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)

Clinical studies of ARDS have been successful in determining the most common predisposing clinical disorders and the natural history of this syndrome. Sepsis, gastric aspiration, and major trauma are the most frequently associated high-risk factors. Overall mortality is in the range of 60% to 70%, but is even higher if ARDS is associated with sepsis, severe acidemia, or decreased renal function. It is evident that multisystem failure is responsible for death in many patients, as well as secondary pulmonary and extrapulmonary infections. Pathologic studies have provided descriptive information regarding the acute, subacute, and chronic phases of the syndrome, but little insight into the precise pathogenesis of the initial lung injury or the progressive fibrosing alveolitis and lung destruction that develops in some patients. There has been considerable circumstantial evidence from clinical studies implicating the neutrophil as a potentially important mediator of the early changes in lung endothelial and epithelial permeability. However, not all investigators have found the same alterations in neutrophil function in the circulation or in the lavage from the lungs of patients with ARDS. Also, the heterogeneous etiologies of ARDS make it difficult to be sure that there is a final common pathway for acute lung injury in all ARDS patients. In addition, there are a host of mediators, including products of complement activation and arachidonic acid metabolism, that may be important in amplifying the inflammatory response. Also, abnormalities of surfactant production and collagen turnover, as well as impaired host defenses in the lung, may contribute to the progressive respiratory failure that occurs in some ARDS patients, even though the acute, exudative phase of lung injury has resolved. Future human studies may provide useful information about the mechanisms of the acute lung injury through studies of circulating plasma markers, blood elements, and lavage fluids from high-risk patients. On the other hand, samples of cells and mediators from the airspaces with lavage still may not reflect the critical interactions of mediators and cells with the lung endothelium that lead to the protein-rich pulmonary edema that characterizes the first phase of ARDS. Thus, experimental studies must continue to study the details of the early phases of acute lung injury (see article by Flick, page 455). Finally, it is clear that treatment designed to reduce the severity and the incidence of ARDS must be started early, since the syndrome develops so rapidly in high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathophysiology of the adult respiratory distress syndrome. What have we learned from human studies? 333 57

Although catecholamine inotropic drugs are often used to support the circulation of critically ill patients with hypoxemic respiratory failure, their effect on the pulmonary circulation and on gas exchange is incompletely understood. In order to improve our understanding of the effects of these drugs on the pulmonary circulation, we made measurements of total and regional intrapulmonary shunt (Qs/Qt), distribution of pulmonary blood flow, and pulmonary hemodynamics before and after infusions of dopamine (n = 6, 5 micrograms/kg/min), dobutamine (n = 6, 10 micrograms/kg/min), isoproterenol (n = 6, 0.1 micrograms/kg/min), or saline in dogs with unilobar oleic acid-induced pulmonary edema. In addition to permitting determination of the overall hemodynamic and gas exchange effects of these drugs, this preparation allowed measurement of changes in distribution of pulmonary blood flow between normal and edematous lung. In 6 dogs given dobutamine, mean cardiac output (CO) increased by 1 liter/min, while pulmonary arterial pressure (PPA) increased by 2 mm Hg with no change in pulmonary vascular resistance (PVR) or distribution of pulmonary blood flow. There was a 5% increase in mean Qs/Qt which, because of the lack of evidence of pulmonary vasoactivity, was attributed to time or to increased CO. Isoproterenol produced a similar increase in CO, but reduced PPA and PVR indicating pulmonary vasodilator activity. Pulmonary vasodilation was most prominent in edematous lung, resulting in an increase in relative blood flow to the edema lung lobe and a substantial increase in Qs/Qt, exceeding the increase in all other groups. Dopamine, similarly increasing CO, did not change overall PVR but reduced fractional blood flow to the edema lobe by 3.4% of CO. Neither Qs/Qt nor PaO2 changed significantly in this group. The differing effects of these agents on pulmonary hemodynamics, intrapulmonary blood flow distribution, and gas exchange have potentially significant implications affecting the choice of drug used for circulatory support in hypoxemic respiratory failure.
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PMID:The pulmonary vascular effects of dopamine, dobutamine, and isoproterenol in unilobar pulmonary edema in dogs. 333 8

