Background: Results of ACTH stimulation test (ACTHst), pre- and post-trilostane serum cortisol concentrations (SCCs), urine concentration (urine-specific gravity [USG]), and urine cortisol : creatinine ratios (UCCRs) are common variables used to monitor trilostane treatment of dogs with pituitary-dependent hyperadrenocorticism (PDH). However, none has consistently discriminated dogs receiving an adequate dose (A) from those overdosed (O) or underdosed (U). Objectives: To assess and compare recommended monitoring variables, including serial SCCs in a cohort of dogs with PDH treated with trilostane. Animals: Privately owned dogs with PDH (n = 22) and 3 healthy dogs (controls). Methods: Prospective, multicenter, 2-day study. On day “a” (randomized): ACTHst was completed. Day “b” (>2 to <7 days later): SCCs were assessed −0.5 hours, immediately before, and 1, 2, 2.5, 3, 3.5, 4, 6, 8, and 12 hours after trilostane administration. On the first study day, urine collected at home was assessed for USG, UCCR and owner opinions regarding PDH were categorized as: A (clinical signs resolved), U (remains symptomatic), or ill (possible O). Results: At 27 pairs of evaluations, 7 dogs were categorized as A, 19 U, and 1 possible O (excluded from the study). There was overlap in SCC results from the A and U dogs at every time point. Results of USG, UCCR, and ACTHst did not discriminate A from U dogs. Trilostane suppresses SCC within 1 hour of administration and its duration of action in most PDH dogs is <8 hours. Conclusions and Clinical Importance: No single variable or group of variables reliably discriminated A dogs from U dogs during trilostane treatment for PDH.

To compare survival in dogs with recurrent or metastatic insulinomas that were treated with palliative therapy, alone or in combination with toceranib phosphate and to assess tolerability of the co...

Background Systemic hypertension (SH) is common in dogs with hyperadrenocorticism (HAC) however there are not many studies assessing its prevalence and risk factors. Objectives To determine the prevalence and severity of SH in dogs with HAC and its association with clinical and laboratory findings to identify potential risk factors. Animals Sixty‐six client owned dogs with spontaneous HAC. Methods Retrospective cross‐sectional study. Medical records of dogs with HAC were reviewed. Systolic blood pressure (SBP) was measured using Doppler ultrasonography. Clinical signs, physical examination findings and clinicopathologic data (CBC, serum biochemistry and electrolytes, urinalysis and urinary culture, and adrenal function tests) were reviewed for analysis. Results Prevalence of SH (≥150 mm Hg) was 82% (54/66) and prevalence of severe SH (≥180 mm Hg) was 46% (30/66). All dogs with thrombocytosis had SH (P = .002), and a platelet count ≥438 × 10³/μL was 100% specific and 61.1% sensitive to predict SH (AUC = .802, P = .001). Median potassium levels were lower in hypertensive dogs (4.1 mEq/L, range 3.1‐5.4 mEq/L) than in normotensive ones (4.5 mEq/L, range 4.0‐5.0 mEq/L) (P = .007). Dogs with UPC ≥ 0.5 had higher median SBP than those without proteinuria (P = .03). Dogs with concurrent diabetes mellitus seemed to have a reduced risk of SH (OR = .118, 95%CI = .022‐.626, P = .02). Conclusions and Clinical Importance Systemic hypertension is common in dogs with HAC and is frequently severe. Blood pressure should be routinely assessed in these dogs, especially if thrombocytosis, proteinuria or low potassium concentrations are present.

Background Systemic hypertension (SH) is common in dogs and humans with hypercortisolism and can persist after treatment. Objectives To evaluate changes in prevalence of SH and systolic blood pressure (SBP) in dogs with pituitary‐dependent hyperadrenocorticism (PDH) during the first year of trilostane treatment, its relationship with disease control and selected laboratory variables, and their response to antihypertensive treatment. Animals Fifty‐one dogs with PDH treated with trilostane Q12h. Methods Prospective case series study. Dogs were evaluated at diagnosis (T0) and 1, 3, 6, and 12 months (T12). Dogs were classified as nonhypertensive (SBP < 160 mm Hg) or hypertensive (SBP≥160 mm Hg) and subclassified according to target organ damage (TOD) risk. Hypertensive dogs were treated with benazepril and, if control of SH was not achieved, amlodipine was added. Results Prevalence of SH decreased from T0 (36/51) to T12 (17/37; P = .01). Changes in SBP during the study were influenced by the risk of TOD at T0. In severely hypertensive (SBP ≥ 180 mm Hg) dogs, the decrease in SBP was more pronounced whereas in normotensive (SBP < 140 mm Hg) dogs SBP increased slightly (P = .00). Blood pressure was not associated with disease control. Antihypertensive treatment was needed in 31/51 dogs, and in 13/31 dogs additional SH control with amlodipine was required. One third of nonhypertensive dogs at T0 required treatment with benazepril because SH developed during follow‐up. Conclusions and Clinical Importance In dogs with PDH, SBP should be measured at every visit, regardless of disease control or SBP at diagnosis. More than 1 drug may be necessary to manage SH in affected dogs.

The incidence of surgical site infection (SSI) following mastectomy in female dogs remains poorly characterized, despite its relevance to postoperative outcomes and patient welfare. This retrospective cohort study aimed to determine the incidence of SSI and identify associated clinical and surgical risk factors in dogs undergoing mastectomy procedures at a veterinary teaching hospital between 2013 and 2022. SSI diagnosis was based on the Centers for Disease Control (CDC) criteria and identified structured passive surveillance of medical records. Univariate logistic regression was carried out to screen for potential risk factors, followed by multivariate analysis of selected variables. Among 376 mastectomy procedures performed in 306 dogs, 33 SSIs were detected, resulting in an overall incidence of 8.8% (95% CI: 6.1–12.1). The majority were superficial infections (93.9%), with only two cases classified as deep SSI; no organ/space infections were recorded. Prolonged anaesthesia duration (p = 0.041) and intraoperative hypothermia (p = 0.026) were independently associated with increased SSI risk. These findings indicate that the incidence of SSI after canine mastectomy is comparable to that reported for other clean surgeries. Prolonged anaesthesia and hypothermia represent modifiable risk factors, highlighting the importance of perioperative temperature control and optimized anaesthetic management. No significant associations were observed with patient-related variables, mastectomy type, or wound soaker catheter use, supporting its safe inclusion in multimodal analgesia.