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

Two cases of pathologically confirmed miliary pulmonary tuberculosis complicated with ARDS were presented. Both had systemic lupus erythematous and used maintenance dose of corticosteroid. Case one developed respiratory distress and severe hypoxemia one day postpartum and chest radiograph revealed nodular and miliary infiltrations and pleural effusion. The patient was intubated and placed on a volume-cycled ventilator. A FIO2 of 70% and a PEEP of 0.98 kPa were required to maintain the oxygen tension at 6.95 kPa. The effective compliance of the lung decreased progressively and the patient died 5 days later. Autopsy revealed disseminated tuberculosis extensively involving the lungs, the liver and kidney. The alveoli were filled with edematous fluid with formation of hyaline membranes and micro-atelectasis. Case two developed respiratory distress and pulmonary edema at the third month of pregnancy. Cardiopulmonary arrest occurred when trying to intubate the patient. Postmortem needle puncture of the lungs and liver revealed charges comparable with tuberculosis and ARDS. In considering the relatively high incidence of pulmonary tuberculosis in China, the percentage of miliary tuberculosis as a potential cause of ARDS might not be very low. It is important to maintain a high index of suspicion for this treatable precipitating disorder and initial appropriate therapy early enough in patients with ARDS.
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PMID:[The adult respiratory distress syndrome associated with miliary tuberculosis]. 273 72

This article reviews the phenomenon of surfactant inactivation by soluble proteins. Following surfactant treatment of preterm lambs, the initial clinical response was not maintained. The surface tensions that were low in the lungs following surfactant treatment increased to high values concurrently with the return of severe respiratory failure. The surface properties of the surfactant that remained in the airways and alveoli could be restored if the soluble proteins were removed. These soluble proteins inactivated different surfactants to different degrees and the interaction was very concentration dependent. The proteins entered the lungs of the preterm lamb because of the tendency of these lungs to form pulmonary oedema. Similar surfactant inactivation occurred in the lungs of infants with respiratory distress syndrome. A variety of manipulations influenced the formation of proteinaceous pulmonary oedema, suggesting that new therapeutic strategies could be developed to treat infants with RDS.
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PMID:Protein leaks and surfactant dysfunction in the pathogenesis of respiratory distress syndrome. 274 83

The purpose of this study was to see if lung vascular protein permeability is greater in preterm lambs with respiratory distress than it is in lambs without lung disease. We measured pulmonary vascular pressures, lung lymph flow, and concentrations of protein in lymph and plasma of 10 chronically catheterized preterm lambs (gestation 133 +/- 1 d) for 2-4 h before and for 4-8 h after delivery by cesarean section. All lambs were treated with mechanical ventilation after birth and received a constant intravenous infusion of glucose-saline solution at an hourly rate of 10 ml/kg. Respiratory failure developed in six lambs, in which there was a sustained threefold postnatal increase in lung lymph flow and lymph protein flow, with an even greater increase in pleural liquid drainage. Concentrations of protein in lymph and pleural liquid were almost identical, averaging approximately 75% of the plasma protein concentration. In the four preterm lambs without lung disease, lymph flow and lymph protein flow were either near or below fetal values by 6-8 h after birth, and there was little or no pleural liquid drainage. Extravascular lung water averaged 7.3 +/- .8 g/g dry lung in lambs with respiratory failure compared to 4.8 +/- .5 g/g dry lung in lambs without lung disease. Thus, pulmonary edema with abnormal leakage of protein-rich liquid from the lung microcirculation into the interstitium is an important pathological feature of the respiratory disease that often occurs after premature birth.
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PMID:Lung fluid balance in lambs before and after premature birth. 276 Feb 1

