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PubMed1991

[An experimental models in the evaluation of the effect of the amniotic fluid].

Fetal life develops in a fluid environment. Amniotic fluid is not inert. It contains proteins, hormones, fetal urine and electrolytes, known to interact with a variety of fetal processes such as wound healing, intestinal growth, etc. Interest in its study has been increasing recently. In order to determine the effect of amniotic fluid, intra-amniotic and extra-amniotic fetuses should be compared. We describe a model that allows isolation of a fetal portion from amniotic fluid. Sixty 23-day pregnant rabbits were operated on. Surgery was performed in two fetuses of each mother. One fetus was replaced into the amniotic sac; the other was sutured along its waist to the histerotomy orifice, leaving the caudal half of the fetus in an extra-amniotic position. The mothers continued their pregnancy and were sacrificed on day 30. Maternal survivance rate was 82 per 100. Twelve intra-amniotic fetuses (FIA) and nine extra-amniotic fetuses (FEA) were obtained, as well as 16 nonoperated littermates that served as controls. The average weight of FIA fetuses was 31 g, FEA fetuses weighed 37 g and controls 36 g. The difference was not statistically significant between any of the groups. This model allows the study of a variety of fetal conditions in the absence of amniotic fluid. The survivance rate of this technique of extrauterine fixation has been 75 per 100.

Amniotic Fluid↗
PubMed1975

Bacterial growth inhibition by amniotic fluid. III. Demonstration of the variability of bacterial growth inhibition by amniotic fluid with a new plate-count technique.

The ability of 50 human amniotic fluid samples to inhibit the growth of Escherichia coli was measured with a new semimicro plate-count technique. A range from bacterial growth-sustaining fluid to bactericidal fluid was observed. When the inhibitory capacities of the fluid samples were correlated with gestational age, a progressive increase was obtained with maximum inhibitory capacity at 36 to 40 weeks. All fluid samples obtained before 20 weeks' gestation were capable of supporting bacterial growth. Fluid samples of 36 to 40 weeks' gestation were all bactericidal or bacteriostatic. More variability in inhibitory capacity was seen after 40 weeks, with an over-all loss of inhibition observed.

Amniocentesis↗
PubMed2000

Amniotic fluid embolism.

Amniotic fluid embolism is a rare occurrence, with no single pathognomonic clinical or laboratory finding. Diagnosis is based on clinical presentation and supportive laboratory values. We describe the case of a 17-year-old nulliparous woman at 27 weeks' gestation who had uterine bleeding, hematuria, hemoptysis, hypotension, dyspnea, and hypoxemia within 30 minutes of vaginal delivery. Laboratory values revealed diffuse intravascular coagulation. Chest films were consistent with adult respiratory distress syndrome. Pulmonary artery catheterization revealed moderately increased pulmonary capillary wedge pressure. Supportive measures, including oxygenation, fluid resuscitation, and plasma, were administered. Central hemodynamic monitoring and inotropic support were necessary. Our patient recovered uneventfully and 6 weeks later was living an unrestricted life-style.

Adolescent↗
PubMed1982

[Assessment of fetal lung maturity by immunological measurement of fetal pulmonary surfactant apoproteins in amniotic fluid (author's transl)].

The pulmonary surfactant consists of phospholipid and 10% apoprotein. The lipid fraction has been extensively studied. The protein fraction, however has not been completely dissolved. We isolated the surfactant from autopsy human lung washing fluid and amniotic fluid. By SDS-polyacrylamide gel electrophoresis, the molecular weights of the two surfactant apoproteins were estimated to be approximately 36,000 and 16,000. The identity of surfactant fractions from both lung washing and amniotic fluid was demonstrated by immunodiffusion and immunoelectrophoresis. The pulmonary surfactant apoproteins in amniotic fluid was measured by using Laurell rocket immunoelectrophoresis. The pulmonary surfactant became detected from 32 week gestation in amniotic fluid, and its concentration increased significantly at 36 week gestation. The coefficient of correlation between surfactant apoprotein and shake test was 0.76, and that of between apoprotein and disaturated lecithin (DSL) was 0.61. Amniotic fluid contaminated with blood or meconium are often false positive results in shake test or DSL concentration. On the other hand, the apoprotein determination by Laurell's method, which however was too complicated to perform clinically, gave reliability regardless of the contamination.

