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Background: Impacts of delivery modes on the subsequent risk of coronary heart disease (CHD) in pregnant women have not been elucidated., Materials and Methods: Data of women who had undergone cesarean delivery (CD cohort) or vaginal delivery (VD cohort) between January 2000 and December 2012 from Taiwan Health Insurance Database were analyzed. All subjects were tracked until December 31, 2013. For women with multiple deliveries, only the first delivery data were included. Study end point was the diagnosis of new-onset CHD after delivery., Results: In total, 51,765 subjects (CD cohort: n = 17,839; VD cohort: n = 33,926) were included. During 1-14 years of follow-up, the incidence rate of new-onset CHD in the CD cohort was significantly higher than in the VD cohort (1.3% [231/17,839] vs. 0.8% [257/33,926], p < 0.001; effect size: 0.30). Analysis revealed that the subsequent risk of CHD in the CD cohort was significantly higher than in the VD cohort (adjusted hazard ratio [HR] = 1.28, 95% confidence intervals [CI]: 1.06-1.55, p = 0.012). We performed sensitivity tests by excluding subjects who had undergone CD due to nonmedical reasons from the CD cohort. The remaining subjects were named as the *CD cohort. Analysis also revealed a higher subsequent risk of CHD in the *CD cohort than in the VD cohort (adjusted HR = 1.32, 95% CI: 1.08-1.60, p = 0.006)., Conclusions: Women who had undergone primary CD, especially those who had undergone CD due to medical reasons, were associated with an ∼30% higher risk of CHD than those who had undergone VD.

Characteristic signs of malignant hyperthermia (MH) include unexplained tachycardia, increased end-tidal carbon dioxide (Etco₂) concentration, metabolic and respiratory acidosis, and an increase in body temperature above 38.8°C. We present the case of a patient with highly probable MH. In addition to sinus tachycardia and metabolic and respiratory acidosis, this patient also had a negative arterial to Etco₂ gradient and an increased requirement for minute ventilation to maintain a normal Etco₂ concentration, with signs of increased CO₂ production. Despite these signs of MH, the patient's rectal temperature monitoring equipment did not show an increase in temperature, although the temperature measured in the mouth was increased. This case illustrates the unreliability of measuring rectal temperature as a means of reflecting body temperature during MH and the usefulness of increased CO₂ production signs in helping to diagnose MH., (Copyright © 2014. Published by Elsevier B.V.)

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., (Copyright © 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.)

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.

We report an 82-year-old male patient who developed complete atrioventricular block (CAVB) with severe bradycardia 1 hour after craniotomy. After emergency placement of a transvenous pacemaker, the patient's heart rate was restored. Serial assays of serum cardiac enzymes, echocardiography and serum digoxin concentration did not show evidence of myocardial infarction, myocardial injury, or drug toxicity. Tracing back past history, neither syncope nor arrhythmia of any form was noted. A neurogenic heart disorder, high vagal tone, and aging possibly contributed to this cardiac event in this patient. CAVB, although uncommon, is a disastrous complication following craniotomy, and needs aggressive and instantaneous management.

Background: The authors conducted this prospective study to determine the incidence, potential routes, and risk factors of microbial colonization of epidural catheter used for postoperative pain control., Methods: Two-hundred five patients with epidural analgesia for postoperative pain were studied. On removal of the catheter, five samples were sent for culture: the infusate, a swab from inside the hub of the epidural catheter connector, a swab from the skin around the catheter insertion site, the subcutaneous segment, and the tip of the catheter. Clinical data related to the catheter insertion, management, and general patient conditions were collected., Results: The positive culture rates for the subcutaneous and tip segments of the catheter were 10.5% and 12.2%, respectively. The most common organism in the culture was coagulase-negative staphylococcus. There was a strong linear relationship between bacterial colonization in the skin around the catheter insertion site and growth from the subcutaneous and tip segments of catheter (P = 0.000). Catheter-related events at ward, blood transfusion, and positive culture from the skin at the insertion site were risk factors for bacterial colonization of epidural catheters. Inflammation at catheter insertion site, catheter indwelling time, and level of catheter insertion were not predicators for epidural catheter colonization., Conclusions: 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.

Background: A period of hypothermia before ischemia (hypothermic preconditioning) induces a delayed phase of ischemic tolerance in rat brain. However, whether hypothermic preconditioning induces an acute phase (within a few hours after the hypothermia) of ischemic tolerance remains unknown. This study was designed to determine the time window of the hypothermic preconditioning-induced acute phase of neuroprotection, which is useful information for situations during surgery with anticipated ischemic episodes, and its involved mechanisms., Methods: Survival of Purkinje cells in rat cerebellar slices was evaluated after a 20-min oxygen-glucose deprivation (OGD, in vitro simulated ischemia) followed by a 4-h recovery. Mild hypothermia (33 degrees C) for 20 min was applied at various times before the OGD., Results: The hypothermia applied immediately to 3 h before the OGD equally effectively reduced OGD-induced Purkinje cell death/injury. Glibenclamide, a selective KATP channel blocker; 8-cyclopentyl-1,3-dipropylxanthine, a selective adenosine A1 receptor antagonist; and farnesyl protein transferase inhibitor III, a selective inhibitor to reduce Ras farnesylation, abolished hypothermic preconditioning-induced neuroprotection when applied during the hypothermia. OGD increased the expression of high-mobility group I(Y) proteins, which are nuclear transcription factors to enhance the expression of putatively damaging proteins such as cyclooxygenase-2, in cerebellar slices. This increase was attenuated by hypothermic preconditioning., Conclusions: 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.