Complications after a median sternotomy incision, which is used currently in most open heart surgery, are serious, although it is infrequent. Reconstruction of the sternal defect resulting from dehiscence of median sternotomy is still big challenge to the most plastic surgeons. Since vascularized greater omentum was transposed to eliminate mediastinal wound problems, many vascularized regional muscle flaps became mainstay in reconstruction of median sternotomy wound. We treated 13 patients with median sternotomy dehiscence between October of 1993 and March of 1998. In two patients, the wound problems were so confined to superficial tissue that debrided and closed primarily. Eleven patients with deep wound infection were managed with vigorous debridement of all necrotic tissues and resultant defects were covered with regional muscle flaps: rectus myocutaneous flap(3) and bilateral pectoralis advancement flap(8). We used the pectoralis major advancement flaps without counter incision at humeral insertion site and the dissections were limited only medial to the anterior axillary line to preserve the axillary fold. In five patients with larger defects, we elevated muscle and cutaneous flaps separately to make these flaps more mobile. Large portion of two rectus abdominis flaps could not survive, whereas pectoralis advancement flaps had mo special wound problems. Only one patient developed fistula due to remained wire, regardless to flap surgery.
Debridement ; Fistula ; Humans ; Omentum ; Rectus Abdominis ; Sternotomy* ; Thoracic Surgery ; Wound Infection ; Wounds and Injuries

PURPOSE: Myotonic dystrophy, also known as dystrophia myotonica (DM), is an autosomal dominant disorder with 2 genetically distinct forms. DM type 1 (DM1) is the more common form and is caused by abnormal expansion of cytosine/thymine/guanine (CTG) repeats in the DM protein kinase (DMPK) gene. Our study aimed to determine whether the age of onset is correlated with CTG repeat length in a population of pediatric patients with DM1. METHODS: We retrospectively identified 30 pediatric patients with DM1 that underwent DMPK testing, of which the clinical data of 17 was sufficient. The cohort was divided into 2 subgroups based on the clinical phenotype (congenital-onset vs. late-onset) and number of CTG repeats ( < 1,000 vs. ≥1,000). RESULTS: We found no significant difference between the age of onset and CTG repeat length in our pediatric patient population. Based on clinical subgrouping, we found that the congenital-onset subgroup was statistically different with respect to several variables, including prematurity, rate of admission to neonatal intensive care unit, need for respiratory support at birth, hypotonia, dysphagia, ventilator dependence, and functional status on last visit, compared to the late-onset subgroup. Based on genetic subgrouping, we found a single variable (poor feeding in neonate) that was significantly different in the large CTG subgroup than that in the small CTG subgroup. CONCLUSION: Clinical variables exhibiting statistically significant differences between the subgroups should be focused on prognosis and designing tailored management approaches for the patients; our findings will contribute to achieve this important goal for treating patients with DM1.
Age of Onset ; Cohort Studies ; Deglutition Disorders ; Genetic Association Studies ; Genotype ; Humans ; Infant, Newborn ; Intensive Care, Neonatal ; Muscle Hypotonia ; Myotonic Dystrophy ; Myotonin-Protein Kinase ; Parturition ; Phenotype ; Prognosis ; Retrospective Studies ; Ventilators, Mechanical

PURPOSE: The purpose of this study is to suggest predictive ultrasonographic finding of papillary thyroid microcarcinoma (PTMC) with lymph node metastasis (LNM), compared to PTMC without LNM. MATERIALS AND METHODS: This study included 93 patients (79 women, 14 men; mean age 46.0 +/- 10.6 years) with surgically proven PTMC. Twenty patients had LNM and 73 patients did not have LNM on surgical specimens. The following ultrasonographic characteristics were evaluated: tumor location, size, shape, echogenicity, margin, presence of calcification, and presence of capsular abutment. Univariate analysis and multivariable stepwise logistic regression analysis were performed for comparison of these characteristics in regard to the presence of LNM in order to determine predictors of LNM. RESULTS: Two factors were significantly related to LNM: presence of capsular abutment (p = 0.0011) and tumor size (cutoff value: > or = 5 mm, p = 0.0058). Lateral lymph node metastasis (LLNM) showed a significant association with macrocalcification (p = 0.015), presence of capsular abutment (p = 0.0104), tumor size (cutoff value: > or = 7 mm, p = 0.002), and upper location of thyroid nodule (p= 0.0255). Presence of capsular abutment was an independent predictive factor for LNM (Odds ratio: 14.83, p = 0.010). Tumor size was an independent predictive factor for LLNM (Odds ratio: 2.102, p = 0.010). CONCLUSION: Presence of capsular abutment and tumor size are important ultrasonographic predictors for LNM or LLNM in patients with PTMC.
Carcinoma, Papillary ; Female ; Humans ; Logistic Models ; Lymph Nodes ; Neoplasm Metastasis ; Thyroid Gland ; Thyroid Neoplasms ; Thyroid Nodule

