The intramedullary nailing for the fractured tibia has been used in selected cases of fresh diaphyseal fracture and non-union. However, with modern technical improvements, the indications could be expanded considerably. With interlocking nailing technic we can treat various types of tibia fracture, which were unsuitable for intramedullary nailing previously. Stability can be achieved with transverselyinserted bolts which anchor the implant directly to the cortical bone, thereby controllinglength, alignmentandrotation of the fracture as well as permitting early joint motion and weight bearing. Between May 1985 and Feb. 1988, interlocking nailings were performed for 54 cases oftivial fractures, of which 40 cases were acute fracture and 10 were non-union and 4 weremalunion. We obtained the following results ; 1. Closed nailing technic was accomplished in 40 cases and 14 cases were opened. 2. Dynamic and static interlocking nailings were done in 8 and 46 cases respectively. 3. Full weight could be borne on 5th postoperative day in transverse or short oblique fracture cases, 2 weeks in nonunion and malunion cases and 4 weeks in comminuted or segmental fracture cases. 4. The mean fracture healing period was 11.5 weeks in dynamic interlocking cases and 13 weeks in static nailing cases. 5. According to the functional classification of Klemm and Borner, out of 54 cases 36 were excellent, 14 were good, 3 were fair and one was poor.
Classification ; Fracture Fixation, Intramedullary ; Fracture Healing ; Joints ; Tibia ; Weight-Bearing

BACKGROUND: Pulmonary thromboembolism is relatively frequent and potentially fatal. However, it is commonly misdiagnosed. The incidence of pulmonary thromboembolism is not decreasing despite advances in diagnosis and effective prophylatic measures. Its potential for significant sequela necessitates a prompt diagnosis and treatment. Unfortunately, there are many difficulties and problems regarding accurate diagnosis. There is a low prevalence of deep vein thrombosis and pulmonary thromboembolism in Korea and only few reports on this subject are available. METHOD: The clinical features of 36 patients, who were diagnosed with pulmonary thromboembolism at the Korea University medical center, were reviewed. RESULTS: 1) There was no significant difference in prevalence between men an women, and the mean age was 50.9 years in men 59.2 years in women. 2) The frequent causes of pulmonary thromboembolism were malignancies (22.2%), surgery (22.2%), and heart disease(8.2%). Specific causes were not identified in 33.3%. 3) The most common symptom was dyspnea(72.2%), and the most common sign was tachypnea(61.1%). 4) The EKG findings were normal in 28.6%, and S1Q3T3 pulmonale pattern in 25.7%, ST or QRS changes in others. 5) The chest X-ray findings indicated pulmonary infiltation in 37.5%, cardiomegaly in 15.6%, pleural effusion in 12.5%, and normal in 27.8%. The perfusion lung scan showed a high probability in 66.7%, and intermediate or low probability in 33.3%. 6) The pulmonary arterial pressure(PAP) in the high probability groups was 57.9mmHg with a higher mortality rate(35%). CONCLUSION: Pulmonary thromboembolism is not uncommon in Korea and its clinical features do not differ greatly from those reported in the literature. When pulmonary thromboemblism of unknown causes are diagnosed, a search for an occult malignancy is recommended. Rapid diagnosis and treatment are achieved when thromboemblism is suspected.
Academic Medical Centers ; Cardiomegaly ; Diagnosis ; Electrocardiography ; Female ; Heart ; Humans ; Incidence ; Korea ; Lung ; Male ; Mortality ; Perfusion ; Pleural Effusion ; Prevalence ; Pulmonary Embolism* ; Thorax ; Tomography, Spiral Computed ; Venous Thrombosis

