Early childhood general anesthesia exposure associated with later developmental delay: A national population-based cohort study.

Exposure to general anesthesia has been reported to induce neurotoxicity, impair learning, memory, attention, motor functions, as well as affect behavior in adult rodents and nonhuman primates. Though many have speculated similar effects in humans, previous literature has shown conflicting findings. To investigate the differences in risk of developmental delay among young children exposed to general anesthesia compared to matched unexposed individuals, a population-based cohort study was conducted with a longitudinal dataset spanning 2000 to 2013 from the Taiwan National Health Insurance Research Database (NHIRD). Procedure codes were used to identify children who received anesthesia. For each exposed child, two unexposed children matched by gender and age were enrolled into the comparison cohort. Neurocognitive outcome was measured by the presence of ICD-9-CM codes related to developmental delay (DD). Cox regression models were used to obtain hazard ratios of developing DD after varying levels of anesthesia exposure. After excluding 4,802 individuals who met the exclusion criteria, a total of 11,457 children who received general anesthesia before two years of age was compared to 22,914 children (matched by gender and age) unexposed to anesthesia. Increased risk of DD was observed in the exposure group with a hazard ratio (HR) of 1.320 (95% CI 1.143-1.522, P < 0.001). Subgroup analysis demonstrated further elevated risks of DD with multiple anesthesia exposures (1 anesthesia event: HR 1.145, 95% CI 1.010-1.246, P = 0.04; 2 anesthesia events: HR 1.476, 95% CI 1.155-1.887, P = 0.005; ≥3 anesthesia events: HR 2.222, 95% CI 1.810-2.621, P < 0.001) and longer total anesthesia durations (Total anesthesia <2 hours: HR 1.124, 95% CI 1.003-1.499, P = 0.047; Total anesthesia 2-4 hours: HR 1.450, 95% CI 1.157-1.800, P = 0.004; Total anesthesia > 4 hours: HR 1.598, 95% CI 1.343-1.982, P < 0.001) compared with children unexposed to anesthesia. These results suggest that children exposed to general anesthesia before two years of age have an increased risk of DD. This risk is further elevated with increased frequency of anesthesia, and longer total anesthesia duration. The findings of this study should prompt clinical practitioners to proceed with caution when assessing young patients and planning managements involving procedures requiring general anesthesia.

Extensive spinal cord ischemia following endovascular repair of an infrarenal abdominal aortic aneurysm: a rare complication.

Postoperative paraplegia secondary to spinal cord ischemia (SCI) is an extremely rare and devastating complication of endovascular repair in abdominal aortic aneurysm (AAA) surgery. The reported incidence is only 0.21 % worldwide. This case of postoperative paraplegia occurred in a 60-year-old man immediately following endovascular repair of an infrarenal AAA. Postoperative magnetic resonance imaging showed multiple foci of SCI involvement from C5 to L1. However, neither cerebral spinal fluid drainage nor steroid therapy was effective; he was eventually admitted with no improvement in his neurological status. The mechanism remains multifactorial until now and needs more attention in perioperative management. We report the first case involved in the most significantly extensive SCI after endovascular repair of an infrarenal AAA.

Ultra-low-dose naloxone enhances the antinociceptive effect of morphine in PTX-treated rats: regulation on global histone methylation.

OBJECTIVE: Epigenetic reprogramming may have a possible role in neuropathic pain development; the present study examined the global patterns of lysine histone modification. In this serial study we analyzed the levels of histone 3 lysine 4 monomethylation, histone 3 lysine 4 dimethylation, and histone 3 lysine 9 trimethylation in pertussis toxin (PTX)-induced thermal hyperalgesic rat spinal cords. METHODS: Male Wistar rats implanted with an intrathecal catheter received a single intrathecal PTX (1 µg in 5 µl saline) injection. Four days later, they were randomly assigned to receive either a single injection of saline, or ultra-low-dose naloxone (15 ng in 5 µl saline), followed by morphine (10 µg in 5 µl saline) injection 30 minutes later. RESULTS: The results showed that PTX injection induced thermal hyperalgesia and significant increase of global histone methylation in the spinal cords. Intrathecal morphine alone did not affect the thermal hyperalgesia and global histone methylation. In contrast, intrathecal administration of ultra-low-dose naloxone plus morphine significantly attenuated the PTX-induced thermal hyperalgesia and down-regulated the global histone methylation. CONCLUSION: The results suggest that ultra-low-dose naloxone might be clinical valuable for neuropathic pain management via regulating global histone modification.