Radiofrequency ablation (RFA) is a new, minimally invasive modality that serves as an alternative to surgery in patients with thyroid tumors. The Task Force Committee of the Korean Society of Thyroid Radiology developed recommendations for the optimal use of RFA for thyroid tumors in 2012 and revised them in 2017. Herein, we review and summarize the 2017 thyroid RFA guideline and compare it with the 2012 thyroid RFA guideline.
Advisory Committees ; Catheter Ablation ; Humans ; Thyroid Gland ; Thyroid Neoplasms ; Thyroid Nodule ; Ultrasonography

Objective: To compare core needle biopsy (CNB) and repeat fine-needle aspiration (rFNA) to reduce the rate of diagnostic surgery and prevent unnecessary surgery in nodules initially diagnosed as atypia/follicular lesions of undetermined significance (AUS/FLUS). Materials and Methods: This study included 231 consecutive patients (150 female and 81 male; mean age ± standard deviation, 51.9 ± 11.7 years) with 235 thyroid nodules (≥ 1 cm) initially diagnosed as AUS/FLUS, who later underwent both rFNA and CNB. The nodules that required diagnostic surgery after the biopsy were defined using three different scenarios according to the rFNA and CNB results: criterion 1, surgery for low-risk indeterminate (categories I and III); criterion 2, surgery for high-risk indeterminate (categories IV and V); and criterion 3, surgery for all indeterminate nodules (categories I, III, IV, and V). We compared the expected rates of diagnostic surgery between CNB and rFNA in all 235 nodules using the three surgical criteria. In addition, the expected rates of unnecessary surgery (i.e., surgery for benign pathology) were compared in a subgroup of 182 nodules with available final diagnoses. Results: CNB showed significantly lower rates of nondiagnostic, AUS/FLUS, and suspicious for malignancy diagnoses (p ≤ 0.016) and higher rates of follicular neoplasm or suspicious for a follicular neoplasm (p < 0.001) and malignant diagnoses (p = 0.031). CNB showed a significantly lower expected rate of diagnostic surgery than rFNA for criterion 1 (29.8% vs. 48.1%, p < 0.001) and criterion 3 (46.4% vs. 55.3%, p = 0.029), and a significantly higher rate for criterion 2 (16.6% vs. 7.2%, p = 0.001). CNB showed a significantly lower expected rate of unnecessary surgery than rFNA for criterion 1 (18.7% vs. 29.7%, p = 0.024). Conclusion CNB was superior to rFNA in reducing the rates of potential diagnostic surgery and unnecessary surgery for nodules initially diagnosed as AUS/FLUS in a scenario where nodules with low-risk indeterminate results (categories I and III) would undergo surgery.

Mitochondrial diseases (MDs) are genetic disorders with diverse phenotypes that affect high-energy-demand organs, notably the central nervous system and muscles. Epilepsy is a common comorbidity, affecting 40%–60% of patients with MDs and significantly reducing their quality of life. This review discusses the different treatment modalities for epilepsy in patients with MDs. Advances in genetic sequencing have identified specific mutations in mitochondrial and nuclear DNA, enabling more precise diagnoses and tailored therapeutic strategies. Anti-seizure medications and dietary interventions, such as ketogenic diets and their variants, have been effective in reducing seizures and improving mitochondrial function. Emerging treatments include gene therapy, mitochondrial transplantation, and antioxidants such as EPI-743, which protect mitochondrial integrity and improve neurological function. Additionally, therapies that promote mitochondrial biogenesis, such as bezafibrate and epicatechin, are being explored for their potential to enhance mitochondrial proliferation and energy production. Gene therapy aims to correct genetic defects underlying MDs. Techniques like mitochondrial gene replacement and using viral vectors to deliver functional genes have shown promise in preclinical studies. Mitochondrial transplantation, an emerging experimental technique, involves transferring healthy mitochondria into cells with dysfunctional mitochondria. This technique has been demonstrated to restore mitochondrial function and energy metabolism in preclinical models. Patient-derived induced pluripotent stem cells can model specific mitochondrial dysfunctions in vitro, allowing for the testing of various treatments tailored to individual genetic and biochemical profiles. The future of mitochondrial medicine is promising, with the development of more targeted and personalized therapeutic strategies offering hope for improved management and prognosis of mitochondrial epilepsy.

