CASE REPORT Transient intracardiac thrombi in amniotic fluid embolism S. Porat a , D. Leibowitz b , A. Milwidsky a , D.V. Valsky a , S. Yagel a , E.Y. Anteby a, * Introduction Amniotic fluid embolism is an uncommon and lethal obstetric complication. Its prevalence has been estimated as 1:8000 – 1:80,000. 1 Its hallmarks are hypotension, respira- tory failure, disseminated intravascular coagulation and neurologic symptoms. The clinical picture sometimes in- cludes only a part of this triad and establishing a definite diagnosis is often difficult. Mortality rates have been reported that range from 26% in the California database 2 to 60–80% of cases in earlier series. 1,3 Severe morbidity, mostly neurological, may affect 85% of survivors. 3 It is possible that the dismal outcome of AFE is related to under-diagnosis of mild cases, so that only the severe cases are reported. The pathophysiology of AFE is thought to resemble that of anaphylaxis and septic shock, 3 and hence the term anaphylactoid reaction of pregnancy was coined. Although activation of the coagulation system is a major part of this syndrome, thrombotic manifestations accom- panying AFE have only rarely been described. 4,5 Activa- tion of the coagulation mechanism is usually explosive, resulting in consumption of coagulation factors. The con- sequences of this activation are usually haemorrhagic as a part of disseminated intravascular coagulation. In this case, the use of echocardiography during the acute phase of AFE enabled us to detect large asymptomatic intracardiac thrombi that disappeared within a few days. A 35 year old healthy woman, gravida 7, para 5 was admitted to the delivery room for elevated blood pressure measurements along with a new-onset headache at 37 þ 1 weeks of her spontaneous dichorionic twin gestation. Her past medical history was unremarkable and past obstetric history included five normal spontaneous vaginal deliveries and one spontaneous miscarriage. The current pregnancy had been uneventful. Physical and laboratory work-up on admission including urinary protein, liver function tests, uric acid and full blood count were all within the normal range. Because the first twin was in a breech presentation, a caesarean section was performed under spinal anaesthesia. Following the delivery of the second twin, while the patient was receiving oxytocin infusion as the sole medication, sudden cardiovascular collapse was noted. A wide complex bradycardia of 40 bpm was seen on the monitor with an unmeasurable non-invasive blood pressure and oxygen saturation. The patient was unconscious and gasping. Im- mediate resuscitation (CPR) was initiated using atropine, adrenaline, intubation, manual ventilation and closed car- diac massage. First measurement of end-tidal CO 2 was 10 mmHg. No signs of intra-abdominal or retroperitoneal bleeding were detected. After 5–10 minutes of CPR, the patient returned to sinus rhythm and her blood pressure returned to normal. Immediate echocardiographic evalua- tion was ordered in order to investigate the cause of the sudden collapse. While awaiting the echocardiographer, and within 30 minutes of the onset of cardiovascular collapse, a clinically significant haemorrhage developed. Bleeding was noted from the uterine incision and from the vagina with an overall estimated blood loss of 800 mL. Trans- thoracic echocardiography demonstrated normal left and right ventricle size and function without pericardial effu- sion and a suspected right atrial mass. Trans-oesophageal echo revealed a highly mobile, non-obstructive, elongated (2.5 cm), echodense mass in the right ventricle outflow tract (RVOT) (Figure 1). Mild to moderate tricuspid regur- gitation with a peak gradient of 25 mmHg was observed. In addition, a prominent Eustachian valve was seen in the right atrium (Figure 2). Coagulation tests indicated a severe coagulation distur- bance with activated partial thromboplastin time (aPTT) > 180 seconds, international normalized ratio (INR) of 4.7, fibrinogen 43, D-Dimer 5.6 (normal <0.5). Six units of fresh frozen plasma, 40 units of cryoprecipitate, 6 units of platelets and 2 units of packed red blood cells were transfused, resulting in a cessation of bleeding, and improve- ment in coagulation studies, with an aPTT of 34 seconds and an INR of 1.54. The patient was transferred to the ICU intubated, haemo- dynamically stable, with minimal coagulopathy. Presumed diagnosis was amniotic fluid embolism. Over the next 12 hours tachycardia worsened, and her abdomen became BJOG: an International Journal of Obstetrics and Gynaecology May 2004, Vol. 111, pp. 506–510 D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology www.blackwellpublishing.com/bjog a Department of Obstetrics and Gynaecology, Hadassah University Hospital — Mt. Scopus, Jerusalem, Israel b Department of Internal Medicine, Hadassah University Hospital — Mt. Scopus, Jerusalem, Israel * Correspondence: Dr E. Y. Anteby, Department of Obstetrics and Gynaecology, Hadassah University Hospital — Mt. Scopus, PO Box 24035, 91240 Jerusalem, Israel. DOI:10.1111/j.1471-0528.2004.00102.x