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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.
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PMID:[Examinations to phenomenon of shock-lung (author's transl)]. 0 60

Diffuse pulmonary edema, capable of arising in the absence of hemodynamic disorders is rare in infectious disease. They take on two different clinical appearances: a) acute edema of the lung with the syndrome of asphysia, b) a subacute dyspneic pneumonia with hypoxemia and hypo or normocapnia. These initial disorders can be followed by progressive respiratory failure secondary to the development of diffuse interstitial lesions with fibrosis and intra-alveolar hyaline deposits. The bronchiolo-alveolar lesions which induce a fibrin rich exudate are directly caused by the patogenic agent: myxovirus, essentially influenzae, and more rarely adeno or herpes virus. The role of bacteria and of certain parasites is more debateable.
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PMID:[Pulmonary edemas of infectious origin]. 0 55

Pulmonary edema, cardiac enlargement, and respiratory insufficiency may occur in patients with acute pancreatitis. The mechanisms are complex and incompletely understood, but probable etiologic factors include fluid overload, left ventricular failure, impaired respiratory excursion and microatelectasis, and a nonspecific response of the lung to various types of pulmonary injury including hypotension, intravenous crystalloids, and the effects of circulating pancreatic enzymes. Recognition of the association of pulmonary edema and respiratory insufficiency with pancreatitis is importance because early treatment with positive pressure breathing, careful fluid management and diuretics, and corticosteroids may prevent the development of irreversible respiratory failure.
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PMID:Pulmonary edema and respiratory insufficiency in acute pancreatitis. 12 91

Ten infants and children with respiratory failure, receiving standard maintenance water requirements, were treated on 13 occasions with intravenously given furosemide (1 to 2 mg/kg) because of continued impairment of oxygenation despite conventional therapy. Pulmonary auscultation and radiographs were normal or typical of the primary diagnosis. After a five-fold increase in urine output the mean Po2 rose from 61 mm Hg at a mean FiO2 of 0.7 to 140 mm Hg at an FiO2 of 0.65. The Pco2 decreased from 46 to 38 mm Hg. Interstitial pulmonary edema in these patients can be related to both their lung disease and impaired water tolerance during ventilatory therapy.
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PMID:Edema of the pulmonary interstitium in infants and children. 23 52

In a 49 year old man with blast crisis and massive leukocytosis due to chronic myelogenous leukemia, severe hypoxic respiratory failure developed despite a normal chest film. Correction of hypoxemia was observed after reduction of the white blood cell count by hydroxy-urea therapy. A similar episode occurred prior to death, and necropsy examination revealed extensive plugging of the pulmonary vasculature by leukemic blast cells but no infection or pulmonary edema. An inverse linear correlation was demonstrated between the peripheral white blood cell count and the efficiency of oxygen transfer in the lung as determined by the arterial to alveolar oxygen tension ratio. We postulate that mechanical obstruction and/or leukocyte mediated capillary endothelial injury caused the severe leukocyte mediated capillary endothelial injury caused the severe hypoxemia. Abnormalities of pulmonary gas exchange may be common in leukemic patients with markedly increased leukocyte counts.
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PMID:Reversible respiratory failure due to intravascular leukostasis in chronic myelogenous leukemia. Relationship of oxygen transfer to leukocyte count. 29 38

Acute fulminating pulmonary edema developed in three patients after acute airway obstruction secondary to tumor, strangulation, and interrupted hanging (one case each). The common etiologic factor was vigorous inspiratory effort against a totally obstructed upper airway. Acute pulmonary edema followed the event in minutes to hours and required ventilatory assistance to maintain oxygenation. All patients eventually responded to fluid restriction, diuretics, and steroids. One case was complicated by aspiration of gastric contents following respiratory failure. To our knowledge, this condition is previously unreported in English literature. We presume that the pathogenesis is related to alveolar and capillary damage, induced by the severe negative pressure generated by attempting to inspire against the closed upper airway.
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PMID:Pulmonary edema as a complication of acute airway obstruction. 33 33

Twenty-nine patients with acute renal failure following bites by snakes of the genera Crotalus and Bothrops were treated in an Intensive Care Unit (ICU). Eight were given conservative treatment. Peritoneal dialysis was necessary in 21 patients, and hemodialysis in one of these. The main complications occurring while the patients were in the ICU were pulmonary edema (5 cases), respiratory failure (4), cardiac arrest (4), and hypovolemic shock (1 case). Three patients died with respiratory and hemodynamic disturbances while in the ICU, one of them during the polyuric phase. Twenty-four patients were discharged from the hospital with no clinical or laboratory evidence of renal failure. Two patients developed bilateral cortical necrosis of the kidney. One of them died in the general ward after interruption of dialysis and the other was discharged from the hospital with chronic renal failure. It was not possible to perform a kidney transplantation. The importance of the ICU in the recovery of such patients is stressed.
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PMID:Intensive care unit treatment of acute renal failure following snake bite. 45 41

Close relationships between progressive respiratory failure, roentgenographic signs of pulmonary opacification and decreases in the difference between colloid osmotic pressure of plasma and the pulmonary artery wedge pressure (colloid-hydrosatic pressure gradient) were demonstrated in 49 critically ill patients with multisystem failure, in patients in shock. The potential importance of this relationship is underscored by the observation that fatal progression of pulmonary edema was related to a critical reduction in the colloid-hydrostatic pressure gradient to levels of less than 0 mm Hg. More often, reduction in colloid osmotic pressure rather than increases in left ventricular filling pressure (pulmonary artery wedge pressure) accounted for the decline in colloid-hydrostatic pressure gradient. Routine measurement of colloid osmotic pressure, preferably in conjunction with pulmonary artery wedge pressure, is likely to improve understanding of the mechanisms of acute pulmonary edema.
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PMID:Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure. 64 30

Pulmonary oedema has been reported in severe cases of acetyl salicylic acid (ASA) poisoning. Liberal use of intravenous fluids, to establish a forced diuresis, is usually thought to be the precipitating cause. A case of severe ASA poisoning and respiratory failure was found to have increased pulmonary vascular resistance and signs of intravascular hypercoagulability. The patient recovered rapidly on mechanical ventilation with a positive endexpiratory pressure of 18 cm H2O and systemic steroids.
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PMID:Adult respiratory distress syndrome precipitated by massive salicylate poisoning. 73 81

The possible association between acute respiratory failure and disseminated intravascular coagulation was examined in eight patients with severe acute respiratory failure--a condition characterized by tachypnea, right to left intrapulmonary shunting of blood greater than 30 per cent of cardiac output, increased pulmonary artery pressure with low or normal pulmonary artery wedge pressure and roentgenologic interstitial pulmonary edema. Treatment consisted of mechanical ventilation with positive end expiratory pressure sufficient to minimize intrapulmonary shunting. There was no abnormality in platelet concentration fibrin split product concentration, fibrinogen concentration, prothrombin time or activated partial thromboplastin time during the period of most severe respiratory failure in any patient. However, mean platelet concentration fell to 90,000+/-9,000 per cubic millimeter, less than 0.001, and mean fibrin split product levels rose to 60+/-10 micrograms per milliliter, p less than 0.05, the fourth day after the onset of acute respiratory failure. No significant change occurred in other coagulation parameters. Disseminated intravascular coagulation developed in none of the patients nor was there any correlation between coagulation abnormalities and severity of acute respiratory failure that would suggest a cause and effect relationship.
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PMID:Acute respiratory failure and intravascular coagulation. 78 44


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