The Fibrinolytic Enzyme System After Trauma and in Patients With Fat Embolism

Rennie, A. M.; Ogston, D.; Cooke, Rhian; Douglas, A.G.

doi:10.1302/0301-620x.56b3.421

Cited by 12 publications

(6 citation statements)

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“…The changes most frequently described have been the reduction of kalcemia and platelets, the increase of platelet adherence, the prolonged times of activated partial prothrombin and thromboplastin, the release of FDPs (fibrin degradation products), and the reduction of circulating fibrinogen (8,16,17,20,22,24,27,39,74) . Those changes, however, do not occur in all FES cases (27,30,75) and, when they do, are usually subtle (27,76) . Thus, the majority of the recent authors think that laboratory changes suggesting DIVC shall be attributed mainly to coagulation changes that usually accompany a severe trauma than to a potential FES (22,74,75) .…”

Section: Laboratory Changesmentioning

confidence: 94%

“…In fact, it is not uncommon to find laboratorial changes compatible to DIVC syndrome in some cases of FES (22,27,45,74) , yet the occurrence of the hemorrhagic syndrome secondary to this consuming coagulopathy is extremely rare (13) . On the other hand, there are well established FES case series, in which the authors did not manage to detect laboratory changes characterizing DIVC in none of the patients (30,75) . For the great majority of researchers, therefore, DIVC is considered as an infrequent phenomenon, which can or cannot occur in conjunction with FES (13,27,74,76) .…”

Section: "Biochemical Phase"mentioning

confidence: 98%

“…For the great majority of researchers, therefore, DIVC is considered as an infrequent phenomenon, which can or cannot occur in conjunction with FES (13,27,74,76) . Furthermore, the fact that DIVC is a common complication in polytraumatism patients is well known, regardless of the presence of absence of FE (22,75) . So, today, it is considered that DIVC and FES are two independent morbid conditions, but they may coexist in a same patient, which certainly compromises diagnosis.…”

Section: "Biochemical Phase"mentioning

confidence: 99%

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Embolia gordurosa: uma revisão para a prática ortopédica atual

et al. 2005

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A embolia gordurosa (EG) é a oclusão de pequenos vasos por gotículas de gordura, geralmente originadas nas fraturas do fêmur, tíbia e bacia, e nas artroplastias do joelho e quadril. Normalmente não causa danos aos órgãos atingidos, a menos que seja maciça. Em poucos casos a EG evolui para a "síndrome da embolia gordurosa" (SEG) a qual afeta principalmente os pulmões e o cérebro, embora qualquer órgão ou estrutura do organismo possa ser afetada. A gordura embolizada é hidrolizada pela lipase, originando os ácidos graxos livres (AGL) que agem toxicamente sobre o endotélio capilar e que intensificam a ação das integrinas as quais acentuam a adesividade dos neutrófilos às células endoteliais, facilitando a ação das enzimas proteolíticas dos lisossomas desses neutrófilos sobre o endótelio. O resultado dessas reações é a ruptura da rede capilar seguida de hemorragia e edema nos órgãos afetados. A SEG apresenta desde insuficiência respiratória e alterações neurológicas variadas até convulsões e coma profundo. O diagnóstico da SEG é puramente clínico, não existindo nenhum exame laboratorial que o confirme. Dentre os exames de imagens, apenas a ressonância magnética cerebral demonstra claramente as áreas do edema perivascular e dos infartos. O tratamento da EG com inúmeras drogas não apresentou resultados positivos; no entanto, a medida mais requisitada para a SEG é a assistência ventilatória. A mortalidade é quase de 100% nas formas fulminantes; aproximadamente de 20% nas formas sub-agudas e não há mortalidade na forma sub-clínica. Para prevenir a SEG é fundamental evitar o choque e a hipóxia desde a cena do acidente, e proceder à fixação precoce das fraturas, o que diminui a incidência de SARA e a mortalidade pós-trauma.

