The authors' results suggest that bacterial migration along the epidural catheter track is the most common route of epidural catheter colonization. Maintaining sterile skin around the catheter insertion site will reduce colonization of the epidural catheter tip.

Accumulated evidence suggests that the C-C motif chemokine ligand 5 (CCL5) modulates migration of inflammatory cells in several pathological conditions. This study tested the hypothesis that lack of CCL5 would modulate the recruitment of inflammatory cells to painful, inflamed sites and could attenuate pain in a murine chronic neuropathic pain model. Nociceptive sensitization, immune cell infiltration, multiple cytokine expression, and opioid peptide expression in damaged nerves were studied in wild-type (CCL5 +/+) and CCL5-deficient (CCL5 -/-) mice after partial sciatic nerve ligation (PSNL). Results indicated that CCL5 -/- mice had less behavioral hypersensitivity after PSNL. Macrophage infiltration and proinflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and interferon-γ) in damaged nerves following PSNL were significantly decreased in CCL5 -/- mice. Conversely, several antiinflammatory cytokine (IL-4 and IL-10) proteins were significantly increased in CCL5 -/- animals and the expression of enkephalin, β-endorphin, and dynorphin mRNA was significantly lower than in wild-type control mice. These results represent the first evidence that CCL5 is capable of regulating the pathway that controls hyperalgesia at the level of the peripheral injured site in a murine chronic neuropathic pain model. We demonstrated that lack of CCL5 modulated cell infiltration and the proinflammatory milieu within the injured nerve. Attenuated behavioral hypersensitivity in CCL5 -/- mice observed in the current study could be a result of decreased macrophage infiltration, mobilization, and functional ability at injured sites. Collectively, the present study results suggest that CCL5 receptor antagonists may ultimately provide a novel class of analgesics for therapeutic intervention in chronic neuropathic pain.

Hypothermic preconditioning induces an acute phase of neuroprotection. This neuroprotection depends on activation of the signaling molecules, adenosine A1 receptors, KATP channels, and Ras. Inhibition of putatively damaging proteins via the effects of hypothermic preconditioning on high-mobility group I(Y) expression may also be involved in hypothermic preconditioning-induced neuroprotection.

Relapsing polychondritis (RP) is a rare disease that is characterized by recurrent inflammation and destruction of cartilage and connective tissues. RP can have significant airway pathology that may require procedures to maintain airway patency and thus may have serious implications for anesthesiologists. Anesthesiologists must be prepared to deal with the possible complications that may occur during airway manipulation in patients with RP. Here, we present a case of life-threatening bilateral tension pneumothorax and tension pneumoperitoneum that developed after a tracheal tear during Montgomery T-tube insertion in a patient with tracheal stenosis due to RP. Correct diagnosis was delayed due to a misdiagnosis of airway obstruction. As a result, we emphasize that bilateral tension pneumothorax should be considered during refractory cardiac arrest in patients with increased airway pressure. A high index of suspicion and adequate management are mandatory for patients to survive these life-threatening complications.