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Amniotic fluid embolus: a review of the literature.

PURPOSE: To review the literature since 1979 to determine the natural history, etiology, diagnosis and potential treatment of amniotic fluid embolus (AFE). SOURCE: English language articles and books published between June 1976 and June 1998 were identified by a computerized medline search using the title or text word amniotic fluid embolus. This same search strategy was repeated and updated to October 1999 by an independent individual using both Medline and Embase. The search was also expanded to include Science Citation Index listing Morgan's 1979 review article. All relevant publications were retrieved and their bibliographies were scanned for additional sources. PRINCIPAL FINDINGS: Randomized controlled trials are not possible with amniotic fluid emboli. The majority of the literature consists of clinical reports combined with occasional limited reviews. Knowledge obtained from these reports suggests that amniotic fluid emboli present as a spectrum of disease that ranges from a subclinical entity to one that is rapidly fatal. Because cases are sporadic and the diagnosis is often unconfirmed, little progress has been made towards understanding its etiology or defining the risk factors. Present management is empirical and directed towards the maintenance of oxygenation, circulatory support and the correction of coagulopathy. CONCLUSION: Amniotic fluid embolus continues to be a life-threatening but potentially reversible complication unique to pregnancy. It cannot be predicted nor prevented. Review of the literature reveals that there are no standardized investigational methods or protocols to confirm the diagnosis in suspected cases.

Adult↗

Amniotic fluid embolus. A report of two cases resulting in maternal survival.

Two cases of amniotic fluid embolus resulted in patient survival. Both were manifested by fetal bradycardia, respiratory distress and disseminated intravascular coagulopathy. Rapid diagnosis and treatment and anticipation of subsequent events, especially coagulopathy, appear to offer the best chance of a successful outcome.

Adult↗

Successful pregnancy after suspected anaphylactoid syndrome of pregnancy (amniotic fluid embolus). A case report.

BACKGROUND: Limited information is available on the recurrence risk of anaphylactoid syndrome of pregnancy. CASE: A successful pregnancy followed suspected anaphylactoid syndrome of pregnancy. CONCLUSION: A review of the literature revealed five cases of successful subsequent pregnancies following anaphylactoid syndrome of pregnancy. No instances of recurrent anaphylactoid syndrome of pregnancy have been reported.

Adult↗

Histological changes in placenta villi in some types of pathological pregnancy.

The examinations were carried out on 3 placentas from normal pregnancies and 12 placentas from pathological pregnancies (gestosis, cholestasis, type A diabetes pregnancies and premature outflow of amniotic fluids). Placenta sections were fixed in glutaraldehyde and subsequently embedded in Epon 812. Semithin sections 1 mu thick were stained with methylene blue and azure. Moreover, changes in terminal villi were assessed. In comparison with the control placentas changes in blood vessels, stroma and syncytiotrophoblast were found.

Adult↗

Ultrastructural changes in the syncytiotrophoblast in some types of pathological pregnancy.

The studies were performed on 12 placentas from pathological pregnancies (gestosis, cholestasis, type A diabetes pregnancies, premature outflow of amniotic fluids) and 3 placentas from normal pregnancies. Ultrathin sections were stained by the Reynold's method and evaluated under the electron microscope BS-500 (Tesla). The changes found in syncytiotrophoblast were the following: the increase or the decrease in its thickness, increase in basal membrane thickness, decrease in the number or lack of pinocytic vesicles and superficial microvilli, damage of mitochondria.

Cholestasis↗

Amniotic fluid embolus: a review of the research literature.

The diagnosis of Amniotic Fluid Embolus (AFE) is often missed clinically leading to the incorrect attribution of a major post-partum haemorrhage, which may accompany AFE, to uterine atony. This paper reviews the research on AFE with particular emphasis on the clinical presentation and diagnosis; both before and after death. It begins by dealing with the difficulty of defining AFE due to confusion about the underlying pathophysiological events. As this paper will demonstrate, the theory that AFE is an embolic event is no longer valid. A description of the clinical manifestations is provided so that these can be explained by the contemporary theory of AFE as an 'anaphylactoid' reaction. Finally, the difficulties of diagnosis, particularly laboratory diagnosis, will be discussed. The research indicates that it is not possible to accurately diagnose AFE, either, pre or post mortem, by any currently available laboratory tests. Because of better diagnosis it is now known that AFE in not uncommon and, if it is diagnosed early, a much higher rate of intact survival can be achieved than was previously thought possible.

Diagnosis, Differential↗

Maternal mortality in South Carolina from 1970 to 1984: an analysis.