Infection, hemorrhage and adult respiratory distress syndrome (ARDS) are pulmonary complications occurring after remission induction therapy for acute leukemia. The aim of this study was to analyze the incidence of these causes by serial roentgenogram, clinical, microbiological and laboratory tests in 21 patients (pts) with relapsed acute leukemia (18 X myeloid, 3 X lymphoblastic), an AML-pt (acute myeloid leukemia) suffering from secondary leukemia, and three pts with primary refractory leukemia following treatment with intermediate (IM) and high-dose cytosine arabinoside (HD-Ara C), in combination with amsacrine (AMSA)(n = 19), etoposide (VP 16) (n = 5) or Mitoxantrone (n = 1). Eleven out of 25 pts developed pulmonary complications, one of them with massive hemoptysis and roentgenographic signs of pulmonary bleeding, one suffering from protracted shock after a tumor lysis syndrome, two pts showing symptoms of a cardiogenic pulmonary edema complicating severe Candida pneumonia in one case and legionnaires' disease in the other. Seven of the eleven pts had a non-cardiogenic pulmonary edema with respiratory failure 1-14 days after cessation of induction or consolidation therapy. In six of the seven, there were no signs of cardiogenic, infectious or metabolic reasons, including fluid overload, for the pulmonary edema, one had as a contributing factor a Candida infection of the lung. Three of the seven patients recovered, four died (two following IM and two after HD-Ara C). Other adverse side effects, clearly attributable to HD-Ara C, included delirious state (n = 3), generalized erythema (n = 3), acute pancreatitis (n = 2), acute abdomen (n = 1) and conjunctivitis in almost all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-cardiogenic pulmonary edema complicating intermediate and high-dose Ara C treatment for relapsed acute leukemia. 336 72

We studied the role of O2 supply and demand factors for producing diaphragmatic failure in a canine model of cardiogenic shock with pulmonary edema. We produced pulmonary edema with oleic acid and then hypotension with cardiac tamponade and followed the animals until respiratory failure began, which was defined by a 50% fall in frequency of breathing and diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease in the diaphragmatic electromyogram. Regional blood flows were measured with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di) (ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi) and the arterial and phrenic venous O2 contents. With oleic acid-induced pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/- 31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2 +/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98 (P less than 0.05) due to increased O2 extraction and no significant change in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/- 0.23 due to the combined effects of small declines in Qdi and the arterial O2 content but remained higher than control even though the energy demands returned to control values. In conclusion, when cardiogenic shock is added to pulmonary edema VO2 di and energy output do not increase further and eventually fall.
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PMID:Diaphragmatic energetics and blood flow during pulmonary edema and hypotension. 339 91

Hybridoma cells were obtained by fusing spleen cells from mice, immunized against the 15 kDa porcine surfactant apoprotein, with a myeloma cell line. Adult mice were inoculated intraperitoneally with this hybridoma; mice that were not inoculated or were inoculated with myeloma cells served as controls. Lung-thorax compliance was measured at various intervals after inoculation. The animals were then killed for histologic-morphometric evaluation of alveolar air expansion, inflammatory reaction in the pulmonary parenchyma, and intraalveolar edema. In the hybridoma group, the mice developed respiratory failure 9 days after inoculation, with markedly reduced lung-thorax compliance, lung congestion, alveolar collapse, hemorrhagic pulmonary edema, and hyaline membranes. Morphometric data from the same animals showed reduced volume density of alveolar air, and increased volume densities of intraalveolar "fluid" (edema) and tissue components. These lung lesions are similar to those in the adult respiratory distress syndrome.
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PMID:Respiratory failure in mice caused by a hybridoma making antibodies to the 15 kDa surfactant apoprotein. 339 79

Pulmonary calcinosis is a recognized complication of renal failure. The resulting pulmonary compromise may be severe or even fatal. The potential contribution of hypercalcemia, hyperphosphatemia, and increased calcium-phosphorus product to the development of pulmonary calcinosis has been controversial. We describe four patients (ages 2 1/4 to 18 years) who had severe pulmonary calcinosis and respiratory failure within three to five days after renal transplantation. Initial clinical and roentgenographic findings suggested noncardiogenic pulmonary edema. Marked pulmonary hypertension was present in the two patients in whom pulmonary artery pressure data were available. Other clinical features in common included poor allograft function with persistent uremia requiring dialysis and evidence of moderate to severe secondary hyperparathyroidism. In three of the patients, the calcium-phosphorus product increased markedly after transplantation, to peak values of 122 to 147. This increase occurred at the same time as the onset of respiratory failure. Peak serum calcium levels were 10.0 to 11.0 mg/dL and peak serum phosphorus levels were 9.2 to 13.5 mg/dL. All patients died of respiratory failure five to 58 days after transplantation. The posttransplantation period may be a time of increased risk of potentially fatal pulmonary calcinosis in pediatric renal transplant recipients. The diagnosis should be considered in any patient with respiratory failure of unknown cause following renal transplantation.
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PMID:Pulmonary calcinosis after renal transplantation in pediatric patients. 352 Dec 66

