Amniotic fluid embolus: An update
Amniotic fluid embolism: an update
Click here to view full-size graphic
By Alfredo Gei, MD, and Gary D.V. Hankins, MD
With an associated maternal mortality rate of 61% and long-term neurologic complications in most surviving women and infants, AFE warrants special vigilance in evaluating symptoms and instituting treatment. This review describes a wide range of diagnostic and therapeutic modalities.
The amniotic fluid, which protects the unborn fetus from its surrounding environment, is normally isolated from the maternal intravascular compartment. When this isolation is disrupted in one way or another, a systemic maternal reaction can ensue, affecting the heart, lungs, and brain. The dramatic hemodynamic-respiratory, CNS, and hematologic phenomena that characterize this reaction can be lethal to both mother and fetus.
The syndrome we know as amniotic fluid embolism (AFE) is one of the most serious complications of pregnancy and delivery, one that is still associated with high mortality in the developed world. Fortunately the condition is rare, but as other causes of maternal death such as hemorrhage and infection are brought under control, the relative frequency of AFE as a cause of death continues to rise.1
Given the unpredictable and unexpected nature of AFE, every obstetrician should be prepared to include this condition in differential diagnosis of acute respiratory or cardiac symptoms during labor and establish prompt therapeutic measures to optimize the chances for intact survival of both mother and infant.
The presence of fetal cellular debris in the maternal circulation, associated with maternal complications, was reported for the first time in the 1920s by Ricardo Meyer from Brazil.2 In the United States, Steiner and Lushbaugh described autopsy findings for eight cases in 1941.3 Until 1950, only 17 cases had been reported; since then, more than 400 cases have been documented, probably as a result of increased awareness among practitioners.4,5 But these numbers have to be viewed with caution: After correcting for possible confounding variables, researchers have concluded that some of the cases reported earlier were not really AFE.
In an effort to better understand this condition, several animal models have been developed.6 However, extrapolations from these studies to human beings cannot be easily made, since not all the findings in animals are consistent with the clinical manifestations observed in humans.7
Recently, the term anaphylactoid syndrome of pregnancy has been proposed instead of AFE, to better characterize this condition as a multisystemic reaction to toxins rather than an embolic phenomenon.8
The true incidence of AFE may not be known.6 The disparity between reported figures is large, with rates ranging from 1 in 8,000 to 1 in 83,000 deliveries.3,6,8,9 A recent study from California reports an incidence of 1 per 20,646 deliveries; this figure is slightly higher than but still consistent with other reports.10-13 It is plausible that growing awareness of the syndrome, rather than a true increase in incidence or idiosyncrasies in obstetric practice, is responsible for these differences.
AFE constitutes the leading cause of mortality during labor and the first few postpartum hours.13 Maternal death usually occurs because of sudden cardiac arrest, hemorrhage due to coagulopathy, or acute respiratory distress syndrome (ARDS) and multiple organ failure.6
It has been estimated that between 5% and 18% of all maternal deaths are due to AFE, a rate of about 7.8 to 12 deaths per million births.6, 9, 12-15 The condition is rare enough that despite systematic research in an autopsy series, no evidence of AFE was noted among 14 maternal deaths from 26,000 deliveries.4
For women diagnosed as having AFE, mortality rates ranging from 26% to as high as 86% have been reported.6,10,16 The variance in these numbers is explained by dissimilar case definitions and possibly improvements in intensive care management of affected patients, as pointed out in a recent report.10 The first well-documented case with ultimate survival was published in 1976, although a handful of surviving patients with presumptive diagnoses of AFE have been reported since 1947.12, 17-20
Although significant progress has been made in the past 70 years since AFE was brought to physicians' attention, unanswered questions remain about the syndrome.