Mitochondrial diseases (MDs) are genetic disorders with diverse phenotypes that affect high-energy-demand organs, notably the central nervous system and muscles. Epilepsy is a common comorbidity, affecting 40%–60% of patients with MDs and significantly reducing their quality of life. This review discusses the different treatment modalities for epilepsy in patients with MDs. Advances in genetic sequencing have identified specific mutations in mitochondrial and nuclear DNA, enabling more precise diagnoses and tailored therapeutic strategies. Anti-seizure medications and dietary interventions, such as ketogenic diets and their variants, have been effective in reducing seizures and improving mitochondrial function. Emerging treatments include gene therapy, mitochondrial transplantation, and antioxidants such as EPI-743, which protect mitochondrial integrity and improve neurological function. Additionally, therapies that promote mitochondrial biogenesis, such as bezafibrate and epicatechin, are being explored for their potential to enhance mitochondrial proliferation and energy production. Gene therapy aims to correct genetic defects underlying MDs. Techniques like mitochondrial gene replacement and using viral vectors to deliver functional genes have shown promise in preclinical studies. Mitochondrial transplantation, an emerging experimental technique, involves transferring healthy mitochondria into cells with dysfunctional mitochondria. This technique has been demonstrated to restore mitochondrial function and energy metabolism in preclinical models. Patient-derived induced pluripotent stem cells can model specific mitochondrial dysfunctions in vitro, allowing for the testing of various treatments tailored to individual genetic and biochemical profiles. The future of mitochondrial medicine is promising, with the development of more targeted and personalized therapeutic strategies offering hope for improved management and prognosis of mitochondrial epilepsy.

Mitochondrial diseases (MDs) are genetic disorders with diverse phenotypes that affect high-energy-demand organs, notably the central nervous system and muscles. Epilepsy is a common comorbidity, affecting 40%–60% of patients with MDs and significantly reducing their quality of life. This review discusses the different treatment modalities for epilepsy in patients with MDs. Advances in genetic sequencing have identified specific mutations in mitochondrial and nuclear DNA, enabling more precise diagnoses and tailored therapeutic strategies. Anti-seizure medications and dietary interventions, such as ketogenic diets and their variants, have been effective in reducing seizures and improving mitochondrial function. Emerging treatments include gene therapy, mitochondrial transplantation, and antioxidants such as EPI-743, which protect mitochondrial integrity and improve neurological function. Additionally, therapies that promote mitochondrial biogenesis, such as bezafibrate and epicatechin, are being explored for their potential to enhance mitochondrial proliferation and energy production. Gene therapy aims to correct genetic defects underlying MDs. Techniques like mitochondrial gene replacement and using viral vectors to deliver functional genes have shown promise in preclinical studies. Mitochondrial transplantation, an emerging experimental technique, involves transferring healthy mitochondria into cells with dysfunctional mitochondria. This technique has been demonstrated to restore mitochondrial function and energy metabolism in preclinical models. Patient-derived induced pluripotent stem cells can model specific mitochondrial dysfunctions in vitro, allowing for the testing of various treatments tailored to individual genetic and biochemical profiles. The future of mitochondrial medicine is promising, with the development of more targeted and personalized therapeutic strategies offering hope for improved management and prognosis of mitochondrial epilepsy.

Mitochondrial diseases (MDs) are genetic disorders with diverse phenotypes that affect high-energy-demand organs, notably the central nervous system and muscles. Epilepsy is a common comorbidity, affecting 40%–60% of patients with MDs and significantly reducing their quality of life. This review discusses the different treatment modalities for epilepsy in patients with MDs. Advances in genetic sequencing have identified specific mutations in mitochondrial and nuclear DNA, enabling more precise diagnoses and tailored therapeutic strategies. Anti-seizure medications and dietary interventions, such as ketogenic diets and their variants, have been effective in reducing seizures and improving mitochondrial function. Emerging treatments include gene therapy, mitochondrial transplantation, and antioxidants such as EPI-743, which protect mitochondrial integrity and improve neurological function. Additionally, therapies that promote mitochondrial biogenesis, such as bezafibrate and epicatechin, are being explored for their potential to enhance mitochondrial proliferation and energy production. Gene therapy aims to correct genetic defects underlying MDs. Techniques like mitochondrial gene replacement and using viral vectors to deliver functional genes have shown promise in preclinical studies. Mitochondrial transplantation, an emerging experimental technique, involves transferring healthy mitochondria into cells with dysfunctional mitochondria. This technique has been demonstrated to restore mitochondrial function and energy metabolism in preclinical models. Patient-derived induced pluripotent stem cells can model specific mitochondrial dysfunctions in vitro, allowing for the testing of various treatments tailored to individual genetic and biochemical profiles. The future of mitochondrial medicine is promising, with the development of more targeted and personalized therapeutic strategies offering hope for improved management and prognosis of mitochondrial epilepsy.