http://informahealthcare.com/jmf ISSN: 1476-7058 (print), 1476-4954 (electronic) J Matern Fetal Neonatal Med, 2015; 28(7): 793–798 ! 2014 Informa UK Ltd. DOI: 10.3109/14767058.2014.932766

ORIGINAL ARTICLE

Amniotic fluid embolism: antepartum, intrapartum and demographic factors Alex Fong1, Cindy T. Chau1, Deyu Pan2, and Dotun A. Ogunyemi3 1

Department of Obstetrics and Gynecology, University of California, Irvine Medical Center, Orange, CA, USA, 2Research – Life Sciences Institute, Charles Drew University of Medicine and Science, Los Angeles, CA, USA, and 3Department of Obstetrics and Gynecology, William Beaumont School of Medicine, Oakland University, Rochester, MI, USA Abstract

Keywords

Objective: To describe the incidence, antepartum, intrapartum and postpartum risk factors, and mortality rate of amniotic fluid embolism (AFE). Methods: We used 2001–2007 California health discharge data to identify cases of AFE by ICD-9 codes. Results: Of 3 556 567 deliveries during the time period, we identified 182 cases of AFE, resulting in a population incidence of 5.1 in 100 000. Twenty-four of the cases resulted in death, giving a case fatality rate of 13.2%. Non-Hispanic blacks had a higher than 2-fold odds of developing AFE. AFE increased significantly with maternal age, most significantly after age 39. Cardiac disease had a nearly 70-fold higher association with AFE, cerebrovascular disorders had a 25-fold higher association, while conditions such as eclampsia, renal disease, placenta previa and polyhydramnios had nearly 7- to 13-fold higher associations. Classical cesarean delivery, abruption placentae, dilation and curettage, and amnioinfusion were all procedures highly associated with AFE. Conclusion: Several antepartum and peripartum conditions and procedures are associated with significantly higher risks of amniotic fluid embolism. This information may contribute to a better understanding of the pathophysiology of AFE and potentially help identify those at the highest risk of developing this morbid condition.

Amniotic fluid embolism, California, incidence, outcomes, population-based study

Introduction Amniotic fluid embolism (AFE), also known as anaphylactoid syndrome of pregnancy, is a rare yet potentially catastrophic condition that occurs during pregnancy or shortly after delivery. The estimated incidence ranges from 2.2 to 7.7 per 100 000 deliveries in countries such as the US, UK, Australia and in Canada [1–3]. The mortality rate ranges between 0.5 and 1.7 deaths per 100 000 deliveries in developed countries and 1.8–5.9 per 100 000 in developing countries [4]. In the US, it has been cited as the cause for 7.5% of maternal deaths [5]. The diagnosis of AFE is primarily on a clinical basis and that of exclusion. It is assumed that a breach in the physical barriers between maternal and fetal compartments have occurred, leading to leakage of amniotic fluid through endocervical veins, uterine trauma sites and placental attachment sites. It is characterized by sudden cardiovascular collapse (cardiac arrest, shock or severe hypotension with

Address for correspondence: Alex Fong, MD, Clinical Instructor, Department of Obstetrics and Gynecology, University of California, Irvine, 101 The City Drive South, Building 56, Suite 800, Orange, CA 92869, USA. Tel: 714 456 6807. E-mail: [email protected]

History Received 20 March 2014 Revised 9 May 2014 Accepted 5 June 2014 Published online 27 June 2014

associated respiratory distress or need for mechanical ventilation), altered mental status (seizure or coma) and disseminated intravascular coagulation (DIC) [6]. Another proposed mechanism includes that of an anaphylactic reaction induced by fetal material leaked into maternal circulation. Laboratory tests are non-specific and its pathogenesis remains poorly understood. Management is supportive. There is no sufficient data to identify superiority in different treatment modalities. However, there is consensus that maximum supportive therapy, including correction of coagulopathy, oxygenation and significant hemodynamic support may decrease risk of ischemic consequences [7,8]. The primary intent of our study was to perform a comprehensive surveillance of all antepartum and peripartum factors associated with AFE in California, specifically including intrapartum procedures which have not been previously investigated, such as amniotomy, intrauterine pressure catheter placement and amnioinfusion. The secondary objectives of our study were to describe sociodemographic factors of AFE (such as age and race/ethnicity) and trends over time. Given the high mortality of AFE, we sought to identify whether there were any potentially modifiable risk factors, including those during labor, which

