A 30-year-old woman died with massive pulmonary microvascular leukostasis immediately after cesarean hysterectomy. We postulated that this might have resulted from amniotic fluid embolization and, therefore, tested amniotic fluids as activators of granulocytes and the plasma complement system. Normal human amniotic fluid failed to aggregate granulocytes, provoke a respiratory burst, or attract the cells chemotactically. However, amniotic fluid activated complement when incubated with normal pfasma. The ability to activate complement resided in lipid-rich particulate material in the fluid, and activation proceeded mainly (but probably not exclusively) via the alternative complement pathway. Amniotic fluids varied widely in their ability to activate complement, with the most potent samples derived from women with distressed pregnancies. Plasma samples from donors also varied widely in their ability to be activated by amniotic fluid, and many of the most activatable plasma samples derived from gravid women. We propose that amniotic fluid embolization can, like "shock lung" syndrome, have a leukostatic early phase, and that complement and granulocyte activation on embolization of amniotic fluid can contribute to the pulmonary collapse characteristic of that syndrome, especially when a potently activating fluid is combined with a potently activatable plasma.
|Original language||English (US)|
|Number of pages||7|
|Journal||The Journal of laboratory and clinical medicine|
|State||Published - Dec 1984|