For years, it was held that the showering of microscopic fetal debris particles (microembolization) during an AFE episode caused acute occlusion of a large part of the mother's pulmonary microvasculature.2,21-23 The assumption was that the characteristic respiratory distress and cyanosis were manifestations of acute cor pulmonale. The first hemodynamic assessments of patients with AFE revealed elevated pulmonary capillary wedge pressure (PCWP), decreased left ventricular stroke work index (LVSWI), mild to moderate increases in mean pulmonary arterial pressures (MPAP), and variable increases in central venous pressure (CVP).24-29 These findings are consistent with left-sided (rather than right-sided) heart failure. It was also noted that both the anterograde (shock) and retrograde (pulmonary edema) manifestations correlated fairly well with the degree of negative inotropism and left-sided heart failure.
In order to reconcile some of the animal model data with human findings, a biphasic hemodynamic response in humans has been postulated.28 The initial reaction of the pulmonary vasculature to amniotic fluid exposure may be transient vasospasm, pulmonary hypertension, and profound hypoxia. To date, however, no direct evidence of these reactions has been documented, probably due to the delay between the onset of symptoms and the insertion of a pulmonary artery catheter.30
It is currently believed that the presence of fetal debris in the maternal pulmonary circulation is merely evidence of fluid passage within the maternal circulation.21,28-30 The contribution, if any, of these fetal particles to the pathophysiology of AFE may be through the release of arachidonic acid metabolites at the lung level, induced by the capillary damage of microemboli.31
Given the hemodynamic findings described above and early experimental data suggesting that anaphylaxis plays a role in the syndrome, a significant effort has been directed to the study of the amniotic fluid components and their potential vascular, inotropic, and hemostatic effects.3,4, 32-40 It is conceivable that the toxins responsible for the anaphylactoid reaction of AFE have multiple interactions and that no single mediator plays a greater role than another. Evidence also suggests that these mediators have sources other than the amniotic fluid, such as plasma components, pulmonary endothelium, and leukocytes.1,32,34,37,38, 40,41
Clinically, the reaction to AFE comprises three distinct phases. The first phase of reaction to maternal exposure to AF has three predominant manifestations:
(1) respiratory, including respiratory distress and cyanosis;
(2) hemodynamic, with pulmonary edema and shock; and
(3) neurologic, including seizures, confusion or coma.
These presentations can occur separately or in combination, and in different degrees.
Of patients who survive the initial acute cardiorespiratory insult, 40% to 50% enter the second phase, characterized by coagulopathy and hemorrhage. In some women this may be the first and only clinical manifestation.
In the third phase, the acute symptoms are over and tissue injury (brain, lung, or renal) is for the most part already established. Depending on the magnitude of the event and the maternal physiologic reserve, the patient may or may not recover from her injury. During this convalescent period, which may last weeks, affected patients can die as a result of severe lung or brain injury, multisystemic organ failure, or infections acquired in the intensive care unit.
Figure 1 presents a chronology of these pathogenic events and Figure 2 illustrates the pathophysiology of AFE.
Until recently, the diagnosis of AFE was made by a pathologist, based on a finding in maternal tissue of epithelial squamous cells, lanugo hair, fat derived from vernix caseosa, mucin derived from infant's intestinal mucus, or bile derived from meconium.2,3 Increased awareness of the syndrome's existence has resulted in earlier diagnoses, aggressive intervention, and probably a better chance of survival.
Symptoms and signs. The symptoms and signs associated with AFE are fairly vague and nonspecific.3, 6, 9, 14, 16,42,43 The combination of signs and symptoms and their temporal relationship make the diagnosis presumptive. In particular, hemorrhage and fetal distress have been neglected as presenting symptoms that sometimes precede other manifestations. As to be expected, several cases that are clear exceptions to the classical presentation have also been reported.46-48 Suspect AFE when confronted with any pregnant patient who has sudden onset of respiratory distress, cardiac collapse, seizures, unexplained fetal distress, and abnormal bleeding (Table 1).
Clinical conditions associated with AFE. Although we are not aware of casecontrol studies, multiple case and series reports have suggested an association between AFE and certain obstetric and nonobstetric conditions. The most frequently cited are onset of labor, rupture of membranes, fetal death, trauma, and uterine overdistention by multiple gestation, polyhydramnios or fetal macrosomia.3,6,9,11,13,16,23,30,44 Nevertheless, these and other frequently cited risk factors are not consistently observed and at the present time experts agree that this condition is not preventable.6, 8
Diagnostic modalities. Different methods have been described and used with variable degrees of success to support the clinical diagnosis of AFE. Table 2 provides a detailed description of these diagnostic aids. This knowledge may assist clinicians in obtaining the appropriate samples and better communicating with a laboratory that can assist and direct them in the investigation.