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Methods This is a retrospective study using California hospital discharge data provided by the California Office of Statewide Health Planning and Development (OSHPD) from 2001 to 2007. The publicly available data set comprises all cases where a patient is treated and discharged from a licensed general acute care hospital in California. The information contains details regarding demographics, hospital of treatment, diagnoses, specific procedures undergone and particulars of the patient’s stay, such as source of funding, length of stay and disposition at time of discharge. Hospital discharge data from OSHPD has previously been used in publications as well as undergone validation specifically in pregnancy related conditions [9–11]. The localInstitutional Review Board granted exempt approval because of the de-identified, retrospective design. A total of 3 556 567 million deliveries were extracted from inpatient California discharge data using delivery codes. We identified cases of amniotic fluid embolism using International Classification of Diseases, 9th Revision (ICD9) codes of 673.0x. We performed a comprehensive surveillance of the ICD-9 manual to identify all antepartum, obstetric and labor-related variables and procedures in order to analyze their associations with AFE. Conditions arising during pregnancy such as gestational diabetes (648.8x) and preeclampsia (642.4x–642.6x) were identified using their respective ICD-9 codes 630-677 (‘‘Complications of pregnancy, childbirth, and the puerperium’’). For certain other antepartum conditions found both during and outside of pregnancy, we utilized additional ICD-9 codes as necessary from outside of pregnancy. For example, thyroid disease was coded using ICD-9 codes 240.x–246.x in addition to the pregnancy-related 648.1x code. ICD-9 procedure codes were used to identify procedures performed (e.g. cesarean delivery 74.0x–74.9x, forceps/vacuum/breech delivery 72.0x–72.9x) When calculating raw incidence and trends on the small number of cases of AFE during the time period, we used the unadjusted population (3 556 567 deliveries, 182 cases of AFE). In order to ascertain the population to only reproductive-age women, we eliminated subjects 515 years of age (the lower limit of reproductive age as defined by the World Health Organization), and patients 455 years of age [12]. We also eliminated cases missing race/ethnicity in order to exclude possible confounding from absent data. The two groups used for our comparative analyses were subjects with AFE versus those without AFE. For comparison of continuous variables, we used Student’s t-test and Pearson’s chi-square or Fisher’s exact test for discrete variables. Cochran–Armitage was used for determining trends over time. We also performed a multivariable logistic regression analysis for adjustment of covariates in determining antepartum/peripartum associations of AFE. For all morbidities, we adjusted for age, race/ethnicity, insurance type, year of delivery, diabetic disease, hypertensive disease and cardiac disease, unless the variable being adjusted was the morbidity itself. This was done in order to try to establish

an independent relation between AFE and each peripartum outcome. Results were expressed in odds ratios (ORs) and 95% confidence intervals (CI). SPSS 20.0 (IBM Corp, Armonk, NY) was used for statistical analysis.

Results Of the 3 556 567 deliveries during the study period, there were 182 cases of amniotic fluid embolism, resulting in an unadjusted population incidence of 5.1 in 100 000. The yearly incidence of AFE showed no trend in change over time (p ¼ 0.97), with the yearly incidence fluctuating between 4.47 to 6.89 cases per 100 000 (Figure 1). Twenty-four out of 182 cases resulted in death, giving a case fatality rate of 13.2%. As seen in Figure 2, this also demonstrated no significant temporal trend (p ¼ 0.29). After eliminating cases due to missing age, race/ethnicity or extremes of age, 2 770 781 total deliveries remained for morbidity analysis, with 133 of these complicated by AFE. Table 1 shows a comparison of baseline study population characteristics between subjects with and without AFE. There were statistically significant differences between the two groups in their age and race/ethnicity breakdown. Non-Hispanic blacks comprised more than twice as much of the proportion of AFE subjects (9.8%) compared to their non-AFE counterparts (4.4%). A significantly larger percentage of subjects with AFE were of advanced maternal age (37.6% versus 17.2%, p50.001). Subjects with AFE demonstrated a trend of being less likely to have private insurance (42.9% versus 51.1%, p ¼ 0.06). The mean length of hospital 8 Incidence (cases per 100,000)

could give a better understanding of this rare and morbid disease.

