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• W2022706819 abstract "Amniotic fluid embolism (AFE) is a rare, catastrophic complication of pregnancy that occurs in the setting of a disrupted barrier between the amniotic fluid and maternal circulation. The onset of signs and symptoms is swift and dramatic, classically marked by dyspnea, hypoxemia, and hypotension, followed by cardiopulmonary collapse. Coagulopathy and hemorrhage are common and often occur after the clinical diagnosis is made. Mortality remains high despite aggressive therapeutic interventions. We describe a perplexing case of AFE in which isolated coagulopathy was the initial presentation. Case Report The patient was a healthy, 23 year-old secundigravid, nulliparous woman at 37 wk gestation who was admitted to our labor and delivery unit in active labor. Her antepartum obstetric history was unremarkable. On admission, the patient's arterial blood pressure was 132/87 mm Hg, and her temperature was 36.4[degree sign]C orally. Her initial hematocrit and platelet count were 42% and 241,000 cells/[micro sign]L, respectively. Her cervix was dilated 5 cm, and contractions occurred every 90-120 s. The fetal heart monitor revealed a reassuring tracing. One hour after admission, amniotomy was performed, and clear fluid was noted. Because the external tocodynamometer was unable to detect contractions, an intrauterine pressure catheter was inserted at that time. Thirty minutes later, a continuous lumbar epidural catheter was placed uneventfully, and 0.125% bupivacaine 10 mL and fentanyl 50 [micro sign]g were given incrementally. Analgesia was maintained with a solution of 0.125% bupivacaine and 2 [micro sign]g/mL fentanyl at the rate of 10 mL/h. Approximately 3 h after admission, the patient's cervix was completely dilated, and expulsive efforts were initiated. One hour later, her temperature increased from 38.1[degree sign]C to 39.1[degree sign]C. The patient was given ampicillin 2 g and gentamicin 100 mg IV for presumed chorioamnionitis. At this point, the fetal heart tracing revealed tachycardia and severe variable decelerations during contractions. Gingival and epidural catheter site bleeding in addition to epistaxis were noted on placing the patient in the knee-chest position, which was initiated to improve the fetal dysrhythmias. During this time, the patient's blood pressure and heart rate were 146/86 mm Hg and 133 bpm, respectively. The fetal heart tracing demonstrated no improvement; the patient was then transported to the delivery suite for a trial of forceps delivery. The epistaxis was controlled with direct pressure to her nostrils, and it resolved in the delivery suite. Coagulation studies were obtained and sent to the laboratory. The patient underwent a low-outlet forceps delivery resulting in a viable male infant (Apgar scores of 6 and 8 at 1 and 5 min, respectively). The second stage of labor lasted for 3.5 h. Immediately after the delivery of an intact placenta without evidence of retroplacental clots, postpartum hemorrhage ensued from uterine atony. Over the next 60 min, the patient received oxytocin (100 U IV), methylergonovine (0.2 mg intrauterine), and.15-methylprostaglandin F2-alpha (0.5 mg IM). Laboratory studies were consistent with disseminated intravascular coagulation (DIC): prothrombin time >60 s, partial thromboplastin time >150 s, D-dimer >8.0 [micro sign]g/mL, fibrin split products >40 [micro sign]g/mL, platelets 85,000 cells/[micro sign]L. The patient's condition quickly deteriorated. She became disoriented and unresponsive, for which she underwent endotracheal intubation. Of note, the patient maintained adequate oxygenation throughout this time, with pulse oximetry revealing 98%-100% saturation with 0.5 fraction of inspired oxygen. Packed red blood cells and platelets were administered, followed by fresh-frozen plasma. The patient then became hypotensive despite the rapid administration of crystalloid, colloid, and blood products and incremental dosing of ephedrine and phenylephrine. Resuscitation continued while central venous and arterial catheters were placed. Because of the acuity of events and time course, however, no central venous or pulmonary artery pressure monitoring was obtained, and vasoactive infusions were omitted in favor of bolus injections. The pulse oximetry tracing later diminished, and arterial blood gas analysis confirmed hypoxemia despite ventilation with 1.0 fraction of inspired oxygen. The patient experienced cardiopulmonary arrest immediately thereafter, and despite aggressive resuscitative efforts, including transfusion