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Prevention and treatment of postpartum hypertension

  1. Laura Magee1,*,
  2. Peter von Dadelszen2

Editorial Group: Cochrane Pregnancy and Childbirth Group

Published Online: 30 APR 2013

Assessed as up-to-date: 12 FEB 2013

DOI: 10.1002/14651858.CD004351.pub3


How to Cite

Magee L, von Dadelszen P. Prevention and treatment of postpartum hypertension. Cochrane Database of Systematic Reviews 2013, Issue 4. Art. No.: CD004351. DOI: 10.1002/14651858.CD004351.pub3.

Author Information

  1. 1

    British Columbia Women's Hospital and Health Centre, Departments of Internal Medicine (UBC) and Specialized Women's Health (BC Women's Hospital), Vancouver, British Columbia, Canada

  2. 2

    University of British Columbia, Department of Obstetrics and Gynaecology, Vancouver, BC, Canada

*Laura Magee, Departments of Internal Medicine (UBC) and Specialized Women's Health (BC Women's Hospital), British Columbia Women's Hospital and Health Centre, 4500 Oak Street, Suite 1U59, Vancouver, British Columbia, V6H 3N1, Canada. lmagee@cw.bc.ca.

Publication History

  1. Publication Status: New search for studies and content updated (no change to conclusions)
  2. Published Online: 30 APR 2013

SEARCH

 

Background

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

The hypertensive disorders of pregnancy are associated with increased morbidity and mortality. Research has focused on the antenatal complications, for both mother and baby, and the risks and benefits of administering antihypertensive therapy prior to delivery (Abalos 2007; Duley 2002). There is very little information on how best to manage postpartum hypertension, regardless of type or severity, to optimise maternal safety and minimise hospital stay.

The true prevalence of postpartum hypertension is difficult to ascertain, but the importance of monitoring women in the puerperium was highlighted by the Confidential Enquiries into Maternal Deaths in the United Kingdom (Conf Enq 94-96), in which roughly 10% of maternal deaths due to a hypertensive disorder of pregnancy occurred in the postpartum period (Tan 2002). In the 1997 to 1999 triennial report, one of 15 deaths was attributed to severe hypertension that developed only postpartum in a woman with antenatal pre-eclampsia (Conf Enq 97-99). Other complications of severe postpartum hypertension include stroke, and possibly, eclampsia. In a survey of all cases of eclampsia in the United Kingdom, 1992, it was shown that 44% of eclampsia occurs in the postpartum period, usually in the first 48 hours after delivery (Douglas 1994). Women with postpartum hypertension may also experience longer hospital stays and possibly, heightened anxiety about their recovery.

Blood pressure rises progressively over the first five postnatal days, peaking on days three to six after delivery (Bayliss 2002; Walters 1986). This pattern of blood pressure is thought to result from mobilisation, from the extravascular to the intravascular space, of the six to eight litres of total body water and the 950 mEq of total body sodium accumulated during pregnancy. Excretion of urinary sodium (i.e., natriuresis) has been observed on days three to five postpartum (Davison 1984), and it has been postulated that this may result from an increase in atrial natriuretic peptide (ANP). ANP has roles in natriuresis and inhibition of aldosterone, angiotensin II and vasopressin (Bond 1989) and has been observed to rise during the first week postpartum (Castro 1994).

What causes a postpartum recurrence or de novo (i.e., new) postpartum presentation of hypertension is not known. Perhaps an attenuated increase in ANP plays a role. Five women with de novo postpartum hypertension were seen to have significantly lower ANP levels, compared with 10 normotensive controls (Nagai 1997). Another possibility is a failure to observe the expected postpartum fall in serum angiotensin I, an inactive intermediate of angiotensin II which is a potent vasoconstrictor. This was observed in 10 women with postpartum hypertension (recurrent or de novo) (Mizutani 1993).

There are iatrogenic causes of postpartum hypertension. Bromocriptine, to inhibit lactation, was withdrawn from the American market in 1994, because of numerous case reports of intracerebral haemorrhage and other vasospasm-mediated adverse events (such as myocardial infarction). It is plausible that the administration of non-steroidal anti-inflammatory drugs (NSAIDs) for postpartum analgesia may contribute to the risk of postpartum hypertension by stimulating sodium retention (Makris 2004).

