Amniotic Fluid Embolism

A, Aguillón; Andjus, Theophile; Grayson, Arthur; Race, George J.

doi:10.1097/00006254-196210000-00001

Cited by 32 publications

(5 citation statements)

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“…Thus, when assessing the etiologic triggers of patients with DIC as a group, amniotic fluid embolism is quite rare. The risk factors associated with development of amniotic fluid embolism (Table 3) consist of older age, multiparity, marked exaggeration of uterine contraction following rupture of the uterine membranes, or markedly exaggerated uterine contraction due to the use of oxytocin (pitocin) or other uterine stimulatory agents, cesarean section, uterine rupture, high cervical laceration, premature separation of the placenta, and intrauterine fetal death (2,23,24). Other factors have been spontaneous rupture of the fetal membranes and blunt trauma to the abdomen (25,26).…”

Section: Amniotic Fluid Embolismmentioning

confidence: 99%

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

Bick

2002

Clin Appl Thromb Hemost

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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.

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Section: Amniotic Fluid Embolismmentioning

confidence: 99%

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

Bick

2002

Clin Appl Thromb Hemost

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“…21,22 The risk factors associated with the development of amniotic fluid embolism are depicted in Table 2, in cluding marked exaggeration of uterine contraction following rupture of the uterine membranes or due to the use of oxytocin or other uterine stimulatory agents. 18,23,24 The syndrome can, on rare occasions, occur late in pregnancy, but most commonly occurs during labor in 80% of patients; in only up to 20% of pa tients does the syndrome occur before labor begins and before rupture of the amniotic sac. 25,26 Twentyfive percent of women will die within 1 hour of devel oping this syndrome and up to 80% of patients will die within the first 9 hours.…”

Section: Etiology Acute Dicmentioning

confidence: 99%

Disseminated Intravascular Coagulation and Related Syndromes: A Clinical Review

Bick

1988

Semin Thromb Hemost

172

470

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“…Disorders of coagulation and fibrinolysis have been shown to be a more constant feature of amniotic fluid embolism than of any other condition in obstetrics. It is usually agreed that blood incoagulability occurs in 30-45% of women who survive the first hours of AFE (3,6,10,29). The changes in the essential blood factors resulting from AFE are compatible with those seen after disseminated intravascular coagulation (28), a process causing activation of the coagulation and/or fibrinolytic systems which is called intravascular pathological proteolysis in modern nomenclature.…”

Section: The Uterine Wall Tmentioning

confidence: 99%

“…Despite all treatment measures, 75°/o of the mothers usually die within 6 hours (29). If the woman survives the initial profound shock, there is a 30-45% risk of her developing blood incoagulability, with the possibility of death from hemorrhagic shock (3,6,10,29).…”

Section: Introductionmentioning

confidence: 99%

Amniotic Fluid Embolism: A Review of the Literature with Two Case Reports

Lalos

Schoultz

1977

Intl J Gynecology & Obste

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Amniotic fluid embolism (AFE) is a rare but dramatic obstetric complication. In this study, the pathogenesis of AFE and the disorders of coagulation and fibrinolysis and postmortem gross pathologic and histologic findings resulting from it are reviewed. The 2 case histories examined in this report exemplify different clinical courses of amniotic fluid embolism. In the first case, there was a predominant activation of the coagulation system, with a fatal outcome. In the second case, generalized fibrinolysis dominated, and the woman survived. Finally, the authors wish to emphasize that the administration of fibrinogen is an incorrect approach to the management of this syndrome. A combination of Macrodex and heparin might be effective in preventing the formation of microthrombi, but increased fibrinolysis has to be treated by a sufficiently high dose of fibrinolytic inhibitors.

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Amniotic Fluid Embolism

Cited by 32 publications

References 0 publications

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

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

Disseminated Intravascular Coagulation and Related Syndromes: A Clinical Review

Amniotic Fluid Embolism: A Review of the Literature with Two Case Reports

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