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

The time course of leukotriene generation in the adult respiratory distress syndrome (ARDS) was investigated by measurement of urinary leukotriene E4 (LTE4) excretion, the major urinary LT metabolite in humans. Sequential measurements were made in nine subjects entered into the study within 48 h of the onset of ARDS, defined by an arterial/alveolar PO2 ratio of less than 0.3 and radiographic evidence of diffuse bilateral pulmonary edema. Initial urinary LTE4 excretion was significantly elevated (1.250 +/- 0.050 ng/mg creatinine sulphate; n = 7) compared with a non-ARDS postoperative group (0.254 +/- 0.114 ng/mg; n = 5) and normal control subjects (0.035 +/- 0.010 ng/mg; n = 12). LTE4 excretion in the first 24 h was estimated to be 6.9 micrograms, representing a release of 0.1 micrograms/kg/h of peptido leukotrienes into the bloodstream. These values were physiologically important based on a comparison with the increased urinary LTE4 excretion observed after antigen-induced bronchoconstriction in allergic asthmatics (baseline LTE4, 0.06 +/- 0.04 ng/mg; postantigen, 0.56 +/- 0.14 ng/mg; 0.17 micrograms LTE4/24 h; n = 8). In subjects with ARDS, this pathologic LTE4 excretion persisted during a subsequent 5-day study period. Leukotriene E4 excretion was associated with persistent abnormalities in gas exchange, pulmonary edema, and lung compliance, suggesting an important role for peptido leukotrienes in the pathophysiology of ARDS.
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PMID:Persistent generation of peptido leukotrienes in patients with the adult respiratory distress syndrome. 165 Jan 52

The alterations in lung glutamine (GLN) metabolism that occurs in the endotoxin-injured lung were studied in rats and subsequently correlated with flux changes that occur in patients with the adult respiratory distress syndrome (ARDS). Measurements in animals were made at various time-points following the administration of endotoxin, while studies in surgical patients were done in a group of healthy controls, in patients with "early" sepsis who had normal chest x-ray films, and in patients with radiographic and physiologic evidence of ARDS. In healthy control rats, net amounts of GLN are released by the lungs into the systemic circulation. This release rate doubled 30 minutes after intravenous endotoxin (1,580 +/- 320 nmol GLN/100 g BW/min vs. 736 +/- 179 in controls, p less than 0.01) but glutamine synthetase activity was unchanged, suggesting an outpouring of cellular glutamine stores. Two hours after endotoxin treatment, this accelerated fractional release of glutamine by the lungs was no longer detected. By the 12-hour time-point, the lungs reversed to an organ of net glutamine balance (234 +/- 248 nmol/100 g BW/min, p less than 0.05 vs. controls and ENDO30 min) despite a more than two-fold increase in glutamine synthetase activity (p less than 0.01). Simultaneously, lung weights were increased by 21% (p less than 0.01) and histologic examination showed an interstitial infiltrate and pulmonary edema. Similar observations were made in humans; patients with "early" sepsis exhibited a marked increase in lung glutamine release, while patients with ARDS demonstrated glutamine balance across the lungs (4,030 +/- 910 nmol GLN/kg BW/min vs. 637 +/- 496 in ARDS, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glutamine metabolism by the endotoxin-injured lung. 167 90

Fifty-four children from the Jerusalem area were studied prospectively following scorpion envenoming. Their ages ranged from 11 months to 10 years. Severe symptoms (convulsions, brain oedema, shock, respiratory distress and myocarditis) were encountered in 19. Respiratory distress was the main feature in 17 of the children, in two cases owing to pulmonary oedema and in a third because of adult respiratory distress syndrome and myocarditis; mechanical ventilation was required in three cases. The severity of the symptoms and signs was not related to sex, age, weight, interval between scorpion sting and admission or to the type of offending scorpion; it was most likely dependent upon the susceptibility of the individual and/or the dose of venom injected by the scorpion. Intravenous antivenom quickly reversed the symptoms, and no side-effects were seen in the patients studied. The two patients who died had not received the antivenom intravenously. We recommend that specific antivenom should be given intravenously in all children who show significant symptoms. Furthermore, a longer period of observation is necessary following scorpion sting in this age group.
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PMID:Scorpion sting in children in the Jerusalem area: a review of 54 cases. 171 20

