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Central diabetes insipidus in an African Grey parrot

Simon R. StarkeyDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Catherine WoodDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Ricardo de MatosDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Eric C. LedbetterDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Abstract

Case Description—A 5.5-year-old sexually intact female African Grey parrot (Psittacus erithacus) was evaluated for a 1-year history of pronounced polyuria and polydipsia. The bird also had a 1-month history of signs of mild depression and mydriasis.

Clinical Findings—Physical examination revealed a thin body condition and incomplete bilateral mydriasis. Other examination findings as well as CBC and screening radiography results were unremarkable. Plasma biochemical analysis revealed mild hypernatremia. The bird had a 3.3% loss in body weight over 170 minutes during a water deprivation test, and urine osmolality remained low. After IM administration of 0.9 μg of desmopressin, the rate of weight loss decreased substantially and urine osmolality increased 300% over the following 200 minutes.

Treatment and Outcome—Initial attempts to treat the bird with orally administered desmopressin failed to correct the polydipsia and polyuria. Ultimately, IM administration of 24 μg of desmopressin/kg (10.9 μg/lb) every 12 hours yielded a noticeable reduction in water consumption and urine production over a 6- to 8-hour period. Eight months later, the bird was returned for a recheck examination, at which time it was in good health and continued to respond to the medication. Despite continued response to the medication, right-sided internal ophthalmoparesis was detected 16 months after the initial diagnosis.

Clinical Relevance—To the authors' knowledge, central diabetes insipidus in birds has not been reported. The condition should be considered in birds with clinical signs of disease similar to those in mammals. Long-term IM administration of desmopressin may be a viable treatment option.

Abstract

Case Description—A 5.5-year-old sexually intact female African Grey parrot (Psittacus erithacus) was evaluated for a 1-year history of pronounced polyuria and polydipsia. The bird also had a 1-month history of signs of mild depression and mydriasis.

Clinical Findings—Physical examination revealed a thin body condition and incomplete bilateral mydriasis. Other examination findings as well as CBC and screening radiography results were unremarkable. Plasma biochemical analysis revealed mild hypernatremia. The bird had a 3.3% loss in body weight over 170 minutes during a water deprivation test, and urine osmolality remained low. After IM administration of 0.9 μg of desmopressin, the rate of weight loss decreased substantially and urine osmolality increased 300% over the following 200 minutes.

Treatment and Outcome—Initial attempts to treat the bird with orally administered desmopressin failed to correct the polydipsia and polyuria. Ultimately, IM administration of 24 μg of desmopressin/kg (10.9 μg/lb) every 12 hours yielded a noticeable reduction in water consumption and urine production over a 6- to 8-hour period. Eight months later, the bird was returned for a recheck examination, at which time it was in good health and continued to respond to the medication. Despite continued response to the medication, right-sided internal ophthalmoparesis was detected 16 months after the initial diagnosis.

Clinical Relevance—To the authors' knowledge, central diabetes insipidus in birds has not been reported. The condition should be considered in birds with clinical signs of disease similar to those in mammals. Long-term IM administration of desmopressin may be a viable treatment option.

A 5.5-year-old DNA-sexed female African Grey parrot (Psittacus erithacus) was evaluated by the Avian and Exotic Animal Service at Cornell University's Hospital for Animals for a 1-year history of progressive PUPD and a 1-month history of signs of mild depression and concurrent mydriasis. The owner reported that the bird consumed approximately 1 L of water daily and produced voluminous droppings consisting mostly of urine. The bird was captive bred, hand reared, and purchased at 2 months of age by the present owner. It was housed alone in a large, commercially made powdercoated cage and was fed a mixture of a commercial pelleted food supplemented with limited table foods and a seed-and-nut mixture. The owner had 12 other birds in the home; however, these birds did not have direct contact with the parrot. The bird was not receiving any medication at the time of evaluation. Results of a CBC and plasma biochemical analysis performed by the referring veterinarian 3 months previously were within reference limits.

Physical examination revealed the bird was alert and in fair body condition, with mild to moderate atrophy of the pectoral muscles (body condition score, 2/5). The feathers and integument were in excellent condition, although there was some soiling of the contour feathers in the region of the vent. Voluminous watery droppings, consisting predominantly of urine, were evident on the bottom of the bird's travel cage.