A case is reported of rapidly resolving pulmonary oedema following post-extubation laryngospasm in a 23 year-old healthy man who underwent emergency resection of a rectal polyp. The laryngospasm occurred immediately after extubation and resolved after administration of curare. The patient was reintubated and auscultation disclosed bilateral coarse and moist rales. Chest X-ray displayed a right pulmonary opacity. Because of the deteriorating respiratory status, mechanical ventilation was used with positive end-expiratory pressure for 18 h. Chest examination, chest X-ray and arterial blood gas levels improved steadily and the patient was discharged 24 h later. Pulmonary oedema associated with upper airway obstruction seems to be related to hypoxic pulmonary vasoconstriction and the largely subatmospheric transpulmonary pressure gradients generated while trying to breathe against a closed glottis. In addition, this increased negative intra-alveolar pressure was responsible for significant changes in cardiovascular function: right ventricular blood volume, right ventricular ejection fraction and left ventricular after-load increased, while left ventricular ejection fraction decreased. These changes favoured a rise in left atrial and pulmonary blood volumes, with transudation of fluid from the capillaries into the alveoli. Because of the severe consequences of respiratory failure, any patient who suffers acute upper airway obstruction should be observed in the recovery room for at least 3 h in order not to miss this rarely developing, but fortunately rapidly reversible, syndrome.
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PMID:[Pulmonary edema after laryngospasm]. 355 82

The course of 177 consecutive patients with severe salicylate self-poisoning treated in an intensive care unit (ICU) during a period of 15 years is presented. On admission, cerebral depression was observed in 61% respiratory failure was present in 47%, acidosis in 36% and cardiovascular function was impaired in 14%. A mortality rate of 15% was observed, which was proportionally higher in patients more than 40 years old and in patients with delayed diagnosis. Twenty-seven patients died and an autopsy was performed on 26 patients. The main autopsy diagnosis was ulcers of the gastrointestinal tract in 46%, pulmonary oedema in 46%, cerebral oedema in 31% and cerebral haemorrhage in 23%.
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PMID:Acute salicylate self-poisoning in 177 consecutive patients treated in ICU. 359 Dec 55

There is evidence from pediatric tertiary care centers in the United States that childhood deaths from asthma in hospitalized patients are becoming increasingly rare, while asthma mortality outside the hospital appears to be on the rise. When a young outpatient with asthma dies, the event is apt to be sudden and unanticipated and the victim is likely to be a preadolescent or adolescent who has suffered from asthma most of his or her life and who, despite ongoing bronchodilator therapy, requires hospitalizations for treatment of status asthmaticus. Patients in this age cohort have a strong tendency to underuse, overuse, or neglect to use prescribed medications, possibly as a gesture of emerging independence or because of the depression engendered by a chronic illness. In some instances serious psychosocial pathology accounts for noncompliance. For a patient with chronic asthma with a high-risk profile, any departure from an ongoing treatment regimen may result in respiratory failure. Pathologic complications of asthma may also act to upset the precarious physiologic equilibrium these patients have established. Unsuspected chronic pneumonia may lead to further increases in a chronically high degree of oxygen desaturation. Hypoxic seizures during an asthma attack may precipitate pulmonary edema. Tension pneumothorax has an even greater fatality potential for high-risk patients with asthma than it has for other patients with asthma, and pulmonary hypertension with cor pulmonale may develop because of chronic hypoxia. Some sudden deaths in children with chronic, severe asthma are unassociated with any of the above, making it necessary to entertain still other hypotheses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An analysis of fifteen childhood asthma fatalities. 362

Of 210 multiple trauma patients admitted to our Intensive Care Unit (ICU), 12 (5%) presented with severe hypoxemic respiratory failure needing mechanical ventilation with an FIO2 of 1.0 because of severe intrapulmonary shunting (IS). Five (42%) of these patients survived and two (17%) died because of their underlying respiratory failure. We found a mean of three etiologic factors in each patient to account for their IS. Nonsurvivors had a lower cardiac index than survivors when they first needed FIO2 of 1.0 and ARDS was more frequent among this group. All patients who survived were in severe hypoxemic respiratory failure in the first 5 days post-trauma; all patients who needed FIO2 of 1.0 later than 5 days post-trauma died. Data collected for patients with similar degree of respiratory failure in coronary care ICU (n = 18), in medical ICU (n = 19), and surgical ICU (n = 21) demonstrated that multiple trauma patients with severe hypoxemic respiratory failure were younger and were hospitalized and ventilated for longer periods of time. In multiple trauma patients, as for patients with cardiogenic pulmonary edema, death was seldom related to respiratory failure itself. We concluded that severe hypoxemic respiratory failure in trauma patients is usually of mixed etiologies. It is a serious cause of morbidity in these patients; however, mortality is seldom directly related to this condition. Severe IS occurring shortly after trauma is of better prognosis than late IS.
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PMID:Mortality and morbidity related to severe intrapulmonary shunting in multiple trauma patients. 365 78


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