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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
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PMID:Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome. 37 80

In a retrospective analysis of 18 patients with sepsis and adult respiratory distress syndrome, we found that high plasma epinephrine and noradrenalin levels were associated with severe defects in oxygenation that accompany this disease. The result of previous experimental work support the concept that high plasma catecholamine levels augment already existing defects in the ventilation to perfusion ratio and increases the measured intrapulmonary shunt fraction. The results of this study do not, however, delineate whether or not the relationship between high circulating plasma catecholamine levels and severe adult respiratory distress syndrome is causal or simply a measurement of two indexes which reflect the severity of the underlying disease process.
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PMID:Plasma catecholamine levels and pulmonary dysfunction in sepsis. 43 84

The course of intrauterine infections are illustrated and 5 maternal deaths reported. Early lung complications were predominant, described as shock lung or septic pneumonia. Renal complications or disseminated intravascular coagulation were absent or developed late. In contrast to gram negative sepsis there was a frequent association with premature rupture of the membranes, which indicates the danger of this event. On microbiology gram positive rods were found more frequently than a mixed flora. The morphology of intrauterine infection is similar to those of puerperal sepsis although the clinical course is quite different. This indicates a change in infectious pattern during the last centuries.
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PMID:[Intrauterine infections in pregnancy. The significance of premature rupture of the membranes and early lung complications]. 45 59

Pulmonary alterations after shock and sepsis, described clinically as shock lung or adult respiratory distress syndrome, are of great importance in intensive care. Pathogenetically an alteration of the surfactant system of the lung is often discussed. Since phospholipids are constituents of lung surfactants, phospholipid metabolism is investigated in experimental peritonitis in rats in our laboratory. 15 hours after inducing a peritonitis, the lung incorporates more oleic acid than that in animals of the reference group. 33 hours after inducing peritonitis, the capacity of the lung to incorporate choline and fatty acids is markedly reduced, histologically the lungs represent morphological equivalents of the so-called shock lung at this time. Therefore we conclude, that an alteration of phospholipid metabolism with a diminished and/or altered synthesis of lung surfactant plays, at least in part, an important role in the pathogenesis of respiratory distress in sepsis and peritonitis.
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PMID:Altered metabolism of phospholipids in the lung of rats with peritonitis. 58 Aug 12

Fifteen patients (range of ages, 18 to 35 years) who survived an acute episole of the adult respiratory distress syndrome caused by mechanical or thermal injuries, sepsis, and shock were studied during 1 to 30 months after recovery. The patients had had no previous pulmonary diseases, and only two had been smokers. All of the patients were asymptomatic, and their chest x-ray films were normal on follow-up examination. Tests of pulmonary function revealed mild abnormalities which consisted of reduction of pulmonary volumes, decreased carbon monoxide diffusing capacity, and a mild increase of alveolar-arterial oxygen pressure gradients in the early stage ofter recovery. Improvement was noted after a few months, but eight patients still had mild reduction of pulmonary volume after one to two years. No correlation could be established between the severity of the adult respiratory distress syndrome, therapy with mechanically assisted ventilation, the duration of exposure to supplemental oxygen, the fractional concentration of oxygen in the inspired gas, and the degree of residual functional defect.
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PMID:Pulmonary function following the adult respiratory distress syndrome. 68 80

We report an evaluation of the effect of postive-end-expiratory-pressure (PEEP) on improving pulmonary oxygenating capacity in the adult respiratory distress syndrome (ARDS), when the latter is associated with generalized gram-negative sepsis. Fifty-seven cases treated in our RICU with PEEP ventilation (April 1972 to January 1975) were retrospectively reviewed. Oxygenating capacity improvement was evaluated in terms of the changes in PaO2/FIO2 and AaDO2 (FIO2 = 1.0). Both the short term (2-3 hours from the initiation of PEEP) and the overall effects of PEEP were evaluated. A mean PEEP of 5.6 cm H2O initially increased PaO2/FIO2 by a mean of 94 torr and decreased AaDO2 (FIO2 = 1.0) by 105 torr in the 28 nonseptic patients. In the 29 septic patients, 5.1 cm H2O PEEP initially increased PaO2/FIO2 by 32 torr and decreased AsDO2 (FIO2 = 1.0) by 38 torr. The differences between the septic and nonseptic patients were statistically significant (P less than 0.001). Likewise, the long-term effect of similar levels of PEEP was in increasing PaO2/FIO2 by 142 torr and by 75 torr in the nonseptic and septic patients, respectively. The final reduction in AaDO2 (FIO2 = 1.0) was 163 torr and 87 torr in the nonseptic and septic patients, respectively. These differences between patient groups were also statistically significant (P less than 0.02). Mortality during PEEP was 15/29 and 3/28 in the septic and nonseptic patients, respectively. Overall mortality in the septic and nonseptic groups was 18/29 and 5/28, respectively. We conclude that ARDS with sepsis constitutes a more severe pulmonary insult than ARDS without sepsis, and/or that generalized sepsis creates a more prolonged pulmonary insult that makes it less amenable to PEEP. Thus, high levels of PEEP may be needed to treat ARDS associated with sepsis.
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PMID:The effect of PEEP on oxygenating capacity in acute respiratory failure with sepsis. 78 54

