Multimodal Pain Control Reduces Narcotic Use after Outpatient Abdominoplasty: Retrospective Analysis in an Ambulatory Surgery Practice.

Despite dominating fewer headlines, the opioid epidemic continues to plague society. Surgeons have the responsibility to change their opioid prescribing habits while maintaining adequate patient comfort. This study examines the transition to a multimodal, perioperative protocol in an ambulatory surgery setting for abdominoplasty patients. We hypothesized that using multimodal analgesia could significantly reduce narcotic consumption. Methods: The authors retrospectively compared one surgeon's consecutive abdominoplasty patients over 24 months. The control group received primarily narcotic medications to manage pain, and the treatment cohort was given a multimodal protocol for perioperative analgesia. Results: Demographic data, surgical time, and postanesthesia care unit time between the groups were similar. Although the mean intravenous narcotic decreased in the operating room and postanesthesia care unit for the treatment group, it failed to achieve statistical significance. The treatment cohort was prescribed two-thirds less oral narcotic than the control (251 versus 787 mean morphine milligram equivalents P < 0.001). Ten patients in the treatment cohort used no oral narcotics compared to one in the control (P = 0.002), and only four narcotic refills were given in the treatment group compared to 36 in the control (P < 0.001), suggesting that the treatment group had better pain control despite taking fewer narcotics. Conclusions: Optimally utilizing multimodal medications effectively reduces narcotic consumption while effectively managing postoperative pain from abdominoplasty in a private practice, ambulatory surgery setting. Surgeons must change their prescribing habits if we are going to make progress in the war against the opioid crisis.

Hearing loss caused by CMV infection is correlated with reduced endocochlear potentials caused by strial damage in murine models.

Congenital cytomegalovirus (CMV) infection is a significant cause of neonatal hearing loss. However, at the cochlear level, the anatomical lesions and pathophysiological mechanisms that underlie hearing loss are still not clearly understood. In murine models of CMV infection, we have observed early damage to the capillary networks in stria vascularis, as well as hearing loss manifested in ABR threshold elevations. Our experimental hypothesis is that strial damage causes a reduced endocochlear potential (EP) resulting in impaired haircell activation and consequent hearing loss. We have studied strial damage, EP, and ABR threshold elevations in two mouse models (BALB/c and C57BL6 strains) infected with murine CMV. Neonatal (P3) pups were inoculated with murine CMV (2µl of 200pfu) by intra cerebral injection. Control mice were saline injected. At 6 weeks, ABR thresholds to tonal stimuli at 8, 16 and 32 kHz were determined for each ear. At 8 weeks a sub-group of treated and control animals was prepared for study of cochlear capillary networks using scanning electron microscopy of corrosion cast specimens. In a second group, at 8 weeks, EP measurements from both cochleas were made. We report that in both mouse strains, CMV infection caused capillary loss in the stria vascularis, initially at the cochlear apex, and extending to lower cochlear turns in some subjects. After CMV infection, in both BALB/c and C57BL6 mice, reduced EPs and ABR threshold elevations were observed, and there was a within-animal correlation between loss of EP and ABR threshold elevations across the sound frequencies tested. These results suggest that CMV induced damage to stria vascularis results in EP reduction that is correlated with ABR threshold elevations. Extrapolating to the human condition, we suggest that strial damage and its physiological consequences may contribute to the initial hearing loss in congenital CMV infection. The early involvement of cochlear capillary damage may encourage a focus on therapeutic interventions that can prevent vascular damage, or subsequently promote vascular healing or angiogenesis.

Effects of ganciclovir treatment in a murine model of cytomegalovirus-induced hearing loss.

OBJECTIVE: To determine whether ganciclovir (GCV) treatment reduces sensorineural hearing loss in cytomegalovirus (CMV)-infected mice. The effects of GCV on viral load, absolute neutrophil count (ANC), and outer hair cell (OHC) integrity were also investigated. METHODS: Infected BALB/c mice were inoculated with murine CMV on postnatal day 3. Those treated with GCV received an intraperitoneal injection twice a day for 14 days. Auditory thresholds were assessed using distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) testing 4 weeks after inoculation. Temporal bones were used for determination of viral load by quantitative polymerase chain reaction and hair cell quantification by scanning electron microscopy. ANCs were completed by an automated hematology analyzer, with manual review for confirmation. RESULTS: GCV-treated CMV-infected mice had lower ABR (P < 0.0001, Kruskal-Wallis test) and DPOAE (P < 0.0001) thresholds compared to CMV-infected untreated mice, indicating that GCV protected mice from CMV-induced hearing loss. Viral load in infected populations undergoing GCV treatment was significantly decreased (P = 0.03) relative to untreated mice. GCV treatment alone had no effect on ABR and DPOAE compared to untreated, uninfected controls (P = 0.1, P = 0.24, respectively). GCV-treated mice received increased protection from OHC loss when compared to untreated groups, with total OHC losses of approximately 7% and 14%, respectively (P < 0.05). Neutropenia was absent after 7 days of GCV treatment. CONCLUSION: Ganciclovir effectively ameliorated SNHL and partially protected from OHC loss in a preclinical model of congenital CMV infection, seemingly by reducing viral load. LEVEL OF EVIDENCE: NA Laryngoscope, 130:1064-1069, 2020.

Role of Free Radical Formation in Murine Cytomegalovirus-Induced Hearing Loss.

OBJECTIVES: The goal of the study was to determine whether reactive oxygen species (ROS) mediates cytomegalovirus (CMV)-induced labyrinthitis. STUDY DESIGN: Murine model of CMV infection. SETTING: University of Utah laboratory. SUBJECTS AND METHODS: Nrf2 knockout mice were inoculated with murine CMV. Auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAEs) were then performed on these and uninfected controls. BALB/c mice were inoculated with murine CMV to determine whether a marker for ROS production, dihydroethidium (DHE), is expressed 7 days after inoculation. Finally, 2 antioxidants-D-methionine and ACE-Mg (vitamins A, C, and E with magnesium)-were administered 1 hour before and after infection in inoculated mice for 14 days. Temporal bones were harvested at postnatal day 10 for DHE detection. ABR and DPOAE testing was done at postnatal day 30. Scanning electron microscopy was also performed at postnatal day 30 to evaluate outer hair cell integrity. RESULTS: Nrf2-infected mice had worse hearing than uninfected mice (P < .001). A statistically significant increase in DHE fluorescence was detected in BALB/c-infected mice as compared with uninfected mice 7 days after inoculation. D-methionine- and ACE-Mg-treated mice demonstrated an attenuation of the DHE fluorescence and a significant improvement in ABR and DPOAE thresholds when compared with untreated infected controls (P < .0001). Scanning electron microscopy demonstrated less outer hair cell loss in the treated versus untreated infected controls. CONCLUSION: These results demonstrate for the first time that excessive ROS mediates CMV-induced hearing loss in a mouse model.