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Probable amniotic fluid embolism after first-trimester pregnancy termination. A case report.

A patient collapsed immediately after dilatation and curettage for pregnancy termination. Disseminated intravascular coagulation supervened rapidly. Although the diagnosis of amniotic fluid embolism has remained unproven, it is the most likely explanation for the chain of events. We recommend rupture of the membranes prior to curettage or the administration of an oxytocic agent.

Abortion, Induced↗

Serological and immunohistochemical diagnosis of amniotic fluid embolism.

The purpose of this study was to evaluate whether serological assays and immunohistochemical staining, employing antibody TKH-2, are sensitive methods for the serological and histologic diagnosis of amniotic fluid embolism (AFE). TKH-2 is a sensitive antibody directed to sialyl Tn (STN), NeuAcalpha2-6GalNAc. Nineteen samples of maternal sera with clinical AFE and 120 control sera and 15 specimen of formalin-fixed, paraffin-embedded lung tissue sections were examined in this study. Tissue sections were stained using the streptavidin-biotin-immunoperoxidase method. The concentration of STN in serum was measured by an immunoradiometric competitive inhibition assay using the monoclonal antibody TKH-2 in a one-step procedure. Remarkable positive TKH-2 stainings were easily seen within the pulmonary vasculature in 14 of the 15 (93%) patients with AFE. The serum STN levels (mean+/-SD) in patients with AFE (110.8+/-48.1 U/ml) showed significantly higher concentrations compared with those of patients with non-AFE (17.3+/-2.6 U/ml) (p <0.01). Seventeen of 19 sera (89%) were diagnosed as AFE by serum TRH-2 level. We conclude that both TKH-2 immunostaining and serum STN assay are sensitive methods to diagnose patients with AFE.

Antigens, Tumor-Associated, Carbohydrate↗

[Amniotic fluid embolism].

A 38-year old quintipara with an unremarkable medical history suddenly complained of nausea during delivery, became pulseless and cyanotic, and lost consciousness. The ECG showed evidence of tachycardia, ventricular extrasystoles, and right-ventricular strain. Within 30 min there were also hemorrhage and a consumption coagulopathy (Table 1). Kerato-hyaline cell material was found in central-venous blood. Following cardiopulmonary resuscitation, emergency cesarean section, hemotherapy (Table 2), and intensive care (acute renal failure, ARDS, sepsis) the patient was able to be released with no permanent sequelae. The etiology, epidemiology, and clinical aspects of amniotic fluid embolism are discussed.

Adult↗

Survival from DIC following amniotic fluid embolism. Successful treatment with a serine proteinase inhibitor; FOY.

A 30-year-old multigravida of 38 weeks gestation bled profusely at delivery. Coagulation studies revealed disseminated intravascular coagulation and a diagnosis of amniotic fluid embolism was made. Treatment consisted of transfusion of whole blood and administration of a synthetic serine proteinase inhibitor, FOY. Approximately two hours after administration of the latter, bleeding began to cease and vital signs became stable. The patient survived without sequelae.

Adult↗

Oximetry for amniotic fluid embolism detection in mini-pigs: tail or snout?

The continuous, non-invasive real-time monitoring of arterial oxygenation (pulse oximetry) has become a standard of care in both human and veterinary medicine. It allows reliable, simple and inexpensive assessment of the arterial oxygenation status. In pigs, commonly used sites for oximetry-probe placement are the ear, snout or tongue, while more recently the 'pig-tail oximetry' has been suggested. In a study regarding the coagulation system during amniotic fluid embolism (AFE) in mini-pigs, we compared tail and snout for oximetry-probe placement and compared them with the 'gold standard': blood-gas analysis (BGA). In both the AFE group and the control group, the tail measurements were slightly lower and the snout measurements were slightly higher than the BGA results. In the experimental model used, both tail and snout measurements were able to detect a temporary desaturation immediately after amniotic fluid embolism (AFE). Blood-gas analysis (BGA) performed on blood drawn from a large artery missed the event. Clinically, there is no significant difference between snout and tail as oximetry-probe placement sites: both are reliable oximetry sites in mini-pigs.

Animals↗

Rapid diagnosis of amniotic fluid embolism.

Acute respiratory failure developed in a 19-year-old primigravida 7 hours after undergoing cesarean section. The diagnosis of amniotic fluid embolism was established by viewing fragments of vernix caseosa in a pulmonary artery blood sample. Forty-eight hours after the cytologic diagnosis had been made, amniotic fluid material was no longer present in pulmonary arterial blood. The patient underwent supportive care in an intensive care setting and recovered completely.

