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)

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

We evaluated the role of sulfidopeptide leukotrienes as mediators of endotoxin-induced respiratory failure in pigs. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized 10- to 14-wk-old pigs at 5 micrograms/kg the 1st h followed by 2 micrograms.kg-1.h-1 for 3 h in the presence and absence of LY171883, a specific leukotriene D4 (LTD4)/LTE4 receptor antagonist. Endotoxin caused hemoconcentration, granulocytopenia, decreased cardiac index, systemic hypotension, pulmonary hypertension, increased pulmonary vascular resistance, bronchoconstriction, hypoxemia, increased permeability of the alveolar-capillary membrane, pulmonary edema, and increased plasma concentrations of thromboxane B2 (TxB2), prostaglandin F2 alpha (PGF2 alpha), and 6-keto-PGF1 alpha. LY171883 did not modify endotoxin-induced cardiopulmonary and hematologic abnormalities, except for a modest attenuation of pulmonary hypertension (at 1 h) and increased pulmonary vascular resistance (at 1-2 h). Ex vivo stimulation of whole blood with calcium ionophore caused large increases in plasma concentrations of TxB2, PGF2 alpha, and LTB4. These increases were not significantly modified in blood derived from pigs treated with LY171883, indicating no inhibition of cyclooxygenase or 5-lipoxygenase. We conclude that LTD4 and LTE4 are not important mediators of endotoxin-induced lung injury in anesthetized pigs, although they may contribute modestly to pulmonary vasoconstriction.
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PMID:Effect of LY171883 on endotoxin-induced lung injury in pigs. 197 87

Adult respiratory distress syndrome (ARDS), or noncardiac pulmonary edema, is a form of acute hypoxemic respiratory failure. The goals of treatment for patients with ARDS are to provide supportive therapy, to reverse the underlying etiology or pathology, and to prevent subsequent complications. Supportive therapy consists of supplemental oxygen, positive end-expiratory pressure, and, often, mechanical ventilation. The reversal of the underlying pathology varies according to the etiologic origin of ARDS. Complications from ARDS include stress ulcers, which occur when gastric aggressive and defensive functions become unbalanced. Antacids and cytoprotective agents are used for stress ulcer prophylaxis, but histamine H2-receptor antagonists are now regarded as the standard of care. Because all the marketed H2-receptor antagonists are efficacious, choice of the agent is based on the adverse effect profile and drug interactions. No definitive data currently exist linking stress ulcer prophylaxis regimens that raise intragastric pH to a significant risk for nosocomial pneumonia.
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PMID:Pathophysiology, monitoring, and management of the ventilator-dependent patient: considerations for drug therapy, emphasis on stress ulcer prophylaxis. 198 Jan 84

We reviewed 88 episodes of cardiogenic pulmonary edema (CPE) treated with mechanical ventilation to define the clinical features that predict in-hospital mortality. Fifty-six patients survived to hospital discharge. APACHE II scores were not helpful in prediction. Multiple logistic regression models to predict outcome were developed using variables present at the time of intubation and 24 hours later. The model at the time of intubation indicated mortality was related to systolic blood pressure less than 130 mm Hg, the presence of anterior myocardial infarction, use of calcium channel blockers, age, and absence of prior hospitalization for CPE. A model using additional variables available 24 hours later showed that mortality was related only to the need for vasopressor medication at 24 hours, and systolic blood pressure at intubation less than 130 mm Hg. The predictive power of these models was confirmed by applying them to 46 additional patients. The variables contained in these models suggest that the prognosis of patients with CPE treated with mechanical ventilation depends primarily on the severity of acute left ventricular injury. Variables relating the degree of respiratory failure, however, were not predictive of mortality. These multiple logistic regression models provide a means to compare patients with CPE for quality assessment purposes and for studies of treatment regimens, and may also provide information useful to patient and family counseling regarding the value of continued aggressive intensive care.
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PMID:Acute cardiogenic pulmonary edema treated with mechanical ventilation. Factors determining in-hospital mortality. 201 82

Epileptic seizures may be rapidly followed by neurologic pulmonary edema (NPE). While the outcome of respiratory failure may be spontaneously favourable, in some cases death may occur due to respiratory and/or neurologic dysfunction. Two patients with NPE are described, one of whom survived without treatment and is in good health. In the other the outcome was rapidly fatal despite prompt and vigorous medical treatment.
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PMID:[Neurogenic pulmonary edema complicating a generalized epileptic crisis]. 210 93

