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)

Children who have been exposed to smoke in a confined space or who have soot or burns, however minimal, on the face should be admitted to hospital. Respiratory distress may be delayed, but if it is progressive the patient should be curarised, intubated, and mechanically ventilated. Unless ventilation continues for 48 hours, followed by 24 hours' spontaneous respiration against a positive airway pressure, stridor and pulmonary oedema may recur. An endotracheal tube small enough to allow a leak between it and the oedematous mucosa must be passed to prevent laryngeal damage and subsequent subglottic stenosis. High humidity of inspired gases keeps secretions fluid and the endotracheal tube patent. A high oxygen concentration compensates for deficient oxygen uptake and transport caused by pulmonary lesions and the presence of poisonous compounds interfering with oxygen transport. Dexamethasone to minimise cerebral oedema and antibiotics to reduce the incidence of chest infections should be given.
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PMID:Management of airway complications of burns in children. 58 69

Acetazolamide is a useful prophylactic for acute mountain sickness causing marked reduction in headache, nausea, vomiting, weakness, etc. Improvements correlate with increased arterial oxygen concentrations, reduction in proteinuria and peripheral oedema and other objective measures of acute mountain sickness. Evidence that Acetazolamide is beneficial for pulmonary oedema or cerebral oedema is scanty because of the lower frequency of these severe forms of mountain sickness. Dexamethasone, used prophylactically, also reduces the symptoms of acute mountain sickness partly due to its euphoric effect. Use of Acetazolamide as a treatment for established acute mountain sickness has been investigated. Large doses of Acetazolamide increase arterial oxygen levels over a few hours and this leads to a reduction of symptoms but data is limited and faster acting carbonic anhydrides inhibitors such as Methazolamide may be preferable in an emergency situation. There is no comparison of the effectiveness of Acetazolamide with other drugs used for treating acute mountain sickness such as steroids and calcium channel blocking drugs. Also, there is no data on drug combinations which could have additive effects and thereby be more beneficial than individual drugs.
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PMID:Acetazolamide and high altitude diseases. 148 96

Intravenous Paf-acether (Paf, 15-80 micrograms kg-1) killed conscious Swiss mice in a dose-dependent manner, without causing platelet aggregation in the lung microvasculature, or pulmonary oedema. Propranolol (0.01-10 mg kg-1, i.p.) potentiated the effects of an LD20 of Paf dose-dependently, while the beta 1-adrenoceptor selective antagonist, metoprolol, was three orders of magnitude less potent in this respect. Salbutamol (1 mg kg-1, i.p.) provided complete protection against an LD80 of Paf. High doses of indomethacin, aspirin, benoxaprofen and FPL 55712 given i.p. failed to inhibit the effects of an LD80 of Paf, while BW 755C (50-100 mg kg-1) exerted a dose-dependent protection and benzydamine (50 mg kg-1) and nordihydroguaiaretic acid (200 mg kg-1) were partially active. Dexamethasone (1-5 mg kg-1, s.c.) exerted a dose-dependent protection, when administered at least 4 h before Paf. In mice anaesthetized with urethane, Paf (1-30 micrograms kg-1) produced hypotension which was not clearly dose-related. The effects of the highest dose were also tested on the resistance of the lungs to inflation and found to produce bronchoconstriction. It may be concluded that pharmacological manipulation of beta 2-adrenoceptors modulates Paf-induced death in mice, while arachidonate metabolites of the cyclo-oxygenase pathway and peptidoleukotrienes do not appear to be involved. However, lipoxygenase products, distinct from peptidoleukotrienes, may play a role in this phenomenon. It is suggested that bronchoconstriction, probably associated with cardiovascular effects, is a major determinant of the acute toxicity of Paf in mice.
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PMID:Paf-acether-induced death in mice: involvement of arachidonate metabolites and beta-adrenoceptors. 288 Jun 24

