Citations

Purpose The purposes of this study were to determine the frequency of acute and subacute complications (within 6 months) of arthroscopic knee procedures in patients aged 17 years or younger and to determine associated risk factors. Methods We identified all patients aged 17 years or younger who underwent arthroscopic knee procedures at our institution from 1997 to 2009. Patient demographic and surgical data were collected from the medical and surgical records, with specific focus on intraoperative and postoperative complications. Results During the study period, 1,002 knee arthroscopies were reviewed. The overall complication rate was 14.7%. Major complications occurred in 21 surgeries (2.1%) and included the following: septic arthritis (n = 3, 0.3%), wound complication requiring operative revision (n = 9, 0.9%), arthrofibrosis requiring manipulation (n = 4, 0.4%), other unplanned subsequent surgery (n = 4, 0.4%), and death (n = 1, 0.1%). Surgeries with an anesthesia time of 265 minutes or greater ( P = .026), operative time of 220 minutes or greater ( P = .013), or tourniquet time of 114 minutes or greater ( P < .001) and surgeries with 3 or more Current Procedural Terminology codes ( P = .003) had a statistically significant increase in risk of major complications. The incidence of minor complications was 12.6%, which included persistent effusion/hemarthrosis requiring arthrocentesis (n = 59, 5.9%) and superficial wound infection (n = 18, 1.8%). Conclusions Major complications after knee arthroscopy in children and adolescents are rare, but minor complications are more common. If possible, surgeons should avoid prolonged anesthesia, surgery, and tourniquet times. The pediatric patient's medical and family history should be reviewed to identify important risk factors. Level of Evidence Level IV, therapeutic case series.

Abstract Cancer-associated inflammation is a molecular key feature in pancreatic ductal adenocarcinoma. Oncogenic KRAS in conjunction with persistent inflammation is known to accelerate carcinogenesis, although the underlying mechanisms remain poorly understood. Here, we outline a novel pathway whereby the transcription factors NFATc1 and STAT3 cooperate in pancreatic epithelial cells to promote KrasG12D-driven carcinogenesis. NFATc1 activation is induced by inflammation and itself accelerates inflammation-induced carcinogenesis in KrasG12D mice, whereas genetic or pharmacologic ablation of NFATc1 attenuates this effect. Mechanistically, NFATc1 complexes with STAT3 for enhancer–promoter communications at jointly regulated genes involved in oncogenesis, for example, Cyclin, EGFR and WNT family members. The NFATc1–STAT3 cooperativity is operative in pancreatitis-mediated carcinogenesis as well as in established human pancreatic cancer. Together, these studies unravel new mechanisms of inflammatory-driven pancreatic carcinogenesis and suggest beneficial effects of chemopreventive strategies using drugs that are currently available for targeting these factors in clinical trials. Significance: Our study points to the existence of an oncogenic NFATc1–STAT3 cooperativity that mechanistically links inflammation with pancreatic cancer initiation and progression. Because NFATc1–STAT3 nucleoprotein complexes control the expression of gene networks at the intersection of inflammation and cancer, our study has significant relevance for potentially managing pancreatic cancer and other inflammatory-driven malignancies. Cancer Discov; 4(6); 688–701. ©2014 AACR. This article is highlighted in the In This Issue feature, p. 621