Hypervolemia from fluid overload with resultant pulmonary edema is thought to be a frequent cause of Adult Respiratory Distress Syndrome (ARDS). However, ARDS may also occur as a result of the hypovolemic shock of surgery or trauma. To develop an appropriate rationale for fluid therapy in high-risk surgical patients, the relationship between fluid balance, hemodynamics, the onset of ARDS by physiologic criteria (shunt greater than or equal to 20%, and/or PaO2/FiO2 ratio less than 250) and the onset of pulmonary infiltration (PI) associated with ARDS were examined. Fifty patients were prospectively followed from admission throughout their hospitalizations; 38 (76%) had trauma and 12 (24%) were postoperative. Cardiac index, central venous pressure (CVP), wedge pressure (WP), and shunt (Qsp) were measured. All chest x rays were read by one staff radiologist who was blinded to the patients' identities. PI was graded from "0" to "4" (0 = no PI, 4 = maximum PI). The first x ray reading of "2" or greater was used as the time of onset of PI. ARDS by physiologic criteria occurred in 29 of 50 (58%) patients; 27 of these 29 (94%) also developed +2 or greater PI. The mean onset times of ARDS and of +2 PI were 40 +/- 41 hours and 40 +/- 38 hours, respectively. The ARDS patients had a significantly smaller net positive fluid balance than the non-ARDS patients over the first 40 hours after admission (+6,831 ml +/- 4,909 ml vs 12,440 ml +/- 7,817 ml, (P less than 0.01)).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship between ARDS, pulmonary infiltration, fluid balance, and hemodynamics in critically ill surgical patients. 174 95

Twenty years have now elapsed since Ashbaugh and Petty first described the syndrome of acute respiratory failure associated with a wide spectrum of clinical conditions. During the past two decades, significant advances have emerged in our understanding of the clinical conditions associated with the syndrome and the pathophysiological changes affecting the alveolar-capillary membrane responsible for the characteristic non-cardiogenic pulmonary edema. Recent data have reaffirmed the notion that mortality rates in ARDS remain in excess of 60 percent, essentially unchanged since the first description of the syndrome, despite all the advances in critical care medicine in the intervening years. The incidence of ARDS has been difficult to establish because of lack of agreement on precise definition criteria. The lack of agreed definition criteria has hampered evaluation of the natural history of the syndrome, its epidemiology and mortality rates, and the efficacy or otherwise of a variety of therapeutic interventions. This review will highlight a recent, clinically appropriate, expanded definition of ARDS. New understandings of the roles of sepsis and multi-system organ failure in mortality associated with ARDS will be discussed. Several mediators, both locally in the lung and in the systemic circulation, have been implicated in the pathophysiology of ARDS. This review will discuss the evidence for and against neutrophils, platelets, cytokines derived from mononuclear cells and macrophages, complement, prostaglandins/leukotrienes, oxygen-derived radicals, and a variety of proteases. Current treatment strategies for ARDS are designed to increase tissue oxygen delivery by increasing arterial oxygen tension and cardiac output while simultaneously attenuating the pulmonary and systemic injury by appropriate pharmacologic and surgical interventions. Recent data advocating pharmacological augmentation of cardiac index and oxygen delivery will be highlighted. The persistently high mortality rates of 60-70 percent in patients with established ARDS have provoked recurring interest in new techniques of providing mechanical ventilation. Most studies have shown, however, that mortality in ARDS patients is attributable mainly to sepsis and multi-system organ failure rather than primarily to respiratory failure. Established and speculative intervention to reduce sepsis and multi-system organ failure associated with ARDS will be featured in the review.
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PMID:Acute respiratory distress syndrome--two decades later. 181 55