Pulmonary edema after ascent to altitude is well recognized but its pathogenesis is poorly understood. To determine whether altitude exposure increases lung vascular permeability, we exposed rats to a simulated altitude of approximately 14,500 feet (barometric pressure [Pb] 450 Torr) and measured the pulmonary transvascular escape of radiolabeled 125I-albumin corrected for lung blood content with 51Cr-tagged red blood cells (protein leak index = PLI). Exposures of 24 and 48 h caused significant increases in PLI (2.30 +/- 0.08 and 2.40 +/- 0.06) compared with normoxic controls (1.76 +/- 0.06), but brief hypoxic exposures of 1-13 h produced no increase in PLI, despite comparable increases in pulmonary artery pressure. There were associated increases in gravimetric estimates of lung water in the altitude-exposed groups and perivascular edema cuffs on histologic examination. Normobaric hypoxia (48 h; fractional inspired oxygen concentration [FIO2] = 15%) also increased lung transvascular protein escape and lung water. Dexamethasone has been used to prevent and treat altitude-induced illnesses, but its mechanism of action is unclear. Dexamethasone (0.5 or 0.05 mg/kg per 12 h) started 12 h before and continued during 48 h of altitude exposure prevented the hypoxia-induced increases in transvascular protein escape and lung water. Hemodynamic measurements (mean pulmonary artery pressure and cardiac output) were unaffected by dexamethasone, suggesting that its effect was not due to a reduction in pulmonary artery pressure or flow. The role of endogenous glucocorticoid activity was assessed in adrenalectomized rats that showed augmented hypoxia-induced increases in transvascular protein escape, which were prevented by exogenous glucocorticoid replacement. In summary, subacute hypoxic exposures increased pulmonary transvascular protein escape and lung water in rats. Dexamethasone prevented these changes independent of reductions of mean pulmonary artery pressure or flow, whereas adrenalectomy increased pulmonary vascular permeability and edema at altitude. Increases in vascular permeability in hypoxia could contribute to the development of high-altitude pulmonary edema and endogenous glucocorticoids may have an important influence on pulmonary vascular permeability in hypoxia.
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PMID:Hypoxia-induced increases in pulmonary transvascular protein escape in rats. Modulation by glucocorticoids. 319 58

Acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) continue to cause significant morbidity and occasional deaths among mountain recreationists and residents. Descent to lower altitude is still considered the treatment of choice, but an increased role for medical therapy is emerging. Acetazolamide is currently the drug of choice for prevention of AMS, and probably HAPE as well. Numerous studies have demonstrated the drug's effectiveness when it is started 12 to 24 hours before ascent. Suggestions for indications, dosage, and regimen vary with different authors. Lower dosage offers adequate protection with fewer side effects. Acetazolamide has still not been adequately studied for treatment of altitude illness. Oxygen effectively treats HAPE and mild AMS, but is not as useful for cerebral edema. Dexamethasone recently was found effective for treatment of AMS, including early cerebral edema, but not for advanced cerebral edema. Side effects limit its use for prophylaxis, but dexamethasone offers an alternative to acetazolamide for those with sulfa intolerance.
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PMID:Medical therapy of altitude illness. 330 58

Endotoxin (500 micrograms/kg)-treated rats are very tolerant to hyperoxia (greater than 95% O2, 1 ATA). We have now attempted to determine if dexamethasone given to rats 1 h before a usually lethal dose of endotoxin would diminish endotoxin's lethality without substantially abrogating its capacity to confer tolerance to hyperoxia. Endotoxin (20 mg/kg) given alone killed 70-80% of air- or O2-breathing rats within 24 h; dexamethasone (0.6 mg) given 1 h before endotoxin decreased mortality at 24 h to 10-15%. About 90% of the rats that were alive 24 h after receiving dexamethasone plus endotoxin (20 mg/kg) survived 72 h of hyperoxia. Dexamethasone plus endotoxin (10 mg/kg) provided as much protection against pulmonary edema resulting from 72 h of hyperoxia as did 500 micrograms/kg endotoxin alone. Tolerance to hyperoxia produced by dexamethasone plus high-dose endotoxin was accompanied by a rise in the activity in the lung of antioxidant enzymes. We conclude that dexamethasone protects rats against the lethal effects of high doses of endotoxin without interfering with endotoxin's capacity to engender tolerance to hyperoxia.
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PMID:Dexamethasone protects against high-dose endotoxin without loss of tolerance to oxygen. 370 Mar 5