Recombinant interleukin 2 (rIL-2) administration, a new form of therapy for patients with far-advanced cancer, is associated with a "third space" syndrome, i.e., pulmonary edema, respiratory distress, and hypoxemia, which limits the dose and duration of treatment. To extend our knowledge regarding this toxicity, we established a sheep chronic lung lymph fistula model and measured hemodynamics, arterial blood gases, caudal mediastinal (lung) lymph flow (QL), and blood and lung lymph cellular changes before, during, and after (recovery) a 3-day continuous rIL-2 infusion (9 x 10(5) U/kg). Moderate systemic hypotension, mild pulmonary hypertension, and an increase in alveolar-arterial PO2 gradient was present on day 3 of rIL-2 infusion. QL increased from a base line of 1.9 +/- 0.2 to a maximum of 4.3 +/- 1.1 ml/15 min on day 3 of rIL-2 infusion. At no time was there a change in lymph-to-plasma protein ratio. The leukocyte count increased significantly to 16.1 +/- 4.5 x 10(3) cells/mm3 at recovery day 1. The percentage of blood lymphocytes decreased significantly by day 1 of rIL-2 infusion, returned to base-line levels on day 3, and significantly increased on day 2 of recovery. Lung lymph lymphocytes decreased significantly on days 1 and 2 of rIL-2 infusion. There was a shift in their size; i.e., their area increased from 32 +/- 7 to 57 +/- 19 micron 2 (P less than 0.05) by day 2 of rIL-2 infusion. By day 1 of recovery, lung lymph lymphocyte counts increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiorespiratory and cellular changes with interleukin 2 infusion in sheep. 278 28

We measured airway blood flow in unanesthetized sheep under control conditions and after lung injury induced by inhalation of cotton smoke. Blood flows in trachea, carina, main stem bronchi, intraparenchymal bronchi, and whole lung were measured by injection of radioactive microspheres. In 10 control sheep mean blood flow (+/- SD) was trachea, 17.2 +/- 10.5; main stem bronchi, 17.5 +/- 7.6; and whole lung (parenchyma inclusive of all small intraparenchymal airways), 20.5 +/- 11.9 ml.min-1/100 gm tissue weight. After injury, measurements were made 8 to 30 hours after smoke inhalation when respiratory distress was evident by arterial oxygen tensions of less than 60 mm Hg. Inhalation injury had little effect on cardiac output or blood flow to peripheral tissue. However, after inhalation injury airway blood flow (n = 6) was increased nine times in trachea, eight times in main stem bronchi, twelve times in intraparenchymal bronchi, and two times in whole lung. The increased airway blood flow resulted from a selective vasodilation of the airway vasculature because arterial driving pressures were unchanged by inhalation injury. Other investigators have shown that the microvascular permeability of the bronchial circulation is remarkably sensitive to inflammation, and the present experiments suggest that a selective vasodilation of the airway vasculature is another aspect of the airway response to inflammation. Increased airway blood flow through a leaky microvasculature may increase capillary filtrate from the bronchial circulation and contribute to the pulmonary edema of inhalation injury.
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PMID:Effects of inhalation injury on airway blood flow and edema formation. 292 Dec 58

We report the case of a healthy one-month-old male infant who underwent an uneventful endotracheal anaesthetic for hernia repair. During transport to the recovery room (a less than 30 second trip), the endotracheal tube in the spontaneously breathing infant became obstructed, possibly due to impaction of the tip in the right main bronchus. Restoration of the airway was followed by fulminant pulmonary oedema. Several days of vigorous respiratory and pharmacologic therapy were required for resolution of the infant's respiratory distress. We review other reported cases of acute airway obstruction associated with pulmonary oedema in children and briefly describe the proposed mechanisms. The difficulties of gauging proper endotracheal tube depth in the infant are noted. This case report demonstrates the importance of continuous monitoring during patient transport to the recovery room.
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PMID:Negative pressure pulmonary oedema secondary to airway obstruction in an intubated infant. 304 56