Although the maternal mortality rate in South Carolina has decreased at an impressive and statistically significant rate over the past 15 years, the overall rate is still 77% higher than in the United States as a whole. Certain epidemiologic variables related to the maternal deaths were analyzed statistically for three five-year periods: 1970-1974, 1974-1979, and 1980-1984. Deaths were more frequent in older, nonwhite, single mothers. Amniotic fluid embolus and ectopic pregnancy have become the leading causes of death. Maternal mortality declined more rapidly in smaller hospitals than in larger ones, probably due to the transfer of high-risk patients. Improved obstetric techniques and practice have reduced these mortality rates thus far. If rates are to decrease still more, this trend must continue along with a sustained effort to provide comprehensive prenatal care to indigent pregnant women in a regionalized perinatal care system.

Embolism, Amniotic Fluid↗

Amniotic fluid embolus.

Amniotic fluid embolus remains among the most fatal obstetrical emergencies, with an extremely high maternal and fetal death rate. There is no way to predict who is at risk for this often catastrophic malady. Increased awareness by the medical community of the signs and symptoms of AFE may allow us to provide earlier aggressive treatment to these patients. Early recognition and treatment remain the best way to start early aggressive intervention aimed at successful outcomes for both mother and child.

Embolism, Amniotic Fluid↗

Intrapartum emergencies.

Intrapartum emergencies are challenging to all perinatal nurses because of the increased risk of adverse outcomes for the mother and fetus. Perinatal emergencies, such as seizures, amniotic fluid embolus, hemorrhage, and uterine rupture, create physiological challenges and trigger intrinsic survival techniques. The pregnant uterus becomes a vital source of blood volume during hypovolemic events because it is not considered a vital organ. The pregnancy itself may become burdensome, and birth may occur as an intrinsic maternal compensatory mechanism. The resultant fetal hypoxemia may also stress the fetus into initiating labor. During extensive oxygen desaturation and decompensation, the focus should be on maternal stabilization, which will subsequently enhance fetal stabilization. Clinical assessments, critical thinking, decision making, and resource allocation must be quick and appropriate to increase the likelihood of a positive outcome for the mother, fetus, and neonate.

Abruptio Placentae↗

Nitrotyrosine immunostaining correlates with increased extracellular matrix: evidence of postplacental hypoxia.

Nitrotyrosine residues (NT), an index of oxidative stress arising from peroxynitrite formation and action, are found in placental vasculature of pregnancies complicated by pre-eclampsia (PE) or pregestational insulin-dependent diabetes mellitus (IDDM). This study correlates conventional placental pathology with NT immunostaining in 20 cases of perinatal mortality (13 stillbirths and seven cases of neonatal mortality) associated with PE, IDDM, amniotic fluid infection syndrome (AFIS), or from fetal/neonatal demise not related to these conditions (congenital anomalies) (n = five/group). Patients with PE have more decidual arteriolopathy and Tenney-Parker change, while patients with IDDM and ascending infection have more villous cytotrophoblastic hyperplasia. Archival paraffin-embedded placental sections were immunostained for NT for correlation with clinical features and H&E histological findings. The intensity of immunostaining for NT varied from absent (n = 7) to 1+ (n = 5) or 2+ (n = 8). All eight placentae with 2+ staining showed increased villous extracellular matrix (ECM), compared to none of five with 1+ staining and two of seven with no staining (chi2 = 14.3, P = 0.001). There was no statistically significant difference in the percentage of stem villi with luminal vascular abnormalities (5.7 vs 10 vs 35.7 per cent, F = 2.3, P = 0.1). Our data show that increased production of reactive oxygen species by placental tissue may be associated with increased extracellular matrix, itself produced by fibroblasts under the influence of oxygen. NT immunostaining may therefore help differentiate those cases of perinatal morbidity/mortality associated with post-placental hypoxia provided that the secondary impact of intrauterine fetal death can be excluded by future studies.

Adult↗

Shock in pregnancy: pathophysiology and morphologic findings.

Sepsis and non-septic shock in pregnancy show characteristic modifications which are caused a) by physiologic changes in hemostasis primarily in the third trimester of pregnancy, b) by etiologic distinctions of shock regarded as pregnancy-specific, c) by hemodynamic changes in the circulation during pregnancy, d) by the ability of the healthy, young organism to compensate adequately. In the dead fetus syndrome and in non-septic shock, i.e., in amnionic fluid embolism and in abruptio placentae, the clinical picture is often governed by marked secundary fibrinolysis. Retroplacental hematoma, the characteristic feature of premature placental separation, remains controversial as either the cause or sequela of the hemostatic disorder. Etiologic, pathogenetic, and morphologic similarities exist between septic abortion, chorioamnionitis, and puerperal sepsis, but the varying response of the maternal organism during the course of pregnancy leads to different clinical and morphologic pictures. Due to a decrease in fibrinolytic activity as a consequence of pregnancy, the hypercoagulability state in a septic endotoxic shock predisposes the kidneys to bilateral renal cortical necrosis, principally in the amnion infection syndrome.

Abortion, Septic↗