• Journal of Korean Neurosurgical Society
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• v.60 no.1
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• pp.118-124
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• 2017

Brain abscess commonly occurs secondary to an adjacent infection (mostly in the middle ear or paranasal sinuses) or due to hematogenous spread from a distant infection or trauma. Pulmonary arteriovenous fistulas (AVFs) are abnormal direct communications between the pulmonary artery and vein. We present two cases of brain abscess associated with asymptomatic pulmonary AVF. A 65-year-old woman was admitted with a headache and cognitive impairment that aggravated 10 days prior. An magnetic resonance (MR) imaging revealed a brain abscess with severe edema in the right frontal lobe. We performed a craniotomy and abscess removal. Bacteriological culture proved negative. Her chest computed tomography (CT) showed multiple AVFs. Therapeutic embolization of multiple pulmonary AVFs was performed and antibiotics were administered for 8 weeks. A 45-year-old woman presented with a 7-day history of progressive left hemiparesis. She had no remarkable past medical history or family history. On admission, blood examination showed a white blood cell count of 6290 cells/uL and a high sensitive C-reactive protein of 2.62 mg/L. CT and MR imaging with MR spectroscopy revealed an enhancing lesion involving the right motor and sensory cortex with marked perilesional edema that suggested a brain abscess. A chest CT revealed a pulmonary AVF in the right upper lung. The pulmonary AVF was obliterated with embolization. There needs to consider pulmonary AVF as an etiology of cerebral abscess when routine investigations fail to detect a source.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.183-190
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• 1997

Tocolytics are agents widely used in the treatment of premature labor to inhibit uterine contractions. Ritodrine is most commonly used tocolytic agent and acts by increasing intracellular cyclic adenosine monophosphate, which decreases the activity of myosin light-chain kinase, the rate-limiting enzyme in the signal network leading to contraction. Physiologic effects associated with the use of ritodrine are due to their effect on bera-l as well as beta-2 receptors. Some of maternal complications of therapy are rachycardia, hyperglycemia, hypokalemia, lactic acidosis, myocardial ischemia, and pulmonary edema. Tocolytics induced pulmonary edema is a serious complication that can lead to marternal death, although infrequent, The incidence varies from 0.5% to 5% of those receiving these agents. Predisposing factors include the concommitant use of corticosteroid, twin gestation, fluid overload (particularly with saline), and anemia. Several mechanisms have been postulated, but the pathogenesis is uncertain. It is suggested that both types of mechanism, hydrostatic and permeability induced, might be involved. The association of tocolytic therapy with pulmonary edema appears to be unique to the pregnant state, because this complication has never been reported in asthmatic patients exposed to high dosages. We report a case of tocolytic induced pulmonary edema developed in 24 hours after delivery.

• The Journal of Korean Medicine
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• v.15 no.2 s.28
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• pp.173-183
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• 1994

The results about effects of Maecmoondongtang on the pulmonary function of $SO_2$ exposed rats were summerized as follows: 1. Maecmoondongtang reavealed significant effect on decrease of the lung weight in pulmomary edema of rats. 2. Maecmoondongtang reavealed very significant effect on decrease of the TBA value of lung. 3. It was recognized Maecmoondongtang had signiftcant effect on decrease of glycoprotein contents in trachea. 4. It was recognized maecmoondongtang had significant effect on decrease of mucos area in tracheal epithelium. 5. Maecmoondongtang had effects on recovery of the cillia cells of tracheal epithelium and inhibition of mucous secretion. According to the above result. it was recognized Gamimaecdongtang had significant effect on decrease of lung weight in pulmonary edema. the TBA value. glycoprotein contents in trachea. and mucous area in tracheal epithelium. and recovery of the cillia cells of tracheal epithelium. and inhibition of mucous secretion. So I think we can take advantage of this medicine very usefully for treatment of pulmonary edema. pheumonia. acute and chronic bronchitis etc.

• Journal of Chest Surgery
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• v.7 no.2
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• pp.145-152
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• 1974

The effect of reticuloendothelial hyperfunction on hypothermic preservation of lung was studied in dogs. In order to evaluate the viability after hemodynamic_ load in preserved isolated lung, observations were made on the rate of increase in weight, degree of edema,compliance and surface activity of lung. The results obtained as follows: l. In the group of activating of the reticuloendothelial system by injection of sodium thiosulfate intravenously before pneumonectomy and infusion of naphthionine through the pulmonary artery before hypothermic preservation of isolated lung the limit of preservation was eight hours whereas four hours in non-treated control group. 2.Therefore the method of activating of the reticuloendothelial system before and after pulmonary resection seems effective in preserving for prolonging the period of preservation of lung by means of inhibition of pulmonary edema. 3. Pulmonary surface activity is expected to be valuable as a method in evaluation of the viability of preserved lung along with compliance and rate of increase in weight of lung.

• Journal of Medicine and Life Science
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• v.18 no.3
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• pp.61-65
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• 2021

Although re-expansion pulmonary edema (RPE) is rare (incidence rate <1%), it is associated with a mortality rate of >20%; therefore, early diagnosis and treatment are important. We report a case of RPE following chest tube insertion in a patient with spontaneous pneumothorax. We have specifically focused on the mechanism underlying RPE and the possible etiology. An 82-year-old man with a history of chronic anemia, chronic obstructive pulmonary disease, diabetes mellitus, and hypertension was referred to the emergency department for management of recurrent right-sided pneumothorax. We performed emergency closed thoracostomy for suspected tension pneumothorax, which led to stabilization of the patient's vital signs; however, he coughed up frothy pink sputum accompanied by severe right-sided chest pain 30 min postoperatively. The patient showed new-onset right pulmonary consolidation on chest radiography, as well as desaturation, tachycardia, and tachypnea and was diagnosed with RPE. He was transferred to the intensive care unit for mechanical ventilation and supportive treatment using diuretics, ionotropic agents, and prophylactic antibiotics. RPE gradually resolved, and the patient was extubated 3 days after admission. He has not experienced recurrent pneumothorax or pulmonary disease for 4 months. We emphasize the importance of RPE prevention and that aggressive ventilator care and supportive treatment can effectively treat RPE following an accurate understanding of the underlying pathogenetic mechanisms and risk factors.

