![]() Phase 2 occurs in patients who survive the initial insult, and is characterised by left ventricular failure, endothelial activation and leakage, and DIC. Pulmonary obstruction can be exacerbated by the formation of microthrombi in the pulmonary vasculature once DIC has developed. The pulmonary artery pressure rises, and right ventricular failure ensues with subsequent microvascular damage and hypotension. Phase 1 can last about 30 min and is thought to follow the initial entry of amniotic fluid into the circulation. There is a temporal relationship between the two main pathophysiological theories. This is not entirely understood, but the presence of tissue factor and platelet-activating factor, and complement activation, may have a role in the development of DIC. In addition, the activation of the coagulation cascade supports the immunological theory. ![]() Reduced concentrations of C3 and C4 in AFE, in conjunction with the presence of respiratory distress, make it highly likely that complement has an important role in the pathophysiology. Another suggested trigger for mast-cell degranulation is complement activation. A possible explanation is the fact that mast cells degranulate mostly in the lungs, and therefore, the tryptase concentrations are not raised in the systemic circulation. Mast-cell degranulation, which occurs on exposure to fetal antigens, is similar to that in anaphylaxis, but studies have failed to show a significant increase in serum mast-cell tryptase after AFE. The amniotic fluid itself contains numerous immunologically active and prothrombotic substances, including platelet-activating factor, interleukins, complement factors, and tumour necrosis factor-alpha. ![]() This theory emerged initially from the similarities between AFE, systematic inflammatory response syndrome, and anaphylaxis. Currently, it is thought that AFE results from immunological activation secondary to exposure to fetal antigens.
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