The Clinical Significance of Fibrinogen Degradation Products

Bick, Rodger L.

doi:10.1055/s-2007-1005060

Cited by 56 publications

(71 citation statements)

References 62 publications

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“…The systemically circulating FDP interfere with fibrin monomer polymerization; this further impairs hemostasis and may lead to hemorrhage [3][4][5]. The subsequent fragments (D and E) have a high affinity for platelet membranes and induce a profound platelet function defect, which may contribute to clinically significant hemorrhage [3][4][5][73][74][75]. FDP and D-dimer, discussed later, induce synthesis and release of monocyte/macrophage-derived IL-1, IL-6 and plasminogen activator inhibitor-type 1; IL-1 and IL-6 induce additional vascular endothelial damage and disruption, thus more endorgan damage, and elevated plasminogen activator inhibitor-1 inhibits fibrinolysis, leading to accelerated thrombus formation [70].…”

Section: Consequences Of Systemic Thrombin Activitymentioning

confidence: 99%

“…The precipitation of fibrin monomer may cause endorgan damage due both to primary parenchymal damage and to microvascular occlusion. Also, this may impair reticuloendothelial clearance of FDPs, activated clotting factors, and circulating so- The platelet-rich microthrombi are later replaced by hyaline (fibrin) microthrombi [73]. Hyaline microthrombi cause three types of endorgan damage; globular hyaline microthrombi, which may be seen on PAS-stained peripheral blood smears and are polymerized complexes of fibrinogen, fibrin, their degradation products and many intermediates [3,5], intravascular hyaline microthrombi, which are typically seen by pathologists at postmortem examination in DIC patients; these intravascular hyaline microthrombi are homogeneous, compact, intravascular hyaline structures oriented parallel to the blood flow, which occasionally contain platelets or white cell fragments, are easily seen by PAS staining, trichrome staining, tryptophan staining, and fluorescein-labeled antifibrinogen antiserum staining and by electron microscopy [109,110], and pulmonary hyaline membranes, which are also a form of hyaline microthrombus and are highly polymerized complexes of fibrinogen, fibrin, their degradation products, and all types of intermediates [111,112].…”

Section: Morphological Findings In Dicmentioning

confidence: 99%

“…These degradation products are only 'diagnostic' of plasmin biodegradation of fibrinogen or fibrin, and are therefore only indicative of the presence of plasmin [3][4][5]73]. The protamine sulfate or ethanol gelation tests for circulating soluble fibrin monomer are usually positive [3,5,69,125,126].…”

Section: Global Coagulation Tests In Dicmentioning

confidence: 99%

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Disseminated Intravascular Coagulation

Bick¹,

Arun²

1999

Pathophysiol Haemos Thromb

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Disseminated intravascular coagulation (DIC) is a complex disorder, with pathophysiology being variable and highly dependent upon the triggering event(s), host response(s) and comorbid conditions. As a result of these complicated interactions, the clinical expression and laboratory findings are varied, thereby affecting the specifics of diagnosis and therapeutic approaches. The highly complex and variable pathophysiology of DIC often results in a lack of uniformity in clinical manifestations, a lack of consensus in the specific appropriate laboratory criteria of diagnosis, and a lack of specific therapeutic modalities. Indeed, recommendations for therapy are often difficult because the morbidity and survival is more dependent on the specific cause of DIC and because the generally used specific therapeutic approaches, which include for example heparin, low-molecular-weight-heparin antithrombin concentrate and protein C concentrate, have never been subjected to objective prospective randomized trials, except antithrombin concentrates. An analysis of the complex and varied pathophysiological events in DIC provide objective guidelines and criteria for the clinical diagnosis, the laboratory diagnosis, and the definition of severity. These data compounded by an understanding of complex and varied pathophysiology can be used for objective evaluation of therapeutic responses and results. DIC is an intermediary mechanism of disease usually seen in association with well-defined clinical disorders. The pathophysiology of DIC serves as an intermediary mechanism in many disease processes, which sometimes remain organ specific. This catastrophic syndrome spans all areas of medicine and presents a broad clinical spectrum that is confusing to many. Most physicians consider DIC to be a systemic hemorrhagic syndrome; however, this is only because hemorrhage is evident and often impressive. Less commonly appreciated is the profound microvascular thrombosis and sometimes, large vessel thrombosis. The hemorrhage is often simple to contend with in patients with fulminant DIC, but it is the small- and large-vessel thrombosis, with impairment in blood flow, ischemia, and associated end-organ damage that usually leads to irreversible morbidity and mortality. In conclusion, the pathophysiological mechanisms, clinical, and laboratory manifestations of DIC are complex in part due to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents, and agents which can block, blunt or modify cytokine activity and the activity of vasoactive substances appear to be of value. The complexity and variable degree of clinical expression suggests that therapy should be individualized depending o...

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Section: Consequences Of Systemic Thrombin Activitymentioning

confidence: 99%

Section: Morphological Findings In Dicmentioning

confidence: 99%

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Disseminated Intravascular Coagulation

Bick¹,

Arun²

1999

Pathophysiol Haemos Thromb

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“…In the borderline of activation and clinical manifestation, we believe that evaluation of coagulation times, AT activity, FDP and fibrinogen levels should be helpful for an appropriate establishment of diagnosis (Bick 1982).…”

mentioning

confidence: 99%

“…Uncontrolled bleeding is therefore a result of deficiency of coagulation factors, coming along with platelet depletion plus the anticoagulant properties of FDP's (Hardaway 1966;Ryan 1976;Green and Thomas 1994;Maruyama et al 2004). Plasmin seems to be a very important substance in this system, because it acts in fibrin degradation with formation B_beta 15-42 and related peptides and D-dimer and also in degradation of other coagulation factors (Owen and Bowie 1977;Bick 1982;Stokol et al 2000;Boisvert et al 2001;Monreal 2003). The fluido-coagulation balance is basically a balance of two dominant mediators -thrombin and plasmin.…”

mentioning

confidence: 99%

Disseminated Intravascular Coagulopathy of the Dog

Vlašín¹,

Raušer²,

Fichtel³

et al. 2004

Acta Vet. Brno

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Use of streptokinase for the salvage of a free flap: Case report and review of the use of thrombolytic therapy

et al. 1987

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This is the first case report of the clinical use of intraoperative streptokinase to promote free flap salvage. A latissimus dorsi free flap was mobilized to cover a scalping type injury. After 4 1/2 hours of ischemia and recurrent thrombosis, streptokinase was perfused into the thoracodorsal artery (7,500 units of streptokinase in 30 cc of normal saline). The free flap was exposed to this concentration of streptokinase for 10 minutes followed by drainage of the venous effluent in order to avoid possible deleterious systemic effects of the streptokinase. Good flow throughout the free flap resulted, and the flap remained viable, providing good coverage for the patient's skull. Controversies regarding the no-reflow phenomena and the use of various thrombolytic agents are discussed.

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The Clinical Significance of Fibrinogen Degradation Products

Cited by 56 publications

References 62 publications

Disseminated Intravascular Coagulation

Disseminated Intravascular Coagulation

Disseminated Intravascular Coagulopathy of the Dog

Use of streptokinase for the salvage of a free flap: Case report and review of the use of thrombolytic therapy

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