AFE is a rapidly lethal condition.14 To limit its associated mortality and morbidity, supportive care must be initiated with the same promptness and aggressiveness as the presentation of AFE itself.12 Even when the diagnosis is not pinpointed, the reality of an acute and life-threatening situation is usually self-evident. Multiple and simultaneous interventions are needed for an acutely ill obstetric patient, regardless of the cause of illness (Table 3). Therefore, give high priority to asking for help and informing the surrounding ancillary personnel, including those in nursing and anesthesia. You also need to make sure that the patient's relatives are escorted gently but firmly out of the room.
The patient's position does not need to be modified except for the displacement of the hips to a left lateral decubitus, to ensure the best possible uterine perfusion.22,61 Since shock often develops quickly after the onset of symptoms, having the bed flat or in slight Trendelenburg position will improve the venous return and CNS perfusion. The head of the bed needs to be removed in anticipation of intubation or imminent CPR. A backboard should also be ready.
Oxygen should be administered by any means available at concentrations of 100%.5,7 As in any other condition when oxygenation and airway patency may be compromised due to seizures, shock, or severe respiratory distress, securing an airway through endotracheal intubation is advisable.5,6 When a patient is cyanotic or unconscious, procuring an arterial blood sample for gases is a waste of time, unless the sample is obtained while securing an arterial line to assist cardiorespiratory assessment.
Electrocardiographic appraisal is cardinal in these patients, to detect and treat potentially lethal arrythmias, given that most patients with AFE initially have electromechanical dissociation or bradycardia.8 Obviously, resuscitation measures need to be instituted immediately if the patient has a cardiac arrest. Someone in the room should record the time of events. As in any situation when a pregnant patient experiences cardiac arrest, the interval from the arrest to delivery of a viable fetus is of paramount importance for the intact survival of an unborn child.5,8
Arrangements should be made to transfer the patient from labor and delivery to an ICU setting after initial resuscitation measures are taken and upon return of vital signs. However, if she is not being transferred to an obstetric intensive care bed, a decision concerning potential delivery should ideally precede the transfer to either a medical or surgical ICU. In these latter two units, the necessary equipment or expertise to monitor a fetus or perform a bedside C/S is not typically available. Also keep in mind that full stabilization before transfer is unlikely, so that this task will often entail transferring a woman who is in shock, while anesthesia or maternal-fetal medicine physicians start pressor infusions.
Once in the ICU, hemodynamic monitoring with a pulmonary artery catheter is often helpful for assessment and to guide pharmacologic support.22,28 Additionally, blood samples from a "wedged" catheter may be obtained and sent to the laboratory to help confirm the clinical diagnosis.7,21,26,50-53 This procedure is important in a setting where the manifestation of AFE closely resembles that of pulmonary thromboembolism. It can persuade clinicians not to waste time with pulmonary angiograms and thrombolytics, as well as lead them to anticipate coagulopathy before the symptoms occur. 55
A team approach to the clinical problems will prove invaluable to the patient. A liberal use of consultants is recommended, including those from intensive care, pulmonology, cardiology, hematology, anesthesiology, and neurology, as needed.
