ObjectiveTo report the development of a tension pneumomediastinum during mechanical ventilation of a young Irish Wolfhound with aspiration pneumonia.Case SummaryA 9‐month‐old intact female Irish Wolfhound was presented for clinical signs consistent with aspiration pneumonia. Evaluation of her pedigree and clinical signs prompted suspicion of Irish Wolfhound rhinitis bronchopneumonia syndrome as a contributing factor. Despite supportive care for bronchopneumonia, progressive hypoxemia and increased work of breathing required mechanical ventilation (MV). Development of a pneumothorax 36 hours after initiation of MV necessitated bilateral thoracostomy tubes. Cardiovascular decline persisted despite resolution of the pneumothorax and 1 hour later the dog was humanely euthanized. On necropsy, severe pneumomediastinum was identified without other evidence of barotrauma. Necropsy results suggested tension pneumomediastinum as the cause of pneumothorax and cardiovascular deterioration.New or Unique Information ProvidedPneumomediastinum has not been described in dogs receiving MV. This case highlights the importance of rapid detection of pneumomediastinum during MV, as the complication can quickly become life‐threatening.
The pharmacokinetics of dantrolene and its active metabolite, 5-hydroxydantrolene, after a single oral dose of either 5 mg/kg or 10 mg/kg of dantrolene were determined. The effects of exposure to dantrolene and 5-hydroxydantrolene on activated whole blood gene expression of the cytokines interleukin-2 (IL-2) and interferon-γ (IFN-γ) were also investigated. When dantrolene was administered at a 5 mg/kg dose, peak plasma concentration (Cmax) was 0.43 µg/ml, terminal half-life (t1/2) was 1.26 hrs, and area under the time-concentration curve (AUC) was 3.87 µg hr/mL. For the 10 mg/kg dose, Cmax was 0.65 µg/ml, t1/2 was 1.21 hrs, and AUC was 5.94 µg hr/mL. For all calculated parameters, however, there were large standard deviations and wide ranges noted between and within individual dogs: t1/2, for example, ranged from 0.43 to 6.93 hrs, Cmax ratios ranged from 1.05 to 3.39, and relative bioavailability (rF) values ranged from 0.02 to 1.56. While activated whole blood expression of IL-2 and IFN-γ as measured by qRT-PCR was markedly suppressed following exposure to very high concentrations (30 µg/mL and 50 µg/mL, respectively) of both dantrolene and 5-hydroxydantrolene, biologically and therapeutically relevant suppression of cytokine expression did not occur at the much lower drug concentrations achieved with oral dantrolene dosing.
Objective: Evaluate the clinical utility of the systemic inflammatory response syndrome (SIRS) criteria in dogs and cats presenting to an emergency room (ER).
A 5-month-old male intact Great Pyrenees was presented for an acute onset of severe neurologic signs (stupor, absent menace, intermittent head turn to the left). The patient's history included possible naproxen ingestion with a maximum ingested dose of 59 mg/kg, exceeding the reported dose of >50 mg/kg known to cause neurologic signs. Blood sampling for baseline bloodwork was performed, and intravenous lipid emulsion (ILE) was subsequently administered, for treatment of the suspected toxicosis. Due to severe and life-threatening neurologic signs, other methods of decontamination were contraindicated and unlikely to be effective; extracorporeal therapy was also unavailable. Complete resolution of neurologic signs occurred 30 min after completion of ILE therapy. At this time, the owners found the missing naproxen tablets after returning home and the bloodwork results returned revealing findings consistent with hepatic encephalopathy. The fasted blood ammonia concentration immediately prior to ILE administration was 702.1 μg/dL (reference interval, RI: 24–36 μg/dL) and decreased to 194.1 μg/dL 24 h later. In the first 24 h, the patient also received three doses of lactulose, N-acetylcysteine, and intravenous fluids. The patient was subsequently diagnosed with a single, large intrahepatic portosystemic shunt via computed tomography and underwent an endovascular coil embolization procedure. Given the rapid and dramatic improvement in severe neurologic signs after ILE therapy alone, it is strongly suspected that this treatment resulted in improvement of hepatic encephalopathy.
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