Postpartum hypertension may represent a continuation of an antenatal hypertensive disorder (regardless of type), or the appearance of a new hypertensive disorder after delivery. Although it is recognised that antenatal hypertension may continue into the postpartum period, the incidence with which this occurs and for what duration, have been poorly defined. For clarification, hypertension is defined as a blood pressure of 140/90 mmHg or more. Mild-to-moderate hypertension is usually defined as a blood pressure of 140 to 169/90 to 109 mmHg, and severe hypertension as 170/110 mmHg or more. Hypertension in pregnancy (or the puerperium) is classified as: pre-existing hypertension (defined as that which antedated pregnancy or appeared before 20 weeks' gestation); gestational hypertension without proteinuria (defined as hypertension that appeared at or after 20 weeks, with less than 0.3 grams/day of urinary protein); gestational hypertension with proteinuria (also known as 'pre-eclampsia' or 'toxaemia'); or pre-eclampsia superimposed on pre-existing hypertension. Eclampsia is included in the pre-eclampsia category, and is defined as an otherwise unexplained seizure in a woman with pre-eclampsia.

 

Prevention of postpartum hypertension for high-risk groups

Women delivered with pre-eclampsia appear to be at increased risk of postpartum hypertension (Tan 2002). This was recognized by JS Henry in 1936, who pointed out that, "... in toxaemic patients, the postpartum fall [in blood pressure] to normal is very variable, but is apt to take longer in eclamptics and in pre-eclamptics" (Henry 1936). In the no treatment arm of a randomised controlled trial comparing furosemide with no treatment, 26% of women with pre-eclampsia were observed to be on antihypertensive therapy at the time of hospital discharge (Ascarelli 1999). An observational study of 67 women with either proteinuric or non-proteinuric gestational hypertension found that 50% of women had a blood pressure greater than 150/100 mmHg on day five postpartum (Walters 1987). In women who develop pre-eclampsia antenatally, postnatal hypertension lasted approximately two weeks (mean ± standard deviation (SD) of 16 ± 9.5 days). Although blood pressure dropped significantly in the first two weeks postpartum, there was substantial variability between women (Bowler 2002; Ferrazzani 1994). Women at increased risk for recurrence of hypertension after delivery were those who delivered preterm, and those multiparous women with higher uric acid levels or blood urea nitrogen (Ferrazzani 1994). In a study of 80 women with pregnancy-induced hypertension, the risk of developing postpartum morbidity increased with higher levels of urinary albumin and urinary immunoglobulin G (IgG), measured in the antepartum and intrapartum periods. In this study, postpartum morbidity was defined as one or more of the following: (1) need for greater than 24 hours of maternal postpartum intensive care or parenteral magnesium sulphate administration; (2) need for postpartum parenteral antihypertensive medication for blood pressure greater than 160/110 mmHg; (3) postpartum blood pressure of greater than 140/90 for more than three days; and/or (4) need for oral antihypertensive medication at the time of hospital discharge (Eden 1986).

Compared with women with pre-eclampsia, fewer women with gestational hypertension appear to have postpartum hypertension. Also, the duration of this hypertension appeared to be shorter (mean ± SD of six days, SD 5.5 days) than in women with pre-eclampsia. Again, the duration was highly variable (Ferrazzani 1994). Multiparous women with higher uric acid and blood urea nitrogen appeared to be at higher risk (Ferrazzani 1994).

It is not known whether or not antihypertensives should be routinely re-instituted postpartum among women with antenatal hypertension in order to prevent postpartum hypertension. No international guidelines give guidance in this regard.

 

Treatment of postpartum hypertension

The incidence of de novo postpartum hypertension has also been poorly defined. In an observational study of 136 primarily Caucasian women who were normotensive antenatally, 12% had a diastolic blood pressure (dBP) greater than 100 mmHg during the first five postpartum days, with an average rise in blood pressure of 6 mmHg systolic and 4 mmHg diastolic (Walters 1986). In contrast, postpartum hypertension occurred in only 3.5% of 210 Nigerian women who were normotensive during pregnancy. However, excluded were women who were hypertensive within 48 hours of delivery. Of note, is the fact that of the two thirds of women who became hypertensive within six weeks postpartum, 70% did so between days two and seven postpartum (Ojugwu 1993). Long-term follow-up was available for only 35 of the women (17%), most of whom developed gestational hypertension (N = 8) or recurrent isolated postpartum hypertension (N = 17) in subsequent pregnancies. Finally, in a case-control study of women readmitted to hospital with postpartum pre-eclampsia after a normotensive pregnancy (versus controls who were normotensive throughout pregnancy and the postpartum period), a rise in mean arterial pressure of more than 10 mmHg between the intrapartum and postpartum periods was associated with a greater than threefold increased risk of readmission postpartum with severe pre-eclampsia or eclampsia (Atterbury 1996).

