Right ventricular and right atrial enlargement may be observed, along with signs of myocardial damage and tachycardia. 2) Chest X-ray: May show no abnormalities. Approximately 70% of patients exhibit mild pulmonary edema, presenting as bilateral diffuse punctate infiltrates distributed around the hilar regions, mild pulmonary enlargement, and possible cardiac shadow enlargement.
3) Oxygen saturation:
A sudden drop often indicates pulmonary embolism.
① Platelet count <100×10⁹/L;
② Prolonged prothrombin time (PTT) – a 10-second increase is diagnostically significant;
③ Plasma fibrinogen <1.5 g/L confirms diagnosis; actual severity is often greater. Clark et al. reported 8 cases with undetectable fibrinogen or the lowest levels recorded in their laboratory's history;
④ Clot observation: Place 5 mL of normal maternal blood in a test tube and observe clot formation in an incubator for 8–12 minutes. Patients with low fibrinogen show poor coagulation, minimal clots after 30 minutes, and diffuse platelets indicating significantly low platelet count with secondary fibrinolysis;
⑤ Prolonged bleeding and clotting times;⑥ Increased fibrin degradation products, with positive results in the plasma protamine sulfate coagulation test (3P test) and ethanol gel test.
Since amniotic fluid embolism primarily results from amniotic fluid and its cellular components entering maternal circulation, causing pulmonary vascular embolism and spasm, the presence of fetal components—such as fetal squamous epithelial cells, lanugo, and mucus—in maternal blood, uterine vessels, and lung tissue is considered diagnostic. The positive rate in maternal blood is approximately 50%,while autopsy positivity reaches 73%.
2) Detection of Sialyl-N-acetylgalactosamine (SialylTn) Antigen in Maternal Serum and Lung Tissue:
With recent advances in immunological techniques, this represents a novel diagnostic approach for amniotic fluid embolism. The monoclonal antibody TKH-2 recognizes oligosaccharide structures within mucinous glycoproteins in amniotic fluid.Using immunoblotting, TKH-2 can detect extremely low concentrations of SialylTn antigen in meconium supernatant. The antigen recognized by TKH-2 is not only abundant in meconium but can also be detected in clear amniotic fluid via immunohistochemical analysis.
3) Tissue Anticoagulant Factor Assay:
As previously noted,the cellular components of amniotic fluid are not the primary cause of amniotic fluid embolism. Instead, certain humoral factors such as tissue factor-like procoagulants and leukotrienes play a crucial role in the pathophysiological process. Approximately 40% of patients develop fatal coagulation disorders following amniotic fluid embolism. The procoagulant activity of tissue factor can be antagonized by anti-tissue factor protein. Therefore, theoretically, detecting tissue factor in maternal blood could serve as a basis for distinguishing amniotic fluid embolism from other obstetric disseminated intravascular coagulation (DIC) conditions.
4) Measurement of Mast Cells in Lung Tissue:
Recent literature extensively reports on the pathogenesis of amniotic fluid embolism, suggesting it arises from an allergic reaction to fetal components in amniotic fluid. This triggers mast cell degranulation, releasing histamine, tryptase, and other mediators that induce severe pathophysiological changes in the body.