BACKGROUND: The dominant innervation of airway smooth muscle is parasympathetic fibers which are carried in the vagus nerve. Activation of these cholinergic nerves releases acetylcholine which binds to M3 muscarinic receptors on the smooth muscle causing bronchocontraction. Acetylcholine also feeds back onto neuronal M2 muscarinic receptors located on the postganglionic cholinergic nerves. Stimulation of these receptors further inhibits acetylcholine release, so these M2 muscarinic receptors act as autoreceptors. Loss of function of these M2 receptors, as it occres in animal models of hyperresponsiveness, leads to an increase in vagally mediated hyperresponsiveness. However, there are limited data pertaining to whether there are dysfunctions of these receptors in patients with asthma. The aim of this study is to determine whether there are dysfunction of M2 muscarinic receptors in asthmatic patients and difference of function of these receptors according to severity of asthma. METHODS: We studied twenty-seven patients with asthma who were registered at Pulmonology Division of Korea University Hospital. They all met asthma criteria of ATS. Of these patients, eleven patients were categorized as having mild asthma, eight patients moderate asthma and eight patients severe asthma according to severity by NAEPP Expert Panel Report 2(1997). All subjects were free of recent upper respiratory tract infection within 2 weeks and showed positive methacholine challenge test(PC 20<16mg/ml). Methacholine provocation tests performed twice on separate days allowing for an interval of one week. In the second test, pre-treatment with the M2 muscarinic receptor agonist pilocarpine(180µg) through inhalation was performed before the routine procedures. RESULTS: Eleven subjects with mild asthma and eight aubjects with moderate asthma showed significant increase of PC20 from 5.30±5.23mg/ml(mean±SD) to 20.82±22.56mg/ml(p=0.004) and from 2.79±1.5mg/ml to 4.67±3.53mg/ml(p=0.012) after pilocarpine inhalation, respectively. However, in the eight subjects with severe asthma significant increase of PC20 from 1.76±1.50mg/ml to 3.18±4.03mg/ml(p=0.161) after pilocarpine inhalation was not found. CONCLUSION: In subjects with mild and moderate asthma, function of M2 muscarinic receptors was normal, but there was a dysfunction of these receptors in subjects with severe asthma. These results suggest that function of M2 muscarinic receptors is different according to severity of asthma.
Acetylcholine ; Asthma ; Autoreceptors ; Humans ; Inhalation ; Korea ; Methacholine Chloride ; Models, Animal ; Muscle, Smooth ; Neurons* ; Pilocarpine ; Pulmonary Medicine ; Receptors, Muscarinic* ; Respiratory Tract Infections ; Vagus Nerve

Cryoglobulinemia is the presence of globulins in the serum that precipitate on exposure to cold temperatures (cryoglobulins). Pulmonary complications of cryoglobulinemia include interstial infiltration, impaired gas exchange, small airway disease and pleurisy. Only one other acute respiratory distress syndrome(ARDS) case has been described in patients with cryoglobulinemia. A 55-years old man was admitted with dyspnea. He had been diagnosed as being a hepatitis B virus antigen carrier 15 years age. On the first admission, chest radiography showed a bilateral pleural effusion and a patchy infiltration on both lungs. On protein-and immuno-electrophoresis, cryoglobulinemia was confirmed. The patient was treated with corticosteroid and plasmapheresis. Forty-five days after the diagnosis, the patient complained of progressive dyspnea and showed a diffuse bilateral pulmonary infiltration on chest radiography. Despite intensive care with mechanical ventilation, the patient died as consequence of hypoxemia and multiple systemic organ failure. On a pathologic examination of the postmortem lung biopsy, multiple necrotizing vasculitis and increased infiltration of the lymphocytes and monocytes were observed. In conclusion, ARDS developed as a result of pulmonary hemorrhage due to cryoglobulinemia-associated vasculitis.
Anoxia ; Biopsy ; Cold Temperature ; Cryoglobulinemia ; Diagnosis ; Dyspnea ; Globulins ; Hemorrhage ; Hepatitis B virus ; Humans ; Critical Care ; Lung ; Lymphocytes ; Monocytes ; Plasmapheresis ; Pleural Effusion ; Pleurisy ; Radiography ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult* ; Thorax ; Vasculitis

BACKGROUND: Goblet cell hyperplasia is a critical pathological feature in hypersecretory diseases of the airways. A bacterial infection of the lung is also known to induce inflammatory responses, which can lead to the overproduction of mucus. Recently, mucin synthesis in the airways has been reported to be regulated by neutrophilic inflammation-induced epidermal growth factor receptor (EGFR) expression and activation. In addition, it was reported that migration of the activated neutrophils is dependent on the matrix metalloproteinases (MMPs), especially MMP-9. In this study, bacterial lipopolysaccharide (LPS)-induced goblet cell hyperplasia and mucus hypersecretion by EGFR cascade, resulting from the MMPs-dependent neutrophilic inflammation were investigated in the rat airways. METHODS: Pathogen-free Sprague-Dawley rats were studied in vivo. Various concentrations of LPS were instilled into the trachea in 300microliter PBS (LPS group). Sterile PBS (300microliter) was instilled into the trachea of the control animals (control group). The airways were examined on different days after instilling LPS. For an examination of the relationship between the LPS-induced goblet cell hyperplasia and MMPs, the animals were pretreated 3 days prior to the LPS instillation and daily thereafter with the matrix metalloproteinase inhibitor (MMPI; 20 mg/Kg/day of CMT-3; Collagenex Pharmaceuticals, USA). The neutrophilic infiltration was quantified as a number in five high power fields (HPF). The alcian blue/periodic acid-Schiff (AB/PAS) stain were performed for the mucus glycoconjugates and the immunohistochemical stains were performed for MUC5AC, EGFR and MMP-9. Their expressions were quantified by an image analysis program and were expressed by the percentage of the total bronchial epithelial area. RESULTS: The instillation of LPS induced AB/PAS and MUC5AC staining in the airway epithelium in a time- and dose-dependent manner. Treatment with the MMPI prevented the LPS-induced goblet cell hyperplasia significantly. The instillation of LPS into the trachea induced also EGFR expression in the airway epithelium. The control airway epithelium contained few leukocytes, but the intratracheal instillation of LPS resulted in a neutrophilic recruitment. A pretreatment with MMPI prevented neutrophilic recruitment, EGFR expression, and goblet cell hyperplasia in the LPS-instilled airway epithelium. CONCLUSION: Matrix metalloproteinase is involved in LPS-induced mucus hypersecretion, resulting from a neutrophilic inflammation and EGFR cascade. These results suggest a potential therapeutic role of MMPI in the treatment of mucus hypersecretion that were associated with a bacterial infection of the airways.
Animals ; Bacterial Infections ; Coloring Agents ; Epidermal Growth Factor* ; Epithelium ; Glycoconjugates ; Goblet Cells ; Hyperplasia ; Inflammation ; Leukocytes ; Lung ; Matrix Metalloproteinases ; MMPI ; Mucins ; Mucus* ; Neutrophils* ; Rats ; Rats, Sprague-Dawley ; Receptor, Epidermal Growth Factor* ; Trachea