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Section: Laboratory Changesmentioning

confidence: 94%

Section: "Biochemical Phase"mentioning

confidence: 98%

Section: "Biochemical Phase"mentioning

confidence: 99%

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Embolia gordurosa: uma revisão para a prática ortopédica atual

et al. 2005

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“…Fibrino lytic activity was higher after surgery or trauma (44). Plasma plasminogen levels were also higher after surgery or trauma (45,46). Low fibrinolytic activity was observed in pregnant women at later months of pregnan cy.…”

Section: Exercise Injury and Pregnancymentioning

confidence: 97%

Physiology of Plasminogen: With Special Reference to Activation and Degradation

Takada

Takada²

1988

Pathophysiol Haemos Thromb

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Plasminogen is said to be synthesized in many organs, but the major source of its production is considered to be the liver. The production of plasminogen is observed in fetal life, but its plasma level is low in new born infants, rising rapidly to attain adult levels in about 13 weeks. The plasma levels do not change much with age. Although the fibrinolytic enzyme system is influenced by many factors such as hormones, exercise, emotion, age, sex, nutritional states etc., the plasma levels of plasminogen are relatively stable. In this presentation we would like to discuss three important subjects related to the physiology of plasminogen. The first subject is the activation pathway of the native form of plasminogen (Glu-plg) by various activators in the plasma or clotted plasma. Glu-plg was not easily activated by activators such as urokinase (UK) or tissue plasminogen activator (t-PA), but activated very easily in the presence of fibrin clot. In the presence of purified clot, Glu-plg was partly activated by activators to Glu-plasmin, but also converted to Lys-plg by preformed plasmin, subsequently being activated to plasmin. Glu-plg I (containing two carbohydrate chains) changed conformation more easily upon interaction with fibrin than Glu-plg II (containing one carbohydrate chain) and Glu-plg I was also more easily activated by activators than Glu-plg II. Although Glu-plg was hardly activated by activators in the plasma, Glu-plg was activated easily in the presence of plasma clot. Results of immunoblotting experiments indicated that Glu-plg was mainly activated by activators directly to plasmin, not via Lys-plg in contrast to purified systems. The second subject is the degradation of plasminogen by elastase. Plasminogen may be degraded by proteolytic enzymes such as cathepsin or elastase. The degradation of plasminogen by elastase is shown to give rise to K1 to K3, K4, and mini-pig (containing K5). We have shown that the degradation rate to Glu-plg by elastase increased in the presence of tranexamic acid, indicating that the conformational change of Glu-plg in the presence of tranexamic acid resulted in the exposure of the hydrophobic regions connecting K3, K4 and K5, thus making them accessible to elastase. Consequently, Lys-plg or conformationally altered Glu-plg (possibly bound to fibrin or FDP) is more easily degraded in vivo. The last subject is relationship between plasma plasminogen levels and fibrinolytic activity in various ages. Although plasma plasminogen levels do not change with age, the fibrinolytic activity lowers. We found that t-PA antigen levels increased, PA inhibitor levels decreased, and PA activity decreased with age. These results suggest that the major factor influencing the activity of fibrinolytic system is not plasminogen but other components such as PA, PA inhibitors or inhibitors of plasmin.

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“…These findings easily lead us to conclude that fat entered the vasculature from the injured bone marrow. Rennie, et al (1974) reported that the changes of the plasminogen level and the platelet count were great in the traumatized patients. Jacobs (1976) found some evidences for intravascular coagulation in experimental dogs.…”

Section: Cases Of Acute Decompression Sicknessmentioning

confidence: 99%

Pulmonary Fat Embolism

Kitano

Kawashima

Torisu

et al. 1980

Orthopedics & Traumatology

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A pathological study of a non-selected autopsy material was performed on fat embolism. Pulmonary fat embolism was found in 53 out of 102 consecutive autopsies. Fat embolism seemed as closely associated with bone fracture and bone marrow embolism. Main source of the embolic fat should be the traumatized tissue, especially the marrow cavity of the fractured bone. The incidence of the case numbers of pulmonary thrombosis had an intimate relationship with severity of pulmonary fat embolism. Intravascular fat droplets were sometimes trapped in fibrin clots. It should be very reasonable to consider that fat embolism contributes to the formation of intravascular thrombi.

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The Fibrinolytic Enzyme System After Trauma and in Patients With Fat Embolism

Cited by 12 publications

References 0 publications

Embolia gordurosa: uma revisão para a prática ortopédica atual

Embolia gordurosa: uma revisão para a prática ortopédica atual

Physiology of Plasminogen: With Special Reference to Activation and Degradation

Pulmonary Fat Embolism

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