Pharmacologic treatment should be guided by hemodynamic parameters and the clinical course. The goals of therapy are: (1) maintenance of systolic blood pressure at or above 90 mm Hg with acceptable peripheral organ perfusion, as manifested by a urine output of 25 mL/hour or more and maintenance of the patient's sensorium; (2) maintenance of arterial PO2 over 60 mm Hg or the hemoglobin saturation at 90% or higher6,48,69; (3) correction of coagulation abnormalities.7,22, 61
Besides the infusion of crystalloids, it is often necessary to use inotropics (rapid digitalization 1 ß adrenergics) and pressors (ephedrine, dopamine, dobutamine, norepinephrine infusions).18,22,24,28,29 After hypotension has been corrected, fluid therapy should be restricted to maintenance levels, to minimize pulmonary edema due to developing ARDS.30 In consideration of the pathogenesis of the AFE reaction, as discussed previously, corticosteroids (hydrocortisone 500 mg IV q 6 hours) have been suggested as potentially helpful.13,14 Therapeutic heparinization to limit intravascular coagulation is controversial; we do not recommend it.11,20,21,30
Anecdotally reported interventions include open cardiac massage, e-aminocaproic acid, cardiopulmonary bypass, infusion of cryoprecipitates, inhaled prostacyclin, inhaled nitric oxide, exchange transfusion, prostaglandin inhibitors, antithrombin III, serine proteinase inhibitor, and leukotriene blocking agents (5-lypo-oxygenase inhibitor).5,13,16,31,33,34,62-68 Although in the near future such therapies can conceivably come to play a role in the management of this condition, at present no specific recommendations can be made for any of these.
The following measures are important in managing AFE.
Ventilation/oxygenation. Mechanical ventilation and high levels of fractional inspired oxygen (FIO2) are frequently necessary to remove CO2 and oxygenate the patient. When high levels of FIO2 are reached (above 0.6) and the patient is still inadequately oxygenated, positive end-expiratory pressure (PEEP) is used for alveolar recruitment and improvement of oxygenation. Commonly, PEEP is started at 5 cm H2O and increased by increments of 2 to 3 cm H2O, with careful assessment of lung compliance, peak airway pressures, blood pressure, and cardiac output, until satisfactory levels of PaO2 are reached or hemodynamic compromise becomes unacceptable.5,13,62
Coagulopathy/hemorrhage. The treatment of the bleeding diathesis in AFE should be adjusted to suit each individual and will depend on repeated laboratory evaluations of the clotting defect.16 Administer packed red blood cells, fresh frozen plasma, cryoprecipitates, and platelets, as needed, to maintain organ perfusion and urinary output and until bleeding secondary to disseminated intravascular coagulation resolves.6,12 Cryoprecipitates are rich in both fibrinogen and fibronectin, the latter facilitating the uptake of cellular and particulate debris (such as amniotic fluid contents) from the blood via the reticuloendothelial system.48,63,64 When transfusing, keep in mind that the shock seen in these patients is out of proportion to the amount of bleeding and that vasopressors are an indicated adjunct to blood replacement.18
If the patient has an epidural catheter, it is prudent to remove it as soon as possible. However, if bleeding occurs around the device, it may be better to leave it in place to tamponade the site until further diagnostic testing. After removal of the catheter, the patient should be monitored closely for any signs of subarachnoid or epidural hemorrhage.69
Data gathered from the National AFE Registry indicate a maternal mortality rate of 61%. In addition, only 15% of affected patients survived without neurologic sequelae.8 In the event of cardiac arrest, the survival rate decreased by approximately half, and only 8% of those survivors were without neurologic impairment.8
The neonatal survival rate after a delivery affected by AFE was 79% according to the Registry, and only half of the surviving infants were neurologically normal. The infant's prognosis was adversely affected by maternal cardiac arrest. The neonatal rate of survival in this subgroup was 68%, with only 32% having a normal neurologic outcome, underlining the importance of prompt intervention for delivery when faced with this complication.8
In contrast, data from a recently published population-based study from California show much lower figures of mortality and morbidity for both mother and infant.10 In this report, 73.6% of the patients and 95% of the neonates (known outcomes) survived, with 87% and 72% intact maternal and neonatal survival, respectively. The large variance between the morbidity and mortality data of the National AFE Registry and the California study may be a result of the significant difference between their methodologies. While the National AFE Registry presents a scrutinized collection of reported cases (including the worse case scenarios), the California study is based on hospital discharge summaries and not on a review of the individual charts. As a result, the latter study may have led to overreporting through the inclusion of cases that might have been interpreted as suspicious or presumptive of AFE, while the former study may have underrepresented mild cases of the condition.
