RESUMO
Study's aims were to characterize subclinical bacteriuria (SB) and sporadic bacterial cystitis (SBC) in dogs with spontaneous hypercortisolism (HC). Prospective cross-sectional design divided patients as newly diagnosed (nâ¯=â¯27), poorly controlled (n â¯=â¯21), well controlled (n â¯=â¯34), and controls (n â¯=â¯19). Urine culture positive results were identified by MALDI-TOF and submitted to antibiogram. Escherichia coli was the most common microorganism (36%). The majority of positive cultures in HC were SB (12.2%). All 4.1% SBC cases were in well controlled HC cases. Bacteriuria correlated with low urine specific gravity and low lymphocyte count. HC degree of control correlated with leukocyturia. SB/SBC cases were treated based in antimicrobial susceptibility leading to microbiological cure in 75% of HC cases. Persistent infections occurred only in SB cases, all by E. coli which became more resistant. SB/SBC prevalence in canine HC is actually lower. Further evidence for current ISCAID guideline contraindication for SB treatment due to HC were provided.
Assuntos
Bacteriúria , Síndrome de Cushing , Cistite , Doenças do Cão , Infecções Urinárias , Animais , Bacteriúria/epidemiologia , Bacteriúria/veterinária , Estudos Transversais , Síndrome de Cushing/veterinária , Cistite/epidemiologia , Cistite/veterinária , Doenças do Cão/tratamento farmacológico , Doenças do Cão/epidemiologia , Cães , Escherichia coli , Estudos Prospectivos , Infecções Urinárias/veterináriaRESUMO
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.