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

Anorectal manometry is now widely performed to evaluate anorectal physiology in a variety of clinical conditions. No adverse consequence related with this procedure has been reported yet. There has been no known guideline or precaution regarding the upper limit of the volume inflating the rectal balloon in measuring maximum tolerable volume. We experienced 2 cases of colorectal rupture during measuring maximum tolerable volume. Both cases were in their early postoperative period, 1 month after low anterior resection due to rectal cancer and 3 months after Delorme's procedure due to rectal prolapse, respectively. The rectal sensory and anorectal motor responses to rectal distension are known to depend on the rate and pattern of distension. Therefore, results of different examiners and laboratories cannot be compared directly unless the pattern and rate of distension are the same. Wide intersubject and intrasubject variations in maximum tolerable volume have been also reported, and differentiation between patients and normal subjects is not necessarily possible. Measuring maximum tolerable volume is painful and unpleasant, and some authors believe that maximum tolerable volume in addition to the other steps of rectal sensations does not contribute any additional information. Based on our experience and literature, we suggest that measuring maximum tolerable volume might be better to be omitted, or if it be done, rectal balloon should be inflated with great care especially in early postoperative period or in those who cannot feel or express their symptoms clearly, such as elderly or infants.
Aged ; Humans ; Infant ; Manometry* ; Physiology ; Postoperative Period ; Rectal Neoplasms ; Rectal Prolapse ; Rupture* ; Sensation

Vasovagal syncope is elicited by the Bezold-Jarisch reflex, triggered by anxiety, emotional stress or pain. It is the result of reflexively increasing parasympathetic tone and decreasing sympathetic tone sensed by chemoreceptor in vagus nerve and mechanoreceptor of ventricle, which causes bradycardia, systemic vasodilatation and profound hypotension. Although it is a transient episode in many cases, it could give rise to cardiac arrest. Diabetic autonomic neuropathy can lead to significant change in blood pressure and pulse rate, bradycardia, hypotension, and even cardiac arrest by increasing the risk of hemodynamic instability under general or regional anesthesia. We have experienced a patient who had once cardiac arrest following after positional change and recovered in a few minutes. The patient was supposed to have diabetic autonomic neuropathy under the emotional stress and anxiety before spinal anesthesia was done. We believe that this is the result of combination between paradoxical Bezold-Jarisch reflex caused by overactivation of parasympathetic nerve system and autonomic nervous system instability precipitated by diabetic autonomic neuropathy.
Anesthesia, Conduction ; Anesthesia, Spinal* ; Anxiety ; Autonomic Nervous System ; Blood Pressure ; Bradycardia ; Death, Sudden, Cardiac* ; Diabetic Neuropathies ; Heart Arrest ; Heart Rate ; Hemodynamics ; Humans ; Hypotension ; Mechanoreceptors ; Reflex ; Stress, Psychological ; Syncope, Vasovagal ; Vagus Nerve ; Vasodilation

Duplication of the ureter occurs in 0.6 to 0.8% of adults and it is sometimes encountered in kidney transplantation. We experienced a case of duplicated uretor in kidney transplantaion, so we reports about it with a brief review of literature.
Adult ; Humans ; Kidney Transplantation* ; Kidney* ; Ureter*

Brugada syndrome is an arrhythmogenic disease that is manifested by specific patterns of right bundle branch block with ST elevation in right precordial (V1-V3) ECG leads causing ventricular fibrillation, leads to a sudden death without organic heart problems. It is an incomplete penetrating autosomal dominant disease that is due to mutation in SCN5A gene, coding for Na+ channel of cardiac muscles. This syndrome is more common and may be endemic in southeast Asia. Although it is a highly risky disease, it's preventive treatment for arrhythmia has not been established yet. We experienced a case of 28 year old man who had wedge resection of lung because of spontaneous pneumothorax under general anesthesia and who was suspected Brugada syndrome based on specific ECG patterns and a family history of his father's sudden death after syncope.
Adult ; Anesthesia, General ; Arrhythmias, Cardiac ; Asia, Southeastern ; Brugada Syndrome* ; Bundle-Branch Block ; Clinical Coding ; Death, Sudden ; Electrocardiography ; Heart ; Heart Arrest ; Humans ; Lung ; Myocardium ; Pneumothorax ; Syncope ; Ventricular Fibrillation

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*