We believe that awareness of the syndrome has facilitated earlier intervention and agree with the authors of the California study that developments in intensive care medicine have favorably affected the outcome of the disease. Nonetheless, we hesitate to assert that these factors alone can explain the disparity. Considering the studies' methodology, it is very possible that more realistic figures lie somewhere in between the rates cited in these two reports.
Markers of prognosis. In a retrospective study, Oi and colleagues measured levels of several inflammatory cytokines in women who survived AFE and those who died from it.1 Levels of IL-6 and IL-8 were significantly higher in patients who died than those who survived. So far, this technique has not been used or evaluated prospectively.
Reproductive future. Normal subsequent pregnancies have been reported in women who had survived an episode of AFE during a previous pregnancy.70,71 But the number of patients is too small to make general statements on prognosis or recurrence risks. Theoretically, risk for recurrence should be low.
AFE is a sudden and unexpected complication of pregnancy. It has a complex pathogenesis and serious implications for both mother and infant and continues to be associated with high rates of morbidity and mortality. Obstetricians should be alert to the symptoms of AFE and strive for prompt and aggressive treatment.
Dr. Gei is a Fellow and Dr. Hankins is Division Chief, Division of Maternal-Fetal
Medicine, Department of Obstetrics and Gynecology, The University of Texas Medical
Branch, Galveston, Tex.
1. Oi H, Kobayashi H, Hirashima Y, et al. Serological and immunohistochemical diagnosis of amniotic fluid embolism. Semin Thromb Hemost. 1998;24:479-484.
2. Attwood HD. The histological diagnosis of amniotic-fluid embolism. J Pathol Bacteriol. 1958;76:211-215.
3. Steiner PE, Lushbaugh CC. Maternal pulmonary embolism by amniotic fluid as a cause of obstetric shock and unexpected deaths in obstetrics. JAMA. 1986;255:2187-2203.
4. Mallory GK, Blackburn N, Sparling HJ, et al. Maternal pulmonary embolism by amniotic fluid. Report of three cases and discussion of the literature. N Engl J Med. 1950;243:583-587.
5. Martin RW. Amniotic fluid embolism. Clin Obstet Gynecol. 1996;39:101-106.
6. Hankins GDV, Clark SL. Amniotic fluid embolism. Fetal and Maternal Medicine Review. 1997;9:35-47.
7. Clark SL. Amniotic fluid embolism. In: Cardiac Problems in Pregnancy. Malden, Mass: Alan R. Liss, Inc; 1990:247-256.
8. Clark SL, Hankins GDV, Dudley DA, et al. Amniotic fluid embolism: Analysis of the national registry. Am J Obstet Gynecol. 1995;172:1158-1169.
9. Högberg U, Joelsson I. Amniotic fluid embolism in Sweden, 1951-1980. Gynecol Obstet Invest. 1985;20:130-137.
10. Gilbert WM, Danielsen B. Amniotic fluid embolism: decreased mortality in a population-based study. Am J Obstet Gynecol. 1999;93:973-977.
11. Sperry K. Amniotic fluid embolism. To understand an enigma. JAMA. 1986;255:2183-2186.
12. Resnik R, Swartz WH, Plumer MH, et al. Amniotic fluid embolism with survival. Obstet Gynecol. 1976;47:295-298.
13. Anderson DG. Amniotic fluid embolism. Am J Obstet Gynecol. 1967;98:336-348.
14. Ratten GJ. Amniotic fluid embolism--2 case reports and a review of maternal deaths from this cause in Australia. Aust N Z J Obstet Gynaecol. 1988;28:33-35.
15. Garland IW, Thompson WD. Diagnosis of amniotic fluid embolism using an antiserum to human keratin. J Clin Pathol. 1983;36:625-627.