Additionally, the bird had mild to moderate bilateral mydriasis in all light conditions, with intact neurologic menace responses and reduced pupillary light reflexes bilaterally. The remainder of the findings of the physical examination were unremarkable. Results of a CBC, plasma protein electrophoresis, and orthogonal whole body radiography performed during the initial consultation were also unremarkable. A concurrent plasma biochemical analysis including determination of bile acids concentration revealed mild hypernatremia (159 mg/dL; reference limits, 134 to 152 mg/dL) and hypophosphatemia (2.9 mg/dL; reference limits, 3.2 to 5.4 mg/dL). Additional diagnostic testing included a PCR assay of whole blood and a combined choanal and cloacal swab to detect psittacine beak and feather disease and Gram staining of feces plus fecal wet mount examination. Results of these tests were within reference limits. A complete urinalysis was performed on the urine fraction of voided droppings obtained from a nonporous surface within 30 seconds after voiding. Results indicated hyposthenuria (specific gravity, 1.003; reference limits, 1.005 to 1.020) but were otherwise within reference limits.1,2

In light of the largely ordinary results of physical examination and screening tests, the etiology of the PUPD could not be readily attributed to organ dysfunction such as overt liver, kidney, or gastrointestinal disease. Diabetes mellitus was considered improbable given the unremarkable plasma glucose concentrations when evaluated at the teaching hospital and the referring veterinarian's practice and the lack of glucosuria when evaluated at the teaching hospital. Metabolic, toxicological, or infectious causes of PUPD were also considered less likely given the results of the preliminary physical and laboratory examinations.

Coelomic endoscopy was considered at this juncture to allow for direct visual evaluation of the serosal surface of the coelomic contents and collection of biopsy specimens. Visualization of the oviduct as well as collection of hepatic and renal biopsy specimens would likely have aided in ruling out a large number of renal, hepatic, or potentially reproductive causes of PUPD. However, this technique was not used, primarily because the history, profound polydipsia (estimated to exceed 2 L/kg/d), laboratory results, and radiographic findings were highly consistent with a diagnosis of CDI, nephrogenic diabetes insipidus, or psychogenic polydipsia.3–5 Whereas psychogenic polydipsia has been diagnosed in an African Grey parrot,3 to the authors' knowledge CDI has not been diagnosed in any avian species. Nephrogenic diabetes insipidus has, however, been diagnosed in a strain of Leghorn chickens and Japanese quail.6–8 With these considerations, a water deprivation and desmopressin response test was planned.

The water deprivation test was conducted at the teaching hospital 1 month after the initial evaluation in accordance with the so-called cage method reported for use in pigeons9 and subsequently used for the diagnosis of psychogenic polydipsia in an African Grey parrot.3 At this time, a physical examination was performed, the results of which remained unchanged from those of the initial examination 1 month previously. The bird was weighed and placed in a stainless steel cage with a nonporous perch at time 0 (0 minutes). Food and water were not available during the test period. Several variables were measured throughout the procedure to ensure the bird's safety and to aid in achieving an accurate diagnosis. Briefly, plasma electrolytes and osmolality were determined at 0 and 170 minutes. Hematocrit was measured at 0, 170, and 480 minutes. Plasma total solids concentration, as determined by refractometry, was determined at 480 minutes. Additionally, the urine portion of droppings containing no gross fecal material was collected opportunistically, within 1 minute after voiding, to measure urine supernatant specific gravity and osmolality. Body weight was also monitored frequently as a key determinant of hydration status.

At 170 minutes, 2.14 μg/kg (0.97 μg/lb) of desmopressina was administered IM. The desmopressin dose was extrapolated from data in a report10 suggesting that an IV bolus of 2.14 μg/kg had no adverse cardiovascular effects in White Leghorn cockerels. Following desmopressin administration, the frequency of droppings noticeably decreased, and the bird only voided twice more at 375 and 610 minutes. The osmolality of these samples was greater than 300% more than that detected prior to desmopressin administration. The test ended at 610 minutes, when the bird had lost a total of 6.4% of its body weight. Fifteen milliliters of a balanced crystalloid solution was immediately administered SC, and the bird was allowed free access to food and water overnight.

