Safe Return to Driving After Volar Plating of Distal Radius Fractures.

PURPOSE: A major concern for patients following distal radius fracture fixation is when they can resume driving. This decision has medical, legal, and safety considerations, but there are no evidence-based guidelines to assist the surgeon. The goal of this study was to observe when patients are capable of safely resuming driving following surgical fixation of the distal radius. METHODS: Patients undergoing volar plating of a distal radius fracture were prospectively enrolled. At approximately 2 and 4 weeks after surgery, patients were administered a driving examination on a closed course and given a subjective questionnaire including visual analog scale scores. All basic functions of vehicle operation were evaluated. Successful completion indicated they would pass a driving evaluation. RESULTS: Twenty-three patients were enrolled. Sixteen (69.5%) passed their first attempt (average of 18.4 days from surgery), another 4 (17.4%) passed their second attempt (31.3 days from surgery), and 3 did not complete the second examination. Patients who failed relied too much on their nonsurgical hand, were not able to control the steering wheel with 2 hands, and reported pain and insecurity when using the operative hand. Of those who passed the second attempt, the first failure was universally attributed to pain. Fifteen patients reported a return to independent driving prior to the first examination (average, 11.3 days). Of the 7 who failed, 6 reported they could control the car in an emergency, and 2 reported they would not feel safe with daily driving. Maximum pain while driving on the visual analog scale was 2.4 of 10 among those who failed compared with 1.3 among those who passed. CONCLUSIONS: Most patients could safely return to driving within 3 weeks of surgery. Pain was the primary limiting factor affecting driving ability. Safe return to driving may be warranted within 3 weeks of distal radius volar plate fixation in some patients. Persistent pain is likely the most important obstacle to a safe return to driving. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognostic IV.

Prostaglandin E2 protects murine lungs from bleomycin-induced pulmonary fibrosis and lung dysfunction.

Prostaglandin E(2) (PGE(2)) is a lipid mediator that is produced via the metabolism of arachidonic acid by cyclooxygenase enzymes. In the lung, PGE(2) acts as an anti-inflammatory factor and plays an important role in tissue repair processes. Although several studies have examined the role of PGE(2) in the pathogenesis of pulmonary fibrosis in rodents, results have generally been conflicting, and few studies have examined the therapeutic effects of PGE(2) on the accompanying lung dysfunction. In this study, an established model of pulmonary fibrosis was used in which 10-12-wk-old male C57BL/6 mice were administered a single dose (1.0 mg/kg) of bleomycin via oropharyngeal aspiration. To test the role of prostaglandins in this model, mice were dosed, via surgically implanted minipumps, with either vehicle, PGE(2) (1.32 µg/h), or the prostacyclin analog iloprost (0.33 µg/h) beginning 7 days before or 14 days after bleomycin administration. Endpoints assessed at 7 days after bleomycin administration included proinflammatory cytokine levels and measurement of cellular infiltration into the lung. Endpoints assessed at 21 days after bleomycin administration included lung function assessment via invasive (FlexiVent) analysis, cellular infiltration, lung collagen content, and semiquantitative histological analysis of the degree of lung fibrosis (Ashcroft method). Seven days after bleomycin administration, lymphocyte numbers and chemokine C-C motif ligand 2 expression were significantly lower in PGE(2)- and iloprost-treated animals compared with vehicle-treated controls (P < 0.05). When administered 7 days before bleomycin challenge, PGE(2) also protected against the decline in lung static compliance, lung fibrosis, and collagen production that is associated with 3 wk of bleomycin exposure. However, PGE(2) had no therapeutic effect on these parameters when administered 14 days after bleomycin challenge. In summary, PGE(2) prevented the decline in lung static compliance and protected against lung fibrosis when it was administered before bleomycin challenge but had no therapeutic effect when administered after bleomycin challenge.