For manifest postpartum hypertension, there is general consensus that severe hypertension should be treated (to prevent acute maternal vascular complications such as stroke), but no such consensus exists for mild-moderate postpartum hypertension (whether de novo or not and regardless of type), needs to be treated. The Canadian Hypertension Society recommends treatment for women with severe hypertension or symptoms, and those with target organ damage and moderate gestational hypertension (i.e., dBP greater than 99 mmHg) three days after delivery (Rey 1997). The American and Australasian guidelines acknowledge the postnatal rise in blood pressure and the possibility that antihypertensive medication may need to be increased in women with antenatal (even chronic) hypertension, but they make no specific recommendations about when treatment should be started and what the therapeutic goal should be (Brown 2000; NHBPEPWG 2000).

Despite widespread use of antihypertensives in the postpartum period, there is limited evidence to support their safety for babies of breastfeeding mothers. A review of the available observational literature (37 reports covering 41 different antihypertensives) concluded that the following drugs have minimal milk to maternal plasma ratios to make breastfeeding acceptable: methyldopa, beta-blockers with high protein binding (e.g., oxprenolol), angiotensin converting enzyme inhibitors and some dihydropyridine calcium channel blockers (Beardmore 2002). All of these drugs are used commonly in the postpartum period.

This review focuses on the benefits and risks of antihypertensive therapy for the prevention or treatment of postpartum hypertension. We will not address other therapeutic approaches (e.g., postpartum curettage) (Hunter 1961; Magann 1993; Magann 1994; Robinson 1964) or magnesium sulphate therapy (Livingston 2003; Ehrenberg 2006).

 

Objectives

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

To assess the relative benefits and risks of interventions to prevent postpartum hypertension, by assessing whether or not 'routine' postpartum administration of oral antihypertensive therapy is better than placebo/no treatment.

To assess the relative benefits and risks of treatment of postpartum hypertension by assessing whether or not:
(i) oral antihypertensive therapy is better than placebo/no therapy for mild-moderate postpartum hypertension; and
(ii) one antihypertensive agent offers any advantages over another for either mild-moderate or severe postpartum hypertension.

 

Methods

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms
 

Criteria for considering studies for this review

 

Types of studies

Randomised controlled trials. Quasi-random designs were excluded.

 

Types of participants

Women with either:
(i) an antenatal hypertensive disorder of pregnancy; or
(ii) women with de novo postpartum hypertension.

Postpartum hypertension was defined as an elevated blood pressure (140/90 mmHg or more) measured twice at least four hours apart, between delivery and six weeks postpartum.

 

Types of interventions

 

For prevention of postpartum hypertension

Comparisons of:
(i) routine postpartum antihypertensive therapy versus placebo/no therapy;
(ii) routine postpartum antihypertensive therapy of one agent versus another.

 

For treatment of postpartum hypertension

Comparisons of:
(i) oral antihypertensive agents with placebo or no therapy; or
(ii) oral antihypertensive agent(s) versus another.

Any pharmacological therapy that was given to reduce blood pressure was acceptable for this review, and was considered as a source of between-trial heterogeneity in outcome. Also recorded were other aspects of postpartum management, including use of non-steroidal anti-inflammatories (NSAIDs), bromocriptine, and/or ergot alkaloids. Interventions used to treat the syndrome of pre-eclampsia (e.g., endometrial curettage) were not included in the review.

 

Types of outcome measures

 

Primary outcomes

 
Maternal outcomes

Measures that evaluated the effectiveness and safety of antihypertensive therapy for the woman:

  • stroke (acute neurological deficit of vascular origin, which lasts more than 48 hours);
  • maternal mortality;
  • severe hypertension (blood pressure of greater than or equal to 170/110 for four hours or more);
  • eclampsia, haemolysis;
  • elevated liver enzymes;
  • low platelets syndrome;
  • the need for additional antihypertensive therapy (according to criteria defined by respective researchers);
  • the need to change therapy due to maternal side-effects of antihypertensive therapy;
  • maternal hypotension
  • duration of postpartum hospital stay (days);
  • incidence of readmission to hospital after discharge postpartum;
  • measures of maternal anxiety or well-being as defined by respective researchers.