of multiple blood products (10 U of packed red blood cells, 6 U of fresh-frozen plasma, 6 pack of platelets), IV calcium, atropine, and epinephrine, followed by open chest cardiac massage, the patient died. The postmortem examination determined AFE as the cause of death, with diffuse extensive capillary and large vessel plugging by squamous cells, mucin, lipid material, and lanugo hairs noted in the lungs. No thromboemboli were observed. Similar amniotic fluid contents were present in the liver and parametrium, with markedly prominent plugging noted in the vasculature of the posterior cervix. Evidence of early myocardial infarction was noted in the right ventricle consistent with acute cor pulmonale. The uterus was intact, and the placenta demonstrated prominent microcalcifications without evidence of chorioamnionitis or abruption. Discussion AFE, first described by Meyer [1] in 1926, is a topic of great concern in obstetrics today because of its dramatic presentation and high rate of mortality. The reported incidence of AFE varies from 1:8,000 [2] to 1:80,000, but a rate between the two figures is most likely. Mortality exceeds 80%, with 25%-50% of deaths occurring within the first hour of diagnosis [3]. AFE can occur only when there is a breech in the barrier between the amniotic fluid and maternal circulation. The three most common routes of entry are the endocervical veins, the placental site, and a uterine trauma site [4]. Postmortem examination of our patient revealed marked plugging of the cervical vasculature by amniotic fluid contents, with significant numbers of acute inflammatory cells noted; thus, the posterior endocervical veins were deemed to be the port of entry. It is noteworthy that traumatic intrauterine pressure catheter placement has been implicated as a risk factor for AFE [5], although there was no evidence of traumatic insertion documented in the patient's chart. The onset of AFE is said to be abrupt, heralded by sudden dyspnea, hypoxemia, cyanosis, and hypotension disproportionate to the amount of blood loss [6]. More than 80% of patients [7] experience cardiopulmonary arrest. Invasive hemodynamic monitoring in patients with AFE reveals decreased cardiac output, increased pulmonary artery pressure, and marked systemic vasodilation [8]. Of those patients who survive the initial hemodynamic collapse, approximately 70% develop noncardiogenic pulmonary edema [9], and 45% develop a severe coagulopathy 30 min to 4 h later [10]. Laboratory evidence of coagulopathy can be seen 30-60 min before the onset of the more classic signs and symptoms of AFE, which suggests that a latency period may be necessary [10]. Although there was no laboratory confirmation of coagulopathy in our patient, the spontaneous gingival and epidural catheter site bleeding and epistaxis noted approximately 120 min before hemodynamic collapse support a coagulopathic state at that time. In a review of 272 cases of AFE, Morgan [11] found excess bleeding in 49%-in 12%, it was the first indication of the ensuing catastrophe. It must be noted, however, that Morgan did not differentiate coagulopathy from hemorrhage, and no mention is made concerning the presentation time of coagulopathy relative to the onset of AFE. Although our patient experienced excess bleeding from uterine atony after delivery, we believe that she was coagulopathic before delivery; further, it may have been the initial presentation of AFE. A recent review of the national registry of AFE patients by Porter et al. [12] identified eight patients in whom isolated acute coagulopathy developed without preceding hypotension, hypoxia, or evidence of placental abruption. Acute hemorrhage occurred post-partum in seven of eight patients, five of whom developed uterine atony. Six patients exsanguinated despite appropriate medical management and blood component transfusion, yielding a mortality rate (75%) similar to that in classic AFE. The authors concluded that fatal DIC in pregnant patients may represent a forme fruste of AFE. The cause of coagulopathy from amniotic fluid is multifactorial. Phillips and Davidson [13] described the procoagulant properties of amniotic fluid, specifically noting increased factor X activity when amniotic fluid is mixed with maternal blood. In addition, Yaffe et al. [14] discussed the increase in thromboplastic activity associated with AFE. Furthermore, although amniotic fluid lacks plasmin and plasmin activator, it contains plasmin proactivator. Weiner [10] speculated that thrombin generation in the pulmonary beds leads to plasmin and kinin production, which, in