Amniotic Fluid↗
PubMed1991

Amniotic fluid embolism.

Amniotic fluid embolism remains an enigmatic and often lethal condition. The pathophysiology is complex, however, from a clinical standpoint. Right or, more commonly, left heart failure is the dominant physiologic aberration. Disseminated intravascular coagulation is often present. The detection of squamous cells in the central circulation of living patients can no longer be considered pathognomonic for this condition.

Embolism, Amniotic Fluid↗
PubMed2004

Amniotic fluid embolism.

Amniotic fluid embolism (AFE) (also known as anaphylactoid syndrome of pregnancy)is a catastrophic condition that occurs during pregnancy or shortly after delivery. It is found throughout the world in developed and undeveloped countries and occurs at an incidence of between 1 in 80000 live births. In the United States, AFE occurs in 1 in 20000 to 80000 deliveries.

Embolism, Amniotic Fluid↗
PubMed2004

Amniotic fluid embolism.

Amniotic fluid embolism is a rare syndrome that can have debilitating and lethal consequences. It is a difficult and somewhat intangible diagnosis that warrants a high index of suspicion by physicians. Prompt and aggressive supportive treatment is required to lessen an otherwise dismal outcome, which may include death and permanent disability. This article provides an account of the protean clinical features, pathogenesis, and principles involved in treatment.

Algorithms↗
PubMed1982

Suppression of cellular immune responses by mouse amniotic fluid.

Mouse amniotic fluid (AF) strongly inhibited the in vitro generation of cell mediated cytolytic responses to allogeneic EL4 tumor cells. Potent immunoregulatory capabilities of AF in utero are suggested by in vitro suppression of immune responses by concentrations below physiological levels and by the inhibition of lytic function late in effector cell differentiation. Finally, suppression was not contingent on the parity of the female or the source of effector cells or of the AF.

Amniotic Fluid↗
PubMed2005

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↗
PubMed1981

Antimicrobic activity of the amniotic fluid.

The amniotic fluid is commonly, though not unanimously, believed to include among its various functions a defensive one, against infections. This is due to the presence of immunoglobulins, immunocompetent cells and such factors like lysozyme, transferrin and zinc. However, evidence of this AF antimicrobic activity had been found only in the second half of the pregnancy period starting from the 20th gestational week. Our study has demonstrated its presence in a very high percentage (58.7%) of AF samples taken in early amniocenteses.

Adult↗
PubMed1983

Immunological and microbiological studies of midtrimester amniotic fluid.

Midtrimester amniotic fluids (MAF) from 73 women undergoing an amniocentesis were studied. The mean immunoglobin G (IgG) level was 34 +/- 14 mg/dl, which is higher than that reported in the third trimester. The maternal serum:MAF IgG ratio was 29 suggesting the blood:MAF barrier is less restrictive than others like the blood:cerebrospinal fluid barrier. Antibodies to herpes simplex virus (HSV) type 1 were detected in 78% of the MAF and the maternal serum:MAF HSV antibody titer ratio was 33. Antibodies to cytomegalovirus (CMV) were found in 84% of the MAF and the maternal serum:MAF CMV antibody titer ration was 40. Whenever either antibody was detected in the maternal serum it was also found in the MAF. No viruses, bacteria, mycoplasma, fungi and chlamyidae were isolated from MAF.

Amniotic Fluid↗
PubMed1989

[Intravascular coagulation in amniotic fluid embolism].

