Nephrogenic Diabetes

 KCS insipidus
 Diabetes Mellitus
 Psychogenic polydipsia
Additional DDX List

 Hyposthenuria
 Hyperparathyroidism
 Hypercalcemia
 VitaminD toxicity
 Hypernatremia
 Hypercalcemia of
 KCS Malignancy
 Hemoconcentration
 Spurious
Additional DDX List

 Hyposthenuria  Diabetes Insipidus

 Hypercalcemia  Renal Failure
 Hypernatremia  Hemoconcentration
 KCS  Spurious
Additional DDX List

 Hypercalcemia  Auto immune

 Hyposthenuria dacryoadenitis
 Hypernatremia  Distemper
 KCS  Systemic sulfonamide
treatment
 Trauma
 Neurogenic
Additional DDX List

 Hypercalcemia  Auto immune

 Hyposthenuria dacryoadenitis
 Hypernatremia  Neurogenic

 KCS
Simplify
PU/PD

RepeatNORMAL
ionized calcium
 Hypercalcemia
 Hyperadrenocorticism NORMAL
Baseline Cortisol
 Hypoadrenocorticism
 Renal Failure ACTH
NORMAL
stimulation
 Diabetes Insipidus
 Psychogenic Polydipsia Technecium
NORMALGFR
 PU/PD

 Diabetes Insipidus
– Nephrogenic Desmopressin Response Test

– Central
 Psychogenic Polydipsia
Diabetes Insipidus

 What is it?
 Anatomy
 Physiology
 Clinical aspects
 Evans and DeLahunta, 2000

Pitutary Gland
Mammillary Infundibulum
Bodies

Evans and DeLahunta, 2000

Evans and DeLahunta, 2000
Boron and Boulpaep, 2003
 ADH is also
known as
AVP
Or
Vasopressin

Boron and Boulpaep, 2003

Renal Collecting Ducts

WATER

Boron and Boulpaep, 2003

Central Vs Nephrogenic

Boron and Boulpaep, 2003

PU/PD

 Central
Diabetes Insipidus
 Nephrogenic Diabetes Insipidus
 Psychogenic Polydipsia
PU/PD
 Central Diabetes Insipidus
– Neoplasia
 Primary pituitary
 Craniopharyngioma
 Meningioma
 Metastatic tumor

– Inflammatory disease
– Trauma
 Nephrogenic Diabetes Insipidus
 Psychogenic Polydipsia
PU/PD
 Central Diabetes Insipidus
 Nephrogenic Diabetes
Insipidus – Pyometra
– Primary- Huskies – Pyelonephritis
– Hypercalcemia – Liver disease
– Diabetes Mellitus – Renal disease
– Hyperadrenocorticism – Hyperthyroidism
– Hypoadrenocorticism – Medullary washout
 Psychogenic Polydipsia
PU/PD

 Central
Diabetes Insipidus
 Nephrogenic Diabetes Insipidus
 Psychogenic Polydipsia
– Young dogs that are kept alone for long
periods of time
Clinical signs of DI

 PU/PD
 Hyposthenuria
 Hypernatremia
– Water Deprived
Clinical signs of DI

 PU/PD
– Reduced water reabsorption in the kidney
 Hyposthenuria
 Hypernatremia
Clinical signs of DI

 PU/PD
 Hyposthenuria
– Salt reabsorption and lack of water reabsorption
 PU/PD
 Hypernatremia
Clinical signs of DI

 PU/PD
 Hyposthenuria
 Hypernatremia
– Result of severe dehydration due to water
loss
– Occurs in animals without access to free water
Back to Princess
 PU/PD

 Diabetes Insipidus
– Nephrogenic Desmopressin Response Test

– Central
 Psychogenic Polydipsia
Desmopressin Response Test

 DDAVP
– Decreased water intake over 24 hrs
– Urine SG increased from 1.003- 1.029
Water intake

eSG
Ur i n

Desmopressin

Time
Diagnosis

 CentralDiabetes Insipidus
 KCS (OU)
 Possible rhinitis
Treatment

 Treatment
– DDAVP (Desmopressin) Synthetic vasopressin
used to treat the symptoms, concentrate urine,
stop PU/PD
 Optimmune (cyclosporine) and NeoPolyDex
ointment, and paralube
Follow up

 Princess returned 11/4/06 with increased

lethargy and increased respiratory rate
 Exam
– Severe Depression
– Masseter muscle atrophy
– No Cranial nerve deficits
– Bloodwork unremarkable
Follow Up

