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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two of 30 patients with esophageal varices had respiratory distress develop within 8-24 h of esophageal sclerotherapy. Evidence of aspiration and sepsis were absent in these two patients with the clinical picture of adult respiratory distress syndrome. To investigate the possible etiologic role of sodium morrhuate in this syndrome, a sheep model was established and pulmonary hemodynamics, lung lymph flow, and albumin concentration were measured before and after the intravenous injection of 2.5-15.0 cm3 of sodium morrhuate. In all 8 animals studied, mean pulmonary artery pressures increased from 11.6 +/- 2.8 to 32.8 +/- 4.9 mmHg (p less than 0.01) 30 s after injection. These pressures returned to baseline values over 120 min. Lymph flow increased from 0.91 +/- 0.89 to 2.8 +/- 1.5 ml/30 min at 90 min postinjection (p less than 0.05) and returned to baseline values in animals monitored for 6-8 h. The lymph/plasma albumin ratio decreased from 0.856 +/- 0.08 to 0.74 +/- 0.01 (p less than 0.05) 120 min postinjection. Pulmonary edema was not evident histologically or gravimetrically (wet/dry weight ratio was 3.65 +/- 0.3 and not different from normal). It was concluded that sodium morrhuate injection in sheep causes marked but transient pulmonary hypertension associated with an increased lymph flow of relatively protein-poor lymph. Sodium morrhuate esophageal sclerotherapy may affect pulmonary hemodynamics and contribute to respiratory difficulties in patients.
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PMID:Acute respiratory failure after sodium morrhuate esophageal sclerotherapy. 660 87

Non-cardiac pulmonary edema comprises all types of pulmonary edema not caused by increase of left ventricular filling pressure and elevated pulmonary capillary pressure. In one year 42 patients at our intensive care unit developed non-cardiac pulmonary edema. In a retrospective study the clinical, radiological and functional changes in patients with non-cardiac pulmonary edema were determined. 76% of the patients had multiple causes for development of non-cardiac pulmonary edema. Sepsis was the most frequent predisposing disease. Over-all mortality reached up to 69%. Additional organ failure caused an increase in mortality. Patients without complications had the best prognosis. Mechanical ventilation (69%), high-dose corticosteroids (50%), hemodialysis with ultrafiltration (33.3%) and hemofiltration (7.1%) were used for treatment of non-cardiac pulmonary edema.
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PMID:[Non-cardiogenic pulmonary edema]. 660 83

We report a case of severe pulmonary embolism in a 37 years old man admitted to the intensive care unit for severe acute respiratory failure. The presenting signs and symptoms were typical for severe pulmonary oedema. Chest radiograph shortly after admission showed local alveolar shadows. In the absence of sepsis, haemodynamic evidence of left ventricular failure on catheterization of the right heart and because of the history of the recent illness, a tentative diagnosis of pulmonary embolism was made. The diagnosis was confirmed by selective pulmonary angiography. The latter demonstrated that pulmonary oedema had been localized only in areas with patent pulmonary arteries and, in addition, confirmed that left ventricular function was normal. Such a pattern of local pulmonary oedema is uncommon in patients and is reminiscent of that observed in animal experiments with severe pulmonary arterial obstruction and overperfusion of unblocked territories. Possible mechanisms of overperfusion oedema are discussed and the hypothesis that humoral factors may increase the permeability of pulmonary microvasculature in cases of severe pulmonary embolism is put forward.
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PMID:[Pulmonary edema in pulmonary embolism]. 670 66

Blockade of the arachidonic acid cascade has been shown to improve survival and hemodynamic alterations in animal models of sepsis and acute respiratory failure (ARF). The effects of intravenous ibuprofen, a cyclooxygenase inhibitor, were observed in 20-30 kg pigs with ARF induced by a continuous LD100 infusion of live Pseudomonas aeruginosa (2 X 10(8)/20 kg/min). Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250-ml tidal volume and 0.5 FiO2. Pigs were randomly assigned to three groups: Group I received 2 bolus infusions of ibuprofen (12.5 mg/kg) at 20 and 210 min after baseline; Group II had Ps. aeruginosa (2 X 10(8) CFU/20 kg/min) only; Group III received Ps. aeruginosa and 12.5 mg/kg of ibuprofen at 20 and 210 min of ARF. Ibuprofen alone caused no significant changes in cardiorespiratory parameters. With Ps. aeruginosa infusion, significant pulmonary hypertension, hypoxemia, increased intrapulmonary shunt fraction, and systemic hypotension occurred. In the septic animals treated with ibuprofen, oxygenation was improved by a significant decrease in shunt, pulmonary edema, and pulmonary hypertension.
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PMID:Effects of ibuprofen on a porcine model of acute respiratory failure. 670 94

