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Tissue damage caused by activated complement and granulocytes in shock lung, post perfusion lung, and after amniotic fluid embolism: ramifications for therapy.

The complement system evolved as a beneficial antimicrobial system. However when activated during extracorporeal perfusion, as with hemodialysis or cardiopulmonary bypass, modest pulmonary dysfunction associated with granulocyte aggregation and embolization can occur. When complement activation is more massive and prolonged as with severe sepsis, trauma and acute pancreatitis or during infusions of amniotic fluid or other lipid-rich suspensions, severe pulmonary damage which we often recognize as shock lung may occur. Therapeutic ramifications of these conclusions are evident. Thus, high doses of corticosteroids (or of non-steroidal anti-inflammatory agents, such as ibuprofen--herein not discussed) have the ability to prevent aggregation and embolization of stimulated granulocytes to patent vessels downstream and also inhibit their production of toxic oxygen radicals. These beneficial properties suggest the use of these agents may be appropriate in shock states, particularly shock lung or during suspected amniotic fluid infusion. Appropriate clinical trials to substantiate this suggestion are awaited with interest.