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

During gram-negative sepsis it is known that endotoxin activates complement by the alternate pathway. The complement anaphylatoxin C5a, a result of this activation, is thought to play a key role in attracting and activating neutrophils in the lungs, leading to the adult respiratory distress syndrome. Complement levels were measured in primates made septic by Escherichia coli infusions. Anti-human C5a antibodies were administered to study their effect on neutrophil-mediated lung injury. Control (I), septic (II) and septic + anti-C5a antibody (III) groups (n = 4) were studied. The antibody-treated group (III) demonstrated a significant attenuation of septic shock and pulmonary edema as has been previously reported. All complement profiles were corrected for varying hemoglobin concentrations. C3, C4, and C5 levels were measured by radial immunodiffusion and were depleted in both septic groups. Once the levels were depleted from the plasma, they did not recover. The depletion of C4 indicates that classical pathway activation also occurred. C3a, C4a, and C5a levels were measured by radioimmunoassay. Significantly increased peak levels were reached in the septic groups 15 min after initiation of the E. coli infusion. There were no significant differences in early peak C3a and C4a levels between groups II and III. However, the mean peak C5a level in group III (anti-C5a antibodies) was 42% lower than that in group II, and after this early peak, C5a levels were not elevated above control levels in group III. The antibody to human C5a was thus shown to be cross-reactive with primate C5a and was specific since C3a and C4a levels were not decreased in group III.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Complement levels in septic primates treated with anti-C5a antibodies. 249 31

Escherichia coli hemolysin has been implicated as a pathogenicity factor in extraintestinal E. coli infections including sepsis. In the present study the effects of intravascular administration of hemolysin were investigated in isolated blood-free perfused rabbit lungs. Low concentrations of the toxin in the perfusate (0.05-5 hemolytic units/ml, corresponding to approximately 5-500 ng/ml), caused a dose- and time-dependent release of potassium, thromboxane A2, and prostaglandin I2, but not of lactate dehydrogenase, into the recirculating medium, as well as a dose-dependent liberation of the prostanoids into the bronchoalveolar space. These events were paralleled by a dose-dependent pulmonary hypertension, and studies with different inhibitors collectively indicated that the vasoconstrictor response was mediated predominantly by pulmonary thromboxane generation. In addition, E. coli hemolysin elicited a protracted, dose-dependent increase in the lung capillary filtration coefficient, which was independent of the prostanoid-mediated pressor response and resulted in severe pulmonary edema formation. We conclude that E. coli hemolysin can elicit thromboxane-mediated pulmonary hypertension combined with severe vascular leakage in isolated lungs in the absence of circulating inflammatory cells and humoral mediator systems, mimicking the key events in the development of acute respiratory failure in states of septicemia.
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PMID:Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. 250 Apr 55

Severe malaria is a major cause of infant and childhood death in the tropics. Effective management relies on rapid diagnosis, prompt administration of parenteral schizonticidal antimalarial drugs, careful fluid balance, prevention of convulsions and early recognition of complications such as hypoglycemia, metabolic acidosis, anemia, pulmonary edema, renal failure, bleeding and supervening bacterial sepsis. The mortality of treated cerebral malaria remains 20%. New, more rapidly acting antimalarials and earlier referral of children with complicated infections should reduce this unacceptable death rate.
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PMID:Management of severe malarial infection. 268 Sep 36

We reviewed in retrospect the records of all patients at our institution in whom peritoneovenous shunts were placed to manage refractory ascites due to chronic liver disease from 1977 through 1986. There was a wide spectrum of underlying liver disease in these 23 patients; most frequent was alcoholic cirrhosis. Five were in modified Child's class A, 14 were in class B, and four were in class C. Fourteen of 23 patients had some complication associated with peritoneovenous shunt placement; clinical consumptive coagulopathy, infection, and gastrointestinal hemorrhage while hospitalized were most frequent. Fifteen of 23 died, 12 while hospitalized or within 1 month of hospitalization. Death in eight patients appeared to be related to shunt placement and was due to sepsis in five, hepatorenal syndrome with an obstructed shunt in one, consumptive coagulopathy in one, and pulmonary edema in one. All modified Child's class C patients, six of seven patients with clinical consumptive coagulopathy, and all patients with a preshunt total bilirubin greater than 3.7 mg/dl died while hospitalized or within 1 month of hospitalization. This review supports studies showing that placement of peritoneovenous shunts for refractory ascites has a high morbidity and mortality in patients with advanced liver disease, and does not support their use in the management of refractory ascites.
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PMID:Poor outcome from peritoneovenous shunts for refractory ascites. 271 11

We have reviewed 108 cases of bacterial endocarditis treated surgically since 1968. The mean age of the patients was 47.7 +/- 15.6 years (+/- SD) (range, 14-79 yr). Seventy-seven percent were male. The most common causative organisms were staphylococci (46%), streptococci viridans group (5%), and other streptococci (20%). Forty-five percent, 25%, and 13% of patients had native aortic valve, native mitral valve, or native double valve (AV/MV) involvement, respectively. Eighteen patients had prosthetic valve endocarditis. No patient underwent surgery for tricuspid valve endocarditis. Seventy-three patients were considered to have active endocarditis (AE) (positive blood or tissue cultures and/or annular abscess). The 35 remaining patients had healed endocarditis (HE). Preoperative complications in patients with either AE or HE were stroke (11%, 11%), renal failure (33%, 3%; p less than 0.001), pulmonary edema (83%, 34%; p less than 0.001), anemia (36%, 8%; p less than 0.01), and inotrope dependence (22%, 6%; p less than 0.05). Hospital mortality for native valve AE was 19.5% (11/56), and for healed endocarditis, 5.7% (2/35). Independent predictors of hospital mortality were inotrope dependence (p less than 0.001), annular abscess (p less than 0.01), pulmonary edema (p less than 0.01), and staphylococcal infection (p less than 0.05). The 5-year actuarial survival for operative survivors was 68.4 +/- 7.5% (AE) and 78.3 +/- 9.2% (HE). We conclude that the operative mortality for patients with continuing sepsis is high and that surgery should be undertaken early in staphylococcal endocarditis. If surgery is successful, then the long-term prognosis is good.
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PMID:The surgical treatment of infective endocarditis. 272 63