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6.89 6

4

5.36

4.94

4.70

4.59

4.93

4.47

2

0 2001

2002

2003

2004 Year

2005

2006

2007

p=0.97

Figure 1. Incidence of AFE during the study period. 35% 30% Incidence

794

31.82%

25% 20% 15%

16.67%

8.82% 11.11% 8.00%

10%

11.54% 8.33%

5% 0%

2001

2002

2003

2004 Year

2005

2006

2007 p=0.29

Incidence defined as cases of AFE resulng in death dividedby all cases of AFE

Figure 2. Incidence of death in cases of AFE during the study period.

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Table 1. Baseline characteristics between subjects with AFE.

Baseline characteristics Age (years) 520 20–24 25–29 30–34 35–39 40–44 45+ Advanced maternal age (35 years) Race/Ethnicity Caucasian Black Native American/Eskimo/Aleut Asian/Pacific Islander Hispanic Private insurance Length of stay (days)

Subjects with AFE (n ¼ 133)

Subjects without AFE (n ¼ 2 770 738)

n (prevalence)

n (prevalence)

p value 50.001

3 24 22 34 34 15 1 50

(2.3%) (18.0%) (16.5%) (25.6%) (25.6%) (11.3%) (0.8%) (37.6%)

55 (41.4%) 13 (9.8%) 0 (0.0%) 18 (13.5%) 47 (35.3%) 57 (42.9%) 8.6 ± 10.2

229 756 648 120 733 257 683 278 389 062 82 676 4589 476 327

(8.3%) (23.4%) (26.5%) (24.7%) (14.0%) (3.0%) (0.2%) (17.2%)

1 057 365 (38.2%) 121 004 (4.4%) 3687 (0.1%) 241 564 (8.7%) 1 347 118 (48.6%) 1 416 725 (51.1%) 2.5 ± 2.2

50.001 0.001

0.06 50.001

Expressed as mean ± standard deviation. Calculations done via chi-square or t-test, where appropriate.

Figure 3. Prevalence of AFE by age.

stay for subjects with AFE was longer by more than six days (8.6 ± 10.2 versus 2.5 ± 2.2 days, p50.001). As seen in Figure 3, there was a marked increase in AFE prevalence with increasing age. Table 2 demonstrates antepartum morbidities and their associations with AFE. AFE prevalence was compared in the presence versus absence of each respective condition. For example, AFE was found in 272.6 cases per 100 000 if cardiac disease was present, compared to only 3.1 cases per 100 000 if cardiac disease was absent. After adjustments for potential confounders, the following factors were found to be significantly associated with AFE: cardiac disease (adjusted OR 69.9, 95% CI 48.1–101.4), cerebrovascular disorders (adjusted OR 25.1, 95% CI 8.6–73.2), pre-existing renal disease (adjusted OR 13.0, 95% CI 5.2–32.6), placenta previa (adjusted OR 7.0, 95% CI 3.5–14.0), polyhydramnios (adjusted OR 6.8, 95% CI 3.0–15.7), stillbirth (adjusted OR 5.8, 95% CI 2.1–15.7), urinary tract infection (adjusted OR 3.4, 95% CI 1.8–6.7) and hypertensive disorders (adjusted OR 2.2, 95% CI 1.3–3.7). Table 3 demonstrates late pregnancy/peripartum variables associated with AFE. Using the same logistic regression adjustment model, the following variables had higher

associations with AFE: amnioinfusion (adjusted OR 3.4, 95% CI 1.6–7.6), induction of labor (adjusted OR 1.6, 95% CI 1.0–2.5), post-delivery curettage (adjusted OR 12.1, 95% CI 3.8–38.6), postpartum hemorrhage (adjusted OR 13.5, 95% CI 9.3–19.5), abruptio placentae (adjusted OR 7.6, 95% CI 4.2–13.9), chorioamnionitis (adjusted OR 6.0, 95% CI 3.6– 10.0), peripartum cardiomyopathy (adjusted OR 110.9, 95% CI 33.6–365.8), low transverse cesarean delivery (adjusted OR 3.4, 95% CI 2.4–4.9), classical cesarean delivery (adjusted OR 6.0, 2.2–16.7), mild preeclampsia (adjusted OR 2.8, 95% CI 1.4–5.8), severe preeclampsia (adjusted OR 3.1, 95% CI 1.4–7.2) and eclampsia (adjusted OR 7.7, 95% CI 2.2–27.1). Death was found to have a nearly 2000-fold higher crude odds association with AFE (adjusted OR 89.5, 95% CI 47.2–169.9). Table 4 demonstrates the racial/ethnic associations of AFE. Non-Hispanic Blacks were found to have a 2.3-fold higher odds of AFE compared to NonHispanic Caucasians. The following factors were not found to be associated with development of AFE on bivariate or logistic regression analysis: pregestational diabetes mellitus, chronic hypertension, pyelonephritis, threatened preterm labor, post-term delivery, fetal growth restriction, macrosomia, oligohydramnios, pre-term premature rupture of membranes, failed induction, failed vacuum/forceps, third/fourth degree lacerations, uterine rupture, venous thromboembolism, shoulder dystocia, bladder repair, hematoma evacuation, manual exploration of uterine cavity, amniotomy, intrauterine pressure catheter placement, cervical laceration repair, asthma, vaginal birth after cesarean, tobacco use, systemic lupus erythematosus, drug dependence, hysterectomy, forceps delivery and vacuum delivery.