16. Morgan M. Amniotic fluid embolism. Anaesthesia. 1979;34:20-32.
17. Cawley LP, Douglass RC, Schneider CL. Nonfatal pulmonary amniotic embolism. Obstet Gynecol. 1959;14: 615-620.
18. Scott MM. Cardiopulmonary considerations in nonfatal amniotic fluid embolism. JAMA. 1963;183:989-993.
19. Tuck CS. Amniotic fluid embolus. Proc R Soc Med. 1972;65:94-95.
20. Chung AF, Merkatz IR. Survival following amniotic fluid embolism with early heparinization. Obstet Gynecol. 1973;42:809-814.
21. Masson RG. Amniotic fluid embolism. Clin Chest Med. 1992;13:657-665.
22. Dudney TM, Elliott CG. Pulmonary embolism from amniotic fluid, fat, and air. Prog Cardiovasc Dis. 1994; 35:447-474.
23. Lau G. Amniotic fluid embolism as a cause of sudden maternal death. Med Sci Law. 1994;34:213-220.
24. Schaerf RH, de Campo T, Civetta JM. Hemodynamic alterations and rapid diagnosis in a case of amniotic-fluid embolus. Anesthesiology. 1977;46:155-157.
25. Masson, RG, Ruggieri J, Siddiqui MM. Amniotic fluid embolism: definitive diagnosis in a survivor. Am Rev Respir Dis. 1979;120:187-192.
26. Dolyniuk M, Orfei E, Vania H, et al. Rapid diagnosis of amniotic fluid embolism. Obstet Gynecol. 1983;61: 28S-30S.
27. Duff P, Engelsjerd B, Zingery LW, et al. Hemodynamic observations in a patient with intrapartum amniotic fluid embolism. Am J Obstet Gynecol. 1983;146:112-115.
28. Clark SL, Montz FJ, Phelan JP. Hemodynamic alterations associated with amniotic fluid embolism: A reappraisal. Am J Obstet Gynecol. 1985;151:617-621.
29. Girard P, Mal H, Laine JF. Left heart failure in amniotic fluid embolism. Anesthesiology. 1986;64:262-265.
30. Clark SL. New concepts of amniotic fluid embolism: a review. Obstet Gynecol Surv. 1990;45:360-368.
31. Reeves WC, Demers LM, Wood MA, et al. The release of thromboxane A2 and prostacyclin following experimental acute pulmonary embolism. Prostaglandins Leukot Med. 1983;11:1-10.
32. Hammerschmidt DE, Ogburn PL, Williams JE. Amniotic fluid activates complement. A role in amniotic fluid embolism syndrome? J Lab Clin Med. 1984;104:901-907.
33. Clark SL. Arachidonic acid metabolites and the pathophysiology of amniotic fluid embolism. Semin Reprod Endocrinol. 1985;3:253-257.
34. Azegami M, Mori N. Amniotic fluid embolism and leukotrienes. Am J Obstet Gynecol. 1986;155:1119-1124.
35. Richards DS, Carter LS, Corke B. The effect of human amniotic fluid on the isolated perfused rat heart. Am J Obstet Gynecol. 1988;158:210-214.
36. Lockwood CJ, Bach R, Guha A, et al. Amniotic fluid contains tissue factor, a potent initiator of coagulation. Am J Obstet Gynecol. 1991;165:1335-1341.
37. Lee HC, Yamaguchi M, Ikenoue T, et al. Amniotic fluid embolism and leukotrienes--the role of amniotic fluid surfactant in leukotriene production. Prostaglandins Leukot Essent Fatty Acids. 1992;47:117-121.
38. El Maradny E, Kanayama N, Halim A, et al. Endothelin has a role in early pathogenesis of amniotic fluid embolism. Gynecol Obstet Invest. 1995;40:14-18.
39. Vedernikov YP, Saade GR, Zlatnik M, et al. The effect of amniotic fluid on the human omental artery in vitro. Am J Obstet Gynecol. 2000;180:454-456.
40. Lunetta P, Penttila A. Immunohistochemical identification of syncitiotrophoblastic cells and megakaryocytes in pulmonary vessels in a fatal case of amniotic fluid embolism. Int J Legal Med. 1996;108:210-214.
41. Fineschi V, Gambassi R, Gherardi M, et al. The diagnosis of amniotic fluid embolism: an immunohistochemical study for the quantification of pulmonary mast cell tryptase. Int J Legal Med. 1998;111:238-243.
