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

A prospective pair-controlled study of maternal, cord blood, and neonatal hematologic findings was done in 50 severely preeclamptic/eclamptic and 50 well-matched normotensive pregnancies. There were no neonatal complications in mature infants. Neonatal complications were similar in premature infants of both study and control group; however, neonatal deaths were higher in the study group. In the study group, there was a poor correlation between maternal and cord blood hematocrit (r = .07), platelet count (r = .11), and fibrinogen (r = .05). In addition, there was no correlation (r = .06) between maternal and cord blood thrombocytopenia. Within each subgroup, abnormal neonatal hematologic findings were usually associated with fetal growth retardation, perinatal asphyxia, acidosis, sepsis, or intracranial hemorrhage. The present findings suggest that abnormal hematologic findings described in neonates of severely preeclamptic/eclamptic pregnancies are the result of associated neonatal complications, rather than a direct consequence of preeclampsia.
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PMID:Maternal-fetal correlations in patients with severe preeclampsia/eclampsia. 663 1

A survey is given on the clinical relevance of microaggregates in stored blood. Initially the pathophysiology of aggregation led by electrostatic and humoral changes on the surface and membrane of the platelets is presented, and the well known pathomechanisms of embolization as well as the functional pulmonary impact of these emboli are discussed. The ever increasing importance of humoral factors is stressed, the mechanic obstruction of pulmonary capillaries by microaggregates having not that clinical importance as the general opinion in earlier days has been. New therapeutic aspects therefore are mentioned: The blockade of aggregation and the release syndrome by adding aspirin, aprotinin or prostaglandin E 1 to the stored blood, pharmacologically influencing the metabolism of arachidonic acid by inhibiting negative effects of prostaglandins (injecting ibuprofen as inhibitor of thromboxane-synthesis) and stimulating positive prostaglandin effects (infusion of prostacyclin), and finally the application of fibronectin (cryoprecipitates) for increasing the RES-function thus also enhancing the clearance of microaggregates, fibrinogen/fibrin complexes and intestinal serotonin. The latter way only, however, is also clinically feasable. The purely mechanical microfiltration should therefore still be used (3 pints of blood at least, pulmonary damage by trauma, shock or sepsis) and the methods of giving aggregate-poor red cell preparations (buffy coat free or saline washed) should be remembered. For the future one could speculate that more or less complete humoral block might be used in conjunction with a "midi-filtration" (Eckert: 40-100 mu diameter standard blood filter).
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PMID:[Clinical relevance of microaggregates in stored blood]. 665 92

161 splenectomies are presented with a morbidity of 14.8% and a total mortality rate of 4.3%. The lethality rate due to severe infections (-3.9%), however, was high and mostly caused by an overwhelming postsplenectomy sepsis, pneumonia or meningitis. 61.5% of the infections were caused by pneumococcus. To drop that high lethality rate after splenectomy we replanted splenic tissue in seven patients. Scintigraphic investigations showed in all cases well vascularised splenic tissue. The immunoglobulins were in a normal range. Howell-Jolly bodies, however, did not disappear in all the patients. From our study as well as from the literature one has to conclude that replanted splenic tissue requires immunologic activity but a reduced capacity for phagocytosis. Therefore, in cases of traumatic injury to the spleen it is necessary to try to preserve as much of the organ as possible either by infrared coagulation, gluing with human fibrinogen or partial splenectomy. If these procedures are impossible a replantation of--50% of the original splenic tissue should be done and several thin homogenised particles replanted intra- or retroperitoneally. Out of that a preoperative vaccination against pneumococcal infection is necessary as well as a postoperative penicillin prophylaxis for about three years.
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PMID:[Splenectomy and reimplantation of splenic tissue in children]. 665 66

A child aged 2 years 3 months with Streptococcus pneumoniae sepsis and pulmonary abscesses had hemolytic-uremic syndrome and acute renal failure develop that required 36 cycles of peritoneal dialysis. A percutaneous renal biopsy specimen taken after dialysis showed mesangial proliferation with interposition, hemorrhagic crescents, and intracapillary thrombosis with fibrinogen and IgM deposition. The atrophic renal tubules showed positive immunofluorescence against peanut agglutinin. Neuraminidase released by pneumococcal organisms is thought to expose the Thomsen-Friedenreich antigen on platelets, erythrocytes, and kidneys, resulting in IgM deposition and binding of peanut agglutinin. Review of the literature showed four other reports involving five children who had hemolytic-uremic syndrome develop secondary to pneumococcal infections.
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PMID:Hemolytic-uremic syndrome associated with Streptococcus pneumoniae. Report of a case and review of the literature. 671 7