The recent 5-year survival rate of patients with lung cancer who underwent resection is significantly higher than that in the previous decade. The main reason for the improved survival rate seems to be due to more accurate staging, however, we cannot detect micrometastases so that distant relapses in many patients occur after operation. In order to control micrometastases, various kinds of surgical adjuvant therapy have been studied. In an attempt to improve resectability rate and survival in patients with locally advanced disease of non-small cell lung cancer, we initiated a pilot study of neoadjuvant (preoperative) therapy. Most of the 31 patients who were entered into the study clinically showed enlarged mediastinal lymph nodes, with or without direct invasion of the primary tumors to mediastinal organs. The response rate of the treatment was 64.5%. Complete resection of the tumor was performed in 14 of 31 (45%) patients and exploratory thoracotomy was done in one patient. Postoperative complications occurred in 6 of those 15 patients who underwent thoracotomy. Three patients suffered from severe complications such as empyema, pulmonary edema or respiratory failure, but recovered eventually. At present, of 15 patients who underwent operation, 9 are alive and free from disease, 2 are alive with relapse and 4 died of relapses. The median survival time was 11.5 and 19 months in non-resected cases and all cases, respectively. Although we cannot draw a conclusion because of the short observation time, we consider that neoadjuvant therapy is worthy of studying.
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PMID:[Surgical adjuvant therapy, especially neoadjuvant therapy of lung cancer]. 216 42

We hypothesized that platelet-activating factor (PAF) and eicosanoids might be important mediators of endotoxin-induced respiratory failure in pigs. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized 10- to 14-wk-old pigs at 5 micrograms/kg the 1st h, followed by 2 micrograms.kg-1.h-1 for 3 h in the presence and absence of SRI 63-675, a specific PAF receptor antagonist. During phase I (i.e., 0-2 h), endotoxin caused pulmonary hypertension and hypoxemia, decreased cardiac index, increased pulmonary vascular resistance, and increased plasma concentrations of thromboxane B2 (TxB2), prostaglandin (PG)F2 alpha, and 6-keto-PGF1 alpha. These phase I effects were attenuated or blocked by SRI 63-675 (10 mg/kg before endotoxin + 3 mg.kg-1.h-1 during endotoxemia). During phase II endotoxemia (i.e., 2-4 h), the PAF receptor antagonist blocked endotoxin-induced pulmonary edema and hypoxemia and increased relative permeability index of the alveolar-capillary membrane. SRI 63-675 also blocked the endotoxin-induced increases in plasma and bronchoalveolar lavage fluid concentrations of leukotriene B4 (LTB4). Ex vivo stimulation of whole blood with calcium ionophore caused large increases in plasma concentrations of TxB2 and LTB4. These increases were not significantly modified in blood derived from pigs treated with SRI 63-675, indicating no inhibition of cyclooxygenase or 5-lipoxygenase and suggesting that the in vivo effects were PAF receptor mediated. We conclude that PAF plays an important role in the release of eicosanoids during endotoxemia and in mediating, either directly or indirectly, endotoxin-induced lung injury in anesthetized pigs.
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PMID:Role of platelet-activating factor and eicosanoids during endotoxin-induced lung injury in pigs. 216 17

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure]. 221 87

Methotrexate, an antifolate cytotoxic drug, is used in anticancer chemotherapy as well as an immuno suppressive in rheumatoid arthritis. It is responsible for numerous secondary effects, amongst which is a characteristic acute pneumonia known since 1969. This pneumonitis has been described in detail, up to the present time in 78 cases gathered in this review. The prevalence of this complication is estimated at around 7%. This pneumonia may occur whatever the age, indication for which methotrexate is prescribed, the route of administration of the product (including the intra-thecal route) and the dose. It includes dyspnoea, fever, (sometimes quite marked) and frequently an acute reversible respiratory failure. Radiologically the opacities are usually diffuse interstitial and symmetrical with a basal predominance with sometimes some confluence and occasionally a pleural reaction. In a small number of cases a transient mediastinal adenopathy has been described. Respiratory function tests show a rapidly developing restrictive syndrome accompanied by hypoxia and hypocapnia. Broncho-alveolar lavage is characterised by hypercellularity with a frank and apparently transitory lymphocytosis. Histologically the most frequent lesion sighted is an extensive acute granulomatous reaction with or without oedema. Most often the outcome is favourable (75% of cases). However 6 deaths due to respiratory failure have been reported. Even though there has not been any formal test, steroid therapy in high dosage seems to accelerate recovery. Progress to an irreversible pulmonary fibrosis is possible but rare. The mechanism of this drug related acute pneumonia is not known but would seem to resemble that of other granulomatosis. Besides this rapidly progressive pneumonitis, methotrexate is responsible for a very small number of cases of severe pulmonary oedema and of acute painful pleurisies.
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PMID:[Pneumopathy caused by methotrexate]. 225 35

A 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
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PMID:Lung fibrosis induced by Thorotrast. 225 23


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