42. Blanc PL, Bethenod JM, Muguet D, et al. Un signe prodromique d'embolie amniotique? Presse Méd. 1985;14:2107.
43. Johnson TR, Abbasi IA, Urso PJ. Fetal heart rate patterns associated with amniotic fluid embolism. Am J Perinatol. 1987;4:187-190.
44. Burrows A, Khoo SK. The amniotic fluid embolism syndrome: 10 years' experience at a major teaching hospital. Aust N Z J Obstet Gynaecol. 1995;35:245-250.
45. Peterson EP, Taylor HB. Amniotic fluid embolism. An analysis of 40 cases. Obstet Gynecol. 1970;35:787-793.
46. Koegler A, Sauder P, Marolf A, et al. Amniotic fluid embolism: a case with noncardiogenic pulmonary edema. Intensive Care Med. 1994;20:45-46.
47. Margarson MP. Delayed amniotic fluid embolism following Cesarean section under spinal anaesthesia. Anaesthesia. 1995;50:804-806.
48. Bastien JL, Graves JR, Bailey S. Atypical presentation of amniotic fluid embolism. Anesth Analg. 1998;87:124-126.
49. Kanayama N, Yamazaki T, Naruse H, et al. Determining zinc coproporphyrin in maternal plasma--a new method for diagnosing amniotic fluid embolism. Clin Chem. 1992;38:526-529
50. Kobayashi H, Ohi H, Terao T. A simple, noninvasive, sensitive method for diagnosis of amniotic fluid embolism by monoclonal antibody TKH-2 that recognizes NeuAc alpha 2-6GalNAc. Am J Obstet Gynecol. 1993;168:848-853.
51. Liu P, Peng W, Zhang A. The value of blood sedimentation test in early diagnosis of amniotic fluid embolism. Chin J Obstet Gynecol. 1997;32:669-670.
52. Tanguy M, Malledant Y, Dormoy D, et al. Diagnostic précoce de l'embolie amniotique. Intérêt de prélèvement veineux central. Presse Med. 1983;12:2398.
53. Masson RG, Ruggieri J. Pulmonary microvascular cytology. A new diagnostic application of the pulmonary artery catheter. Chest. 1985;88:908-914.
54. Lee KR, Catalano PM, Ortiz-Giroux, S. Cytologic analysis with a unique cytologic feature and emphasis on the difficulty of eliminating squamous contamination. Acta Cytologica. 1986;30:177-182.
55. Ricou B, Reper P, Suter PM. Rapid diagnosis of amniotic fluid embolism causing severe pulmonary failure. Intensive Care Med. 1989;15:129-131.
56. Blanc PL, Guibaud S, Bedock B, et al. Diagnostic de l'embolie amniotique par lavage broncho-alvéolaire. Presse Méd. 1987;16:479-480.
57. Cheung AN, Luk SC. The importance of extensive sampling and examination of cervix in suspected cases of amniotic fluid embolism. Arch Gynecol Obstet. 1994;255:101-105.
58. Gross P, Benz EJ. Pulmonary embolism by amniotic fluid. Surg Gynecol Obstet . 1947;85:315-320.
59. Roche WD, Norris HJ. Detection and significance of maternal pulmonary amniotic fluid embolism. Obstet Gynecol. 1974;43:729-731.
60. Ishiyama I, Mukaida M, Komuro E, et al. Analysis of a case of generalized amniotic fluid embolism by demonstrating the fetal isoantigen (A blood type) in maternal tissues of B blood type, using immunoperoxidase staining. Am J Clin Pathol. 1986;85:239-241.
61. Forester D. Amniotic fluid embolism and emergency cardiac care. Ann Emerg Med. 1984;13:1172-1173.
62. Esposito RA, Grossi EA, Coppa G, et al. Successful treatment of postpartum shock caused by amniotic fluid embolism with cardiopulmonary bypass and pulmonary artery thromboembolectomy. Am J Obstet Gynecol. 1990;163:572-574.