The following morning the bird was bright, alert, and responsive and had returned to its pretest weight. A diagnosis of CDI was made on the basis of the rapid development of dehydration and accompanying production of hyposmolar urine prior to desmopressin administration. This diagnosis was supported by the 3-fold increase in urine osmolality and decreased rate of weight loss following desmopressin administration. The presence of hyperosmolar plasma at 0 minutes (327 mOsm/kg; mean ± SD reference value, 305.8 ± 6.5 mOsm/kg) provided additional support for the diagnosis.b The parrot was discharged to the care of its owner later that day with instructions to administer desmopressin PO at 11.5 μg/kg (5.2 μg/lb) once daily. After several days, the owner reported that although the bird seemed brighter and more active, PUPD remained. Increasing the dosage gradually to 93 μg/kg (42.3 μg/lb), PO, every 12 hours over a 2-week period also failed to correct the PUPD. Given the lack of response to orally administered desmopressin, reevaluation at the teaching hospital was recommended.

A recheck examination was performed 3 weeks after performance of the water deprivation test. At this time, physical examination, CBC, plasma biochemistry analysis, protein electrophoresis, and urinalysis were performed. The results of these evaluations were within reference limits; however, the bird's urine was again hyposthenuric (specific gravity, 1.003). Given the continued lack of evidence of other systemic causes of PUPD and the response to IM desmopressin administration during the water deprivation test, it was decided that the route of desmopressin administration at home should be modified. The conjunctival route was considered; however, it was dismissed because the owner would be medicating the bird alone and could not readily administer an accurate volume into the patient's small eyes. As such, the owner was trained in IM injections in birds and directed to administer 4.6 μg/kg (2.1 μg/lb), IM, every 12 hours. The owner was instructed to systematically change the location of the injection sites from day to day and use 29-gauge needles to minimize pectoral muscle irritation and injury. The desmopressin dosage was chosen empirically on the basis of the apparent safety and perceived suboptimal efficacy of the dose administered during the water deprivation test. The efficacy of that dose was considered suboptimal because maximal urine osmolality reached only 362 mOsm/kg, despite data suggesting that similarly sized birds have maximal urine concentrating abilities of 600 to 700 mOsm/kg.11 Additionally, an African Grey parrot with psychogenic polydipsia reportedly had an osmolality of 710 mOsm/kg at a comparable stage of dehydration.3

Over the following 2 weeks, the desmopressin dose was increased to 9.2 μg/kg (4.18 μg/lb), IM, every 12 hours. At this dosage, the bird had a noteworthy reduction in the frequency and volume of urine production for a period of 4 to 5 hours. It had a brighter mentation, and the mydriasis rapidly resolved. The owner estimated that total daily water consumption was approximately 200 mL, which was considerably lower than the approximately 1 L/d before parenteral administration of desmopressin was initiated. The bird continued to respond well to this dose over a period of 7 months, and the duration of action gradually increased to approximately 6 to 8 hours.

The bird was returned to the teaching hospital 8 months after the initial diagnosis of CDI was made. At this time, results of a physical examination, CBC, and plasma biochemical analysis were unremarkable. The bird was alert and neurologically healthy, with no generalized neurologic deficits or behavioral changes noticed upon examination or reported by the owner. The bird was discharged to the owner with instructions to continue administering the desmopressin at 9.2 μg/kg, IM, every 12 hours.

Sixteen months after the initial diagnosis of CDI was made, the bird was reexamined. At this time, the bird was receiving desmopressin at a dosage of 24 μg/kg (10.9 μg/lb), IM, every 12 hours owing to a gradual reduction in efficacy noticed over the preceding 7 months. The owner reported that the bird's clinical signs were well controlled on the higher dose. It was also reported that the owner occasionally chose not to medicate the bird; on those days, the bird had profound PUPD. Results of a CBC and plasma biochemical analysis performed during this examination were within reference limits. Findings of the physical examination were also unremarkable, with the exception of anisocoria with submaximal mydriasis in the right eye. Neurologic menace responses were present, and ocular motility was normal in both eyes. The pupillary light reflex was intact in the left eye and present, but markedly reduced, in the right eye.