Common intracranial complications following head injury are meningitis, usually associated with a basilar skull fracture or open-depressed skull fracture; delayed hematoma; hydrocephalus; and vascular injuries. Prophylactic antibiotics are not recommended for the management of basilar skull fractures. The best means of preventing infection from open-depressed skull fractures is operative debridement and thorough irrigation, though recent evidence suggests that select cases can be safely managed without operation. Serial CT scans should be obtained in severely head-injured patients to identify delayed hematomas. CT and MRI scans obtained several weeks or months after severe head injury frequently reveal enlarged ventricles, though only a small percentage of these patients have clinical hydrocephalus. Those that do, often benefit from a shunt. Vascular injuries frequently are not detected until ischemic symptoms develop hours or days after the injury. Recommended treatment for intimal tears or dissection is full anticoagulation, but in those with cerebral contusions or other intracranial lesions, this may present an unacceptable risk for intracranial hemorrhage. Pulmonary infections frequently occur following head injury, and can be associated with admission to the ICU and intubation. A large percentage of these infections are caused by enteric gram-negative organisms, and aggressive treatment with appropriate antibiotics is necessary. Aspiration of gastric contents is common in head-injured patients and is frequently complicated by bacterial superinfection. The routine use of antacids and H2 blocking agents leads to bacterial colonization of the stomach with anaerobes and gram-negative aerobes. Thus, empiric therapy for aspiration pneumonia should include clindamycin. Sinusitis is a frequent cause of fever and leukocytosis in patients with nasotracheal or nasogastric tubes in place for several days and often subsides spontaneously with removal of the tubes. Pulmonary edema is often caused by excessive fluid administration during resuscitation of these patients, and can be avoided by monitoring central venous pressures. Pulmonary edema may also be caused by ARDS, excessive catecholamine release, or primary cardiac failure. Most of these patients will benefit from early intubation and PEEP. Pulmonary emboli most often originate from deep venous thrombi, and there is increasing evidence that prophylaxis with low-dose heparin and pulsating boots can significantly reduce the incidence of both complications. Erosive gastritis is found in the majority of severely head-injured patients and may be due to ischemia of the gastric mucosa as well as gastric hyperacidity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Complications of head injury and their therapy. 182 50

It is well known that pulmonary influx of neutrophils is involved in lung injury in patients with adult respiratory distress syndrome (ARDS). Neutrophils are major contributors to the self-defence mechanism, however, adverse effects of neutrophils have also been recognized. Recently, we found that a highly toxic substance, 9, 10-epoxy-12-octadecenoate (leukotoxin) is biosynthesized by human neutrophils. This study was designed to investigate whether or not leukotoxin participates in lung injury in ARDS and coagulation abnormality which is often associated with ARDS. Intravenous injection of leukotoxin (100 mumol/kg) caused acute edematous lung injury, which was evidenced by increased lung weight, albumin concentrations, and angiotensin converting enzyme activities in lung lavages. Pulmonary capillary endothelial damage and pulmonary edema were observed by electron microscopy. Moreover, considerable amounts of leukotoxin were detected in lung lavage fluid of rats exposed to pure oxygen for 60 h and patients with ARDS. An increased number of neutrophils and albumin concentrations were also observed in these lavage fluids. Intravenous injection of leukotoxin (100 mumol/kg) induced coagulation abnormalities such as disseminated intravascular coagulation. Increased levels of plasma leukotoxin were detected in ARDS patients with coagulation abnormalities. These results suggest that leukotoxin biosynthesized by neutrophils is an important contributor to lung injury in ARDS and associated coagulation abnormalities.
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PMID:[ARDS and leukotoxin]. 185 3