63. Rodgers GP, Heymach III GJ. Cryoprecipitate therapy in amniotic fluid embolization. Am J Med. 1984;76:916-920.
64. Kumar B, Christmas D. Plasma fibronectin levels in amniotic fluid embolism. Intensive Care Med. 1985;11:273-274.
65. Van Heerden PV, Webb SA, Hee G, et al. Inhaled aerolized prostacyclin as a selective pulmonary vasodilator for the treatment of severe hypoxemia. Anaesth Intens Care. 1996;24:87-90.
66. Tanus-Santos JE, Moreno H. Inhaled nitric oxide and amniotic fluid embolism. Anesth Analg. 1999;88:691-696.
67. Dodgson J, Martin J, Boswell J. Probable amniotic fluid embolism precipitated by amniocentesis and treated by exchange transfusion. British Medical Journal. 1987;294:1322-1323.
68. Taenaka N, Shimada Y, Kawai M, et al. Survival from DIC following amniotic fluid embolism. Successful treatment with a serine proteinase inhibitor; FOY. Anaesthesia. 1981;36:389-393.
69. Sprung J, Cheng EY, Patel S, et al. Understanding and management of amniotic fluid embolism. J Clin Anesth. 1992:235-240.
70. Clark SL. Successful pregnancy outcomes after amniotic fluid embolism. Am J Obstet Gynecol. 1992;167: 511-512.
71. King MB, Harmon KR. Unusual forms of pulmonary embolism.
Clin Chest Med. 1994;15:561-580.
Click here to view full-size graphic
This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Jefferson Medical College and Medical Economics, Inc.
Jefferson Medical College of Thomas Jefferson University, as a member of the Consortium for Academic Continuing Medical Education, is accredited by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians. All faculty/authors participating in continuing medical education activities sponsored by Jefferson Medical College are expected to disclose to the activity audience any real or apparent conflict(s) of interest related to the content of their article(s). Full disclosure of these relationships, if any, would appear on the opening page of the article and below.
CONTINUING MEDICAL EDUCATION CREDIT
This CME activity is designed for practicing obstetrician/gynecologists and other health-care professionals as a review of the latest information in the field. Its goal is to increase participants' ability to prevent, diagnose, and treat important obstetric/gynecologic problems.
Jefferson Medical College designates this continuing medical educational activity for a maximum of one hour of Category 1 credit towards the Physician's Recognition Award (PRA) of the American Medical Association. Each physician should claim only those hours of credit that he/she actually spent in the educational activity.
This credit is available for the period of Januray 15, 2000, to January 15, 2001. Forms received after January 2001 cannot be processed.
Although forms will be processed when received, certificates for CME credits will be issued every four months, in March, July, and November. Interim requests for certificates can be made by contacting the Jefferson Office of Continuing Medical Education at 215-955-6992.
HOW TO APPLY FOR CME CREDIT
1. Each CME article is prefaced by learning objectives for participants to use to determine if the article relates to their individual learning needs.
2. Read the article carefully, paying particular attention to the tables and other illustrative materials.
3. Complete the CME Registration and Evaluation Form below. Type or print your full name and address in the space provided, and provide an evaluation of the activity as requested. In order for the form to be processed, all information must be complete and legible.
4. Send the completed form, with $20 payment if required (see Payment, next page), to:
Office of Continuing Medical Education/JMC
Jefferson Alumni Hall
1020 Locust Street, Suite M32
Philadelphia, PA 19107-6799
5. Be sure to mail the Registration and Evaluation Form on or before January 15, 2001. After that date, this article will no longer be designated for credit and forms cannot be processed.
Jefferson Medical College, in accordance with accreditation requirements, asks the authors of CME articles to disclose any affiliations or financial interests they may have in any organization that may have an interest in any part of their article. The following information was received from the authors of "Amniotic fluid embolism: an update."
Alfredo Gei, MD, and Gary D.V. Hankins, MD, have no information to disclose.
Gary Hankins,Alfredo Gei. Amniotic fluid embolus: An update. Contemporary Ob/Gyn 2000;1:53-66.