A board-certified veterinary ophthalmologist confirmed the ocular findings and performed a complete ophthalmic examination. No additional abnormalities were detected in either eye by slit-lamp biomicroscopy, direct and indirect fundic examination, fluorescein corneal staining, and applanation tonometry. Cranial nerve function was also unremarkable. In light of these findings, a diagnosis of presumed right internal ophthalmoparesis was made, and use of advanced imaging modalities to investigate possible macroscopic causes of the bird's diabetes insipidus and internal ophthalmoparesis was discussed with the owner. Consultation with a board-certified radiologist suggested the most appropriate test would be a magnetic resonance imaging study conducted with a 4-Tesla unit and a specialized coil. This testing was declined owing to the lack of such a unit within a 3-hour drive of the teaching hospital. The bird was discharged to the owner's care with instructions to continue desmopressin administration at 24 μg/kg, IM, every 12 hours.

Follow-up telephone conversations over the subsequent 2 months revealed the bird's CDI continued to be well controlled on the higher dose of desmopressin prescribed during the last physical examination. The bird was drinking amounts of water comparable to those of the owner's other similarly sized parrots. The anisocoria remained stable, but no other neurologic signs developed.

Discussion

Profound polyuria and polydipsia are the hallmark clinical signs of diabetes insipidus in mammals. Central diabetes insipidus is characterized by the production of hyposmolar urine despite strong osmotic stimuli for ADH secretion, a rise in urine osmolality following the administration of exogenous antidiuretic hormone, and the absence of renal disease.4 The disease is considered rare in dogs4 and quite rare in cats, with approximately 15 cases reported in the peer-reviewed literature.12 To date, confirmed CDI has not been reported for any member of the class Aves.

In mammals, CDI can result from decreased production of ADH by the supraoptic and paraventricular nuclei of the hypothalamus or decreased release of ADH from the posterior pituitary gland secondary to neoplasia, trauma, inflammation, infection, or hypothalamopituitary malformations.4,12–14 Primary pituitary gland neoplasia is reportedly the most common cause of impaired ADH release in middle-aged to older animals.4,12 In addition to primary pituitary gland neoplasia, craniopharyngioma and meningioma can cause diabetes insipidus in dogs.13–16 Metastatic, traumatic, inflammatory, and parasitic lesions may also cause diabetes insipidus in dogs and cats.4 In humans and other animals, a certain proportion of CDI cases are considered idiopathic.10,17,18 In these cases, no apparent cause for the lack of ADH production or secretion has been found.

Arginine vasotocin is the avian analog of mammalian ADH and, as in mammals, is produced in the supraoptic and paraventricular nuclei of the hypothalamus and secreted from the posterior pituitary gland in response to osmotic and hypovolemic stimuli.19–22 The hormone has vascular and renal tubular antidiuretic effects that are mediated via V1 and V2 receptors, respectively.23–26 It is therefore likely that, in an analogous manner to the development of CDI in mammals, this condition may develop in birds because of diminished production of AVT by the supraoptic and paraventricular nuclei of the hypothalamus or because of decreased release of AVT from the posterior pituitary gland.

Although there have been several reports27–31 of birds with intracranial neoplasia and PUPD, a water deprivation and desmopressin response test was not performed in any of the affected birds, thus precluding the definitive diagnosis of CDI. It has been speculated that the PUPD observed among some birds with intracranial neoplasia may be the result of a growth hormone excess, decreased AVT production (ie, CDI), or excess production of ACTH.30–32 Several of the affected birds had concomitant or progressive central blindness with unilateral or bilateral mydriasis.28,30,31 Overt exophthalmos was also reported but was not a feature in all birds.

Intracranial neoplasms of birds include ependymal tumors and pituitary gland adenomas and adenocarcinomas of variable incidences, particularly in budgerigars.27–29 Ependymomas have been implicated in CDI in humans,26 and adenomas and adenocarcinomas reportedly cause the condition in cats, dogs, and humans.4,13,33 As such it is probable that several birds with PUPD and intracranial neoplasia reported in the literature did indeed have CDI.

