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Middle East J Anaesthesiol · Jun 2009
Case ReportsSudden cardiac arrest during cesarean section -- a possible case of amniotic fluid embolism.
- Nikooseresht Mahshid, Sadegian Ahmad, Manochehrian Nahid, and Farhanchi Afshin.
- Department of Anesthesiology and Intensive Care, Hamadan University of Medical Sciences, Fatemieh Hospital, Hamadan, Iran. nikoo_mahshid@yahoo.com
- Middle East J Anaesthesiol. 2009 Jun 1;20(2):315-7.
AbstractAmniotic Fluid Embolism (AFE) is a rare obstetric catastrophe that occurs in approximately 1/50,000 pregnancies and has a mortality rate in excess of 80%. AFE is a condition that is poorly understood and often difficult to diagnose. We report a case of a healthy 27-yr-old gravid two, 35 wk gestation parturient with a previous Cesarean section two years previously, and presently admitted for emergent Cesarean section due to premature uterine contractions. Induction of general anesthesias was performed with no problem and a male preterm infant with Apgar 8 at 1 min was delivered. Amniotic fluid was bloody and 40% placental abruption existed. Following delivery of the placenta, patient suddenly became plethoric and O2 saturation began to decrease and no pulse could be palpated! Immediate CPR was successful but she was hemodynamically unstable and signs of right heart strain was obvious. Right jugular venous catheterization was performed, vasopressors were administered. After a two hours period of relatively stable vital signs, patient's reflexes returned to normal, however, profound coagulopathy on lab data was reported and she was treated with 10 unit Packed Red Blood Cells (PRBCs), 10 unit FFP and 8 unit platelets, Sodium bicarbonate, oxytocin and Methergine. The patient remained hemodynamically unstable while laparotomy-hysterectomy was performed to stop the bleeding. Unfortunately attempts were unsuccessful and patient died four hours later in ICU. Post-mortem findings showed signs of Disseminated Intravascular Coagulation (DIC), no fetal squamous cells in pulmonary vasculature were found and special staining of Cytokeratin marker shows no positive cells in lumen of vessels. The post-mortem diagnosis of AFE is challenging to forensic investigators and pathologists and can be confirmed by histological confirmation of amniotic fluid contents in the pulmonary vasculature, although they may be difficult to identify. In recent years it has been suggested that AFE is an anaphylactoid reaction to fetal antigens and an elevated serum tryptase level is increasingly being used to support the diagnosis. Sudden onset of cardiovascular collapse and early signs of right heart strain and fulminant DIC supports the diagnosis of AFE in this case, although no fetal debri could be find in pathologic staining.
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