Discussion Based on this large California birth cohort, the incidence of AFE was found to be 5.1 cases in 100 000. This is similar to the results found in other large studies, where incidences

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Table 2. Antepartum morbidities associated with AFE. Prevalence of AFE (cases per 100000) Morbidity

Condition absent

Cardiac disease Cerebrovascular disorders Pre-existing renal disease Placenta previa Polyhydramnios Stillbirth Urinary tract infection Thyroid dysfunction Hypertensive disorders Multiple pregnancy Hypercoagulable state Diabetes Preterm delivery

3.1 4.7 4.6 4.5 4.6 4.7 4.5 4.6 4.3 4.6 4.4 4.4 4.5

Condition present

(84) (129) (128) (128) (126) (129) (123) (126) (114) (126) (115)

272.6 1075.3 138.5 57.4 45.3 36.9 27.6 21.1 18.9 12.5 11.0 10.6 10.3

Odds ratio

(49) (4) (5) (9) (6) (4) (10) (7) (19) (7) (18)

89.6 233.4 30.0 12.8 9.8 7.9 6.1 4.6 4.4 2.7 2.5 2.4 2.3

(63.0–127.5) (85.9–634.7) (12.3–73.3) (6.5–25.1) (4.3–22.3) (2.9–21.4) (3.2–11.7) (2.1–9.8) (2.7–7.2) (1.3–5.8) (1.5–4.1) (1.5–3.9) (1.4–3.9)

p value 50.001 50.001 50.001 50.001 50.001 0.001 50.001 50.001 50.001 0.008 50.001 50.001 0.001

Adjusted odds ratio 69.9 25.1 13.0 7.0 6.8 5.8 3.4 1.8 2.2 1.5 3.5 1.5 1.4

p value 50.001 50.001 50.001 50.001 50.001 0.001 50.001 0.13 0.002 0.29 0.26 0.11 0.25

(48.1–101.4) (8.6–73.2) (5.2–32.6) (3.5–14.0) (3.0–15.7) (2.1–15.7) (1.8–6.7) (0.8–4.0) (1.3–3.7) (0.7–3.3) (0.4–30.9) (0.9–2.5) (0.8–2.3)

All prevalences expressed as cases per 100 000. Adjusted for: age, race, insurance status, diabetic disease, hypertensive disease and cardiac disease, unless the variable being adjusted is the morbidity itself. Non-significant: pre-gestational diabetes mellitus, chronic hypertension, pyelonephritis, threatened pre-term labor, post-term delivery, fetal growth restriction, macrosomia, oligohydramnios, preterm premature rupture of membranes, failed induction, failed vacuum/forceps, third/fourth degree lacerations, uterine rupture, venous thromboembolism, shoulder dystocia, bladder repair, hematoma evacuation, cervical laceration repair, asthma, vaginal birth after cesarean, tobacco use, systemic lupus erythematosus, drug dependence, hysterectomy, forceps delivery, vacuum delivery. Table 3. Late pregnancy/peripartum variables. Prevalence of AFE (cases per 100 000) Morbidity

Condition absent

Amnioinfusion Induction of labor Post delivery curettage Postpartum hemorrhage Abruptio placentae Chorioamnionitis Peripartum cardiomyopathy Low transverse cesarean delivery Classical cesarean delivery Mild preeclampsia Severe preeclampsia Eclampsia Death

