• Title/Summary/Keyword: Non-cardiogenic pulmonary edema

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Predictors of Cardiogenic and Non-Cardiogenic Causes in Cases with Bilateral Chest Infiltrates

  • Lee, Yeon Joo;Lee, Jinwoo;Park, Young Sik;Lee, Sang-Min;Yim, Jae-Joon;Yoo, Chul-Gyu;Kim, Young Whan;Han, Sung Koo;Lee, Chang-Hoon
    • Tuberculosis and Respiratory Diseases
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    • v.74 no.1
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    • pp.15-22
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    • 2013
  • Background: Differentiating cardiogenic pulmonary edema from other bilateral lung diseases such as pneumonia is frequently difficult. We conducted a retrospective study to identify predictors for cardiogenic pulmonary edema and non-cardiogenic causes of bilateral lung infiltrates in chest radiographs. Methods: The study included patients who had newly developed bilateral lung infiltrates in chest radiographs and patients who underwent echocardiography. Cases were divided into two groups based on the echocardiographic findings: the cardiogenic pulmonary edema group and the non-cardiogenic group. Clinical characteristics and basic laboratory findings were analyzed to identify predictors for differential diagnosis between cardiogenic and non-cardiogenic causes of bilateral chest infiltrates. Results: We analyzed 110 subjects. Predictors of cardiogenic pulmonary edema were higher brain natriuretic peptide (BNP) levels, lower C-reactive protein (CRP) levels on the day of the event (<7 mg/dL), age over 60 years, history of heart disease, and absence of fever and sputum. CRP on the day of the event was an independent factor to differentiate cardiogenic and non-cardiogenic causes of newly developed bilateral chest infiltrates. Also, the validity was comparable to BNP. Conclusion: Clinical symptoms (sputum and fever), medical history (dyslipidemia and heart disease), and laboratory findings (BNP and CRP) could be helpful in the differential diagnosis of patients with acute bilateral lung infiltrates in chest radiographs.

Sodium nitroprusside on acute cardiogenic pulmonary edema in dogs: case reports

  • Han, Mangil;Kim, Yoonhwan;Jeong, Yunho;Ahn, Jin-Ok;Chung, Jin-Young
    • Korean Journal of Veterinary Research
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    • v.62 no.3
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    • pp.22.1-22.4
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    • 2022
  • This study reports the efficacy of the vasodilator sodium nitroprusside (SNP), for treatment of acute cardiogenic pulmonary edema in dogs. For this study, the patients were divided into the SNP only treatment group, the SNP, furosemide and dobutamine treatment group, and non-SNP treatment group. Seven dogs, 6 dogs and 2 dogs were favorable responders in SNP only group, group with SNP, furosemide and dobutamine and non-SNP treatment group, each. The results of this study suggest that SNP can be an effective alternative therapy for dogs with acute cardiogenic pulmonary edema.

A Case of Non-cardiogenic Pulmonary Edema caused by Nitrogen Dioxide Poisoning after Cutting Copper Pipe with an Oxyethylene Torch (산소 에틸렌 토치로 동파이프 절단작업 후 발생한 이산화질소 중독에 의한 비심인성 폐부종 1례)

  • JeGal, Yang-Jin;Ahn, Jong-Joon;Seo, Kwang-Won;Cha, Hee-Jeong;Kwon, Woon-Jung;Kim, Yang-Ho
    • Journal of The Korean Society of Clinical Toxicology
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    • v.4 no.2
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    • pp.175-179
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    • 2006
  • Welders are exposed to a number of hazards including metal fumes, toxic gases, electricity, heat, noise, and radiation such as ultraviolet and infrared light. We encountered a patient who developed non-cardiogenic pulmonary edema within a day after cutting copper pipe with an oxyethylene torch. The patient was a 26-year-old welder. He complained of dyspnea, generalized myalgia, and febrile sensation the following morning. The patient's chest X-ray and chest CT scan showed extensively distributed and ill-defined centrilobular nodules. Both his symptoms and chest X-ray abnormalities improved spontaneously. We attributed the patient's symptoms to non-cardiogenic pulmonary edema due to nitrogen dioxide, reasoning that: 1) the pipe consisted only of copper, according to material safety data sheet (MSDS); 2) a previous report in the literature demonstrated increased nitrogen dioxide levels under similar conditions; 3) the patient's clinical course and radiologic findings were very reminiscent of non-cardiogenic pulmonary edema following accidental exposure to nitrogen dioxide.

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Drug induced Pulmonary Edema (약물 유발성폐부종)

  • Sung, Si-Han;Jang, Hye-Young;Lim, Hoon
    • Journal of The Korean Society of Clinical Toxicology
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    • v.8 no.2
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    • pp.113-121
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    • 2010
  • Purpose: Drug-induced non-cardiogenic pulmonary edema has been reported on in a drug case series. For most of the agents that cause pulmonary edema, the pathogenic mechanisms that are responsible for the pulmonary edema remain unknown. We report here on the cases of suspected drug-induced pulmonary edema and we analyze the clinical characteristics. Methods: We reviewed the medical records of 1,345 patients who had drug adverse effects and drug poisoning from January 2005 to July 2010, and 480 of these patients were admitted to the EM Department. Among them, 17 patients developed abnormal chest radiological findings and they were analyzed for any clinical characteristics, the initial symptoms, securing the airway and the clinical results. Results: Seventeen patients out of 480 (3.54%) developed drug-induced abnormal chest radiographic pulmonary edema; they displayed initial symptoms that included mental change (41.2%), dyspnea (17.6%), vomiting (11.8%), etc, and some displayed no symptoms at all (11.8%). Only 3 patients out of the 11 who died or had severe pulmonary edema were able to obtain an advanced airway prior to their arrival to the EM Department. Clinical recovery was generally rapid and this was mostly completed within 6 hours. The mortality rate was 11.8% (2 of 17 patients), and the causative drugs were found to be propofol (35.3%, 6 of 17 patients), multiple drugs (41.2% or 7 out of 17) and one patient each with ephedrine, ethylene glycol, doxylamine and an unknown drug, respectively. Conclusion: Drug-induced pulmonary edema and deaths are not uncommon, and recovery is typically rapid with few long-term sequelae when drug administration is discontinued. Oxygen therapy and securing the airway must be performed during transportation for patients with pulmonary edema.

