Diagnosis and treatment of canine hypoadrenocorticism

Canine hypoadrenocorticism (Addison’s disease), the ‘great pretender’ of internal medicine, is a disease that should be frequently considered as a differential diagnosis of several clinical presentations, albeit it is less commonly the actual cause of the clinical signs. Hypoadrenocorticism cannot be diagnosed on clinical signs alone and further investigations are always required. There have been some interesting new ideas about diagnostic options for this condition and new treatment options are available for both acute and chronic therapy of the condition in dogs. It is therefore pertinent to review the causes, diagnosis and treatment of hypoadrenocorticism in dogs

Hypoadrenocorticism in an aged cat

A 13-year-old, female, neutered, domestic longhair cat was referred to the hospital with a two-month history of fluctuating weakness, lethargy, inappetence and intermittently soft stools. Physical examination noted variable mentation, mild tachycardia with poor pulse quality and a body condition score of 1/9. In-house haematology and biochemistry abnormalities included a mild neutrophilia, hyponatraemia, and decreased Na:K ratio of 24 and isosthenuric urine (1.012). The cat was admitted to the hospital for intravenous fluid therapy and management of its electrolyte abnormalities. A low basal cortisol (36 nmol/l) was found on analysis of a stored serum sample, and further investigations confirmed the diagnosis of hypoadrenocorticism. Treatment was implemented initially with hydrocortisone and dexamethasone and continued long term with desoxycorticosterone pivalate and oral prednisolone. More than one year since diagnosis, the cat is clinically well and stable on treatment

Combined atypical primary hypoadrenocorticism and primary hypothyroidism in a dog

A dog with combined atypical primary hypoadrenocorticism and primary hypothyroidism is described. The dog presented with waxing and waning, vague complaints since more than a year and had been treated with several drugs without complete resolution of signs. Based on the abnormalities on physical examination, blood examination and abdominal ultrasonography, atypical primary hypoadrenocorticism and primary hypothyroidism were diagnosed. Glucocorticoid supplementation was started and gradually tapered to maintenance rate because of polydipsia. Ten days later, levothyroxine supplementation was started at a very low dose and was gradually increased based on serum total thyroxine concentrations. The dog rapidly improved and recovered completely. Follow-up over a one-year period did not reveal new abnormalities. The presence of combined primary hypoadrenocorticism and primary hypothyroidism has been infrequently described in dogs and may resemble the Schmidt's syndrome in humans

Restored vision in a young dog following corticosteroid treatment of presumptive hypophysitis

Background: Hypophysitis is an umbrella term for a group of disorders involving inflammation of the pituitary gland. A rare occurrence in humans, hypophysitis can produce a range of clinical signs including (but not limited to) visual deficits and diabetes insipidus. Only five cases of canine hypophysitis exist in the literature, all presenting in mature dogs with no visual deficits and a grave outcome. This case report describes the clinical and advanced imaging features of blindness-inducing presumptive hypophysitis in a dog, which rapidly resolved with medical management. Case presentation: A 1-year-and-seven-month-old neutered male Standard Poodle presented with subacute blindness, ataxia, and polyuria/polydipsia (PUPD). Magnetic resonance imaging (MRI) detected a contrast-enhancing pituitary mass with perilesional oedema compromising the optic chiasm. Suspecting neoplasia, anti-inflammatory corticosteroid was commenced prior to radiation therapy planning. Complete resolution of neurological and visual deficits occurred within 12 days of starting steroid treatment. Repeated advanced imaging indicated macroscopic resolution of the lesion. An extended thyroid panel with insulin-like growth factor-1 analysis supported a diagnosis of hypophysitis. Resolution of PUPD was achieved with tapering courses of prednisolone and desmopressin; the dog has since been clinically normal for 14 months and treatment-free for 11 months. Conclusions: To the authors’ knowledge, this is the first instance in which a canine pituitary mass has demonstrated long-term resolution with palliative medical treatment alone, alongside reversal of associated blindness and presumptive diabetes insipidus. We suspect this lesion to be a form of hypophysitis, which should be included among differential diagnoses for pituitary masses, and for subacute blindness in dogs. Where possible, we advocate biopsy-confirmation of hypophysitis prior to timely intervention with anti-inflammatory treatment

Osmotic Demyelination Syndrome after Primary Hypoadrenocorticism Crisis Management

Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineralocorticoids, which leads to electrolyte disorders associated with hyponatremia and hyperkalemia. These disorders can cause hypotension, hypovolemia and shock, putting a patient's life at risk if inadequate hydroelectrolytic supplementation and hormone replacement is provided. Nevertheless, rapid sodium chloride supplementation is contraindicated due to the risk of central pontine myelinolysis induction. The present study aims to describe a thalamic osmotic demyelination syndrome after management of a primary hypoadrenocorticism crisis in a 2-year-old, female West White Highland Terrier. Case: The patient had a presumptive diagnosis of hypoadrenocorticism already receiving oral prednisolone and gastrointestinal protectants in the last 2 days. After prednisolone dose reduction the dog presented a severe primary hypoadrenocorticism crisis treated with intravenous sodium chloride 0.9% solution along with supportive therapy. Four days after being discharged from the hospital, the patient showed severe neurological impairment and went back to the clinic where a neurological examination revealed mental depression, drowsiness, ambulatory tetraparesis and proprioceptive deficit of the 4 limbs, postural deficits, and cranial nerves with decreased response. Due to these clinical signs, a magnetic resonance imaging was performed. It showed 2 intra-axial circular lesions, symmetrically distributed in both thalamus sides, with approximately 0.8 cm in diameter each without any other anatomical changes on magnetic resonance imaging. The images were compatible with metabolic lesions, suggesting demyelination. Furthermore, liquor analysis did not show relevant abnormalities, except for a slight increase in density and pH at the upper limit of the reference range. After treatment, the patient had a good neurological evolution secondary to standard primary hypoadrenocorticism treatment, without sequelae. Discussion: In the present case report, primary hypoadrenocorticism gastrointestinal signs seemed to be triggered by a food indiscretion episode, not responsive to the symptomatic therapies employed. The patient´s breed and age (young West White Highland Terrier bitch) is in accordance with the demographic profile of patients affected by the disease, where young females are frequently more affected. Regarding the probable thalamic osmotic demyelination syndrome documented in this case, is important to notice that myelinolysis or demyelination is an exceedingly rare noninflammatory neurological disorder, initially called central pontine myelinolysis, which can occur after rapid correction of hyponatremia. It has already been observed in dogs after correction of hyponatremia of different origins, including hypoadrenocorticism and parasitic gastrointestinal disorders. Currently, the terms "osmotic myelinolysis" or “osmotic demyelination syndrome" are considered more suitable when compared to the term "central pontine myelinolysis" since it has been demonstrated in dogs and humans the occurrence of demyelination secondary to the rapid correction of hyponatremia in distinct regions of the central nervous system including pons, basal nuclei, striatum, thalamus, cortex, hippocampus and cerebellum. The present case report emphasizes the difficulties for hormonal confirmation of primary hypoadrenocorticism in a patient already on corticosteroid treatment, as well as proposes that the current term osmotic demyelination syndrome replace the term “central pontine myelinolysis” in veterinary literature related to the management of hypoadrenocorticism crisis.Keywords: Addison Syndrome, hyponatremia, osmotic myelinolysis, magnetic resonance imaging

Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management

Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions, and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineralocorticoids, which leads to electrolyte disorders associated with hyponatremia and hyperkalemia. These disorders can cause hypotension, hypovolemia and shock, putting a patient’s life at risk if inadequate hydroelectrolytic supplementation and hormone replacement is provided. Nevertheless, rapid sodium chloride supplementation is contraindicated due to the risk of central pontine myelinolysis induction. The present study aims to describe a thalamic osmotic demyelination syndrome after management of a primary hypoadrenocorticism crisis in a 2-year-old, female West White Highland Terrier. Case: The patient had a presumptive diagnosis of hypoadrenocorticism already receiving oral prednisolone and gastrointestinal protectants in the last 2 days. After prednisolone dose reduction the dog presented a severe primary hypoadrenocorticism crisis treated with intravenous sodium chloride 0.9% solution along with supportive therapy. Four days after being discharged from the hospital, the patient showed severe neurological impairment and went back to the clinic where a neurological examination revealed mental depression, drowsiness, ambulatory tetraparesis and proprioceptive deficit of the 4 limbs, postural deficits, and cranial nerves with decreased response. Due to these clinical signs, a magnetic resonance imaging was performed. It showed 2 intra-axial circular lesions, symmetrically distributed in both thalamus sides, with approximately 0.8 cm in diameter each without any other anatomical changes on magnetic resonance imaging. The images were compatible with metabolic lesions, suggesting demyelination. Furthermore, liquor analysis did not show relevant abnormalities, except for a slight increase in density and pH at the upper limit of the reference range. After treatment, the patient had a good neurological evolution secondary to standard primary hypoadrenocorticism treatment, without sequelae. Discussion: In the present case report, primary hypoadrenocorticism gastrointestinal signs seemed to be triggered by a food indiscretion episode, not responsive to the symptomatic therapies employed. The patient´s breed and age (young West White Highland Terrier bitch) is in accordance with the demographic profile of patients affected by the disease, where young females are frequently more affected. Regarding the probable thalamic osmotic demyelination syndrome documented in this case, is important to notice that myelinolysis or demyelination is an exceedingly rare noninflammatory neurological disorder, initially called central pontine myelinolysis, which can occur after rapid correction of hyponatremia. It has already been observed in dogs after correction of hyponatremia of different origins, including hypoadrenocorticism and parasitic gastrointestinal disorders. Currently, the terms “osmotic myelinolysis” or “osmotic demyelination syndrome” are considered more suitable when compared to the term “central pontine myelinolysis” since it has been demonstrated in dogs and humans the occurrence of demyelination secondary to the rapid correction of hyponatremia in distinct regions of the central nervous system including pons, basal nuclei, striatum, thalamus, cortex, hypoppocampus, and cerebelum. The present case report emphasizes the difficulties for hormonal confirmation of primary hypoadrenocorticism in a patient already on corticosteroid treatment, as well as proposes that the current term osmotic demyelination syndrome replace the term “central pontine myelinolysis” in veterinary literature related to the management of hypoadrenocorticism crisis