Adolescent↗

Cytologic diagnosis of amniotic fluid embolism. Report of a case with a unique cytologic feature and emphasis on the difficulty of eliminating squamous contamination.

A case of amniotic fluid embolism diagnosed cytologically from maternal right heart blood in a patient who survived is presented. Eosinophilic granular material with adherent leukocytes was present in abundance. This material has not been previously described in this setting. The difficulty in eliminating squamous contaminants, which might easily be interpreted as originating from the amniotic fluid, is discussed.

Adult↗

Lung mass due to amniotic fluid embolism--an intrathoracic complication of pregnancy.

A 29-year-old woman with right chest pain was admitted for radiographic investigation and found to have a round mass in the right lower zone. This was initially suspected to be a hydatid lung cyst but was confirmed as a cystic mass by computed tomography and duly excised. Histologic examination revealed an amniotic fluid embolism. The patient had had a stillbirth three months earlier.

Adult↗

Determining zinc coproporphyrin in maternal plasma--a new method for diagnosing amniotic fluid embolism.

We measured the concentration of zinc coproporphyrin I (ZnCP-I), a characteristic component of meconium, in maternal plasma by fluorometry after HPLC. We obtained plasma samples from 89 women: 35 at weeks 10-40 of normal pregnancy, 41 shortly after normal delivery, 4 from patients with amniotic fluid embolism (AFE), and 9 from non-AFE patients with intra- or postpartum shock caused by genital bleeding. The plasma ZnCP-I concentration was 97 (SD 83, range 38-240) nmol/L in the AFE patients, 11 (SD 9.2) nmol/L in the non-AFE patients, 12 (SD 7.9) nmol/L during normal pregnancy, and 26 (SD 10) nmol/L shortly after normal delivery. We suggest that measuring ZnCP-I in maternal plasma by fluorometry on HPLC is a rapid, noninvasive, and sensitive method for diagnosing AFE and propose 35 nmol/L as the cutoff value for the ZnCP-I concentration in maternal plasma for the diagnosis of AFE.

Adult↗

Amniotic fluid embolism: a case report and review.

A 41-year old primigravida underwent caesarean section because of foetal distress following prostin induction of labour. Intraoperative coagulopathy, haemorrhage and hypotension necessitated a hysterectomy. Subsequently, she developed respiratory and renal failure, requiring mechanical ventilation and haemodialysis. She made a full recovery. The likely diagnosis was amniotic fluid embolism (AFE), a rare complication of pregnancy with a variable presentation, ranging from cardiac arrest and death through to mild degrees of organ system dysfunction with or without coagulopathy. The differential diagnosis includes pre-eclamptic toxaemia/pregnancy-induced hypertension, anaphylaxis and pulmonary embolism. There is no diagnostic test for AFE; the finding of foetal elements in the maternal circulation is non-specific. Historically, AFE was thought to induce cardiovascular collapse by mechanical obstruction of the pulmonary circulation. It is now thought that a combination of left ventricular dysfunction and acute lung injury occur, with activation of several of the clotting factors. An immunological basis for these effects is postulated. There is no specific therapy and treatment is supportive. The mortality of the condition remains high.

Adult↗

[Amniotic fluid embolism--a case report with positive outcome].

While inducing delivery, shock occurred in a 23-year old primipara (41 weeks and 5 days of gestation). She showed symptoms of cyanosis, unconsciousness and asystoly. During cardiopulmonary resuscitation an emergency Caesarean section was performed. The resuscitation had to be continued for 1.5 hours and was followed by severe haemorrhage. Hysterectomy had to be performed, because the substitution of packed red blood cells, whole blood, fresh frozen plasma and other blood derivatives could not stop bleeding. Although the prognosis seemed to be very poor, mother and child survived without any physical damage or neurological deficit until now. Because of the clinical pattern we diagnosed an AFE syndrome (amniotic fluid embolism).

Blood Loss, Surgical↗

[A case of fatal amniotic fluid embolism].

A 31-year-old pregnant woman (multipara), who was near the expected date of birth, was found dead in the joint flat by her partner. She was lying beside the bed and showed burns on the front of the body caused postmortem by contact with a radiator. Autopsy revealed a rupture of the fetal membranes, the inner layers of the uterus and a large vein. After centrifugation, the supernatant of the blood from the right half of the heart was turbid and contained small corpuscular amniotic fluid components. The diagnosis of amniotic fluid embolism could be confirmed histologically. In the pulmonary vessels of the mother meconium, lanugo hairs and epidermic scales could be demonstrated; in addition the fetal horny lamellae were confirmed immunohistochemically (using monoclonal antibody against cytokeratin).

Adult↗