T-2 toxin, a major trichothecene mycotoxin, was administered intravenously to rats. At a dose of 0.75 mg/kg two thirds of the animals died. In animals that received dexamethasone (1.6 mg/kg IV) either 30 min before or 1 h after the toxin, there was a more than fourfold reduction in lethality rate. Dexamethasone injected 3 h after the toxin was less effective. At a lethal dose of T-2 toxin (1 mg/kg IV) pretreatment with dexamethasone only delayed death, whereas lethality rate was barely affected (9/10 vs 10/10 in controls). Dexamethasone markedly reduced the incidence of lung edema and diarrhea. The incidence of hemorrhages, however, was not reduced by dexamethasone. Gastrointestinal bleeding was even more frequent in treated rats than in controls.
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PMID:Dexamethasone decreases lethality of rats in acute poisoning with T-2 toxin. 401 4

Children with a history of exposure to smoke in a confined space or showing soot or burns, however minimal, on the face should be admitted to hospital. Respiratory distress may be delayed, but if it is progressive the patient should be curarized, intubated, and mechanically ventilated. Ventilation should be continued for a minimum of 48 hours, followed by 24 hours of spontaneous respiration against a positive airway pressure. It treatment is stopped sooner, a recurrence of stridor and pulmonary oedema is likely. It is mandatory to pass an endotracheal tube small enough to allow a leak between it and the oedematous mucosa, in order that laryngeal damage and subsequent subglottic stenosis may be avoided. It is important tu use high humidity of inspired gases to keep secretions fluid and the endotracheal tube patent. Dexamethasone should be given to minimise cerebral oedema and antibiotics to reduce the incidence of chest infections.
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PMID:Inhalation injury to the respiratory tract of children. 722 Oct 6

Severe malaria remains a major cause of mortality in the world. Malaria can mimic many diseases and there is no absolute diagnostic clinical features. High index of suspicion is clue for clinical diagnosis. Previous travel history to endemic area should be elicited in all, and in particular, febrile patients. Management of severe malaria needs potent antimalarial drug and intensive care. Artemisinin derivatives can be of altemative use to quinine. Dexamethasone and mannitol have no beneficial value in the management of cerebral malaria. In pulmonary oedema patients whose hydration assessments are difficult to monitor, central venous pressure evaluation may be useful. Acute renal failure patients may need dialysis until uraemic syndrome subsides or patients can void urine. Most severe malaria patients have thrombocytopenia; however, platelet concentrate transfusion is indicated only in patients with systemic bleeding. Morbidity and mortality will be reduced in severe malaria patients with early diagnosis and prompt treatment.
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PMID:Guideline in management of severe malaria. 1125 92

All-trans retinoic acid (ATRA) induces complete remission in patients with acute promyelocytic leukemia (APL). However, ATRA sometimes causes retinoic acid syndrome (RAS) characterized by respiratory distress, pleural effusions, fever and weight gain. To investigate the pathophysiology of RAS, we generated an animal model by injecting an APL cell line, NB4, into immunodeficient mice. When NOD/scid mice were injected intravenously with fully differentiated NB4 cells (1 x 10(7)) and then given a daily administration of ATRA, three of 12 mice died of pulmonary edema within 14 days. Pathologically, dilated lung capillary vessels and alveolar effusions were observed. After the injection, NB4 cells were detected in the lung within 2 days and in the pleural effusion later on. The gene expression levels of CXC chemokines (MIP-2 and KC) and ICAM-1 were increased in the lung and heart by the ATRA administration. In immunohistochemical analyses, MIP-2 was clearly detected in alveolar macrophages of the lung in mice with RAS. Dexamethasone treatment prevented the development of RAS and decreased the CXC chemokine mRNA expression in the lung. These findings suggested that the activation of adhesion molecules for leukocytes and expression of CXC chemokines in the lung are closely involved in triggering RAS.
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PMID:Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line. 1474 6


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