Acute hypoxemic respiratory failure (AHRF) can result from diverse lung insults. Toxic oxygen metabolites have been implicated in this clinical condition and in animal models of pulmonary edema. Hydrogen peroxide (H2O2), an oxygen metabolite, mediates tissue injury. We measured H2O2 levels by a spectrophotometric technique in the breath condensate of 68 mechanically ventilated patients; 13 patients with normal lungs undergoing elective surgery had no such detectable levels of H2O2. Fifty-five patients in the ICU meeting criteria for the adult respiratory distress syndrome (ARDS) had a higher concentration of H2O2 in the expired breath condensate than ICU patients without pulmonary infiltrates (2.34 +/- 1.15 vs 0.99 +/- 0.72 mumol/L, p less than 0.005). This marker had a sensitivity of 87.5 percent and a specificity of 81.3 percent in separating the two patient populations. Patients with AHRF and focal pulmonary infiltrates who did not meet criteria for ARDS also had higher concentrations of H2O2 (2.45 +/- 1.55 mumol/L) than patients without pulmonary infiltrates (p less than 0.001). No difference was observed between the expired H2O2 concentrations of patients with ARDS or patients with focal pulmonary infiltrates. Patients with brain injury or sepsis tended to have higher levels of H2O2 regardless of lung pathology. Increased levels of H2O2 are detected in the expired breath of ICU patients with focal lung infiltrates and in ARDS patients, which is consistent with the hypothesis that oxygen metabolites participate in the pathogenesis of ARDS and other forms of AHRF.
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PMID:Increased hydrogen peroxide in the expired breath of patients with acute hypoxemic respiratory failure. 276 20

A case of pulmonary edema in a 34-year-old pregnant woman on corticosteroids and beta adrenergics yielded an unusual radioaerosol/radioperfusion lung image. The image showed normal perfusion but multiple bilateral penetration defects on the radioaerosol study. Factors contributing to this unique pattern include the combined action of corticosteroids and beta-adrenergic agonists, local airway irritation caused by the drying effect of nebulized oxygen, sepsis, or a combination of these factors.
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PMID:Discordant radioaerosol/radioperfusion in drug-induced maternal pulmonary edema. 279 24

Pulmonary edema of sepsis is a consequence of increased transmural conductance for water and proteins at the level of lung microvessels induced by vasoactive endogenous mediators, liberated after activation of complement by bacterial endotoxins. Intermittent opening of interendothelial junctions at the level of post-capillary venules has been implicated as being the pathway for the leaking plasma proteins and water. Microvascular basement membranes and endothelial cell surfaces have fixed anionic charges (AS) which prevent the escape of plasma proteins from the circulation as well as the adhesion of blood cells to the luminal endothelium. The density distribution of these AS was substantially reduced in visceral and systemic microvessels during murine abdominal sepsis. This observation suggest that MOF secondary to sepsis is the consequence of a severe and generalized alteration of the microvascular electronegative charge, induced by liberation of inflammatory mediators.
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PMID:Decreased density distribution of mesenteric and diaphragmatic microvascular anionic charges during murine abdominal sepsis. 284 42

Twenty-four patients with high microvascular permeability pulmonary edema were initially treated by means of conventional supportive therapy for 1-12 days. Continued deterioration was treated by predilutional hemofiltration and induced a dramatic improvement in 22/24 patients. Survival was 92%. Sieving coefficients for autacoids and middle molecular weight vasoactive peptides involved in the development of high microvascular permeability pulmonary edema were higher than 0.88 indicating that clearing from blood of these peptides during one pass through the hemofilter is similar to that obtained during one pass through the pulmonary normal microvasculature. Hemofiltration seems to be a significant breakthrough in the treatment of ARDS secondary to severe sepsis.
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PMID:Hemofiltration in septic ARDS. The artificial kidney as an artificial endocrine lung. 300 79

The decision to use bedside pulmonary artery catheterization for managing patients must involve a careful assessment of the risks compared to the benefits. Complications can be minimized by following specific guidelines for catheter insertion and maintenance. Pulmonary artery catheterization has been shown to be more accurate than clinical assessment alone in critically ill patients for determining the cause of shock (hypovolemic, cardiogenic, or septic) or for assessing the cause of severe pulmonary edema (cardiogenic or noncardiogenic). The diagnosis of cardiac failure in medical or surgical patients with invasive hemodynamic monitoring provides physiologic data that guide pharmacologic treatment that may favorably influence preload and afterload in the failing or ischemic heart. Managing hemodynamics with the aid of pulmonary artery catheterization in patients with the adult respiratory distress syndrome has received considerable attention, but a contribution to better patient outcome has not been established. Similarly, although clinical management of hemodynamic instability in septic shock is facilitated by pulmonary artery catheterization, the mortality remains very high because of the lack of specific therapy to reverse the sepsis syndrome. Adequate volume resuscitation and improved tissue oxygenation are universally accepted goals, but specific hemodynamic endpoints are controversial and direct measurements of tissue oxygenation are not possible. Prospective studies to define the clinical value of pulmonary artery catheterization are needed, but must be designed very carefully in order to identify unequivocally the effect of pulmonary artery catheterization on outcome in critically ill patients.
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PMID:Bedside catheterization of the pulmonary artery: risks compared with benefits. 305 59


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