Perioperative care can be provided for children with SMA safely and effectively with total intravenous or inhaled anesthetics along with the judicious use of opioids to improve patient comfort without increased morbidity. Further prospective studies of standardized anesthetic and perioperative respiratory medical management in this population are required to minimize the decompensation of tenuous preoperative respiratory function.

The administration of ketamine with concurrent noxious stimulation results in the attenuation of the neuroapoptotic response. These findings suggest that concurrent surgery and procedural pain attenuates ketamine-induced neuroapoptosis.

Clinical observation suggests that the number of serious epidural catheter-associated infections have increased recently in children. This increase is likely attributed to an increase in reporting and in frequency of epidural analgesia usage. Estimates of infection rates are difficult to determine primarily because of insufficient study of large pediatric populations. In this retrospective study, the authors investigated the incidence of epidural catheter-associated soft tissue and epidural infections after use of continuous epidural analgesia spanning 17 yr. A total of 10,653 epidural catheters were used in 7,792 children. The majority of catheters, 10,437 (98%), were placed for the management of postoperative pain, and 216 (2%) were placed for the management of chronic pain. The authors identified 13 cases of infections (nine cellulitis, two paravertebral musculature infections, one epidural inflammation, and one epidural abscess) between 3 and 11 days after catheter insertion. The incidence of infection was significantly higher in patients treated for chronic pain (7 of 216 = 3.2%) compared with postoperative pain (6 of 10,437 = 0.06%; P < 0.0001). Surgical drainage of subcutaneous pus was performed in three patients, and medical therapy was administered in the remainder of patients; all patients recovered without sequelae. Although rare, epidural catheter-associated infections remain a serious concern in high-risk children who may benefit the most from epidural analgesia. The findings of the authors support the low rate of epidural infection previously reported despite growing concerns of serious infections in children. These findings highlight the importance of vigilance to early diagnostic indicators of infection and provide practitioners and families with incidence data to guide informed medical decision-making.

Background Delayed cerebral ischemia remains a common and profound risk factor for poor outcome after subarachnoid hemorrhage (SAH). The aim of our current study is to define the role of endothelial nitric oxide synthase (eNOS) in isoflurane conditioning‐induced neurovascular protection after SAH. Methods and Results Ten‐ to 14‐week‐old male wild‐type mice (C57BL/6) as controls and eNOS knockout male mice (strain # 002684) were obtained for the study. Animals underwent either sham surgery, SAH surgery, or SAH with isoflurane conditioning. Anesthetic post conditioning was performed with isoflurane 2% for 1 hour, 1 hour after SAH. Normothermia was maintained with the homeothermic blanket. In a separate cohort, nitric oxide synthase was inhibited by a pan nitric oxide synthase inhibitor, L‐nitroarginine methyl ester. Vasospasm measurement was assessed 72 hours after SAH and neurological function was assessed daily. Isoflurane‐induced changes in the eNOS protein expression were measured. eNOS protein expression was significantly increased by isoflurane conditioning in naïve mice as well as mice subjected to SAH. Vasospasm of the middle cerebral artery and neurological deficits were evident following SAH versus sham surgery, both in wild‐type mice and eNOS knockout mice. Isoflurane conditioning attenuated vasospasm and neurological deficits in wild‐type mice. This delayed cerebral ischemia protection was lost in L‐nitroarginine methyl ester ‐administered mice and eNOS knockout mice. Conclusions Our data indicate isoflurane conditioning provides robust protection against SAH‐induced vasospasm and neurological deficits, and that this delayed cerebral ischemia protection is critically mediated via isoflurane‐induced augmentation of eNOS.

Aneurysmal subarachnoid hemorrhage is a devastating condition causing significant morbidity and mortality. While outcomes from subarachnoid hemorrhage have improved in recent years, there continues to be significant interest in identifying therapeutic targets for this disease. In particular, there has been a shift in emphasis toward secondary brain injury that develops in the first 72 hours after subarachnoid hemorrhage. This time period of interest is referred to as the early brain injury period and comprises processes including microcirculatory dysfunction, blood-brain-barrier breakdown, neuroinflammation, cerebral edema, oxidative cascades, and neuronal death. Advances in our understanding of the mechanisms defining the early brain injury period have been accompanied by improved imaging and nonimaging biomarkers for identifying early brain injury, leading to the recognition of an elevated clinical incidence of early brain injury compared with prior estimates. With the frequency, impact, and mechanisms of early brain injury better defined, there is a need to review the literature in this area to guide preclinical and clinical study.