BACKGROUND: Goblet cell hyperplasia is a critical pathological feature in hypersecretory diseases of the airways. A bacterial infection of the lung is also known to induce inflammatory responses, which can lead to the overproduction of mucus. Recently, mucin synthesis in the airways has been reported to be regulated by neutrophilic inflammation-induced epidermal growth factor receptor (EGFR) expression and activation. In addition, it was reported that migration of the activated neutrophils is dependent on the matrix metalloproteinases (MMPs), especially MMP-9. In this study, bacterial lipopolysaccharide (LPS)-induced goblet cell hyperplasia and mucus hypersecretion by EGFR cascade, resulting from the MMPs-dependent neutrophilic inflammation were investigated in the rat airways. METHODS: Pathogen-free Sprague-Dawley rats were studied in vivo. Various concentrations of LPS were instilled into the trachea in 300microliter PBS (LPS group). Sterile PBS (300microliter) was instilled into the trachea of the control animals (control group). The airways were examined on different days after instilling LPS. For an examination of the relationship between the LPS-induced goblet cell hyperplasia and MMPs, the animals were pretreated 3 days prior to the LPS instillation and daily thereafter with the matrix metalloproteinase inhibitor (MMPI; 20 mg/Kg/day of CMT-3; Collagenex Pharmaceuticals, USA). The neutrophilic infiltration was quantified as a number in five high power fields (HPF). The alcian blue/periodic acid-Schiff (AB/PAS) stain were performed for the mucus glycoconjugates and the immunohistochemical stains were performed for MUC5AC, EGFR and MMP-9. Their expressions were quantified by an image analysis program and were expressed by the percentage of the total bronchial epithelial area. RESULTS: The instillation of LPS induced AB/PAS and MUC5AC staining in the airway epithelium in a time- and dose-dependent manner. Treatment with the MMPI prevented the LPS-induced goblet cell hyperplasia significantly. The instillation of LPS into the trachea induced also EGFR expression in the airway epithelium. The control airway epithelium contained few leukocytes, but the intratracheal instillation of LPS resulted in a neutrophilic recruitment. A pretreatment with MMPI prevented neutrophilic recruitment, EGFR expression, and goblet cell hyperplasia in the LPS-instilled airway epithelium. CONCLUSION: Matrix metalloproteinase is involved in LPS-induced mucus hypersecretion, resulting from a neutrophilic inflammation and EGFR cascade. These results suggest a potential therapeutic role of MMPI in the treatment of mucus hypersecretion that were associated with a bacterial infection of the airways.
Animals ; Bacterial Infections ; Coloring Agents ; Epidermal Growth Factor* ; Epithelium ; Glycoconjugates ; Goblet Cells ; Hyperplasia ; Inflammation ; Leukocytes ; Lung ; Matrix Metalloproteinases ; MMPI ; Mucins ; Mucus* ; Neutrophils* ; Rats ; Rats, Sprague-Dawley ; Receptor, Epidermal Growth Factor* ; Trachea

A 38-year-old woman presented with facial edema with neck vein engorgement for about 45 days. Chest roentgenography showed bulging soft tissue opacities in the right superoanterior mediastinum and a lobulated intraluminal mass was noted in the superior vena cava on the venacavogram. The superior vena cava was incised and the tumor located from the junction of the superior vena cava and internal jugular vein to the right atrial inlet was excised. Grossly, the tumor was myxoid or gelatinous in appearance. A combination of microscopic and immunohistochemical features showed myxoid leiomyosarcoma arising from the wall of the superior vena cava.
Adult ; Bays ; Edema ; Female ; Gelatin ; Humans ; Jugular Veins ; Leiomyosarcoma* ; Mediastinum ; Neck ; Radiography ; Superior Vena Cava Syndrome* ; Thorax ; Veins ; Vena Cava, Superior*

