Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 45-year-old Japanese woman presented with a high fever, a nonproductive coughing, and severe dyspnea, and was admitted to another hospital. During the week prior to hospitalization, she had been given Shosaikoto for treatment of liver dysfunction of unknown etiology. Mycoplasma pneumonitis was initially suspected, so she was treated with antibiotics (clindamycin and minocycline) and received oxygen therapy. Pulmonary insufficiency worsened rapidly, and she was transferred to our hospital. On admission, a chest roentgenogram revealed bilateral alveolar infiltrates predominantly in the medial lung fields. Furosemide and high-dose methylprednisolone were immediately administered, but hypoxemia increased. When the PaO2 was 55.7 Torr while the patient breathed 100% oxygen, mechanical ventilation with positive end-expiratory pressure (PEEP) was started. Arterial blood-gas values improved dramatically, and the chest roentgenogram became clear. Our diagnosis of noncardiogenic pulmonary edema is based on the chest-roentgenographic findings, infiltration of inflammatory cells as seen in two lung-biopsy specimens and bronchoalveolar lavage fluid, the lack of findings of heart failure on physical examination and electrocardiography, and the good clinical response to PEEP. A positive lymphocyte stimulation test in response to Shosaikoto implicated this non-traditional herbal medicine as an etiologic factor in the non-cardiogenic pulmonary edema. Shosaikoto has been identified as the cause of interstitial pneumonia or eosinophilic pneumonia, but pulmonary edema associated with Shosaikoto has not been previously described. This case suggests that methylprednisolone treatment may be insufficient for Shosaikoto-induced pulmonary edema, and that mechanical ventilation with PEEP is very effective.
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PMID:[Pulmonary edema associated with the Chinese medicine shosaikoto]. 986 80

Hexachloroethane (HC) smoke, also known as white smoke, is an obscurant used in numerous military situations. Many adverse health effects are associated with the use of white smoke, some of which are potentially life threatening. Inhalation is the most frequent route of injury. Two deaths among U.S. Army personnel resulted from HC smoke exposure in 1988. As recently as 1997, a United Nations soldier in Bosnia died after an HC smoke canister was discharged in his tent. Injuries are predominantly pulmonary and range from cough and dyspnea to chemical pneumonitis, pulmonary edema, and adult respiratory distress syndrome. In the case presented, a soldier developed pneumomediastinum after exposure to HC smoke. This is the first case reported in the literature of pneumomediastinum associated with HC smoke inhalation.
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PMID:Pneumomediastinum associated with inhalation of white smoke. 1054 33

The purpose of the study was to document the incidence and recurrence rate of pulmonary oedema induced by strenuous swimming (SIPO), and to study the changes in relevant physiological parameters. Thirty-five young men were repeatedly examined over a 2-month period after a swimming time trial in the open sea. A tentative diagnosis of SIPO was made when the swimmer reported shortness of breath accompanied by cough. Twenty-nine events of SIPO were diagnosed in 21 individuals (60% incidence). Oxygen saturation was significantly reduced in SIPO. Mean forced vital capacity (FVC) and FEV(1) were significantly lower in the severe SIPO group. Also, mean FVC and mid-expiratory flows (FEF(25-75%)) obtained 12 months earlier during screening for the programme were lower in individuals who later had SIPO. The ratios of post-swim FVC and FEV(1) values to the corresponding selection examination values were lower in the severe SIPO group. Thus volumes decreased in the SIPO group, besides being lower at the start. Shortness of breath and coughing following strenuous swimming were related to hypoxaemia and reduction in lung volumes, suggesting pulmonary oedema. SIPO was a common and often recurrent phenomenon. Lower initial lung volumes and flows might predict future susceptibility to SIPO.
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PMID:Pulmonary oedema induced by strenuous swimming: a field study. 1085 20

Various drugs are associated with adverse respiratory disorders (ARDs) ranging in severity from mild, moderate to severe and even fatal. Cardioselective and nonselective beta-blockers, calcium antagonists and dipyridamole can induce asthma. ACE inhibitors are mainly associated with cough. Amiodarone is related to a form of interstitial pneumonitis (IP) which can be fatal, tocainidine and flecainidine to a form of IP, and hydrochlorothiazide to a form of IP and pulmonary oedema. Antiasthmatic drugs can be associated with a paradoxical bronchospasm, while leukotriene antagonists are linked to the development of Churg-Strauss syndrome. Nonsteroidal anti-inflammatory drugs including aspirin (acetylsalicylic acid) may induce asthma. Gold is mainly related to IP, penicillamine to IP, systemic lupus erythematosus, bronchiolitis obliterans, and Goodpasture's syndrome. Acute respiratory reactions to nitrofurantoin include dyspnoea, cough, IP, and pleural effusion while IP and fibrosis are common in chronic reactions. Other antibacterials mainly evoke pneumonitis, pulmonary infiltrates and eosinophilia, and bronchiolitis obliterans. ARDs are similar for most categories of cytotoxic agents, with chronic pneumonitis and fibrosis being the most common. Noncardiogenic pulmonary oedema occurs as the most common respiratory complication in opioid agonist addiction. Psychotropic drugs such as phenothiazides, butyrophenones and tricyclic antidepressants can also induce pulmonary oedema. Oral contraceptives may produce asthma exacerbation, while long term use and/or high doses of postmenopausal hormone replacement therapy increase the risk of asthma. Bromocriptine is mainly associated with pleural effusion, while methysergide is usually associated with pleural effusion and fibrosis. Some anorectic agents have been linked to the development of primary pulmonary hypertension. The possibility of the occurrence of ARDs should be taken into account in each individual patient. Although in most cases the adverse effects are unpredictable, they can be reduced to a minimum or prevented if some drugs are avoided or stopped in time.
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PMID:Drug-induced respiratory disorders: incidence, prevention and management. 1094 76

