Apert described acrocephalosyndactyly as a clinical entity in 1906. At first he included a patient with craniofacial deformities combined with syndactyly of both the upper and lower extremities. This is a rare congenital disturbance in the growth of bone and soft tissue affecting principally the head, the hands and the feet. More than 200 cases have been reported in the world literature, and three cases in Korea. Authors experienced one case of the classic pattern of Apert's syndrome and treated surgically for syndsctyly.
Acrocephalosyndactylia ; Congenital Abnormalities ; Foot ; Hand ; Head ; Humans ; Korea ; Lower Extremity ; Syndactyly

No abstract available in English.
Orthopedics

Rectus sheath hematoma of the abdominal wall is a well-recognized, but uncommon condition, caused by a tear in an epigastric vessel and characterized by sudden onset of severe abdominal pain and palpable mass. In most cases, a precipitating cause can be demonstrated. Causes include external trauma, strenuous activities, coughing, lifting, sneezing, vomiting, straining while urinating or defecating, golfing, pregnancy and the puerperium, anticoagulation therapy, infection, chronic diesase, arteriosclerosis, hypertension, prior paracentesis or laparotomy, inadequate hemostasis or excessive retraction in surgery, and idiopathy. Unfortunately, the correct diagnosis often is missed, and the hematoma is found only during an exploratory laparotomy. Treatment should be conservative in most instances. Although the mortality rate for patients with rectus sheath hematoma is low, the condition may be fatal if the volume of the hemorrhage is large and if treatment is delayed. Hence, it should be included in the differential diagnosis of any patient who presents to the emergency department with acute onset of abdominal pain. Our purpose is to familiarlize emergency physicians with the pathophysiology, the diagnosis, and the treatment of rectus sheath hematoma. We describe a patient with fatal rectus sheath hematoma presenting to the emergency department and give a review of the literature.
Abdominal Pain ; Abdominal Wall ; Arteriosclerosis ; Cough ; Diagnosis ; Diagnosis, Differential ; Emergencies ; Emergency Service, Hospital ; Golf ; Hematoma* ; Hemorrhage ; Hemostasis ; Humans ; Hypertension ; Hypovolemia* ; Laparotomy ; Lifting ; Mortality ; Paracentesis ; Postpartum Period ; Pregnancy ; Shock* ; Sneezing ; Vomiting

BACKGROUND: The goal of successful resuscitation is not only to stop the process of ischemia as soon as possible but also to overcome the secondary injury process after resuscitation, which involves a complex interplay of mechanisms. Brain damage accompanying cardiac arrest and resuscitation is frequent and devastating. Cells die by one of two mechanisms: necrosis or delayed neuronal death. Delayed neuronal death may require protein synthesis. Neurons in the CA1 subfield of the hippocampus are selectively vulnerable to death after injury by ischemia and reperfusion. Death of these neurons occurs after an interval of 1 or 2 days. We assessed the effects of a protein synthesis inhibitor, cycloheximide(CHX), on hippocampal neuronal death of rats by using the ventricular fibrillation cardiac arrest(VFCA) model. METHODS: The effect of CHX(3mg/kg, s.c.) on hippocampal neuronal death was studied in two groups of 18 rats each, one group being subjected to a 2-min VFCA and the other to a 3-min VFCA. Each group was divided into three subgroups: control(group I,II) without subcutaneous injection of CHX, 'exp-12' of group I/II treated with CHX 12 hours after return of spontaneous circulation (ROSC), and 'exp-24' of group I/II treated with CHX 24 hours after ROSC. The coronal sections of the hippocampus levels were stained with hematoxylin-eosin after 72 hours of survival. The histologic damage score(HDS) was used to assign a score to the total number of damaged neurons counted in each of the hippocampal CA1 subfields. RESULTS: 1. There were not significan differences in heart rates, blood pressures, blood sugar, and blood gas in group I & II during the pre-arrest steady state or at 5 min and 30 min after ROSC. 2. In group I & II, the HDS, were significantly reduced in rats(I exp-12, 1.1+/-0.6; I exp-24, 1.3+/-0.5; II exp-12, 1.4+/-0.7; and II exp-24, 1.8+/-0.8) treated with CHX 12 hours or 24 hours after ROSC than control rats(I, 2.5+/-0.9, II, 2.9+/-0.8)(p<0.05). CONCLUSION: These results suggest that delayed hippocampal neuronal death from ischemic insult after ventricular fibrillation cardiac arrest followed by resuscitation can be prevented by a protein synthesis inhibitor, CHX. Further experimental studies of the action mechanism of protein synthesis inhibitors to delayed neuronal death and clinical applications are required.
Animals ; Blood Glucose ; Brain ; Heart Arrest* ; Heart Rate ; Hippocampus ; Injections, Subcutaneous ; Ischemia ; Necrosis ; Neurons* ; Protein Synthesis Inhibitors ; Rats* ; Reperfusion ; Resuscitation ; Ventricular Fibrillation*