Severe infections and particularly infectious shock are frequently accompanied by a varying degrees of disseminated intra-vascular coagulation (DIC). The mechanism at work is complex, involving endotoxin or bacterial lipopolysaccharide constituents that damage vascular endothelium and activate intrinsic coagulation, platelet function and the release of leucocyte coagulation-promoting compounds. The activation of coagulation in turn activates prekallikrein and complement and plays a part in shock. The laboratory plays an essential role in diagnosing DIC, determining its repercussions on the parameters of haemostasis and in monitoring its course under antibiotics, which in some cases may be combined with carefully controlled heparin treatment. Sensitive and specific tests are the assays for fibrinogen-fibrin degradation products (FDP) and soluble complexes (SC) using the haemagglutination test or the ethanol test. The platelet count should be combined with measurement of the bleeding time. A varying degree of thrombopenia is frequent but non specific. In cases of septicemia, it is an early warning sign. A selective fall in proaccelerin is an indirect early sign. A fall in antithrombin III (AT III) is considered a good sign of DIC but it does not occur in every case, and is most liable to be present in liver failure. From the FDP and fibrinogen results, it should be clear whether one is dealing with compensated, decompensated or even over-compensated DIC. Diagnosis should be complemented by a careful search for the clinical signs of coagulation and haemorrhage. It is indispensable for investigations to be repeated every 6-12 hours, for the sake both of treatment strategy, which can be extremely difficult, and DIC monitoring.
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PMID:[Diagnosis of defibrination syndromes in infectious pathology]. 673 53

Previous studies have suggested that plasma fibronectin is a component of the physiological antithrombotic mechanism and is related to resistance to cardiopulmonary failure during sepsis. The current study addresses the hypothesis that fibronectin deficiency results in increased sensitivity to thrombosis during sepsis, whereas increased fibronectin results in enhanced resistance. Rats were injected with purified fibronectin, antiserum to fibronectin, antiserum to albumin or vehicle prior to intraaortic infusion of saline, live Escherichia coli (10(7)--10(8)/100 gm) or E coli endotoxin (0.001--0.1 mg/100 gm). Infusion of the higher doses was associated with greater mortality in antifibronectin groups than the other groups. Mean arterial blood pressure fell transiently in all groups following injection of antifibronectin but not following the other pretreatment. Both endotoxin and bacterial infusion resulted in severe thrombocytopenia in antifibronectin-treated animals and to a lesser extent following antialbumin. Fibrinogen consumption was increased in all groups after antifibronectin treatment in bacteria infused animals after pretreatment with antialbumin or fibronectin. Fibrin degradation products were increased by bacterial infusion in animals treated with either antiserum. The current data support a relationship between plasma fibronectin and resistance to thrombosis. The relationship was not as clear-cut as that previously observed for nonseptic thrombotic states.
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PMID:Plasma fibronectin and resistance to thrombosis during sepsis. 675 30

Fibrin has classically been considered a defense mechanism of the peritoneal cavity. We have studied the role of purified fibrin in the pathogenesis of intraperitoneal infection. Implantation of 0.5% bovine fibrin clots containing 2 X 10(8) E. coli into the rat peritoneal cavity reduces the 24-hour mortality rate from 100% to 0% compared to bacteria in a similar volume of saline solution. However, the 10-day mortality rate with fibrin is 90%; 100% develop intraperitoneal abscesses. Animals receiving sterile clots lyse than over 1 to 2 weeks without abscess formation. As few as 10(2) E. coli per fibrin clot produce abscesses, but 10(7) or more are required to produce death; without fibrin less than 10(7) E. coli neither kill nor produce intraperitoneal infections. Both late death and abscess size with 2 X 10(8) E. coli are directly proportional to the fibrin clot size but not the concentration of fibrin in the clot. Operative debridement of the fibrin at 4 or 24 hours completely eliminates abscess formation in surviving animals. In vitro growth of E. coli is neither stimulated nor inhibited by fibrin or fibrinogen. Fibrin delays systemic sepsis, but the entrapped bacteria cannot be easily eliminated by normal intraperitoneal bactericidal mechanisms and abscess formation occurs. Thus radical peritoneal debridement or anticoagulation may reduce the septic complications of peritonitis.
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PMID:Fibrin in peritonitis. I. Beneficial and adverse effects of fibrin in experimental E. coli peritonitis. 699 21