A 48-year-old man with small cell lung cancer developed ARDS, and massive pulmonary edema fluid was obtained with the fiberoptic bronchoscopy. The pulmonary edema fluid to serum ratios of total protein and albumin were 0.72 and 0.85 respectively. The ratio of LDH was higher (2.71), while that of cholesterol was lower (0.11) than that of total protein. Simultaneously, isopropyl N [I-123] p iodoamphetamine (I-123 IMP) and I-131 human serum albumin (I-131 HSA) were injected into this patient. Samples of blood and pulmonary edema fluid were collected to measure the clearance through the pulmonary microvasculature. The time activity curves of I-123 IMP and I-131 HSA in his blood samples revealed almost constant radioactivity from 5 minutes to 120 minutes after injection, while both radioactivity levels in pulmonary edema fluid samples increased with time. The clearance ratio of I-123 IMP to I-131 HSA was constant at each sampling time (mean +/- SD, 1.51 +/- 0.32). The linear correlation between I-123 IMP clearance and I-131 HSA clearance (r = 0.95, p less than 0.01) suggested that the clearance ratio of exudative plasma components may remain unchanged even if pulmonary microvasculature permeability has changed.
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PMID:[Assessment of the permeability of the pulmonary microvasculature using radiotracers in a case of adult respiratory distress syndrome]. 185 5

During pilgrimage season (Hajj) in Saudi Arabia 34 patients with heat stroke (HS) were centrally cannulated to assess their state of hydration and fluid requirement during cooling period. Central venous pressure (C.V.P.) measurements indicated that most victims of heat stroke had normal C.V.P. on arrival at heat stroke centres and may not be fluid depleted. Twenty-two patients (64.7%) had normal or above normal C.V.P. Twelve patients (35.3%) had zero or below zero C.V.P. Six patients (17.6%) had above 10 cmH2O (range 10-26 cmH2O) and could have developed acute congestive heat failure and pulmonary edema if they had been transfused at the standard recommended rate of 3-4 litres of fluid during an average cooling time of 1 h as has been practiced in the heat stroke centres to date. This study also showed that heat stroke patients should not be briskly transfused because the heart may be affected by heat stroke per se and an unmonitored challenge by brisk i.v. therapy during cooling (which on its own increases preload on the heart due to peripheral vasoconstriction) can lead to acute overload problems. An average of 1 litre of normal saline or Ringer's lactate (crystalloids) was sufficient to normalize C.V.P. during the cooling period and to restore an optimal state of hydration without predisposing to congestive cardiac failure and pulmonary edema--the potential to develop disastrous adult respiratory distress syndrome and disseminated intravascular coagulopathy.
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PMID:Are heat stroke patients fluid depleted? Importance of monitoring central venous pressure as a simple guideline for fluid therapy. 185 63

This retrospective study comprises 234 cases of accidental hypothermia (core temperature less than 35 degrees C) hospitalized in 95 Swiss clinics between 1980 and 1987. The most frequent accidents were alpine (n = 78) in origin, followed by cold exposure after injuries (n = 63) and suicide attempts (n = 43). Hypothermia was induced by cold air in 129 cases and by water in 47 cases. Patients were divided evenly between the degree of hypothermia: 75 mild (32-35 degrees C), 79 moderate (28-32 degrees C) and 66 severe (less than 28 degrees C). Among the survivors the coldest patient had a core temperature of 17.5 degrees C and the longest cardiac arrest with a favourable outcome lasted 4.75 hours. Out of the 234 patients 68 died (29%). We assessed all variables relative to outcome, in particular the mechanism of the accident, the mode of cooling, temperature, circulation, age and sex, underlying diseases, rewarming methods, medication and complications during the hospital course. All variables were tested in two multiple regression analysis models (retrospective model n = 181: prospective model n = 128) with regard to significance (p less than 0.05) and survival. Results are expressed with ODD's ratios (OR). The negative survival factors are asphyxia (OR 30), invasive rewarming methods (OR 20), slow rate of cooling (OR 10), asystole on arrival (OR 9), pulmonary edema or ARDS during hospitalization (OR 8), elevated serum potassium (OR 2/mmol/l) and age (OR 1.03/year). The positive survival factors are rapid cooling rate (OR 10), presence of ventricular fibrillation in cardiac arrest patients (OR 9) and presence of narcotics and/or alcohol during hypothermia (OR 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Accidental hypothermia in Switzerland (1980-1987)--case reports and prognostic factors]. 188 13


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