Development of a self-directed sinonasal surgical anatomy video curriculum: Phase 1 validation.

BACKGROUND: Sinusitis is a common outpatient diagnosis made by physicians and is a reason for referral to otolaryngologists. A foundation in basic sinonasal anatomy is critical in understanding sinus pathophysiology and avoiding complications. Our objective in this study was to develop and to validate a self-directed surgical anatomy video for medical students. METHODS: Two multimedia videos were developed highlighting sinonasal anatomy. In Video 1 we included audio narration and radiologic imaging. Video 2 incorporated highlighted images from a sinus surgery video. An assessment was developed to test sinonasal anatomy landmarks, spatial recognition of structures, and their clinical relevance. An expert panel of rhinologists scored face and content validity of the curriculum videos and assessment. Factor analysis was used to separate questions into face and content validity domains, and a one-sample t test was performed. RESULTS: The panel scored face validity (Videos 1 and 2: 4.4/5) and content validity (Video 1: 4.5/5, 0.83; Video 2: 4.3/5, 0.75) significantly higher than a neutral response. There were no statistical differences for face or content validity between videos. The assessment was rated suitable (29%) or very suitable (57%) for testing basic sinonasal surgical anatomy, and the majority (71%) of respondents agreed (14%) or strongly agreed (57%) that the assessment thoroughly covered the sinus anatomy content with which medical students should be familiar. CONCLUSION: We have developed two videos and an assessment that highlight and test sinonasal anatomy. Future studies will aim to identify whether the use of a self-directed video curriculum improves sinonasal anatomy awareness and whether incorporation of surgical endoscopic videos augments training.

Pediatric hereditary angioedema: what the otolaryngologist should know.

PURPOSE OF REVIEW: To review pediatric hereditary angioedema for otolaryngologists, with emphasis on articles within the past 12-18 months. RECENT FINDINGS: Biologic therapies are accepted for adult hereditary angioedema (HAE), but have been studied less for pediatric HAE. Recent literature supports expanded use of biologic agents in pediatrics as acute treatment and prophylaxis. Available agents include plasma-derived C1 esterase inhibitors (C1-INH) (Berinert, Haegarda, Cinryze), recombinant C1-INH (Ruconest), bradykinin B2 receptor inhibitor (Icatibant), and kallikrein inhibitors (Ecallantide and lanadelumab). Of these, only Berinert is Food and Drug Administration (FDA) approved for acute therapy for children under 12 years of age. Ruconest is approved for treatment of acute attacks over age 13. Ecallantide also has FDA approval as acute treatment for age 12 and older, while lanadelumab and Haegarda are prophylactic agents for adolescents. Icatibant lacks FDA approval in patients under 18 years of age. Cinryze has FDA approval only for prophylaxis for children as young as 6 years old. SUMMARY: Pediatric HAE is a potentially life-threatening disease. Targeted biologic agents have gained acceptance in treatment of acute attacks, and their use as prophylactic agents is changing the focus of management from acute intervention to preventive management. While intubation or surgical airway management may still be necessary, early intervention or prophylaxis can decrease morbidity and improve quality of life.

Nodular Lymphocyte-Predominant Hodgkin Lymphoma in Progressive Transformation of Germinal Centers.

Nodular lymphocyte-predominant Hodgkin lymphoma is an uncommon variant of Hodgkin lymphoma. Progressive transformation of germinal centers has been associated with and can develop prior to, concurrent with, or after the diagnosis of nodular lymphocyte-predominant Hodgkin lymphoma. We present a patient with a history of progressive transformation of germinal centers of the right parotid who presented 4 years later with ipsilateral parotid mass and cervical adenopathy. Knowledge of her previous diagnosis raised our concern for lymphoma, influenced our surgical management, and spared the patient additional surgery with risk of facial nerve injury inherent in revision parotidectomy.

Tumor necrosis factor-alpha and apoptosis signal-regulating kinase 1 control reactive oxygen species release, mitochondrial autophagy, and c-Jun N-terminal kinase/p38 phosphorylation during necrotizing enterocolitis.

BACKGROUND: Oxidative stress and inflammation may contribute to the disruption of the protective gut barrier through various mechanisms; mitochondrial dysfunction resulting from inflammatory and oxidative injury may potentially be a significant source of apoptosis during necrotizing enterocolitis (NEC). Tumor necrosis factor (TNF)-alpha is thought to generate reactive oxygen species (ROS) and activate the apoptosis signal-regulating kinase 1 (ASK1)-c-Jun N-terminal kinase (JNK)/p38 pathway. Hence, the focus of our study was to examine the effects of TNF-alpha/ROS on mitochondrial function, ASK1-JNK/p38 cascade activation in intestinal epithelial cells during NEC. RESULTS: We found (a) abundant tissue TNF-alpha and ASK1 expression throughout all layers of the intestine in neonates with NEC, suggesting that TNF-alpha/ASK1 may be a potential source (indicators) of intestinal injury in neonates with NEC; (b) TNF-alpha-induced rapid and transient activation of JNK/p38 apoptotic signaling in all cell lines suggests that this may be an important molecular characteristic of NEC; (c) TNF-alpha-induced rapid and transient ROS production in RIE-1 cells indicates that mitochondria are the predominant source of ROS, demonstrated by significantly attenuated response in mitochondrial DNA-depleted (RIE-1-rho) intestinal epithelial cells; (d) further studies with mitochondria-targeted antioxidant PBN supported our hypothesis that effective mitochondrial ROS trapping is protective against TNF-alpha/ROS-induced intestinal epithelial cell injury; (e) TNF-alpha induces significant mitochondrial dysfunction in intestinal epithelial cells, resulting in increased production of mtROS, drop in mitochondrial membrane potential (MMP) and decreased oxygen consumption; (f) although the significance of mitochondrial autophagy in NEC has not been unequivocally shown, our studies provide a strong preliminary indication that TNF-alpha/ROS-induced mitochondrial autophagy may play a role in NEC, and this process is a late phenomenon. METHODS: Paraffin-embedded intestinal sections from neonates with NEC and non-inflammatory condition of the gastrointestinal tract undergoing bowel resections were analyzed for TNF-alpha and ASK1 expression. Rat (RIE-1) and mitochondrial DNA-depleted (RIE-1-rho) intestinal epithelial cells were used to determine the effects of TNF-alpha on mitochondrial function. CONCLUSIONS: Our findings suggest that TNF-alpha induces significant mitochondrial dysfunction and activation of mitochondrial apoptotic responses, leading to intestinal epithelial cell apoptosis during NEC. Therapies directed against mitochondria/ROS may provide important therapeutic options, as well as ameliorate intestinal epithelial cell apoptosis during NEC.