4.6 4.4 4.7 4.6 4.4 4.3 4.7 2.3 4.7 4.6 4.6 4.7 4.1

(126) (107) (130) (91) (121) (116) (130) (46) (129) (125) (127) (130) (116)

Condition present 16.3 8.0 69.2 57.5 51.8 29.2 1158.3 10.8 69.2 16.4 30.4 158.9 7489.0

(7) (26) (3) (42) (12) (17) (3) (87) (4) (8) (6) (3) (17)

Odds ratio 3.5 1.8 14.8 17.0 11.8 6.8 249.7 4.6 14.84 3.6 6.6 33.9 1933.5

(1.6–7.6) (1.2–2.8) (5.5–40.1) (11.8–24.6) (6.5–21.3) (4.1–11.4) (79.0–789.6) (3.2–6.6) (5.5–40.1) (1.8–7.3) (2.9–14.9) (10.8–106.6) (1141.8–3273.9)

p value

Adjusted odds ratio

p value

0.001 0.005 50.001 50.001 50.001 50.001 50.001 50.001 50.001 0.003 50.001 50.001 50.001

3.4 1.6 12.1 13.5 7.6 6.0 110.9 3.4 6.0 2.8 3.1 7.7 89.5

0.001 0.04 50.001 50.001 50.001 50.001 50.001 50.001 0.001 0.005 0.008 0.001 50.001

(1.6–7.6) (1.0–2.5) (3.8–38.6) (9.3–19.5) (4.2–13.9) (3.6–10.0) (33.6–365.8) (2.4–4.9) (2.2–16.7) (1.4–5.8) (1.4–7.2) (2.2–27.1) (47.2–169.9)

Adjusted for: age, race, insurance status, diabetic disease, hypertensive disease, and cardiac disease, unless the variable being adjusted is the morbidity itself. Table 4. Racial/ethnic associations of AFE.

Odds of AFE

Non-Hispanic Caucasian

Non-Hispanic Blacks

Asian

Hispanic

Native American

1

2.3 (1.2–4.4) p ¼ 0.01

1.6 (0.9–2.7) p ¼ 0.10

1.06 (0.7–1.7) p ¼ 0.82



All results expressed as odds ratio (95% CI). Non-Hispanic Caucasians used as referent group. Adjusted for age, insurance status, diabetic disease, hypertensive disease and cardiac disease.

ranged from 2.0 per 100 000 deliveries in the UK to 7.7 per 100 000 deliveries in the US [1,2]. No significant temporal changes in frequency of AFE were noted in our study, nor any of the aforementioned population-based studies. Given the rarity of the condition, such trends would not necessarily be expected. Increasing maternal age was associated with an increase in AFE prevalence, with a marked rise after age 40 (20.0–32.3 cases per 100 000 in those 440 years of age, compared to 1.5–8.6 cases per 100 000 in 5/¼39 years of age). NonHispanic blacks, compared to Caucasians, had a 2.3-fold

increased prevalence of AFE in our study, a finding which was also noted in a study by Abenhaim et al. [1], which reported data on 3 million US deliveries. We also demonstrate several pre-pregnancy, antepartum and peripartum conditions associated with AFE, with many of these findings reflected in other similar population-based studies. For example, induction of labor, preeclampsia/ eclampsia, placenta previa and abruptio placentae were associated with AFE in numerous publications, including other national databases from the US and Canada [1,13,14]. Specifically, our results demonstrate that the hypertensive

