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

Abstract

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.

Amniotic Fluid Embolism in Sweden, 1951–1980

“…The known predisposing factors for AFE are multiparity, hypertonic labor, fetopelvic disproportion, laceration of the birth canal, low insertion of the placenta with pathology of the endocervical veins, excessive amounts of amniotic fluid, abruptio placentae, cord entanglement, and oxytocin administration [5,6,12,27,[30][31][32]. These risk factors were also found in the Swedish cases.…”

“…It is rather the amniotic fluid stained with meconium that is patho genic [37], The fulminant syndrome of AFE follows the ultimate common pathway of shock lung such as fat embolism, postperfu sion lung with aggregation of platelets and granulocytes, and activation of the comple ment system [38,39], The source of throm boplastin in AFE syndrome is not only the microaggregates, but also the amniotic fluid itself [12,27], Violent pulmonary hypertension, a severe fall in lung complicance, arterial hypoxemia, and a drastic fall in cardiac output are ob served in the syndrome [31,[40][41][42], The main cause of death in AFE is cardiorespira tory arrest. Immediate resuscitation and sup portive measures for the hemodynamic dis turbances are of utmost importance for the patient's survival [5], Some 30-45% of the patients who survive the first hours of the syndrome will develop severe blood incoagulability [5,6], Thrombo plastin is the origin of the complication, caus ing intravascular pathological proteolysis with predominant activation of the coagula tion system. Blood volume substitution and supplementation of coagulation factors are of importance, but other supportive measures are still under debate [11,27,39,43,44], Sub stitution with fibrinogen has been questioned [6,11,21,45], Fibrinolysis is a late conse quence of AFE.…”

“…Immediate resuscitation and sup portive measures for the hemodynamic dis turbances are of utmost importance for the patient's survival [5], Some 30-45% of the patients who survive the first hours of the syndrome will develop severe blood incoagulability [5,6], Thrombo plastin is the origin of the complication, caus ing intravascular pathological proteolysis with predominant activation of the coagula tion system. Blood volume substitution and supplementation of coagulation factors are of importance, but other supportive measures are still under debate [11,27,39,43,44], Sub stitution with fibrinogen has been questioned [6,11,21,45], Fibrinolysis is a late conse quence of AFE. When present, it should be counteracted with aminocaproic acid or trancxamic acid [6,45], The controversy over heparin continues.…”

“…Blood volume substitution and supplementation of coagulation factors are of importance, but other supportive measures are still under debate [11,27,39,43,44], Sub stitution with fibrinogen has been questioned [6,11,21,45], Fibrinolysis is a late conse quence of AFE. When present, it should be counteracted with aminocaproic acid or trancxamic acid [6,45], The controversy over heparin continues. It has been recommended by some as a therapy [45^47], but others have pointed out the disadvantage that heparin will exacerbate the problem of bleeding and rec ommend instead substitution with anti thrombin III [48].…”

“…The clinical symptoms of AFE were de scribed in detail 40 years ago: sudden and profound shock, dyspnea, cyanosis, appre hension, seizures and the failure of rapid blood coagulation [3], By its symptoms the condition could therefore be diagnosed with confidence [3,[5][6][7][8][9], Findings on chest roent genograms and lung scans have also been proposed as evidence for AFE [10,11].…”