Determination of ChloraPrep® drying time before neuraxial anesthesia in elective cesarean delivery. A prospective observational study.

BACKGROUND: ChloraPrep® is a skin antiseptic commonly used before neuraxial anesthesia. It is believed that skin must be allowed to dry to prevent nerve damage by seeding ChloraPrep® solution into the neuraxis. We aimed to determine ChloraPrep® drying time in pregnant women before initiation of neuraxial anesthesia. METHODS: In 18 parturients undergoing elective cesarean delivery the skin 'wetness' after standardized ChloraPrep® application was prospectively assessed by blotting the skin with tissue paper and observing for residual orange tint. The isopropyl alcohol drying time was indirectly assessed by measuring the alcohol vapor concentration above the skin with a volatile organic compound analyzer. The primary outcome was the time measured from the end of skin preparation until tissue paper was no longer stained with orange tint. The secondary outcome was the time measured from the end of skin preparation until an abrupt reduction of isopropyl alcohol vapor concentration indicating that no further significant evaporation of alcohol was occurring. RESULTS: The mean ChloraPrep® drying time assessed by blotting the skin with tissue paper was 123 s (SD 32 s, 95% CI 107 to 140 s, range 85-195 s). The estimated isopropyl alcohol drying time was 82 s (95% CI 77.4 to 86.3 s). CONCLUSION: Our results suggest that ChloraPrep® drying time may be longer than the current manufacturer-recommended guideline of three minutes. The amount of ChloraPrep® used, application methods, patient characteristics, and environmental factors could influence the drying time.

Deep hypothermia therapy attenuates LPS-induced microglia neuroinflammation via the STAT3 pathway.

Deep hypothermia therapy (HT) is a standard method for neuroprotection during complex pediatric cardiac surgery involving extracorporeal circulation and deep hypothermic cardiac arrest. The procedure, however, can provoke systemic inflammatory response syndrome (SIRS), one of the most severe side effects associated with pediatric cardiac surgery. To date, the cellular inflammatory mechanisms induced by deep HT remain to be elucidated. Therefore, we investigated the effects of deep HT (17°C) and rewarming on the inflammatory response in lipopolysaccharide (LPS) stimulated BV-2 murine microglia. Additionally, we also investigated the application of Stattic, a signal transducer and activator of transcription 3 (STAT3) activation inhibitor, as an alternative to physical cooling to attenuate the LPS-induced inflammatory response. Deep HT had no cytotoxic effect but attenuated microglia migration. IκBα degradation was delayed by deep HT resulting in the attenuation of pNF-κB p65 migration into the nucleus and significant decreases in pro-inflammatory IL-6, TNF-α, and MCP-1 expressions and secretions, as well as decreased anti-inflammatory IL-10 and SOCS3 expressions. Additionally, pStat3 was significantly down regulated under deep hypothermic conditions, also corresponding with the significant reduction in IL-6 and TNF-α expressions. Similar to the effects of HT, the application of Stattic under normothermic conditions resulted in significantly reduced IL-6 and TNF-α expressions. Moreover, attenuation of the inflammatory response resulted in decreased apoptosis in a direct co-culture of microglia and neurons. HT reduces the inflammatory response in LPS-stimulated BV-2 microglial cells, alluding to a possible mechanism of therapeutic hypothermia-induced neuroprotection. In the future, attenuating the phospho-STAT3 pathway may lead to the development of a neuroprotectant with greater clinical efficacy.