A 27-year-old woman with 39 week gestation was admitted because of cough and dyspnea accompanied by massive right-sided pleural effusion. Following the right thoracocentesis, about 2000 ml of bloody pleural effusion was drained. Just after the thoracocentesis, the fetal heart rate (FHR) temporarily showed a variable deceleration pattern but the rate was restored spontaneously. One hour later, cough and dyspnea became worse. Changes in FHR pattern indicated the premature separation of the normally implanted placenta. Accordingly, an emergency cesarean section was performed under general anesthesia. Massive foamy tracheal secretion was drained from the tracheal tube during surgery. As her chest X-ray showed signs of pulmonary edema in the right lung, her status was diagnosed as reexpansion pulmonary edema (RPE). She was transferred to the intensive care unit and treated with mechanical ventilation, prednisolone and diuretics. Extubation was performed on the 2nd day after the surgery. On reexpansion of the collapsed lung, it is always necessary to consider not only the hemodynamic changes just after reexpansion but also RPE following reexpansion.
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PMID:[Perioperative management for emergency cesarean section of a patient with reexpansion pulmonary edema]. 1102 58

Transfusion-related acute lung injury (TRALI) is a second most serious complication of the blood transfusion. It is a group of symptoms and signs such as dyspnoea, hypotension, cyanosis, cough, elevated temperature, fever and lung oedema that usually develops within an hour or two after transfusion. The full stage clinical presentation is developed between 4th and 6th hours after transfusion. The syndrome is caused by leucoagglutinins or by other lymphocytotoxic antibodies specific for some antigens present on the donor's leukocytes. Alveoles of the lung are the main place of the pathological changes such as intra-alveolar oedema, haemorrhage, hyaline membrane formation, alveolar cell hypertrophy and scant interstitial inflammation. Chest X-ray showed bilateral pulmonary infiltrates but without vascular congestion and with normal cardiac silhouette comparing to the status before transfusion. The syndrome has to be distinquished from pulmonary oedema caused by acute cardial insufficiency, overhydration, trauma and sepsis.
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PMID:[Acute lung injury related to blood transfusion]. 1143 32

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Negative pressure pulmonary edema due to upper airway obstruction following extubation is a well-recognized problem. However, frank pulmonary hemorrhage as a manifestation of upper airway obstruction is uncommon. We report a case of significant pulmonary hemorrhage and negative pressure pulmonary edema in an intubated patient. Bronchoscopy showed a collection of blood in the right lower lobe of the lungs, suggesting a localized source of bleeding. There have been two previously reported cases of pulmonary hemorrhage after upper airway obstruction. One suggested that the bleeding was due to damage to the pulmonary capillaries, the other that it was due to disruption of the bronchial vessels. We feel that in our case there was some indication that the pulmonary bleeding was a result of bronchial vessel damage. A number of factors might have been involved in its development, including negative pulmonary pressure, recent respiratory tract infection, and positive airways pressure (due to coughing).
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PMID:Pulmonary hemorrhage in association with negative pressure edema in an intubated patient. 1147 96

Quinine sulfate, which has been available for many years, has not been implicated definitively in the development of pulmonary toxicity. A variety of adverse effects, however, have been reported with quinine administration. A 45-year-old woman with longstanding rheumatoid arthritis experienced wheezing, severe anxiety, breathlessness, cough, orthopnea, mild fever, chills, and pleuritic chest discomfort after taking a single dose of quinine for nocturnal leg cramps. Radiographic imaging demonstrated diffuse, bilateral pulmonary infiltrates suggestive of pulmonary edema. No cause other than acute quinine ingestion could be identified despite thorough cardiac and infectious disease evaluations. Clinicians should be aware of a possible association between quinine sulfate and pulmonary toxicity.
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PMID:Transient pulmonary infiltrates possibly induced by quinine sulfate. 1206 69

A 45-year-old patient developed shortness of breath, intensive cough, hemoptysis, chest pain and acute bilateral pulmonary infiltrates following the inhalation of crack-cocaine. The bronchoalveolar lavage and transbronchial biopsy revealed infiltrations of polymorphonuclear neutrophils and the formation of foreign body granulomas. The diagnosis of a crack-syndrome was made and the patient rapidly improved under temporary discontinuation of cocaine inhalation and symptomatic therapy. Crack-cocaine is the free-base of cocaine-hydrochloride and its chemical properties allows it to be inhaled tobacco-like. Therefore the lungs become the principal organs exposed and affected. In addition to our findings, diffuse damage of the alveolar wall and capillary injury due to vasoconstriction and toxic action were reported, in some cases rapidly progressing into pulmonary oedema and ARDS. As the consumption of crack cocaine in Germany has markedly increased over the past decade, a higher prevalence of the reported syndrome has to be assumed.
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PMID:[Crack-syndrome: the pulmonary complications of inhaled cocaine. A review a propos a case report]. 1244 9


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