When initially evaluated, the bird in this report had mydriasis that resolved after treatment with desmopressin at 9.2 μg/kg, IM, every 12 hours. The owner did not report subsequent ophthalmic abnormalities, and none were detected at the 8-month recheck. Assessment of avian pupils and the pupilary light reflex is hindered by conscious control of the iris attributable to the striated nature of the sphincter and dilator muscles of the pupil.34 However, the pupilary light reflex can be evaluated, particularly among birds that are acclimated to their environment and not overly excited.34 During the initial assessment of the parrot, the mydriasis persisted in all lighting conditions and was observed over a period of several hours. Additionally, the bird's owner reported that the condition was also evident in the bird's home environment. This latter observation reduced the likelihood of mydriasis secondary to a stress-induced state of heightened sympathetic tone. As such, it is speculated that the bilateral mydriasis reported by the owner and observed during the first and second examinations at the teaching hospital was due to increased sympathetic tone secondary to a hypovolemic state induced by untreated and then suboptimally treated CDI. This supposition is supported by the rapid and long-lasting resolution of the mydriasis once an appropriate dose of desmopressin was administered.

At the 16-month recheck examination, anisocoria was noticed by the attending veterinarian and confirmed by a veterinary ophthalmologist. This condition was characterized by right-sided mydriasis associated with a reduced pupillary light response and no detectable visual impairment. This lesion was deemed secondary to internal ophthamolparesis resulting from partial parasympathetic denervation of the iris because mechanical impairment or structural abnormalities of the iris were not detected during ophthalmic examination and the bird did not have a history of exposure to pharmacological agents or toxicants that could affect pupil function. This condition is uncommonly reported in veterinary medicine and develops secondary to incomplete paralysis of the intraocular muscles. Internal ophthalmoparesis is a sign of lower motor neuron dysfunction observed when there is disease of the parasympathetic nucleus of cranial nerve 3, the ciliary ganglion, or the pre- or postganglionic fibers of the parasympathetic fibers innervating the iris and ciliary body.35 An intracranial meningioma was associated with internal ophthalmoparesis in the absence of external ophthalmoplegia or paresis or cavernous sinus syndrome in 1 of the 4 reported cases of internal ophthalmoparesis in dogs.35 As such, it is possible that the development of internal ophthalmoparesis in the bird described in this report happened secondary to the growth of an intracranial neoplasm that was also responsible for the CDI. Unfortunately, this hypothesis could not be confirmed without more readily available advanced imaging techniques or gross necropsic and histologic evaluation. Consequently, the possibility of a congenital abnormality of the hypothalamo-pituitary axis, trauma, or previous inflammation or infection as the cause of CDI in our parrot cannot be ruled out.

In the bird of this report, a diagnosis of CDI was made on the basis of the profound PUPD in the absence of any of the common causes of PUPD in birds, as well as the bird's response to a water deprivation and desmopressin response test. It should be considered that urinalyses and urine osmolality measurements in birds are likely affected by the physiologic process whereby urine may flow via retrograde peristalsis from the urodeum into the coprodeum and distal portion of the colon.36 This process is believed to play an important role in water homeostasis through colonic absorption of water and sodium.36 It may lead to considerable differences between the osmolality of ureteral urine obtained by catheterization and from cage samples, particularly in conditions of dehydration. Indeed, in a study9 of dehydrated pigeons, urine from cage samples was 30% more concentrated than that obtained via ureteral canulization. That finding supports the diagnosis of CDI in the parrot by further accentuating the profoundly hyposmolar nature of urine voided during the first 145 minutes of the water deprivation test despite the presence of hyperosmolar plasma. The > 12-month follow-up period and the recurrence of clinical signs when the owner failed to administer the exogenous desmopressin represented additional evidence to support the diagnosis. In addition, the development of anisocoria, characterized by mydriasis and internal ophthalmoparesis of the right eye, after 16 months of follow-up strengthens the accuracy of the diagnosis by suggesting an intracranial lesion in the region of the hypophysis.

ABBREVIATIONS

ADH

Antidiuretic hormone

AVT

Arginine vasotocin

CDI

Central diabetes insipidus

PUPD

Polyuria and polydipsia

a.

DDAVP, Aventis Pharmaceuticals, Bridgewater, NJ.

b.

Tully TN, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, La: Unpublished data, 2009.

References

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    • Search Google Scholar
    • Export Citation
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    Pollock C. Diagnosis and treatment of avian renal disease. Vet Clin North Am Exot Anim Pract 2006;9:107128.

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    • Crossref
    • Search Google Scholar
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Contributor Notes

Drs. Starkey and Woods' present address is Center for Avian and Exotic Medicine, 568 Columbus Ave, New York, NY 10024.

Address correspondence to Dr. Starkey (srs45@cornell.edu).