Original Research
Association of Nonsteroidal
Antiinflammatory Drugs and Postpartum
Hypertension in Women With Preeclampsia
With Severe Features
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Oscar A. Viteri, MD, Joey A. England, MD, Mesk A. Alrais, MD, Kayla A. Lash, MD, Maria I. Villegas, MD,
Olaide A. Ashimi Balogun, MD, Suneet P. Chauhan, MD, and Baha M. Sibai, MD
OBJECTIVE: To estimate whether nonsteroidal antiin-
flammatory drugs (NSAIDs) are associated with persistent
postpartum hypertension in a cohort of women with
preeclampsia and severe features.
METHODS: We conducted a retrospective cohort study
at a single, tertiary center from January 2013 to December
2015. All women diagnosed with severe preeclampsia
who remained hypertensive for greater than 24 hours
after delivery were included. The primary outcome was
the rate of persistent postpartum hypertension, defined
as systolic blood pressure 150 mm Hg or greater or
diastolic 100 mm Hg or greater (or both), on two
occasions, at least 4 hours apart. Secondary outcomes
included severe maternal morbidity: pulmonary edema,
renal dysfunction, stroke, eclampsia, and intensive care
unit admission. Additional outcomes included length of
postpartum hospital stay, receipt of narcotics, and hospi-
tal readmission. Multivariable logistic regression was
performed to adjust for confounders. Adjusted odds
ratios (ORs) are reported for applicable study outcomes.
From the Division of Maternal-Fetal Medicine, Department of Obstetrics,
Gynecology and Reproductive Sciences, McGovern Medical School at the
University of Texas Health Science Center at Houston, Houston, Texas.
Presented at the 37th Annual Meeting of the Society for Maternal-Fetal Medicine,
January 23–28, 2017, Las Vegas, Nevada.
Each author has indicated that he or she has met the journal’s requirements for
authorship.
Corresponding author: Oscar A. Viteri, MD, Division of Maternal-Fetal
Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences,
McGovern Medical School, The University of Texas Health Science Center at
Houston, 6431 Fannin Street, Suite 3.264, Houston, TX 77030; email: Oscar.
A.ViteriMolina@uth.tmc.edu.
Financial Disclosure
The authors did not report any potential conflicts of interest.
© 2017 by The American College of Obstetricians and Gynecologists. Published
by Wolters Kluwer Health, Inc. All rights reserved.
ISSN: 0029-7844/17
830 VOL. 130, NO. 4, OCTOBER 2017
Copyright ª by The American College of Obstetricians
and Gynecologists. Published by Wolters Kluwer Health, Inc.
Unauthorized reproduction of this article is prohibited.
RESULTS: Of the 399 women with severe preeclampsia,
324 (81%) remained hypertensive 24 hours after delivery.
Two hundred forty-three (75%) received NSAIDs (either
ibuprofen or ketorolac) and 81 (25%) did not. After
multivariable logistic regression, the likelihood of reach-
ing a blood pressure of 150 mm Hg systolic or 100 mm
Hg diastolic (or both), on two occasions, at least 4 hours
apart, was similar between those who received NSAIDs
compared with those who did not (70% compared with
73%; adjusted OR 1.1, 95% CI 0.6–2.0). Similarly, puer-
peral occurrence of pulmonary edema (3% compared
with 10%; OR 4.4, 95% CI 1.5–13.1), renal dysfunction
(5% compared with 8%; OR 1.7, 95% CI 0.6–4.8), eclampsia
(1% compared with 0%; P5.34), or intensive care unit
admission (3% compared with 8%; OR 2.4, 95% CI
0.8–7.1) was similar between the groups. There were no
differences in the rate of narcotic use (89% compared
with 75%; adjusted OR 0.6 95% CI 0.18–1.70).
CONCLUSION: In this cohort of women with pre-
eclampsia and severe features before delivery, NSAIDs
were not associated with increased rates of persistent
postpartum hypertension.
(Obstet Gynecol 2017;130:830–5)
DOI: 10.1097/AOG.0000000000002247
P
ostpartum pain from uterine involution, birth canal
trauma, or surgery affects four million women
in the United States annually.1 Nonsteroidal antiin-
flammatory drugs (NSAIDs) are the preferred agents
for postpartum pain as a result of their effectiveness,2
breastfeeding compatibility,3 and reduction in
narcotic use.4
Although effects of NSAIDs on blood pressure
(BP) in normotensive individuals are minimal,5
studies in nonpregnant patients with chronic hyper-
tension have showed that NSAIDs are associated with
OBSTETRICS & GYNECOLOGY
increased systolic and diastolic BP. This effect is pro-
nounced in those chronically treated with b-blockers
and angiotensin-converting enzyme inhibitors (perhaps
as a result of increased prostaglandin synthesis in
response to reflex-pressor mechanisms6,7) but not with
calcium channel blockers.5,8–10 Purported mechanisms
for NSAID-induced hypertension include inhibition of
prostaglandin-mediated vasodilation,11 induction of
cytochrome-P450 breakdown of arachidonic acid into