BACKGROUND: Many inflammatory mediators and collagenases are involved in the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The increase of matrix metalloproteinase-9 (MMP-9, gelatinase-B) produced mainly by inflammatory cells was reported in many ALI models and ARDS patients. Cyclic mechanical stress also can induce MMP-9 production from alveolar macrophages and connective tissue cells. In this study, the expression of MMP-9 in ventilator-induced lung injury (VILI) model and the effects of matrix metalloproteinase inhibitor (MMPI) on VILI were investigated. METHODS: Eighteen Sprague-Dawley rats were divided into three groups: low tidal volume (LVT, 7mL/Kg tidal volume, 3 cmH2O PEEP, 40/min.), high tidal volume (HVT, 30mL/Kg tidal volume, no PEEP, 40/min) and high tidal volume with MMPI (HVT+MMPI) groups. Mechanical ventilation was performed in room air for 2 hours. The 20 mg/Kg of CMT-3 (chemically modified tetracycline-3, 6-demethyl 6-deoxy 4-dedimethylamino tetracycline) was gavaged as MMPI from three days before mechanical ventilation. The degree of lung injury was measured with wet-to-dry weight ratio and acute lung injury score. Expression of MMP-9 was studied by immunohistochemical stain with a mouse monoclonal anti-rat MMP-9 IgG1. RESULTS: In the LVT, HVT and HVT + MMPI groups, the wet-to-dry weight ratio was 4.70+/-0.14, 6.82+/-1.28 and 4.92+/-0.98, respectively. In the HVT group, the ratio was significantly higher than other groups (p<0.05). Acute lung injury score measured by five-point scale was 3.25+/-1.17, 12.83+/-1.17 and 4.67+/-0.52, respectively. The HVT group was significantly damaged by VILI and MMPI protects injuries by mechanical ventilation (p<0.05). Expression of MMP-9 measured by four-point scale was 3.33+/-2.07, 12.17+/-2.79 and 3.60+/-1.95, respectively, which were significantly higher in the HVT group (p<0.05). CONCLUSION: VILI increases significantly the expression of MMP-9 and MMPI prevents lung injury induced by mechanical ventilation through the inhibition of MMP-9.
Acute Lung Injury ; Animals ; Collagenases ; Connective Tissue Cells ; Humans ; Immunoglobulin G ; Lung Injury ; Macrophages, Alveolar ; Matrix Metalloproteinase 9 ; Mice ; MMPI ; Rats* ; Rats, Sprague-Dawley ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Stress, Mechanical ; Tidal Volume ; Ventilator-Induced Lung Injury*

BACKGROUND: Diffuse panbronchiolitis(DPB) is a chronic inflammatory lung disease that presents as coughing, copious sputum, exertional dyspnea, which progresses to bronchiectasis. The pathogenesis of bronchiectasis is controlled by inflammatory mediators, which are closely related to mucus hypersecretion, goblet cell dysplasia. In recent studies, the epidermal growth factor receptor(EGFR) system was reported to be associated with this process. It was hypothesized that a relationship exists between goblet cell dysplasia, EGFR expression, and inflammatory mediators produced by neutrophil. METHOD: Alcian blue/periodic acid -Schiff(AB/PAS) stain, MUC5AC, EGFR, CD16 immunohistochemical stain were examined to investigate a role for the EGFR system in a mucus hypersecretion in DPB using the lung biopsy specimens from 13 DPB patients and 6 controls. RESULTS: In the DPB group, the AB/PAS- and MUC5AC-stained areas were 8.31+/-3.36%, 11.46+/-4.68%, respectively. In the control group, the AB/PAS- and MUC5AC-stained areas were 50.5+/-5.77%, 53.3%+/-6.67%, which was significantly larger than in the DPB group (each comparison, p<0.05). The percentage of EGFR expression was 9.54+/-4.95% in the DPB group, but zero in of the control group. The extent of neutrophilic infiltration was 71.92+/-3.71/5HPF in the DPB group and 45.0+/-5.73/5HPF in the control group, which was statistically significant(p=0.002). CONCLUSION: The EGFR system is highly related to goblet cell dysplasia, mucus hypersecretion and neutrophilic inflammation in DPB.
Biopsy ; Bronchiectasis ; Cough ; Dyspnea ; Epidermal Growth Factor* ; Goblet Cells* ; Humans ; Inflammation ; Lung ; Lung Diseases ; Mucus ; Neutrophils ; Receptor, Epidermal Growth Factor* ; Sputum