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Subphenotypes of Acute Respiratory Distress Syndrome: Advancing towards Precision Medicine

  • Andrea R. Levine;Carolyn S. Calfee
    • Tuberculosis and Respiratory Diseases
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    • v.87 no.1
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    • pp.1-11
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    • 2024
  • Acute respiratory distress syndrome (ARDS) is a common cause of severe hypoxemia defined by the acute onset of bilateral non-cardiogenic pulmonary edema. The diagnosis is made by defined consensus criteria. Supportive care, including prevention of further injury to the lungs, is the only treatment that conclusively improves outcomes. The inability to find more advanced therapies is due, in part, to the highly sensitive but relatively non-specific current syndromic consensus criteria, combining a heterogenous population of patients under the umbrella of ARDS. With few effective therapies, the morality rate remains 30% to 40%. Many subphenotypes of ARDS have been proposed to cluster patients with shared combinations of observable or measurable traits. Subphenotyping patients is a strategy to overcome heterogeneity to advance clinical research and eventually identify treatable traits. Subphenotypes of ARDS have been proposed based on radiographic patterns, protein biomarkers, transcriptomics, and/or machine-based clustering of clinical and biological variables. Some of these strategies have been reproducible across patient cohorts, but at present all have practical limitations to their implementation. Furthermore, there is no agreement on which strategy is the most appropriate. This review will discuss the current strategies for subphenotyping patients with ARDS, including the strengths and limitations, and the future directions of ARDS subphenotyping.

A Case of Cavitary Lung Lesion as a Consequence of Smoke Inhalation Injury (흡입화상 치료과정에서 생긴 공동성 폐 병변)

  • Shin, Hyun Won;Kim, Cheol Hong;Eom, Kwang Seok;Park, Yong Bum;Jang, Seung Hun;Kim, Dong Gyu;Lee, Myung Goo;Hyun, In-Gyu;Jung, Ki-Suck;Lee, Eil Seong
    • Tuberculosis and Respiratory Diseases
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    • v.60 no.5
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    • pp.564-570
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    • 2006
  • Toxic gases and soot deposition as a consequence of smoke inhalation can cause direct injury to the upper and lower airways and even to the lung parenchyma. A delay in proper and prompt therapy can be detrimental to critically ill burn patients with an inhalation injury. Therefore, serial chest radiography is an important diagnostic tool for pulmonary complications during treatment. The radiographic findings of the chest include normal, consolidation, interstitial and alveolar infiltrates, peribronchial thickening, atelectasis, cardiogenic and non-cardiogenic pulmonary edema, and a pneumothorax as acute complications of smoke inhalation. In addition, bronchiectasis, bronchiolitis obliterans and pulmonary fibrosis can occur as late complications. We encountered a case of 44-year-old male who presented with acute lung injury after an inhalation injury. He required endotracheal intubation and mechanical ventilation due to respiratory failure. He was managed successfully with conservative treatment. Later, a cavitary lesion of the left upper lobe was observed on the chest radiography and computed tomography, which was complicated by massive hemoptysis during the follow-up. However, the cavitary lesion disappeared spontaneously without any clinical consequences.

Transient Change of Electrocardiogram in Two Young Women With Salicylate Intoxication - Two Cases Report - (아스피린 중독에 의한 심전도 변화 2례)

  • You Je-Sung;Park Jong-Woo;Choi Young-Hwan;Cho Young-Soon;Cho Kwang-Hyun;Park Jun-Seok;Chung Sung-Pil;Lee Hahn-Shick
    • Journal of The Korean Society of Clinical Toxicology
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    • v.4 no.1
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    • pp.44-47
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    • 2006
  • Symptoms of aspirin overdose may vary from acid-base disturbance, electrolyte abnormality, non-cardiogenic pulmonary edema, chemical hepatitis, seizure to cardiac toxicity. Cardiac adverse effects from aspirin are uncommon but there are reports of arrhythmia, cardiopulmonary arrest, and myocardial infarction. We report 2 cases of young women with aspirin overdose who exhibited ischemic changes on their ECGs a few hours after the ingestion with spontaneous recovery in a few days. First case, a 29 year old woman, presented to the emergency department 6 hours after ingesting 250 tablets of aspirin (325 mg/T). On examination, the temperature was $36.3^{\circ}C$: blood pressure, 105/72mmHg; Pulse, 111/min and respiratory rate, 24/min. Second case, a 27 year old woman, an hour after ingesting 60 tablets (325mg/T). On examination, the temperature was $36.0^{\circ}C$: blood pressure, 102/72 mmHg; pulse, 89/min and respiratory rate, 25/min. In both cases, ECG after 6 hours of ingestion had sinus tachycardia and developed T wave inversion on the anterior leads in the following ECGs. Their initial serum salicylate levels after 6 hours of ingestion were 71.2 mg/dL and 28.4 mg/dL respectively. These salicylate levels were resolving when these ECGs were observed. The ECG changes resolved in the following days and they were discharged without any further symptoms. Further studies are needed, but for the time being, when dealing with salicylate overdose, transient cardiac depression should be kept in mind to avoid adverse ischemic cardiac events.

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