Adoptive immunotherapy, the administration of interleukin-2 (IL-2) and interleukin-2 activated cells, leads to tumor regression in some patients with advanced cancer. Although this new therapeutic modality offers hope for the future, at present, a multitude of toxicities limit the total dose and duration of therapy. Among the toxic side effects a purported third space or vascular leak syndrome is the most serious. In this review, we detail the evidence for a third space syndrome (peripheral edema, ascites, oliguria, elevated serum creatinine levels) and cardiopulmonary dysfunction (hypotension, respiratory distress, pulmonary edema, hypoxemia) with adoptive immunotherapy in human and animal studies. We conclude that IL-2 administration is associated with increased pulmonary microvascular permeability, infiltration of the lung parenchyma with large esterase negative lymphoid cells, hypoxemia, systemic hypotension, positive fluid balance and, in animals, transient pulmonary hypertension. These abnormalities do not seem to be caused by IL-2 directly; the causes may be mediated by IL-2 activated lymphocytes or other IL-2 activated cellular mediators.
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PMID:Cardiopulmonary toxicity of adoptive immunotherapy. 306 15

(1-Sarcosine, 8-isoleucine) angiotensin II was assessed as a therapeutic agent for acute respiratory distress syndrome with oleic acid pulmonary edema in sheep used as an experimental model. Under general anesthesia with controlled mechanical ventilation with 100% oxygen, 32 sheep received oleic acid (0.075 ml/kg) intravenously. After oleic acid infusion, 20 animals were treated with continuous intravenous infusion of the angiotensin II analogue; nine received 300 ng/kg/min, six received 600 ng/kg/min, and five received 2000 ng/kg/min. Cardiopulmonary measurements were repeated every 30 minutes for 270 minutes. According to time-integrated PaO2, six of 15 animals of the groups given 300 and 600 ng/kg/min (43%) did not respond to the treatment. All animals responded in the group given 2000 ng/kg/min. Animals in the latter group had lower Qs/Qt, PaCO2, and airway resistance than had the control animals. Elevation of pulmonary vascular resistance was limited and mean arterial blood pressure was well maintained. These results reveal that (1-Sar, 8-Ile) angiotensin II is effective in the treatment of oleic acid-induced pulmonary edema.
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PMID:Evaluation of (1-sarcosine, 8-isoleucine) angiotensin II as a therapeutic agent for oleic acid-induced pulmonary edema. 308 Aug 19

Sequential lung function was measured in 12 very low-birth weight infants (less than or equal to 1,250 g) within 14 hours of birth, and at daily intervals thereafter for the first week of life, using an esophageal balloon and pneumotachograph system. All infants were clinically free of respiratory distress syndrome and radiographically showed no evidence of atelectasis or pulmonary edema. The alveolar-arterial oxygen tension gradient was high at birth and remained elevated over the period during which arterial blood gases were monitored. Increases of lung compliance and tidal volume between the first day and the end of the first week of life were not significant. Day-to-day determinations of lung compliance revealed an individual and group variability without a definite pattern. Lung resistance measurements indicated no clear trend for the group as a whole, but inspiratory resistance was generally lower than expiratory resistance. Possible causes, in addition to technical factors, that may account for the variability in the pulmonary mechanics of these small infants include an instability of lung volume and uneven distribution of pleural pressure due to chest wall distortion, differences in sleep-state, and alteration in the distribution of body fluids, resulting in a change in lung water. Any or all of these mechanisms may result in an unstable lung, even in an apparently clinically stable very low-birth weight infant.
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PMID:Sequential pulmonary function measurements in very low-birth weight infants during the first week of life. 312 53

We report a case of acute, noncardiogenic pulmonary edema in an 11-year-old boy who suffered strangulation during an altercation. The clinical presentation was characterized by moderate respiratory distress and hemoptysis. Both the radiographic and clinical findings resolved during the three day admission which followed. A review of the literature is presented, and possible pathogenesis is discussed.
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PMID:Acute pulmonary edema after near strangulation. 322 67


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