• Tuberculosis and Respiratory Diseases
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• v.67 no.1
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• pp.59-62
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• 2009

Reexpansion pulmonary edema is not a common phenomenon after chest tube insertion but some reports from 0% to 14%. There are various resulting complications, including acute respiratory distress syndrome. We report a case of focal reexpansion pulmonary edema after chest tube insertion. A 49-year-old male came to the hospital due to ongoing dyspnea and left chest pain for 3 days. On chest X-ray, the patient had a left pneumothrax. We planned to insert a chest tube for symptom relief. To determine whether or not the chest had expanded as a result of the chest tube insertion, the patient underwent repeated chest X-rays the following day. The patient experienced brief respiratory symptoms upon initial suction; a chest PA showed patchy consolidated infiltration at the inserted site. After 5 days of conservative management, the recovered completely.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.313-316
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• 2007

Negative pressure pulmonary edema (NPPE) during anesthetic recovery is a rare, but potentially serious complication for patients who are undergoing different surgical procedures. The proposed mechanism is the generation of high negative pressure during markedly respiratory effort and upper airway obstruction from glottis closure and laryngospasm, and this all leads to pulmonary edema. We report here on a case of a healthy 26-year-old male who immediately developed NPPE and hemoptysis following extubation after partial rib resection due to benign rib tumor; the patient was treated conservatively. We also include a review of the review literatures.

• Tuberculosis and Respiratory Diseases
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• v.56 no.3
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• pp.297-301
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• 2004

A 60-year old male patient admitted with complaints of dyspnea and pleuritic chest pain. The chest X-ray demonstrated right pleural effusion. We planed to do the conventional thoracentesis to evaluate the characteristics of pleural effusion and to relieve the symptom of the patient. Focal reexpansion pulmonary edema was seen on the follow-up chest X-ray. After the 5-day conservative management, the patient recovered without any complications.

• Journal of Chest Surgery
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• v.55 no.1
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• pp.30-36
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• 2022

Background: No consensus exists regarding whether volatile anesthetics are superior to intravenous anesthetics for reducing postoperative pulmonary complications (PPCs) in patients undergoing general anesthesia for surgery. Studies of this issue focused on anatomic pulmonary resection are lacking. This study compared the effects of total intravenous anesthesia (TIVA) versus volatile anesthesia on PPCs after anatomic pulmonary resection in patients with lung cancer. Methods: This retrospective study examined the medical records of patients with lung cancer who underwent lung resection at our center between January 2018 and October 2020. The primary outcome was the incidence of PPCs, which included prolonged air leak, pneumonia, acute respiratory distress syndrome, empyema, atelectasis requiring bronchofiberscopy (BFS), acute lung injury (ALI), bronchopleural fistula (BPF), pulmonary embolism, and pulmonary edema. Propensity score matching (PSM) was used to balance the 2 groups. In total, 579 anatomic pulmonary resection cases were included in the final analysis. Results: The analysis showed no statistically significant difference between the volatile anesthesia and TIVA groups in terms of PPCs, except for prolonged air leak. Neither of the groups showed atelectasis requiring BFS, ALI, BPF, pulmonary embolism, or pulmonary edema after PSM. However, the length of hospitalization, intensive care unit stay, and duration of chest tube indwelling were shorter in the TIVA group. Conclusion: Volatile anesthetics showed no superiority compared to TIVA in terms of PPCs after anatomical pulmonary resection in patients with lung cancer. Considering the advantages of each anesthetic modality, appropriate anesthetic modalities should be used in patients with different risk factors and situations.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.474-483
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• 1992

Background: Regardless of its causes, acute lung injury is characterized pathophysiologically by increased pulmonary arterial pressure and the protein-rich edema. Many inflammatory mediators are known to be involved in the pathogenesis of acute lung injury, including oxygen free radicals (OFR). But the changes in pulmonary capillary pressure in the OFR-induced acute lung injury is not clear. While the pulmonary edema characterized by the movement of fluid and solutes is dependent on the pressure gradient and the alveolar-capillary permeability, the role of pulmonary capillary pressure in the development of pulmonary edema is also not well understood. Method: Male Sprague-Dawley rats were divided into 5 groups: normal control (n=5), xanthine/xanthine oxidase (X/XO)-treated group (n=7), catalase-pretreated group (n=5), papaverine-pretreated group (n=7), and indomethacin-pretreated group (n=5). In isolated perfused rat lungs, the sequential changes in pulmonary arterial pressure, pulmonary capillary pressure by double occlusion method, and lung weight as a parameter of pulmonary edema were determined. Results: Pulmonary arterial pressure and pulmonary capillary pressure were increased by X/XO. This increase was significantly attenuated by catalase and papaverine, but indomethacin did not prevent the X/XO-induced increase. Lung weight gain was also observed by X/XO perfusion. It was prevented by catalase. Papaverine did not completely block the increase, but significantly delayed the onset. Indomethacin had no effect on the increase in lung weight. Conclusion: These data suggest that increased pulmonary capillary pressure by OFR may aggravate pulmonary edema in the presence of increased alveolar-capillary permeability and this may not be mediated by cyclooxygenase metabolites.