metabolites leading to vasoconstriction,12 and
increased renal sodium retention from prostaglandin-
E2 inhibition.13,14 This is important in preeclamptic
women who are at risk for postpartum hypertension
as a result of extravascular to intravascular mobiliza-
tion of 6–8 L of fluid accumulated during pregnancy.15
Based on extrapolation of these data, the 2013
Task Force for Hypertension in Pregnancy developed
by the American College of Obstetricians and Gyne-
cologists (the College) suggested avoiding NSAIDs in
postpartum women with hypertension persisting
greater than 24 hours after delivery.16 The College
also recommends antihypertensives in the puerpe-
rium when BP is persistently 150 mm Hg or greater
systolic or 100 mm Hg diastolic (or both) on at least
two occasions, 4–6 hours apart. However, evidence
on the effects of NSAIDs in otherwise healthy puerperal
women with preeclampsia before delivery remains
conflicting.17–19
We sought to estimate whether NSAIDs are
associated with postpartum hypertension in puerperal
women and antenatal diagnosis of preeclampsia with
severe features.
MATERIALS AND METHODS
This is a retrospective cohort study undertaken at
Children’s Memorial Hermann Hospital, a tertiary
care institution in Houston, Texas, from January
2013 to December 2015. An electronic medical
record chart review was conducted by specialists in
obstetrics and gynecology (M.A.A., K.A.L., M.I.V.)
and maternal–fetal medicine (O.A.V., J.A.E., O.A.A.B.)
to identify all women with preeclampsia with severe
features before delivery who remained hypertensive
after 24 hours postpartum. Eligible study participants
were located using International Classification of
Diseases, 9th Revision codes and hospital databases.
Blood pressure monitoring followed the standard
postpartum unit protocol and was equivalent for
both groups. Hourly BP measurements were taken
while women received magnesium sulfate, and every
4 hours thereafter, unless a systolic BP 150 mm Hg or
greater or diastolic BP 100 mm Hg or greater (or both)
was reached (in which case more frequent monitoring
VOL. 130, NO. 4, OCTOBER 2017
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and Gynecologists. Published by Wolters Kluwer Health, Inc.
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was required). A diagnosis of preeclampsia with
severe features was made based on the current Task
Force Criteria for Hypertension in Pregnancy as
published.16 Postpartum women were categorized
whether they received NSAIDs or not. The primary
outcome was the rate of puerperal women with per-
sistent postpartum hypertension defined as follows:
systolic BP of at least 150 mm Hg or diastolic BP of at
least 100 mm Hg (or both), on two occasions, at least
4 hours apart,16 from 24 hours postpartum until
hospital discharge. Secondary outcomes included
severe maternal morbidity, comprising pulmonary
edema, renal dysfunction (serum creatinine level
greater than 1.1 mg/dL in the absence of other renal
disease), stroke, eclampsia, and intensive care unit
admission as well as length of postpartum hospital
stay, use of narcotics for pain control, and readmission
resulting from hypertension.
Based on a 59% rate of postpartum hypertension
requiring treatment reported in the study by Wasden
et al,18 and assuming a 30% rate increase with the use
of NSAIDs, an a error of 5%, and 90% power, 288
women (144 in each group) were required to show
a clinically significant difference in our primary
outcome. Data were analyzed using Student t test
for continuous variables, x2 or Fisher exact test for
categorical variables, and Mann-Whitney U test for
nonnormally distributed variables as appropriate.
Multivariate logistic regression was performed to
account for confounders noted on univariate analysis
as follows: abnormal laboratory parameters diagnostic
of preeclampsia with severe features,16 gestational age,
and mode of delivery. Crude and adjusted odds ratios
(ORs) and 95% CIs are reported for outcomes of
interest. P,.05 was considered statistically significant.
All analyses were performed in SPSS 24.0. The study
was approved by the McGovern Medical School
institutional review board at The University of
Texas Health Science Center at Houston (HSC-MS-
16-0323).
RESULTS
Of the 399 women diagnosed with antenatal pre-
eclampsia with severe features during the study
period, 324 (81%) remained hypertensive (ie, systolic
BP 140 mm Hg or greater or diastolic BP 90 mm Hg
or greater, or both) 24 hours after delivery. Despite
current Task Force Recommendations, at our institu-
tion, 243 (75%) puerperal women still received
NSAIDs and 81 (25%) did not (Fig. 1). A total of 97
(40%) women received just ibuprofen, 15 (6%)
received just ketorolac, and 131 (54%) received both
NSAIDs.
Viteri et al Postpartum NSAIDs and Preeclampsia 831

