Emergence of Rapid-Onset Ototoxicity Following Three Doses of Vancomycin: A Unique Case Report in the Context of Normal Renal Function and Therapeutic Dosing.

Vancomycin, a potent glycopeptide antibiotic renowned for its efficacy against methicillin-resistant Staphylococcus aureus, also harbors the potential for adverse reactions. While its use is often associated with infusion-related events and nephrotoxicity, ototoxicity has emerged as a noteworthy but rare concern. This adverse effect, characterized by a spectrum of transient to permanent hearing loss or damage, typically surfaces in patients receiving excessive doses, those undergoing concomitant therapy with other ototoxic agents such as aminoglycosides, or individuals with baseline hearing impairment or renal dysfunction. This report highlights the possibility of ototoxicity in the setting of normal renal function and therapeutic dosing. We report a case of a 58-year-old male patient with a complex medical history, who presented with sepsis, respiratory failure, and a constellation of underlying conditions. His treatment regimen encompassed intravenous vancomycin administration, which led to an unexpected development-severe-to-profound bilateral conductive and sensorineural hearing loss after three doses. The absence of concurrent ototoxic agents and Bayesian dosing software predicting an acceptable AUC/MIC ratio complicates the understanding of this adverse event. Amid this complex scenario, the case underscores the evolving landscape of vancomycin-induced ototoxicity, encouraging heightened vigilance, thorough audiometric monitoring, and an in-depth exploration of potential mechanisms underlying this adverse reaction. Early audiometric testing and referral to otolaryngology may allow for early intervention with high-dose steroids to mitigate the ototoxicity.

Evaluation of pulmonary artery banding in the setting of ventricular septal defects and severely elevated pulmonary vascular resistance.

BACKGROUND: Children with pulmonary hypertension secondary to large left-to-right, post-tricuspid valve shunts can eventually have severe and/or irreversible pulmonary vascular disease, yielding them inoperable for conventional surgery. It has been shown, however, that unloading of the pulmonary hypertension can result in remodeling of the pulmonary vasculature and, thus, improvement of the pulmonary hypertension. METHODS: This study explored whether such patients might experience a significant reduction in pulmonary vascular resistance (PVR) after pulmonary artery band (PAB) placement. Pulmonary hypertension hemodynamics were evaluated by cardiac catheterization in 4 patients with pulmonary hypertension secondary to nonrestrictive left-to-right, post-tricuspid valve shunts before and after PAB placement. Two patients with severe pulmonary hypertension who were considered high risk for conventional surgery benefited from PAB placement with a significant reduction in their PVR, permitting subsequent complete intracardiac repair. RESULTS: The medium-term follow-up for these 2 patients demonstrated good outcomes. The PVR failed to improve after PAB placement in the remaining 2 patients, leading to medical therapy for pulmonary hypertension. There was 1 late death, presumably related to pulmonary hypertension. Current practice provides 3 relatively unattractive options for patients with severe pulmonary hypertension secondary to nonrestrictive left-to-right, post-tricuspid valve shunts: transplantation, high-risk intracardiac repair, or palliative medical therapy. CONCLUSION: Our study suggests that a staged approach with initial PAB placement can be considered for select patients with large left-to-right, post-tricuspid valve shunts and high PVR prior to committing them to other high-risk therapeutic options.