Early diagnosis is mandatory in the adult respiratory distress syndromes, particularly in sepsis, and therapy should begin as soon as there is a reasonable suspicion that this problem is developing. Blood-gas changes cannot usually be appreciated clinically until the respiratory problem is quite severe. Accordingly, serial blood-gas analyses should be performed in any septic patient who has an increased chance of developing ARDS. Any deterioration in the patient's condition, blood gases, or ventilatory effort should be considered as an indication for early ventilatory assistance. Control of the primary process, high tidal volumes, PEEP, and careful dehydration are the mainstays of therapy. Serial blood gases and careful observation of the patient's effective compliance are essential to determine the optimal ventilator settings and the optimal PEEP. Early administration of massive steroids should be considered if the patient fails to respond to correction of the underlying etiologic problem (particularly sepsis), careful progressive dehydration, and optimal expansion of the alveoli (using high tidal volumes and/or PEEP).
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PMID:The diagnosis and treatment of acute respiratory failure in sepsis. 104 56

Smoke inhalation, defined as airway or pulmonary parenchymal injury resulting from the inhalation of toxic combustion products, presents with a wide range of severity in patients with and without skin burns. In patients with severe injuries, the diagnosis is obvious on the basis of the history and clinical presentation; in patients with less severe injuries or those in whom the clinical consequences are delayed, diagnostic precision is difficult because diagnostic clues provide only indirect information. There is no specific treatment so diagnosis is not critical for patient management. Patients at risk include 20% to 30% of flame burn victims who should receive vigorous supportive care. The mortality rate of smoke inhalation victims without a burn is < 10%. With a burn the mortality rate is 30% to 50%, suggesting that thermal injury or its treatment is responsible for further lung damage. Endotracheal intubation provides definitive treatment for obstructed or soon-to-be obstructed patients. However the diagnosis of smoke inhalation per se is not an indication for airway intubation and respiratory support; 12% of patients without a burn require intubation versus 62% of those with a burn. A translaryngeal tube can be converted to a tracheotomy safely in burn victims; tracheotomies are easier to manage if burns of the neck are excised and grafted prior to placement. Mechanical ventilation with positive end expiratory pressure (PEEP) is the treatment for the pulmonary injury. The early lesions of smoke inhalation often progress in the context of sepsis and other complications of the burn illness to a clinical state consistent with adult respiratory distress syndrome.
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PMID:Smoke inhalation: diagnosis and treatment. 129 Feb 62

The cardiopulmonary support system is an extracorporeal device that allows for rapid cardiopulmonary support of the critically ill patient in the intensive care unit. It provides immediate and complete support of cardiac and pulmonary functions to maintain perfusion to vital organs in patients who are severely physiologically compromised (eg, in cardiogenic shock, adult respiratory distress syndrome or pulmonary edema). Successful cardiopulmonary support requires systemic anticoagulation, percutaneous venous and arterial cannulation and careful monitoring by the critical care team to maintain adequate tissue perfusion and oxygenation. Although patient mortality can occur secondary to bleeding, embolism or sepsis, this technique provides life-sustaining circulatory and respiratory support until definitive treatment can be initiated.
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PMID:Cardiopulmonary support in the intensive care unit. 835 73

Pulmonary arterial hypertension, defined as a mean pulmonary artery pressure exceeding 20 mmHg has been observed both in experimental animal and human sepsis, even before development of the adult respiratory distress syndrome. In this article we review several mechanisms that have been invoked for the pulmonary arterial hypertension associated with sepsis (and the adult respiratory distress syndrome): obstruction of the pulmonary microcirculation with microthrombi composed of platelets and leukocytes, and active pulmonary vasoconstriction induced by the autonomous nervous system, hypoxia or vasoactive humoral factors ("mediators"). Some of these mediators, in particular serotonin and arachidonic acid metabolites have been the subject of substantial research and therapeutic manipulation. Since pulmonary arterial hypertension imposes an increased afterload to the right ventricle and because right ventricular dysfunction appears to be a major determinant of the outcome of sepsis, the study of the mechanisms involved in pulmonary arterial hypertension may lead to improved management of sepsis and septic shock.
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PMID:Pulmonary arterial hypertension in sepsis and the adult respiratory distress syndrome. 131 81


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