Figure 1. Flow diagram. NSAIDs, nonsteroidal antiin-
flammatory drugs.
Viteri. Postpartum NSAIDs and Preeclampsia. Obstet Gynecol 2017.
No statistically significant differences were noted
in baseline demographic characteristics between the
study groups (Table 1). Puerperal women who
received NSAIDs were more likely to deliver by
cesarean and at a later gestational age; the rate of
laboratory abnormalities was significantly higher
among those who did not receive NSAIDs, particularly
thrombocytopenia (Table 1).
After multivariable logistic regression, women
who received NSAIDs had similar rates of persistent
postpartum hypertension of 150 mm Hg or greater
systolic or 100 mm Hg or greater diastolic (or both),
on two separate occasions, at least 4 hours apart
compared with those who did not receive NSAIDS
(70% compared with 73%; adjusted OR 1.1, 95% CI
0.6–2.0) (Table 2). Rates of this outcome were
similar between groups regardless of mode of delivery
(vaginal591 [64% compared with 63%]; adjusted OR
0.7, 95% CI 0.3–1.9; cesarean5233 [71% compared
with 80%]; adjusted OR 1.4, 95% CI 0.6–3.2).

Table 1. Maternal Baseline Characteristics

Characteristic Received NSAIDs (n5243) Did Not Receive NSAIDs (n581) P

Maternal age (y) 28.966.4 29.865.5 .27

35 or older 49 (20) 15 (19) .19
Younger than 20 15 (6) 2 (3) .26
BMI at delivery (kg/m2) 36.668.2 37.8610 .25
30 or greater 190 (78) 64 (79) .88
40 or greater 72 (30) 28 (35) .41
Race .95
Black 120 (49) 37 (46)
White 47 (19) 19 (24)
Hispanic 15 (6) 5 (6)
Other 61 (25) 20 (25)
Nulliparous 97 (40) 39 (48) .19
Multiple gestation 22 (9) 7 (9) .91
Smoker 9 (4) 5 (6) .36
Illicit drugs 8 (3) 2 (3) 1.00
Chronic hypertension 88 (36) 30 (37) .91
On antihypertensive medication 51 (58) 21 (70) .25
Pregestational diabetes 19 (8) 8 (10) .85
Systemic lupus erythematosus 3 (1) 1 (1) 1.00
Underlying renal disease 6 (3) 4 (5) .28
Gestational diabetes 25 (10) 4 (5) .29
Fetal growth restriction 46 (20) 16 (21) .84
Diagnostic criteria for severe preeclampsia
Severe hypertension 197 (81) 65 (80) .87
CNS symptoms 88 (36) 30 (37) .89
Laboratory abnormalities 20 (8) 23 (28) ,.001
Thrombocytopenia (less than 100,000/microliter)* 6 (30) 19 (83) ,.001
More than 1 feature 86 (35) 38 (47) .07
Received corticosteroids 105 (69) 48 (31) .01
Gestational age at delivery (wk) 33.864.1 32.164.5 .002
Regional anesthesia† 233 (96) 73 (90) .06
Cesarean delivery 184 (76) 49 (61) .008
Breastfeeding 157 (65) 58 (72) .25
NSAIDs, nonsteroidal antiinflammatory drugs; BMI, body mass index; CNS, central nervous system.
Data are mean6SD or n (%) unless otherwise specified.
* Rate of other abnormal laboratory parameters (ie, creatinine level, liver function tests) was similar between the groups.
†
Spinal, epidural, or combined spinal–epidural.