 Treated with fluids overnight

 Urine SG low
– desmopressin was increased to 2 drops in the
evening.
 Chest radiographs (11/6/06)- normal
 MRI- Severe Progressive Depression
 CT
 Endoscopy- no abnormality in nasal cavity
 T1
Contrast
MRI T1
 MRI
T1

DeLahunta, 1983

Princess Pituitary
Normal
MRI

T1 T1

Princess Normal
MRI
T1 T1

Princess Normal
MRI

 Polyostotic aggressive bone lesion

 Otitis media (right side worse)
CT
CT Pterygoid

Princess Normal
 Sphenoid
CT Complex

Princess Normal
 Basisphenoid
CT Bone Lysis

Princess Normal
CT

 Polyostotic aggressive bone lesion

 Otitis Media (right)
Follow Up

 Endoscopy- no abnormality in nasal cavity

?
Princesses depression and lethargy continues and euthanasia was
elected
Necropsy findings

Gross findings
Skull- locally extensive basioccipital bone density
irregularity
Liver- multifocal hepatoma (presumptive)
Kidney (R)- multifocal chronic infarcts
Spleen- focal nodular hyperplasia
Masseter muscle- moderate chronic diffuse muscle
atrophy
Right AV valve- focal hematocyst
 Pituitary
Necropsy Findings

 Histopathology
– Liver- vacuolar
hepatopathy
– spleen- Focal leiomyoma
– Basioccipital bone
 Thinning
– focal medullary cavity
fibroplasia
Evans and DeLahunta, 2000
Histopathology 4X

Cementing Lining

Normal Bone Affected Bone

Histopathology 4X

Blood Vessels

Spindle Cells

Normal Bone Affected Bone

Histopathology 40X
Bone Remodeling Fibroplasia

4X
4X

Cementing Lining
Spindle Cells
Evans and DeLahunta, 2000
Conclusions

 No cause for the changes in the bone were

determined
 The cause of the pituitary disorder was not
found
Speculations

 Inflammatory process or infection causing

locally extensive bone destruction and
secondarily affecting the pituitary and other
parts of the brain.
 An unidentified pituitary neoplasm
 REFERENCES
 1. Authement JM, Boudrieau RJ, Kaplan PM. Transient, traumatically induced, central diabetes insipidus in a dog.
J Am Vet Med Assoc. 1989;194:683-685.
 2. Barr SC. Pituitary tumour causing multiple endocrinopathies in a dog. Aust Vet J. 1985;62:127-129.
 3. Bolger WE, Leonard D, Dick EJ,Jr, Stierna P. Gram negative sinusitis: A bacteriologic and histologic study in
rabbits. Am J Rhinol. 1997;11:15-25.
 4. Boron WF, Boulpaep EL, eds. Medical Physiology: A Cellular and Molecular Approach. 1st ed. Philadelphia,
Pennsylvania: Saunders; 2003.
 5. DeLahunta A. Veterinary Neuroanatomy and Clinical Neurology. 2nd ed. Saunders; 1983.
 6. Evans HE, DeLahunta A. Guide to Dissection of the Dog. 5th ed. Saunders, 2000.
 7. Feldman EC. Central diabetes insipidus in a dog. Mod Vet Pract. 1979;60:615-619.
 8. Feldman EC, Nelson RW. Diagnostic approach to polydipsia and polyuria. Vet Clin North Am Small Anim Pract.
1989;19:327-341.
 9. Goossens MM, Rijnberk A, Mol JA, Wolfswinkel J, Voorhout G. Central diabetes insipidus in a dog with a pro-
opiomelanocortin-producing pituitary tumor not causing hyperadrenocorticism. J Vet Intern Med. 1995;9:361-365.
 10. Harb MF, Nelson RW, Feldman EC, Scott-Moncrieff JC, Griffey SM. Central diabetes insipidus in dogs: 20
cases (1986-1995). J Am Vet Med Assoc. 1996;209:1884-1888.
 11. Neer TM, Reavis DU. Craniopharyngioma and associated central diabetes insipidus and hypothyroidism in a
dog. J Am Vet Med Assoc. 1983;182:519-520.
 12. Nichols R. Polyuria and polydipsia. problems associated with patient evaluation. Probl Vet Med. 1990;2:610-
616.
 13. Ramsey IK, Dennis R, Herrtage ME. Concurrent central diabetes insipidus and panhypopituitarism in a
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 Thanks
 Dr Simpson
 Dr Dykes
 Dr Arauz
 Lisia
 The class of 2007
QUESTIONS ?