fibrin and Vitamin-K-Deficiency

The hemostatic mechanism has evolved to provide efficient protection from traumatic blood loss and yet maintain the blood in a fluid state in the circulation as a whole. Recent advances in biochemistry have provided both detailed understanding of hemostasis and clinically useful coagulation assays to exploit this understanding. Clinicians now have the means to delineate most of the hemostatic problems of clinical significance.

Topics: Blood Coagulation; Blood Coagulation Factors; Blood Coagulation Tests; Factor VIII; Factor X; Factor Xa; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Hemophilia A; Humans; Prothrombin Time; Thrombin; Thrombin Time; Vitamin K Deficiency; von Willebrand Diseases

Topics: Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Tests; Calcium; Factor IX; Factor V; Factor VIII; Factor X; Factor XII; Fibrin; Fibrinogen; Humans; Liver Diseases; Phospholipids; Prothrombin; Prothrombin Time; Thromboplastin; Vitamin K Deficiency

Topics: Blood Coagulation Factors; Blood Platelets; Diagnosis, Differential; Factor VII Deficiency; Fibrin; Fibrinolysis; Hemophilia A; Hemophilia B; Hemorrhage; Humans; Hypoprothrombinemias; Prothrombin Time; Thrombin; Vitamin K Deficiency

After the formation of a platelet-plug, generation of fibrin is necessary for its stabilization. Both congenital and acquired deficiencies of clotting factors occur, leading to retarded formation of fibrin. In congenital disorders, preoperative correction is possible and necessary. In acquired deficiencies, the type and feasibility of correction depends on the cause of the deficiency.

Topics: Blood Coagulation Disorders; Fibrin; Hemophilia A; Hemophilia B; Hemostasis, Surgical; Humans; Vitamin K Deficiency; von Willebrand Diseases

87 newborn infants were studied on their first day of life for defects in the coagulation and fibrinolytic systems. The infants were divided into two diagnostic groups, one with IRDS, the other with mixed neonatal disorders. Factor V, fibrinogen and fibrin/fibrinogen degradation products (FDP) were abnormal more often than any of the other factors examined. The presence or absence of "multiple defects" appeared to depend on the severity of the illness and its ultimate course. Thus 28% of the surviving infants or 85% of those who died had "multiple defects". The pattern of abnormalities did not differ between the infants with IRDS and those with mixed disorders. The "multiple defects" are ascribed to the following mechanisms: (1) impaired synthesis due to vitamin K deficiency and/or liver damage, (2) abnormal proteolytic activity stimulated by tissue damage and causing (a) an activation of the coagulation process (b) activation of the fibrinolytic system, or (c) of both the coagulation and the fibrinolytic systems. Differentiation between these pathways to defective haemostasis are important when deciding upon therapeutic measures in addition to the basic treatment.

Topics: Blood Cell Count; Blood Coagulation; Blood Platelets; Factor V; Factor VIII; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemostasis; Humans; Infant Mortality; Infant, Newborn; Infant, Newborn, Diseases; Male; Plasminogen; Respiratory Distress Syndrome, Newborn; Vitamin K Deficiency

Topics: Adrenal Glands; Asphyxia Neonatorum; Blood Cell Count; Blood Coagulation Disorders; Blood Platelets; Disseminated Intravascular Coagulation; Embryonic and Fetal Development; Fibrin; Fibrinogen; Hemorrhage; Humans; Hypothermia; Infant, Newborn; Liver; Respiration, Artificial; Thromboembolism; Vitamin K Deficiency