Acute Pulmonary Oedema as a Complication of Hypertension During Pregnancy

Hypertension in Pregnancy, Early Online:1–13, 2009 Copyright © Informa UK Ltd. ISSN: 1064-1955 print / 1525-6065 online DOI: 10.3109/10641950902972140

Acute Pulmonary Oedema as a Complication of Hypertension During Pregnancy

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1525-6065 1064-1955 LHIP Hypertension in Pregnancy Pregnancy, Vol. 1, No. 1, June 2009: pp. 1–25

Acute Pulmonary Thornton et al. Oedema During Pregnancy

Charlene E. Thornton,1 Peter von Dadelszen,2 Angela Makris,3 Jane M. Tooher,4 Robert F. Ogle,4 and Annemarie Hennessy1 1

School of Medicine, University of Western Sydney, Sydney, Australia University of British Columbia, British Columbia Women’s Hospital and Health Centre, Maternal-Fetal Medicine Unit, Vancouver, Canada 3 Heart Research Institute, University of Sydney, Sydney, Australia 4 Hypertensive Disorders of Pregnancy Unit, Royal Prince Alfred Women and Babies, Sydney, Australia 2

Objective. To determine rates of and potential causative factors for acute pulmonary oedema (APO) in hypertensive women. Methods. Statistical analysis, including logistic regression, was applied to the individual patient data (IPD) of all hypertensive women who delivered in 2005 at two comparable units. Results. Of 880 cases analysed, there were no women with APO in unit one and 19 women in unit two. The women with APO received larger quantities of intravenous fluids, delivered at earlier gestations, via Caesarean section, following failed induction of labour and had a longer hospital stay. Conclusion. The development of APO in women with hypertension during pregnancy is associated with high levels of intravenous fluid administration. Keywords

Acute pulmonary oedema, Hypertension, Preeclampsia.

INTRODUCTION Hypertensive disorders in pregnancy contribute to significant mortality and morbidity worldwide, and affect 5% of pregnancies. Rapid onset interstitial fluid accumulation in the lungs, acute pulmonary oedema (APO), is a potential complication of maternal hypertension, seen particularly in women with preeclampsia and eclampsia. APO has also been linked to increased maternal age, delivery via Caesarean section, body mass index, parity, undiagnosed

Address correspondence to Charlene E. Thornton, Locked Bag 1797, University of Western Sydney, School of Medicine, Penrith South, DC NSW 1797. E-mail: charlene.thornton@ uws.edu.au

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Thornton et al.

cardiomyopathy (1), multiple gestation, corticosteroid use, colloid therapy and magnesium sulphate (MgSO4) use (2). Endothelial damage, and resulting fluid leakage into the alveolar space, contributes to the development of acute pulmonary oedema in these women (3,4), thus may be in part explained by the endothelial dysfunction seen in women with preeclampsia being an endothelial disease (5). Iatrogenic causes linked to non-restrictive intravenous crystalloid fluid administration policies have also been noted (6). The negative inotropic effect attributed to commonly used anti-hypertensive medications in the obstetric setting, such as nifedipine (7,8) and labetalol (9) has also been questioned as a contributing factor in the development of acute pulmonary oedema. Increasing use of non-steroidal anti-inflammatory drugs (NSAIDS)(10), which can cause fluid retention may also be a contributing factor. Maternal morbidity is currently underreported in the obstetric literature (11). This confounds the ability to both determine rates of acute pulmonary oedema among hypertensive pregnant women and identify potential causative factors. Best estimates of rates are deduced from randomised controlled trials and observational data. This method has inherent problems of accuracy due to issues such as small sample size, and sample and publication biases. Reported rates of acute pulmonary oedema in the obstetric setting vary widely, with rates as high as 0.5% of all deliveries being cited (12). In women with severe disease/HELLP syndrome (haemolysis, elevated liver enzymes, low-platelets), acute pulmonary oedema was seen in between 4.3% (13) and 15% of cases (14,15). In women with eclampsia, the reported rates are between 5% (16) and 33% (6). Acute pulmonary oedema was a contributing cause of death in 17.2% of women affected by hypertension during pregnancy in a recent South African study (17). The aim of this study was to examine the rates of acute pulmonary oedema in two comparable academic tertiary referral obstetric units; the first in Australia and the second in Canada. This is part of a larger study examining the potential of benchmarking obstetric practice to reduce morbidity complicating hypertension in pregnancy.

