Ergonomics in the OR: An Electromyographic Evaluation of Common Muscle Groups Used During Simulated Flexible Ureteroscopy - a Pilot Study.

OBJECTIVE: To assess the effects of different surgeon positions and ureteroscope types on muscle activation as measured by surface electromyography (sEMG) during simulated ureteroscopy in an endourology box-trainer model and the kidney phantom. METHODS: For this exploratory study, sEMG was used to quantify muscle activation of 3 endourology fellows during various ureteroscopic tasks. Electrodes were placed on the ureteroscope-holding side of the following muscles: thenar, forearm flexor, forearm extensor, biceps, triceps, deltoid, and trapezius. Subjects wore fitted lead aprons in an operating room and used a cystoscopy table with surgical drapes and an endoscopic video tower. Trials were completed with a disposable and reusable ureteroscope, both in the standing and sitting positions. Each subject performed an identical set of tasks in a phantom silicone kidney and ureteroscopy box trainer to recreate the procedural components of basketing, navigating a renal collecting system, and dusting. Raw EMG data for each task was processed and normalized as a percent of each subject's maximum voluntary contraction to allow comparison. RESULTS: The forearm extensor was the most heavily utilized muscle. The trapezius and deltoid muscles were activated more during sitting whereas the forearm flexors had increased activity during standing. The heavier reusable ureteroscope had increased forearm extensor activation compared to the disposable ureteroscope. CONCLUSION: Preliminary data show measurable differences in muscle activation based on both surgical posture and type of ureteroscope used. This highlights the need for more extensive EMG studies to identify techniques and equipment to optimize ergonomics and potentially minimize injury during flexible ureteroscopy.

Genetic neutrophil deficiency ameliorates cerebral ischemia-reperfusion injury.

Neutrophils respond rapidly to cerebral ischemia and are thought to contribute to inflammation-mediated injury during stroke. Using myeloid Mcl1 knockout mice as a model of genetic neutrophil deficiency, we investigated the contribution of neutrophils to stroke pathophysiology. Myeloid Mcl1 knockout mice were subjected to transient middle cerebral artery occlusion and infarct size was assessed by MRI after 24h reperfusion. Immune cell mobilization and infiltration was assessed by flow cytometry. We found that myeloid Mcl1 knockout mice had significantly reduced infarct size when compared to heterozygous and wild type control mice (MyMcl1+/+: 78.0mm3; MyMcl1+/-: 83.4mm3; MyMcl1-/-: 55.1mm3). This was accompanied by a nearly complete absence of neutrophils in the ischemic hemisphere of myeloid Mcl1 knockout mice. Although myeloid Mcl1 knockout mice were protected from cerebral infarction, no significant differences in neurological deficit or the mRNA expression of inflammatory genes (TNFα, IL-1ß, and MCP1) were detected. Inhibition of neutrophil chemotaxis using CXCR2 pepducin treatment partially reduced neutrophil mobilization and recruitment to the brain after stroke, but did not reduce infarct size 24h after transient MCA occlusion. These data confirm that neutrophils have an important role in infarct development during stroke pathophysiology, and suggest that complete deficiency, but not partial inhibition, is necessary to prevent neutrophil-mediated injury during stroke.