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disease of pregnancy spectrum was associated with AFE, but that more severe conditions had a higher AFE risk. Cases with mild preeclampsia, severe preeclampsia and eclampsia were associated with 2.8-, 3.1- and 7.7-fold higher odds of developing AFE, respectively. We confirm the lack of a relationship between AFE and several conditions such as tobacco use, thyroid disease, diabetes, preterm premature rupture of membranes, findings which have been described in other studies. These studies also found an association between AFE and instrumental delivery; however, our study was unable to detect this association [1,3,13]. Abenheim et al. [1] specifically found that when instrumental delivery was subdivided by type, only forceps (not vacuum) was associated with a significant increase in AFE. The exact reason for the lack of association in our findings is unclear, but one possibility is the difference in forceps rate in California. According to our data set (data not shown), California’s rate of forceps was nearly two to three times lower than the national average reported by the National Vital Statistics during the study period [15]. We report on the association between AFE and several high risk conditions that have not been investigated in the literature, such as pre-existing renal disease, cardiac disease, peripartum cardiomyopathy, cerebrovascular disorders and postpartum hemorrhage. We also demonstrate a differential risk of AFE by cesarean delivery type – although both low transverse and classical cesarean deliveries were associated with AFE, classical cesarean deliveries had a higher association. Intrapartum procedures such as amniotomy have been associated with AFE in several publications and textbooks, with the belief that disruption of the amniotic sac can cause amniotic fluid to enter the maternal circulation [16–18]. Our findings, in addition to those in two other populationbased studies, have demonstrated no statistically significant association between amniotomy and AFE [1,3]. Hence, based on current available evidence, amniotomy does not appear to pose an increased risk of AFE. We also report for the first time, to our knowledge, on the relationship between AFE and specific intrapartum procedures, such as intrauterine pressure catheter insertion, fetal scalp electrode placement and amnioinfusion using a large population base. Although the former two had nonsignificant associations, amnioinfusion was found to have a more than three-fold higher association with AFE. The relation between amnioinfusion and AFE/cardiovascular collapse has been described previously in the literature, but only via case reports [19,20]. Our finding (along with the six-fold association of polyhydramnios with AFE) supports the theory of uterine distension being a potential pathophysiological basis for the disease; however, the exact nature and extent of this relationship begs further investigation. Our study reflects similar mortality as reported in other population-based studies. Our case fatality rate of 13.2% is similar to those reported in other studies, which demonstrate rates ranging from 11 to 19% in the US, Canada and Australia. Our data was derived from California birth data, which has been previously used in many obstetrical population-

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based studies. Only large population datasets can have the power to detect the relations between a rare condition like AFE and its associated etiologies. However, as with all studies of this nature, we acknowledge there are several limitations. In order to maintain confidentiality, the California OSHPD masked certain variables of patients if they were found to have identical combinations of demographic characteristics (including race, ethnicity). This resulted in a subset of our database being excluded due to omitted data. However, with the large size of the remaining data set (42.7 million total cases, with 133 AFE cases), there was still adequate sample size for many measures. Conversely, the small number of positive cases still decreased the likelihood that we would have sufficient power to detect differences between certain rare outcomes such as hysterectomy and uterine rupture. Unfortunately, in a large database of this nature, it is also impossible to discern the exact temporal relationship between some of the morbidities and AFE. For example, there is a strong association between eclampsia and AFE; however, it is impossible to tell whether the AFE preceded the eclampsia or vice versa. We were not given permission to physically abstract the charts to determine the timing of each respective condition. There may be concerns that inaccuracies will be present when ICD-9 coding is used in any large data set. Yasmeen et al. [9] published a validation on study using older OSHPD data and found that although there was high sensitivity in the coding of delivery types and certain antepartum conditions (multiple gestations, abruption, preeclampsia), other conditions (anemia, obesity, asthma) were less accurately reported. Clark [21] published a recent clinical expert series suggesting that there may be an overestimation of AFE cases in discharge datasets and death certificates. In terms of AFE case ascertainment, Kramer et al. [13] used an algorithm requiring the presence of intensive care-related diagnoses to decrease false positives in selecting true cases of AFE and found that only 40% of AFEcoded cases met their specific diagnostic criteria. We chose not to utilize this algorithm in our study, as we feel it is possible that cases may have been falsely excluded if they did not actually exhibit specific intensive care features, or include the appropriate intensive care coding. AFE is ultimately still a solely clinical diagnosis and is rare enough to where significant co-morbidity would likely be present, regardless of the exact associated diagnoses coded. In conclusion, AFE is a highly morbid condition that is associated with several antepartum conditions. There are socio-demographic predilections in Non-Hispanic blacks and those of advancing maternal age. The estimated incidence and fatality in our study are congruent with those reported in the literature. This is the first study to specifically investigate several intrapartum procedures in relation to AFE, with the notable finding that amnioinfusion does appear to bear an association, suggesting that uterine distension is a plausible etiology. Although there has not been a significant variation in the incidence AFE over time, it would be prudent to exercise caution still in the future, given the recent rise in highly associated morbidities, such as cesarean delivery and placenta accreta [22]. Future research endeavors should focus on pathophysiologic mechanisms of AFE and how to identify

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the highest risk individuals for whom close caution should be exercised.

Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

References 1. Abenhaim HA, Azoulay L, Kramer MS, Leduc L. Incidence and risk factors of amniotic fluid embolisms: a population-based study on 3 million births in the United States. Am J Obstet Gynecol 2008; 199:49 e1–8. 2. Knight M, Tuffnell D, Brocklehurst P, et al. Incidence and risk factors for amniotic-fluid embolism. Obstet Gynecol 2010;115: 910–17. 3. Roberts CL, Algert CS, Knight M, Morris JM. Amniotic fluid embolism in an Australian population-based cohort. BJOG 2010; 117:1417–21. 4. Conde-Agudelo A, Romero R. Amniotic fluid embolism: an evidence-based review. Am J Obstet Gynecol 2009;201:445 e1–13. 5. Berg CJ, Callaghan WM, Syverson C, Henderson Z. Pregnancyrelated mortality in the United States, 1998 to 2005. Obstet Gynecol 2010;116:1302–9. 6. Clark SL, Hankins GD, Dudley DA, et al. Amniotic fluid embolism: analysis of the national registry. Am J Obstet Gynecol 1995;172:1158–67; discussion 1167–9. 7. Rudra A, Chatterjee S, Sengupta S, et al. Amniotic fluid embolism. Indian J Crit Care Med 2009;13:129–35. 8. Annecke T, Geisenberger T, Kurzl R, et al. Algorithm-based coagulation management of catastrophic amniotic fluid embolism. Blood Coagul Fibrinolysis 2010;21:95–100. 9. Yasmeen S, Romano PS, Schembri ME, et al. Accuracy of obstetric diagnoses and procedures in hospital discharge data. Am J Obstet Gynecol 2006;194:992–1001.

J Matern Fetal Neonatal Med, 2015; 28(7): 793–798

10. Fong A, Chau CT, Pan D, Ogunyemi DA. Clinical morbidities, trends, and demographics of eclampsia: a population-based study. Am J Obstet Gynecol 2013;209:229 e1–7. 11. Schmitt SK, Sneed L, Phibbs CS. Costs of newborn care in California: a population-based study. Pediatrics 2006;117:154–60. 12. Gehner MCF, Abraham T. WHO Women’s Health Fact Sheet no. 334. World Health Organization. Available from: http://www. who.int/mediacentre/factsheets/fs334/en/index.html [last accessed 1 December 2013]. 13. Kramer MS, Rouleau J, Liu S, et al.; Maternal Health Study Group of the Canadian Perinatal Surveillance. Amniotic fluid embolism: incidence, risk factors, and impact on perinatal outcome. BJOG 2012;119:874–9. 14. Kramer MS, Abenhaim H, Dahhou M, et al. Incidence, risk factors, and consequences of amniotic fluid embolism. Paediatr Perinat Epidemiol 2013;27:436–41. 15. Martin J, Hamilton BE, Ventura SJ. Births: final data for 2009. Natl Vital Stat Rep 2009. Available from: http://www.cdc.gov/nchs/ data/nvsr/nvsr60/nvsr60_01.pdf [last accessed 1 June 2012]. 16. Mato J. Suspected amniotic fluid embolism following amniotomy: a case report. AANA J 2008;76:53–9. 17. Paterson WG, Grant KA, Grant JM, McLean N. The pathogenesis of amniotic fluid embolism with particular reference to transabdominal amniocentesis. Eur J Obstet Gynecol Reprod Biol 1977;7: 319–24. 18. Hanretty KP. Obstetrics illustrated. Edinburgh, New York: Churchill Livingstone Wordmark; 2003. 19. Dorairajan G, Soundararaghavan S. Maternal death after intrapartum saline amnioinfusion – report of two cases. BJOG 2005;112: 1331–3. 20. Dibble L, Elliott, J. Possible amniotic fluid embolism associated with amnioinfusion. J Matern Fetal Neonatal Med 1992;1:263–6. 21. Clark SL. Amniotic fluid embolism. Obstet Gynecol 2014;123: 337–48. 22. Warshak CR, Ramos GA, Eskander R, et al. Effect of predelivery diagnosis in 99 consecutive cases of placenta accreta. Obstet Gynecol 2010;115:65–9.

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Amniotic fluid embolism: antepartum, intrapartum and demographic factors.

To describe the incidence, antepartum, intrapartum and postpartum risk factors, and mortality rate of amniotic fluid embolism (AFE)...
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