It is suspected, but still unproven, that the increased capillary permeability which accompanies sepsis and contributes to the development of pulmonary edema (PE) involves systemic as well as pulmonary capillaries. We investigated the relationship between the colloid osmotic pressure of serum (COPS) and edema fluid (COPE) in 16 septic and 19 nonseptic patients with severe generalized edema. COPS values of septic and nonseptic patients were not significantly different (14.6 +/- 2.1 and 15.8 +/- 3.4 torr, respectively). However, the COPE of septic patients was 2.4 +/- 0.7 torr while the COPE of nonseptic patients was 1.3 +/- 0.7 torr. The COPE/COPS ratio was 0.165 in septic patients and 0.084 in nonseptic patients. Both of these differences are significant (p less than .001). It was also possible to discriminate septic from nonseptic patients on the basis of the COPE/COPS ratio. Thus, 16/17 determinations in septic patients had a ratio greater than .1, while 17/22 determinations in nonseptic patients showed a ratio less than .1. PE was present in 8/16 septic patients but in only 2/19 nonseptic patients. These data suggest that the increase in capillary permeability during sepsis is generalized.
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PMID:Capillary permeability in septic patients. 674 3

The treatment for pulmonary edema with the adult respiratory distress syndrome is aimed at the early supportive management of hypovolemic shock. The addition of massive corticosteroid dosage, Methylprednisolone Succinate, of 30 mg/kg body wt/dose ever six hours for a 24-48 hour period has been shown in our investigation to be efficacious, particularly in the traumatic and septic shock groups of patients but not in patients with multiple system diseases. Ventilator care utilizing constant positive pressure breathing or constant positive airway pressure in the patient who has spontaneous respirations is of prime importance. The recent utilization of hyperalimentation has also been very effective as an adjunctive therapy and should be used in the management of this problem in the future in conjunction with the steroids. Hemodynamic monitoring employing the specific parameters as delineated in our discussion are all major steps that should be pursued on a routine basis in the vast majority of these patients. The most important factor in the prognosis of this condition is the severity and number of injuries that have occurred at the time of the initial trauma. Other factors affecting the outcome are age, prolonged shock, associated degenerative cardiovascular disease, metabolic imbalance, severe multiple system involvement, and sepsis. We now feel that the utilization of massive corticosteroid therapy is indicated with the first earliest clinical signs of this condition in order to attempt to prevent complications and probably improve survival rate.
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PMID:Acute pulmonary edema with respiratory failure--newer concepts in therapy. 675 Nov 64

Infusion of Escherichia coli endotoxin (0.12-1.5 micrograms/kg) into unanesthetized sheep causes transient pulmonary hypertension and several hours of increased lung vascular permeability, after which sheep recover. To produce enough lung injury to result in pulmonary edema with respiratory failure, we infused larger doses of E. coli endotoxin (2.0-5.0 micrograms/kg) into 11 chronically instrumented unanesthetized sheep and continuously measured pulmonary arterial, left atrial and aortic pressures, dynamic lung compliance, lung resistance, and lung lymph flow. We intermittently measured arterial blood gas tensions and pH, made interval chest radiographs, and calculated postmortem extravascular bloodless lung water-to-dry lung weight ratio (EVLW/DLW). Of 11 sheep 8 developed respiratory failure; 7 died spontaneously 6.3 +/- 1.1 h, and one was killed 10 h after endotoxin infusion. All sheep that had a premortem room air alveolar-arterial gradient in partial pressure of O2 (PAo2-Pao2) greater than 42 Torr (58 +/- 5 (SE) Torr) died. Of eight sheep that had radiographs made, six developed radiographically evident interstitial or interstitial and alveolar edema. Pulmonary artery pressure rose from base line 22 +/- 2 to 73 +/- 3 cmH2O and remained elevated above baseline levels until death. There was an initial fourfold decrease in dynamic compliance and sixfold increase in pulmonary resistance; both variables remained abnormal until death. EVLW/DLW increased with increasing survival time after endotoxin infusion, suggesting that pulmonary edema accumulated at the same rate in all fatally injured sheep, regardless of other variables. The best predictor of death was a high PAo2-Pao2. The marked increase in pulmonary resistance and decrease in dynamic compliance occurred too early after endotoxin infusion (15-30 min) to be due to pulmonary edema. The response to high-dose endotoxin in sheep closely resembles acute respiratory failure in humans following gram-negative septicemia. Respiratory failure and death in this model were not due to pulmonary edema alone.
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PMID:Respiratory failure after endotoxin infusion in sheep: lung mechanics and lung fluid balance. 675 92