BACKGROUND: This study was designed to evaluate the antihypertensive efficacy and safety of nifedipine gastrointestinal system push-pull osmotic pump formulation in patients with mild to moderate essential hypertension. METHODS: After 2 weeks placebo run-in period, nifedipine 60 mg was administered once daily for 8 weeks in thirty-two patients with mild to moderate essential hypertension. RESULTS: At the end point of treatment, sitting blood pressure decreased as much as 33/16mmHg in average and rewarded 88% of efficacy and 69% of normalization. The ambulatoy blood pressure monitoring in 10 patients also revealed 11% decrease in 24 hr mean diastolic blood pressure and 32% decrease in % elevated blood pressure. The most frequent side reactions were constipation in 7 patients and polyuria in 6 patients which were tolerated during entire trial period. There were no significant changes in biochemical parameters and hematologic data, thus making the rate of safety 91% and overall rating of usefulness was 84%. CONCLUSION: Nifedipine GITS 60 mg once daily regimen is well tolerated and effective in the treatment of mild to moderate essential hypertension.
Blood Pressure ; Blood Pressure Monitors ; Constipation ; Humans ; Hypertension* ; Nifedipine* ; Polyuria ; Reward

No abstract available.
Facial Asymmetry*

The objective of this study was to investigate the relationship between insomnia severity, depression, anxiety, and anxiety sensitivity and to find out the explanatory variables that account for the insomnia severity among depression, anxiety, and anxiety sensitivity in general population. 95 mentally healthy volunteers who visit health promotion center of Kangbuk Samsung hospital for their regular medical examination were requested to complete Athens Insomnia Scale, Beck Depression Inventory, State-Trait Anxiety Inventory, and Anxiety Sensitivity Index. Association between total scores of Athens Insomnia scale and other variables (total scores of Beck Depression Inventory excluded item 16, total scores of State Anxiety, total scores of Trait Anxiety, and total scores of Anxiety Sensitivity Scale) was assessed individually with partial correlations adjusted by age and then together using multiple regression analysis. The total scores of Athens Insomnia Scale were significantly associated with total scores of Beck Depression Inventory excluded item 16(r = 0.541, p<0.001), total scores of Trait Anxiety(r = 0.642, p<0.001), total scores of State Anxiety(r = 0.267, p<0.05), and total scores of Anxiety Sensitivity Index(r = 0.312, p<0.01). Total scores of trait anxiety showed the highest correlation with the total scores of Athens Insomnia Scale and was the significant predictor to total scores of Athens Insomnia Scale among the other predictor variables (p<0.001). These results show that insomnia severity is positively correlated with depression, anxiety, and anxiety sensitivity. The correlation was strongest with trait anxiety. In addition, our results suggest that trait anxiety is associated with insomnia severity in general populations.
Anxiety* ; Depression* ; Health Promotion ; Healthy Volunteers ; Sleep Initiation and Maintenance Disorders*

The interstitial lung diseases(ILD) comprises a large, heterogeneous group of disorders characterized by derangement of alveolar walls and alveolar capillary unit causing restrictive pulmonary dysfunction and disordered gas exchange. It is rare, especially in children, and the opinions on investigation and treatments are controversial. The classification of adult ILD is applied to that of children. But considering occurrence during the developing state of lung and immune systems, we should be more cautious because the clinical manifestations and prognosis will be different from those of adults. In 1995, Katzenstein named a unique type of ILD, chronic pneumonitis of infancy (CPI) for the first time. CPI is characterized by marked alveolar septal thickening, striking type II pneumocyte hyperplasia, and eosinophilic alveolar exudate containing numerous macrophages. We report a 14 month-old girl, who had continuing respiratory difficulty and cyanosis after upper respiratory infection, could not sustain oxygen saturation and was finally diagnosed as CPI by histologic examination.
Adult ; Capillaries ; Child ; Classification ; Cyanosis ; Eosinophils ; Exudates and Transudates ; Female ; Humans ; Hyperplasia ; Immune System ; Infant ; Lung ; Lung Diseases, Interstitial* ; Macrophages ; Oxygen ; Pneumocytes ; Pneumonia* ; Prognosis ; Strikes, Employee