METHODS A retrospective individual patient data (IPD) review was conducted in 2006 for the calendar year 2005 at Royal Prince Alfred Women and Babies (RPAWB), Sydney, Australia and British Columbia Women’s Hospital and Health Centre (BCW), Vancouver, Canada. This comparison was undertaken as a component of a larger benchmarking initiative to compare maternal morbidity and perinatal mortality and morbidity between two international units with very similar patient profiles. Potential medical records were identified utilising the International Classification of Disease (ICD) coding system for the codes O.10–O.16, referring to the hypertensive disorders of pregnancy.

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Acute Pulmonary Oedema During Pregnancy

Each medical record was reviewed by one individual (CT) to limit potential bias. Institutional ethics approval was obtained prior to commencement. A database of antenatal, delivery and postnatal details was maintained and women were diagnosed by physical signs and laboratory findings in accordance with the Australasian Society for the Study of Hypertension in Pregnancy (ASSHP) Consensus Statement (18) for consistency of diagnostic grouping. This statement contains the criteria required for a definition of the four types of hypertension in pregnancy; preeclampsia, gestational hypertension, chronic hypertension and superimposed preeclampsia. Outcomes to be compared included age, body mass index, parity, smoking rates, booking blood pressures (BP), maximum antenatal BP, oral anti-hypertensive medication use, intravenous medication use, steroid administration, non-steroidal antiinflammatory drug (NSAID) administration, delivery gestation, delivery type, type and amount of intravenous fluids administered, perinatal mortality rates and final diagnoses. Acute pulmonary edema was defined as a new onset of pulmonary oedema in the presence of a hypertensive disorder of pregnancy occurring within the perinatal period diagnosed by moist crepitant rales, decreased oxygen saturation by pulse oximetry and/or chest X-ray. In discerning a diagnosis of acute pulmonary oedema for the purpose of this review, all relevant medical records were reviewed for the notation of acute pulmonary oedema by the attending physician. Potential cases, as inferred by nursing or physiotherapy entries were only recorded as definite cases if confirmed by medical personnel. Data were analysed by use of student’s t-tests and chi square tests with non-parametric testing where appropriate with SPSS v.14®. A value of p < 0.05 was taken to indicate statistical significance. Logistic regression modelling with goodness-of-fit testing was undertaken to determine associations between potential causative factors and the binary outcome of presence/ absence of APO.

RESULTS There were 472 women at RPAWB and 408 women at BCW diagnosed with one of the four presentations of hypertension in pregnancy stated above. The baseline characteristics and pregnancy outcomes for these women are presented in Table 1 and diagnostic groupings in Table 2. There was no statistical difference in the diagnostic groupings between the two units. During this time period there were no cases of acute pulmonary oedema at RPAWB and 19 cases at BCW. Of the 19 acute pulmonary oedema cases, two occurred in the antenatal period, one occurred during labour and delivery and the remaining 16 occurred in the puerperium. Two women had primary hypertension predating pregnancy and 17 were diagnosed with preeclampsia. None of the women had any known pre-exiting cardiac abnormality. A comparison

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Thornton et al. Table 1: Baseline characteristics and outcomes for all women.

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RPAWB

BCW

SS

Age (mean years ± SD) 32 ± 5.7 33 ± 5.7 Body Mass Index (weight/height2) 26 ± 6.8 26 ± 5.8 (mean units ± SD) Smoking during pregnancy* 9.6% 15.2% Ethnicity* Caucasian 82% 61% Asian 14% 34% Other 4% 5% Parity (% primiparous)* 64% 67% Gestation at booking visit (mean weeks ± SD) 15 ± 6.1 14 ± 6.1 Booking systolic BP (mm Hg mean ± SD ) 118 ± 12.6 118 ± 16.0 Booking diastolic BP (mm Hg mean ± SD) 72 ± 9.7 74 ± 10.3 Highest antenatal systolic BP (mm Hg mean ± SD ) 145 ± 18.7 147 ± 17.3 Highest antenatal diastolic BP (mm Hg mean ± SD) 93 ± 12.2 93 ± 11.7 Anti-hypertensives prescribed antenatally* 52.5% 22.5% Gestation at delivery (mean weeks ± SD) 37.7 ± 3.7 37.3 ± 2.93 Delivered via Caesarean section* 46% 45% Delivered via Caesarean section after 30% 35% attempt at IOL* Intravenous MgSO4 administration* 17% 18% Oral NSAID administration* 6% 78% Steroid administration for fetal lung maturity* 14% 8% Perinatal mortality* 16/1000 18/1000

0.490 0.581 0.013 0.010