832 Viteri et al Postpartum NSAIDs and Preeclampsia OBSTETRICS & GYNECOLOGY

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Table 2. Maternal Outcomes

Received NSAIDs Did Not Receive Adjusted OR

Outcome (n5243) NSAIDs (n581) P OR (95% CI) (95% CI)

Primary outcome* 170 (70) 59 (73) .57 1.2 (0.7–2.1) 1.1 (0.6–2.0)
Severe morbidity†
Pulmonary edema 6 (3) 8 (10) .008 4.4 (1.5–13.1) —‡
Renal dysfunction 11 (5) 6 (8) .30 1.7 (0.6–4.8) —‡
Eclampsia 2 (0) 0 (0) .34 —‡ —‡
ICU admission 8 (3) 6 (8) .12 2.4 (0.8–7.1) —‡
Length of hospital stay (d) 4 (3–5) 4 (2–5) .15 — —
Need for narcotics 216 (89) 61 (75) .003 1.3 (0.6–2.8) 0.6 (0.18–1.70)
Duration of narcotics (d) 3.0 (2–4) 3.0 (2–4) .21 — —
Readmission for hypertension 11 (5) 5 (7) .56 1.4 (0.5–4.1) 1.3 (0.4–4.5)
NSAIDs, nonsteroidal antiinflammatory drugs; OR, odds ratio; ICU, intensive care unit.
Data are n (%) or median (interquartile range) unless otherwise specified.
Data adjusted for: presence of laboratory abnormalities, gestational age, and mode of delivery.
* Rate of puerperal women reaching the treatment threshold for antihypertensive therapy: systolic blood pressure of at least 150 mm Hg or
diastolic blood pressure of at least 100 mm Hg (or both), on two occasions, at least 4 hours apart.
†
There were no cases of maternal stroke or deaths.
‡
Counts are too small to perform logistic regression.

In addition, the rate of those who received de novo
antihypertensive therapy or a second antihypertensive
agent after the first 24 hours postpartum was similar
between the groups (22% compared with 31%;
adjusted OR 1.1, 95% CI 0.5–2.5). Among those
who received NSAIDs and required postpartum anti-
hypertensive therapy, the most common agent used
was nifedipine (25%) followed by labetalol (11%).
Similarly, those who did not receive NSAIDs and
receive antihypertensive therapy were most likely to
receive nifedipine (17%) followed by labetalol (14%).
There were no cases of maternal stroke or deaths
in the study cohort. No significant differences were
noted in the rate of severe maternal morbidity, length
of hospital stay, or need for hospital readmission as
a result of hypertension. In addition, the average
duration of hospital stay was approximately 4.5 days
in both groups. Although postpartum women
receiving NSAIDs were more likely to receive nar-
cotics for pain control on univariate analysis, no
significant differences were noted between the groups
after logistic regression (Table 2).
There were no significant differences in average
systolic or diastolic BP measurements between the
study groups (Fig. 2). Finally, the use of NSAIDs was
not associated with BP changes among whom who
received nifedipine or those who received labetalol
(Fig. 3).
DISCUSSION
In this large cohort of puerperal women with antena-
tal preeclampsia with severe features, the use of
NSAIDs for pain control at or after 24 hours after
delivery was not associated with increased rates of
persistent postpartum hypertension as defined by the
current College Task Force. Furthermore, the use of

Figure 3. The association of nonsteroidal antiinflammatory

Figure 2. Mean blood pressure values in study groups. All
P values ..05. NSAIDs, nonsteroidal antiinflammatory
drugs. Error bars indicate SD.
Viteri. Postpartum NSAIDs and Preeclampsia. Obstet Gynecol
2017.
drugs on blood pressure values in puerperal women
receiving antihypertensives. All P values ..05. Error bars
indicate SD.
Viteri. Postpartum NSAIDs and Preeclampsia. Obstet Gynecol
2017.