Goats, sheep and calves were inoculated intravenously with strain Y3343 of the large colony type of Mycoplasma mycoides subsp. mycoides isolated from a goat with polyarthritis. The goats and sheep died of septicemia (one was killed in extremis) within eight days. The goats had leukopenia and granulocytopenia. Coagulopathy was indicated in some goats; the fibrinogen titer, prothrombin and partial thromboplastin times increased with the progress of disease and the number of platelets decreased dramatically in one goat. Goats and sheep had cellulitis at the site of inoculation, pleural hemorrhages, pneumonia, myocarditis, renal infarcts, glomerulitis, adrenal cortical necrosis, enteritis, focal splenic necrosis, polyarthritis and lymphadenitis. Vasculitis and thrombi were seen occasionally, suggesting that vascular changes, perhaps together with coagulopathy, had a role in pathogenesis. One of two experimental calves developed a slight fever, arthritis and minor inflammation of adrenal tissue. Calves seen less susceptible to the mycoplasma organism given intravenously than do goats or sheep.
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PMID:Experimental infection of goats, sheep and calves with the large colony type of Mycoplasma mycoides subsp. mycoides. 700 31

There is evidence that both bronchoconstriction and accumulation of lung water may contribute to the early alterations in lung function following septicemia. Eigher of these may be mediated by blood components. To assess these proposed mechanisms the changes in hemodynamics, pulmonary mechanics, gas exchange, and gravimetric lung water were measured in the first 4 h after Escherichia coli infusion in the anesthetized dog and baboon. These species were selected because of previously demonstrated differences in the response to gram-negative sepsis. Both species developed systemic hypotension and early hypoxemia. The dogs had early transient increases in venous admixture (Qva/Qt) but not shunt or dead space, while the baboon had a more persistent increase in Qva/Qt and a late increase in dead space, Increases in nonelastic resistance and decreases in lung compliance were preceded or accompanied by decreases in the leukocyte count in both species, but the platelet count, fibrinogen, and total hemolytic complement had different changes in the two species. Postmortem lung analysis revealed increased lung weight in both species but the wet weight-to-dry weight ratio was not increased in either species. The fractional water content of the excess lung mass was less than that of whole blood. Histological examination revealed large numbers of extravasated leukocytes in the lungs, which may be sufficient to explain the increase in lung weight. We conclude that pulmonary edema does not play a role in the early pulmonary response to E. coli bacteremia in either species. The physiological changes observed are more consistent with bronchoconstriction.
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PMID:Role of pulmonary edema in the acute pulmonary response to sepsis. 702 1

The serum concentration of fibrinogen split product D (fragment D; Fg D) is often elevated after trauma and sepsis. Purified human Fg D infused into awake rabbits causes progressive thrombocytopenia and complement depletion, pulmonary dysfunction, increased vascular permeability to albumin, and neutrophil congestion. This study demonstrates the sites of organ sequestration of platelets and neutrophils after Fg D-induced respiratory distress. Washed, 51Cr-labeled rabbit platelets were infused into control (n = 10) and Fg D-infused rabbits (n = 10) Washed, 51Cr-labeled rabbit neutrophils were infused into two additional rabbit groups (control, n = 10; Fg D, n = 10). Four animals from each group were sacrificed at 2 h and six animals at 4 h postinfusion. Four biopsies from the lung, kidney, liver, heart, and spleen of each rabbit were counted for isotope uptake. Data for like groups were analyzed by the Student's t-test. At 2 h platelets that disappear from the circulation begin to sequester in the lung, liver, kidney, and heart of Fg D-infused rabbits (p less than 0.001). Neutrophils are not yet trapped in organ vasculature. However, 4 h postinfusion after thrombocytopenia and complement depletion, platelets are trapped in all organs studied (P less than 0.001) Neutrophils have significantly increased in lung and liver (P less than 0.001). Platelets activated by Fg D in this model sequester before neutrophils, suggesting that the platelet membrane effects of Fg D may initiate organ failure after shock and sepsis.
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PMID:Platelet and neutrophil sequestration after fragment D-induced respiratory distress. 706 54


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