the absence of antiplasmin, perpetuate their own generation. When thrombin generation occurs in an environment of excess plasmin proactivator, a coagulopathy composed of fibrin-fibrinogenolysis-yielding fibrin split products may follow [10]. Excessive production of fibrin split products is implicated in decreased uterine contractility [10], which often occurs in cases of AFE. Indeed, our patient demonstrated evidence of both increased fibrin split products and severe uterine atony with resultant postpartum hemorrhage. AFE is almost always diagnosed on clinical grounds and should not be confused with sepsis, drug reaction, pulmonary aspiration, venous air embolism, pulmonary thromboembolism, or placental abruption [9,15]. Laboratory data may be supportive, but they alone can never diagnose or exclude AFE [9]. Once the diagnosis is made and resuscitative efforts have begun, blood is aspirated from a central venous or pulmonary artery catheter and placed in an anticoagulated test tube. It is then sent for pathologic examination with special stains and dyes (Nile blue A, Papanicolaou, oil red O, and acid mucopolysaccharide) that can demonstrate fetal squamous cells, fat, and mucin [15]. Unfortunately, no differentiation can be made microscopically between fetal and maternal squamous cells. Furthermore, squamous cells have been identified in blood aspirated from pulmonary artery catheters in nonpregnant patients [16]. The identification of mucin, however, seems to be a more sensitive indicator of AFE [15]. Treatment of AFE includes endotracheal intubation and mechanical ventilation with a high inspired concentration of oxygen, inotropic support guided by pulmonary artery catheterization, and correction of coagulopathy. Acute left ventricular dysfunction is the primary hemodynamic insult; thus, therapy should be directed toward improving inotropy [17]. Gillie and Hughes [15] recommend dopamine (2-40 [micro sign]g [center dot] kg-1 [center dot] min-1), dobutamine (2-40 [micro sign]g [center dot] kg-1 [center dot] min-1), and norepinephrine (2-4 [micro sign]g/min) as the drugs of choice for maintaining cardiac output and blood pressure. Fluid therapy should also be guided by central monitoring, avoiding overhydration in these patients, who are predisposed to pulmonary edema. The patient should be ventilated with the highest inspired concentration of oxygen to maintain arterial oxygen saturation greater than 90%. Positive end-expiratory pressure is often helpful in improving oxygenation. Although concern has been raised about adding fuel to the fire of DIC [10], blood component therapy remains the first line of treatment for correcting the coagulopathy associated with AFE. Fresh-frozen plasma, cryoprecipitate, and platelet transfusion are indicated [15], with therapy being guided by the laboratory markers of coagulation and clinical evidence of bleeding. Cryoprecipitate is rich in both fibrinogen and fibronectin, the latter facilitating uptake of cellular and particulate matter (e.g., amniotic fluid contents) from the blood via the reticuloendothelial system. Some have advocated heparinization and administration of thrombolytics [11]. Although most authors today do not recomment the administration of thrombolytics, Weiner [10] recommended administering 3000-5000 U of IV heparin once the diagnosis of AFE has been made. We described a case of AFE that presented atypically as an isolated coagulopathy followed by uterine atony. We speculate that a small tear in the posterior cervix during labor caused amniotic fluid to slowly seed the maternal circulation, being inhibited somewhat by the presence of the fetal head. This may explain the fever and coagulopathy she experienced during labor. Once the fetus was delivered, a larger volume of amniotic fluid may have then entered the circulation, leading to cardiovascular collapse. Although we think that a coagulopathy was the first indication of this patient's AFE, other causes of coagulopathy [18-20], such as placental abruption, preeclampsia, and bacteremia/sepsis must be considered. The latter two processes may have been present to some degree, but they were not likely to have contributed to our patient's death from AFE. This case reinforces that coagulation defects in parturients can encompass a wide differential diagnosis. Successful outcome, albeit uncommon, requires aggressive resuscitation and support." @default.
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• W2022706819 title "Atypical Presentation of Amniotic Fluid Embolism" @default.
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