PURPOSE: Carbamate insecticides are potent cholinesterase inhibitors capable of causing severe cholinergic toxicity. Use of carbamate rather than organophosphate insecticides has been increasing. Compared with organophosphate poisoning, relatively few studies have investigated carbamate-associated acute pancreatitis. We investigated general characteristics and pancreatitis of carbamate poisoning and the predictors, among those readily assessed in the emergency department. METHODS: We performed a retrospective review of consecutive patients, aged over 18 years, who were admitted between January 2008 and April 2012 to an emergency department (ED) of an academic tertiary care center for treatment of carbamate poisoning. Patients who exhibited poisoning by any other material, except alcohol, were excluded. After application of exclusion criteria, patients were divided according to carbamate-induced pancreatitis and non-pancreatitis groups. RESULTS: A total of 41 patients were included in this study. Among these 41 patients, the prevalence of acute pancreatitis was 36.6% (15 patients). Initial blood chemistry tests showed a statistically higher glucose level in the pancreatitis group, compared with the non-pancreatitis group (222, IQR 189-284 vs. 137, IQR 122-175 mg/dL, P<0.05). Regarding clinical courses and outcomes, a significantly higher proportion of patients developed pneumonia [10 (66.7%) vs. 6 (23.1%), P<0.05] and had a longer hospital stay (7 days, IQR 6-12 vs. 5 days, IQR 2-11, P<0.05), but no difference in mortality, in the pancreatitis group vs. the non-pancreatitis group. In multivariate analysis, the initial glucose was showing significant association with the presentation of carbamate-induced acute pancreatitis (odds ratio 1.018, 95% confidence interval 1.001-1.035, P<0.05). CONCLUSION: Carbamate-induced acute pancreatitis is common, but not fatal. Initial serum glucose level is associated with acute pancreatitis.
Blood Glucose ; Carbamates ; Chemistry ; Cholinesterase Inhibitors ; Emergency Service, Hospital ; Glucose ; Humans ; Insecticides ; Length of Stay ; Lipase ; Mortality ; Multivariate Analysis ; Organophosphate Poisoning ; Pancreatitis* ; Pneumonia ; Poisoning* ; Prevalence ; Retrospective Studies ; Tertiary Care Centers

BACKGROUND: A major pathway leading toward neuronal injury following ischemia-reperfusion of the brain involves elevation of extracellular glutamate and activation of glutamate receptors, with a subsequent increase in intracellular calcium, resulting in a generation of free radicals. Oxygen free radicals cause brain injury following resuscitation from cardiac arrest. Oxyradicals produce strand breakage in DNA, which triggers energy-consuming DNA repair mechanisms and activates the nuclear enzyme poly(ADP-ribose) synthetase(PARS). However, excessive PARS activation leads to energy depletion and exacerbation of neuronal damage in cerebral ischemia. METHODS: We investigated the effect of a potent, free-radical scavenger, N-acetylcysteine(NAC), on hippocampal neuronal death in an asphyxial cardiac arrest model of rats. The effect of NAC on hippocampal neuronal death was studied in 32 rats which were subjected to asphyxial cardiac arrest for 7 minutes, followed by resuscitation. The animals were divided into four group(8 rats in each group) as follows: Group I was saline treated for 3 days, Group II was NAC treated for 3 days, Group III was saline treated for 6 days, and Group IV was NAC treated for 6 days. In the NAC-treated groups, NAC(150 mg/kg) was intravenously injected after return of spontaneous circulation. The coronal sections with hippocampus levels were stained with hematoxylin-eosin(H-E) and PARS antibodies at 3 and 6 days after survival. In addition, the levels of myeloperoxidase(MPO) and malondialdehyde(MDA) were determined in the brains of each group. RESULTS: The results are as follows: 1. MPO and MDA levels were significantly lower in the NAC-treated groups, II and IV, than in the saline-treated groups, I and III. 2. The histologic damage score(HDS), as determined by H-E staining, was significantly lower in the NAC-treated groups, II and IV, than in the saline-treated groups, I and III. 3. In PARS immunohistochemical staining, the HDS was significantly lower in the NAC-treated groups, II and IV, than in the saline-treated groups, I and III. CONCLUSION: These results suggest that a free-radical scavenger, N-acetylcysteine, may effectively prevent neuronal damages after reperfusion from asphyxial cardiac arrest in rats. Further studies will be required to examine both the mechanism of the action and the clinical application of NAC in patients with cardiac arrest.
Acetylcysteine* ; Animals ; Antibodies ; Brain ; Brain Injuries ; Brain Ischemia ; Calcium ; DNA ; DNA Repair ; Free Radicals ; Glutamic Acid ; Heart Arrest* ; Hippocampus ; Humans ; Neurons ; Neuroprotective Agents* ; Oxygen ; Poly Adenosine Diphosphate Ribose ; Rats* ; Receptors, Glutamate ; Reperfusion ; Reperfusion Injury ; Resuscitation