Amniotic embolism (AE) was established in 13 (8.13% out of 160 dead pregnant women and parturients. The morphological examination and clinico-anatomical analysis showed that the degree of obstruction of lung microcirculatory bed was of substantial significance for the course of the disease. Intravascular coagulation (IC) was found in 11 (84.6%) of women with AE. Lungs were damaged by microthrombi most frequently and most severely, which was connected with direct contact activation of blood clotting system by the amniotic fluid. Characteristic peculiarities of AE were their jerk-like course with subclinical period of various duration and early secondary activation of the fibrinolytic system. The morphological sign of the latter was the presence of hyaline globules even within the first hour since the clinical onset of AE. IC and the connected with it acute respiratory insufficiency and consumption coagulopathy were the main thanatogenic factors in AE. This imposed dynamic follow-up of coagulation status and fibrinolytic activity combined with timely anticoagulant and antifibrinolytic treatment.

Adult↗
PubMed1987

High resolution proton NMR spectroscopy of human amniotic fluid.

Human amniotic fluid (HAF) is a dynamic system whose characteristics depend on continuous interchanges between fetal and maternal circulations. HAF reflects not only the environment of the fetus but may also provide information about fetal development or pathology. The concentration of HAF constituents varies with gestational age and pathological states. The number of the compounds currently implicated in fetal developmental pathology are relatively few. Currently used assay methods are not adequate to totally explain or predict the complex biochemistry of the fetus. The purpose of this work was to investigate HAF with NMR spectroscopy. In the present study HAF was obtained from 47 women undergoing routine amniocentesis. Cells were separated for karyological analysis and the supernatant was acid-extracted, lyophilized and re-suspended in D20 resulting in a concentration increase over native fluid. 1H NMR spectra were obtained at 360 MHz and 60 MHz. Eighteen compounds including several amino acids, were identified using parallel reference and standard addition protocols. NMR spectroscopy detected compounds of known clinical importance including glucose, leucine, isoleucine, lactate and creatinine. In conclusion, we have demonstrated that a number of physiologically relevant compounds are readily observable in HAF using 1H NMR spectroscopy. This technique can currently provide valuable information regarding HAF composition and has the potential of being used in vivo in the future.

Amniotic Fluid↗
PubMed1993

Quantitative 1H-NMR analysis of amniotic fluid.

Ten amniotic fluid samples (36-38 weeks gestation) are analysed by NMR spectroscopy. Of the species identified in the spectra, valine (mean 198 microM: SEM 57 microM), lactate (9.73 mM; 2.05 mM), alanine (689 microM: 115 microM), acetate (6.87 mM: 1.54 mM), citrate (363 microM: 59 microM), glucose (4.54 mM: 1.28 mM) indoxyl-sulphate (n = 4,270 microM), histidine (n = 6, 125 microM: 31 microM) and formate (n = 4, 92 microM) are quantified using standard addition. The factors governing the detection limits and lowest quantifiable amounts are discussed as are the extension of the work into in vivo magnetic resonance spectroscopy (MRS) in the clinic.

Amino Acids↗
PubMedDate not supplied

Understanding and management of amniotic fluid embolism.

Amniotic fluid embolism (AFE) is a rare obstetric problem characterized by sudden onset of hypotension, hypoxemia, and coagulopathy. This case represents the difficulty in differentiating AFE from other etiologies of cardiopulmonary compromise. The definitive diagnosis of AFE is made at autopsy with the demonstration of fetal cell elements in the pulmonary vasculature. Diagnosis can be highly suspected if squamous cells and other debris of presumed fetal origin are demonstrated in blood aspirated from the central venous or pulmonary artery circulation of symptomatic parturients. Predisposing factors for AFE include advanced maternal age, multiparity, large fetal size, and short tumultuous labor, especially if uterine stimulants are used. Cardiopulmonary resuscitation is the key to the treatment of parturients with AFE. A pulmonary artery catheter can be helpful in diagnosis and hemodynamic management of parturients with AFE.

Adult↗
PubMed1977

Suppression of immunological activities by mouse amniotic fluid.

