Cases reported "Embolism, Amniotic Fluid"

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1/4. serum tryptase analysis in a woman with amniotic fluid embolism. A case report.

    BACKGROUND: Recent studies have noted a striking similarity between amniotic fluid embolism (AFE) and anaphylaxis. serum tryptase levels may therefore serve as a marker of mast cell degranulation in AFE cases. CASE: A 40-year-old woman, gravida 6, para 4, experienced the acute onset of facial erythema, eclampsia-type seizures, severe hypoxia, cardiac arrest and disseminated intravascular coagulation while in early active labor. The patient was declared dead 37 minutes after the onset of resuscitative efforts. At autopsy, fetal squames were found within the pulmonary tree, uterine blood vessels and brain. A peripheral venous blood specimen, obtained approximately one and a half hours postmortem, revealed a tryptase level of 4.7 ng/mL (normal, < 1). CONCLUSION: An elevated serum tryptase level, in conjunction with our patient's clinical history, adds further supporting evidence to the concept of AFE as an anaphylactoid syndrome of pregnancy.
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2/4. 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.
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3/4. The importance of extensive sampling and examination of cervix in suspected cases of amniotic fluid embolism.

    amniotic fluid embolism is an important complication of pregnancy with high mortality. The diagnosis of amniotic fluid embolism is generally made postmortem and rests upon the histological demonstration of amniotic fluid debris, including foetal epithelial squames and hair, in the pulmonary vasculature. We have made the diagnosis of amniotic fluid embolism in two patients by detection of the amniotic fluid debris in the blood vessels of the cervix in their hysterectomy specimens. These two patients presented with profuse primary postpartum haemorrhage and evidence of disseminated intravascular coagulation after uneventful deliveries. amniotic fluid debris were only demonstrated in the blood vessels of the cervix but not in the corpus. This observation emphasizes the importance of a thorough histological examination of the cervix in cases of suspected amniotic fluid embolism.
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4/4. Immunohistochemical identification of syncytiotrophoblastic cells and megakaryocytes in pulmonary vessels in a fatal case of amniotic fluid embolism.

    The histological diagnosis of amniotic fluid embolism (AFE) is based on finding amniotic fluid components in the pulmonary microvasculature. In addition to the distinctive constituents of AFE, placental and decidual tissue fragments as well as isolated trophoblastic cells and megakaryocytes are potentially detectable within pulmonary vessels. The identification of single syncytiotrophoblastic cells (STC), and their differentiation from circulating megakaryocytes (MK) within the lumen of small and medium-sized pulmonary vessels is difficult by classical morphological methods. In a fatal case of AFE, we have successfully detected the simultaneous presence of STC and MK in the pulmonary microvasculature by means of a panel of specific monoclonal (CD61-GpIIIa, beta-hCG) and polyclonal (FVIII-vW, hPL) antibodies. The immunohistochemical analysis for identification of STC and MK should provide more precise data on their incidence and distribution in physiological and pathological conditions as well providing new insights into their physiopathological implications and their correlation with AFE and other gynaecological complications.
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