Trauma‐induced central diabetes insipidus in a cat

Abstract

ERRATUMThis case report was originally published in the AVJ in December 2005 ( Aust Vet J 2005;83:732 -735), but the units for deamino-8-D-arginine vasopressin (DDAVP) were incorrectly given in milligrams instead of micrograms. The paper is reprinted here in full with the correct units for DDAVP. Here a case of trauma-induced central DI in a cat and successful long-term treatment with parenteral DDAVP is described. Trauma-induced central diabetes insipidus in a cat Case reportA 1-year-old neutered male domestic shorthair cat was referred with a 4 week history of polydipsia that began immediately following a fall from an 8 m balcony. Veterinary attention was not sought at the time of the accident because, although mentation was depressed for several minutes, the cat's desire and capacity to consume water over the following hours was perceived by the owner to preclude any serious injury.Daily water intake measured by the owner for 13 consecutive days prior to presentation ranged between 900 and 1500 mL (average 1135 mL/day). Appetite was unchanged and the diet consisted predominantly of commercial tinned food supplemented with a commercial dry food and raw kangaroo meat.Upon presentation, the cat was bright and in good body condition (body condition score 6 out of 9; 9 body weight 6.2 kg). Physical examination, including complete neurological examination, was unremarkable. Urine collected by manual expression of the urinary bladder revealed no chemical abnormalities (Mulitsticks, Bayer) and USG determined by hand-held refractometer was 1.008. Haematological analysis was unremarkable. Biochemical parameters, including electrolytes, were within the reference ranges for normal cats with the exception of mild elevations in albumin (42 g/dL; reference range 27 to 38 g/dL) and alkaline phosphatase (57 IU/L; reference range < 51 IU/L). The following day a complete abdominal ultrasound examination was performed and was unremarkable. Urine was collected by antepubic cystocentesis and repeat urinalysis and urine culture was performed (Medicine and Microbiology Laboratory, University of Queensland). The urine was hyposthenuric (urine specific gravity [USG] 1.004) but otherwise unremarkable.Diabetes insipidus was suspected and a modified water deprivation test was performed (Figure 1).

Central diabetes insipidus following cardiopulmonary arrest in a dog

“…CDI in dogs and cats has been uncommonly reported. Documented causes include neoplasia, pituitary cysts, and inflammatory conditions, and there have been several case reports of CDI post TBI in dogs and cats , . Foley et al described a complex of hypothalamic‐pituitary deficiency secondary to TBI in a 12‐week‐old Great Dane puppy .…”

“…In addition, there are reports of CDI associated with traumatic brain injury (TBI) in dogs and cats. 1,[13][14][15][16][17][18][19][20] In this report, we describe a case of transient partial CDI in an 8-week-old dog that likely incurred ischemic brain injury post cardiopulmonary arrest (CPA) and successful resuscitation.…”

Probable primary polydipsia in a domestic shorthair cat

“…4 NDI can be primary (familial) or secondary (acquired) in dogs; however, no cases of primary NDI have been reported in cats. 2,13 Secondary NDI is caused by renal or metabolic disorders that interrupt the normal interaction of AVP with its tubular receptors in the kidney, disrupt renal tubular function or result in loss of the hypertonic renal medullary interstitial gradient. 4 Several diseases, such as hyperadrenocorticism, 17 pyometra, 18 pyelonephritis, 4 hyperthyroidism 19 and hyperaldosteronism 20 can lead to secondary NDI in the cat.…”

Hypothalamic‐pituitary axis deficiency following traumatic brain injury in a dog

“…Traumatic diabetes insipidus (DI), hypoadrenocorticism, hypothyroidism, growth hormone (GH) deficiency, and sex hormone deficiency have all been reported 1 . There are only a few reports of HPA dysfunction following TBI in the veterinary literature 2–5 . This is the first report of a dog with suspected traumatic panhypopituitarism.…”

“…1 There are only a few reports of HPA dysfunction following TBI in the veterinary literature. [2][3][4][5] This is the first report of a dog with suspected traumatic panhypopituitarism.…”