Pulmonary effects, lung clearance, and tissue retention of blood-borne Pseudomonas aeruginosa were compared in dogs (n = 5) and pigs (n = 5) during continuous 6-hour intravenous infusion of 1.2(10(9)) bacteria/min/20 kg. Control pigs received an equal volume of sterile saline. In contrast to controls, experimental pigs developed pulmonary artery (PA) hypertension (mean, 30 +/- SE 3; baseline, 17 mm Hg) and pulmonary failure manifested by hypoxemia (mean PaO2, 49 +/- 4; baseline, 78 +/- 2 mm Hg; p less than 0.001), increased intrapulmonary shunting (40 to 50%), noncardiogenic pulmonary edema, and congestive atelectasis, a pattern of pulmonary failure very similar to sepsis-induced ARDS in humans. In dogs, PA pressures wee unchanged from baseline, no edema was detected, and comparable hyperventilation was associated with an increase in PaO2 from 77 +/- 4 (baseline) to 87 +/- 2 mm Hg (p less than 0.001). Tissue retention of viable blood-borne organisms in pigs was greatest in the lungs. In dogs, lung retention was minimal and greatest tissue retention occurred in the liver and spleen. We conclude that both lung clearance of blood-borne organisms and bacteremia-induced pulmonary failure are quite host dependent.
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PMID:Bacteremia: host-specific lung clearance and pulmonary failure. 678 63

The ventilatory response in acute lactic acidosis was assessed in 39 patients. In 18 patients, the acidosis was associated with phenformin ingestion and in 21, with other causes such as shock and sepsis, but not pulmonary edema. Arterial blood CO2 tensions and plasma bicarbonate concentrations were compared to those previously found in patients with uncomplicated diabetic ketoacidosis. In most of the lactic acidosis patients, arterial blood CO2 fell within the 95% confidence band calculated from the data in the ketoacidotic patients. Only 1 lactic acidotic patient had a triflingly lower CO2 tension. Shock was present in 8 of the 9 lactic acidotic patients whose CO2 tensions were more than 2 torr above the 95% confidence band.
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PMID:Ventilatory response in patients with acute lactic acidosis. 680 Jul 2

Adult respiratory distress syndrome is becoming more frequent in pediatric age. There are several factors involved in its' etiology. Sepsis is almost invariably present in all patients. Basic mechanism is an increase of pulmonary capillary permeability with production of acute non cardiogenic oedema. The decrease in compliance and functional residual capacity produce a respiratory failure with hypoxemia non-responsive to the increase in FiO2. Pulmonary hypertension and low cardiac output appear once the syndrome has developed. In its' management, cardiorespiratory monitoring is essential. Prophylaxis is based on early treatment of the essential pathological process. Corticoids are only effective if they are administered before development of pulmonary oedema. The treatment is based on: a) Moderate water restriction. b) Early respiratory assistance using PEEP or CPAP. c) Maintenance of adequate oxygen transport. The extracorporeal oxygenation guarantees the oxygen exchange but it does not affect survival. Mortality is 95%. Patients who survive have minimal pulmonary sequelae.
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PMID:[Adult respiratory distress syndrome in childhood]. 681 14


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