Disseminated Intravascular Coagulation: A Review of Etiology, Pathophysiology, Diagnosis, and Management: Guidelines for Care

Abstract

The pathophysiologic 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 pathophysiologic 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 that 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 on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamics and other appropriate clinical parameters. At present, treatment of the triggering event, low-dose heparin or antithrombin concentrate and wise choice of components when indicated appear to be the most effective modes of therapy.

Blood Component Therapy in Obstetrics

“…Obstetric disorders associated with DIC include amniotic fluid embolism, placental abruption, retained products of conception, eclampsia, and abortion [16]. Disseminated intravascular coagulation is commonly associated with obstetric hemorrhage and causes profuse bleeding due to inadequate blood clot formation.…”

Disseminated Intravascular Coagulation in Obstetrics: Ethiopathogenesis and up to date Management Strategies

“…Furthermore, patients exhibit a tendency for severe bleeding associated with the consumption of platelets and coagulation factors (3,4) . Clinically, DIC may lead to a wide range of pictures from unnoticed intravascular thrombosis and microvascular damage to uncontrollable bleeding.…”

Amniotic Fluid Embolism

“…The exact mechanism of this anaphylactoid reaction to amniotic fluid is not clearly understood. Predisposing factors once considered to be associated with AFE include placental abruption, uterine overdistention, fetal death, trauma, turbulent labor oxytocin-stimulated labor, multiparity, male fetus, cesarean delivery, advanced maternal age, prolonged gestation, instrumental vaginal delivery, eclampsia, polyhydramnios, fetal distress, large fetal size, high cervical laceration, premature separation of the placenta and rupture of membranes (12)(13)(14)(15). The presence of a large or dead fetus and meconium staining of the amniotic fluid are also felt to increase the risk (5) ( Table 1).…”