Mouse amniotic fluid (MAF) was shown to be capable of suppressing those antibody responses observed in euthymic or athymic mouse spleen cell cultures to the T-independent antigens dinitrophenylated Ficoll (DNP-Ficoll) and trinitrophenylated lipopolysaccharide (TNP-LPS) and to the polyclonal B-cell activators LPS and purified protein derivative of tuberculin (PPD). Titration experiments demonstrated that the suppressive capacity of MAF for either LPS or DNP-Ficoll responses was maintained up to a MAF dilution of 1:120. Preincubation of spleen cells obtained from athymic mice with MAF for 8 h significantly suppressed polyclonal B-cell activation of such cells induced by LPS, although suppression was greater when MAF was present during the entire culture period. In addition, the suppressive activity that MAF demonstrated for antibody production induced by DNP-Ficoll or LPS was not lost as a result of dialysis. MAF also suppressed the secondary in vitro proliferative responses of lymph node cells sensitized to the T-dependent antigen human gamma globulin (HGG). HGG-induced proliferation of such cells appeared to be more susceptible to suppression effected by MAF than concanavalin-A-induced proliferation.

Amniotic Fluid↗
PubMed1995

Requirements for diagnosis of prenatal cytomegalovirus infection by amniotic fluid culture.

BACKGROUND: Amniotic fluid culture is considered to be the best method for the detection of antenatal cytomegalovirus (CMV) infection and prediction of congenital CMV infection. Recently, however, some false-negative results have been reported. OBJECTIVES: Prediction of congenital CMV infection by amniotic fluid culture with emphasis on false-negative results. STUDY DESIGN: Retrospective study of 42 pregnant women with primary CMV infection. First, estimation of seroconversion related to the gestational age was established. Afterwards, results of amniotic fluid culture were compared either with CMV isolation from biopsies from aborted fetuses, or with viral culture of newborns' urine. RESULTS: In 18 cases (43%), amniotic fluid culture gave negative results which coincided with 18 uninfected newborns. In 18 other cases (43%), amniotic fluid culture was positive for CMV: 7 newborns with CMV viruria and 11 terminations of pregnancy with CMV isolated from fetal biopsies. In the remaining 6 cases, amniotic fluid culture gave negative results, whereas the 6 newborns were all infected. CONCLUSION: Amniotic fluid culture remains an accurate method for the diagnosis of CMV antenatal infection. However, in order to avoid false-negative results, the importance of a correct estimation of the gestational age of seroconversion and of a sufficient interval between primary infection and amniocentesis are stressed.

Journal Article↗
PubMed2006

A hypothesis regarding complement activation and amniotic fluid embolism.

Amniotic fluid embolism, a rare, sudden and often fatal illness of pregnancy may not be a true embolic event resulting from the physical obstruction of the pulmonary vasculature. The high degree of variability in symptoms, the lack of characteristic findings on radiological exam, the absence of a dose-response effect on symptoms, and the occasional occurrence of coagulopathies are not entirely consistent with a physical block to the circulation as the main mechanism of disease. Alternatively, it might be the result of complement activation initiated by fetal antigen leaking into the maternal circulation. This rare immune response may be initiated by a rare pathological antigen, or by common antigens presented uncommonly--in amount, timing, or frequency of entry into the maternal circulation. Some very early evidence in AFE patients supports this hypothesis but is not conclusive. Complement levels remain well within the normal range during uncomplicated parturition. A prior theory that AFE might be a result of maternal anaphylaxis to fetal antigen has much less evidence to support it. The disseminated intravascular coagulation often seen in this and other serious obstetrical illnesses may be a secondary result of complement activation rather than the direct introduction of pro-coagulants into the maternal circulation although the link between the complement and coagulation pathways, if any, remains poorly defined. Through currently available laboratory testing, both the complement hypothesis and the anaphylaxis mechanism are able to be assessed. Direct measurement of serum complement as well as serum tryptase and urinary histamine are readily obtained tests in community hospitals as well as tertiary care hospitals. If the hypothesis proves true, this investigation may be of profound importance to understanding immune tolerance. Rather, than asking why one pregnant woman in 20,000 develops a violent immune reaction to the fetus, a better question is why do not all pregnant women reject the fetus which is a large collection of foreign antigens?

Complement Activation↗