VOL. 130, NO. 4, OCTOBER 2017 Viteri et al Postpartum NSAIDs and Preeclampsia 833

Copyright ª by The American College of Obstetricians

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Unauthorized reproduction of this article is prohibited.
NSAIDs was not associated with increased severe
maternal morbidity, longer duration of hospital stay,
use of narcotics for pain control, or readmission
resulting from hypertension. In addition, unlike
nonpregnant patients with chronic hypertension on
treatment, NSAIDs were not associated with BP
changes in women receiving labetolol.
Concerns about the safety of NSAIDs in hyper-
tensive puerperal women were first raised by Makris
et al,17 who reported six cases of women exposed to
indomethacin or ibuprofen after delivery followed by
hypertensive crises. Comprehensive information was
provided on two of the women exposed to indometh-
acin, who developed severe hypertension between
3 and 5 hours after ingestion, respectively. Although
BP remained labile for up to 2 weeks, no information
was provided on the duration of NSAID treatment or
specific antihypertensive therapy administered.
Importantly, preeclampsia had been diagnosed in
only one of the patients.
Our results are in line with those by Wasden
et al18 who performed a retrospective chart review of
223 women who received magnesium sulfate for
seizure prophylaxis as a surrogate marker for
preeclampsia with severe features and compared them
based on their exposure to NSAIDs. No significant
differences were noted in the average mean arterial
pressure between the study groups. Similarly,
treatment with NSAIDs was not significantly associated
with initiation or dose increases of antihypertensive
medication postpartum, prolonged hospital stay, or
adverse events related to hypertension including
hospital readmission for BP control or central nervous
system symptoms, eclampsia, pulmonary edema, or
intensive care unit admission.
In a recent open-label randomized clinical trial of
ibuprofen compared with acetaminophen, Vigil
de Gracia et al19 studied 113 women after vaginal
delivery with preeclampsia and severe features or pre-
eclampsia superimposed on chronic hypertension.
Although women exposed to ibuprofen were signifi-
cantly more likely to reach a systolic BP of 150 mm
Hg or a diastolic BP of 100 mm Hg 24–96 hours post-
partum compared with those in the acetaminophen
group, the study excluded women delivered by cesar-
ean and had a likelihood of ascertainment bias.
As a retrospective cohort, our study has limita-
tions. Although our overall sample size is adequate to
detect clinically significant differences in the primary
outcome, the study groups were not balanced. Indeed,
the majority of puerperal women in this cohort (75%
[n5243]) received NSAIDs despite current Task
Force guidelines. In addition, this study was not
834 Viteri et al Postpartum NSAIDs and Preeclampsia
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powered to draw firm conclusions regarding rare
but clinically significant outcomes such as pulmonary
edema, renal dysfunction, eclampsia, stroke, or mater-
nal death. Second, data on the duration of NSAIDs or
antihypertensive treatment after hospital discharge
were not available for analysis. This is of importance
because the average length of postpartum hospital
stay in this cohort was 4.5 days and fluid shifts are
more prominent between days 3 and 6 postpartum.20
Lastly, we were not able to demonstrate an association
between NSAIDs and reduced need for narcotics in
the immediate puerperium period. This likely results
from the majority of women in the cohort undergoing
delivery by cesarean and, therefore, being exposed to
more intensive pain control measures.
On the other hand, our study benefits from several
strengths. We conducted a PubMed search from
inception, in English language, and using the terms “pre-
eclampsia,” “postpartum hypertension,” “NSAID,” and
“Task Force” and could not find another study evaluat-
ing the association of NSAIDs on BP in a population of
hypertensive puerperal women with preeclampsia and
severe features before delivery as defined by the current
College Task Force. We were also not able to find
another study that evaluated the association of NSAIDs
on BP among puerperal women receiving antihyperten-
sive therapy. Lastly, the study was conducted on an
ethnically diverse population.
We conclude that in preeclampsia with severe
features before delivery, puerperal use of NSAIDs
was not associated with increased rates of clinically
significant persistent hypertension. It is our opinion
that, given the relative safety of NSAIDs over opioids
in nursing women and because of increasing concerns
regarding narcotic dependence, an adequately pow-
ered randomized clinical trial is warranted to answer
this clinical question before recommendations forfeit-
ing NSAIDs use in this population are made.
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