Acute ST-Elevation Myocardial Infarction During Labor Due to Amniotic Fluid Embolism.

BACKGROUND Amniotic fluid embolism (AFE) is an extremely rare, life-threatening complication of labor that leads to hyper-acute induction of inflammation and disseminated intravascular coagulation (DIC). Usually, acute pulmonary hypertension results in acute right ventricular failure, while DIC manifests by hemorrhagic and ischemic complications, ultimately leading to multi-organ failure and death. CASE REPORT A 30-year-old primigravida and primipara woman with no prior medical history was admitted for labor after intrauterine fetal death at 37 weeks of gestation. After medical birth induction, she had a convulsive seizure and cardiorespiratory arrest. Short mechanical resuscitation was performed before spontaneous circulation returned. Simultaneously occurring severe vaginal hemorrhage and an ST-elevation myocardial infarction (STEMI) triggered the diagnosis of AFE. Laboratory results fulfilled the criteria for DIC, and hemostatic resuscitation and mechanical hemostasis were performed. Transesophageal echocardiography revealed hypokinesia to akinesia of the inferior wall. Owing to the ongoing DIC, coronary angiography could not be performed. After the patient's transfer to the Intensive Care Unit, ST-segment elevations resolved and the myocardial infarct was managed medically. Cardiac magnetic resonance imaging performed 3 months later demonstrated myocardial scarring in 2 different areas. Referring to the coronary artery anatomy in a computed tomography scan of the chest, the infarcted areas correlated with 2 different coronary supply territories. CONCLUSIONS AFE should be considered in women with acute cardiorespiratory failure during labor. This is the first report of a STEMI triggered by an AFE. The 2 separate areas of infarction, corresponding to the 2 different coronary territories, suggest an AFE-related thrombotic/thromboembolic etiology.

Body temperature regulation and outcome after cardiac arrest and therapeutic hypothermia.

OBJECTIVE: Therapeutic temperature modulation is recommended after cardiac arrest (CA). However, body temperature (BT) regulation has not been extensively studied in this setting. We investigated BT variation in CA patients treated with therapeutic hypothermia (TH) and analyzed its impact on outcome. METHODS: A prospective cohort of comatose CA patients treated with TH (32-34°C, 24h) at the medical/surgical intensive care unit of the Lausanne University Hospital was studied. Spontaneous BT was recorded on hospital admission. The following variables were measured during and after TH: time to target temperature (TTT=time from hospital admission to induced BT target <34°C), cooling rate (spontaneous BT-induced BT target/TTT) and time of passive rewarming to normothermia. Associations of spontaneous and induced BT with in-hospital mortality were examined. RESULTS: A total of 177 patients (median age 61 years; median time to ROSC 25 min) were studied. Non-survivors (N=90, 51%) had lower spontaneous admission BT than survivors (median 34.5 [interquartile range 33.7-35.9]°C vs. 35.1 [34.4-35.8]°C, p=0.04). Accordingly, time to target temperature was shorter among non-survivors (200 [25-363]min vs. 270 [158-375]min, p=0.03); however, when adjusting for admission BT, cooling rates were comparable between the two outcome groups (0.4 [0.2-0.5]°C/h vs. 0.3 [0.2-0.4]°C/h, p=0.65). Longer duration of passive rewarming (600 [464-744]min vs. 479 [360-600]min, p<0.001) was associated with mortality. CONCLUSIONS: Lower spontaneous admission BT and longer time of passive rewarming were associated with in-hospital mortality after CA and TH. Impaired thermoregulation may be an important physiologic determinant of post-resuscitation disease and CA prognosis. When assessing the benefit of early cooling on outcome, future trials should adjust for patient admission temperature and use the cooling rate rather than the time to target temperature.