Measures not prespecified were:

  • Maternal end-organ failure (any);
  • Use of NSAIDs for postpartum analgesia;
  • Maternal side effects to antihypertensive medication;
  • Severe maternal hypotension.

 

Secondary outcomes

 
Breastfeeding and neonatal outcomes

  • Proportion of mothers who breastfed their babies and among them, neonatal side-effects such as:

  • bradycardia;
  • hypotension;
  • hypothermia;
  • hypoglycaemia, as defined by respective researchers.

 

Search methods for identification of studies

 

Electronic searches

We searched the Cochrane Pregnancy and Childbirth Group’s Trials Register by contacting the Trials Search Co-ordinator (31 January 2013). 

The Cochrane Pregnancy and Childbirth Group’s Trials Register is maintained by the Trials Search Co-ordinator and contains trials identified from: 

  1. monthly searches of the Cochrane Central Register of Controlled Trials (CENTRAL);
  2. weekly searches of MEDLINE;
  3. weekly searches of EMBASE;
  4. handsearches of 30 journals and the proceedings of major conferences;
  5. weekly current awareness alerts for a further 44 journals plus monthly BioMed Central email alerts.

Details of the search strategies for CENTRAL, MEDLINE and EMBASE, the list of handsearched journals and conference proceedings, and the list of journals reviewed via the current awareness service can be found in the ‘Specialized Register’ section within the editorial information about the Cochrane Pregnancy and Childbirth Group

Trials identified through the searching activities described above are each assigned to a review topic (or topics). The Trials Search Co-ordinator searches the register for each review using the topic list rather than keywords.  

For previous versions of this review, we searched PubMed (2002 to 2009) and MEDLINE (1966 to May 2003), EMBASE (1980 to January 2003) using the search strategies listed in Appendix 1 and Appendix 2.

 

Searching other resources

We searched the bibliographies of retrieved papers and personal files.

We did not apply any language restrictions.

 

Data collection and analysis

For methods used in previous versions of this review see Appendix 3. For this 2013 update, the following methods were used.

 

Selection of studies

Two review authors independently assessed for inclusion all the potential studies we identified as a result of the search strategy. We resolved any disagreement through discussion, or, if required, we consulted a third person.

 

Data extraction and management

We designed a form to extract data. For eligible studies, at least two review authors (S Sadeghi and LA Magee (LAM), or LAM and P von Dadelszen) extracted the data using the agreed form. We resolved discrepancies through discussion or, if required, we consulted a third person. For this update, data were entered into Review Manager (RevMan 2012) software and checked for accuracy.

When information regarding any of the above was unclear, we attempted to contact authors of the original reports to provide further details.

 

Assessment of risk of bias in included studies

Two review authors independently assessed risk of bias for each study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). Any disagreement was resolved by discussion or by involving a third assessor.

 

(1) Sequence generation (checking for possible selection bias)

We have described for each included study, the method used to generate the allocation sequence in sufficient detail to allow an assessment of whether it should have produced comparable groups.

We assessed the method as:

  • low risk of bias (any truly random process, e.g., random number table; computer random number generator);
  • high risk of bias (any non-random process, e.g., odd or even date of birth; hospital or clinic record number);
  • unclear risk of bias.

 

(2) Allocation concealment (checking for possible selection bias)

We have described for each included study the method used to conceal the allocation sequence in sufficient detail and determine whether intervention allocation could have been foreseen in advance, or during recruitment, or changed after assignment.

We assessed the methods as:

  • low risk of bias (e.g., telephone or central randomisation; consecutively numbered sealed opaque envelopes);
  • high risk of bias (open random allocation; unsealed or non-opaque envelopes, alternation; date of birth);
  • unclear risk of bias.

 

(3.1) Blinding (checking for possible performance bias)

We have described for each included study the methods used, if any, to blind study participants and personnel from knowledge of which intervention a participant received. Studies were judged at low risk of bias if they were blinded, or we judged that the lack of blinding could not have affected the results. Blinding was assessed separately for different outcomes or classes of outcomes.

We assessed the methods as:

  • low, high or unclear risk of bias for participants;
  • low, high or unclear risk of bias for personnel.

 

(3.2) Blinding (checking for possible detection bias)

We have described for each included study the methods used, if any, to blind outcome assessors from knowledge of which intervention a participant received. We planned to assess blinding separately for different outcomes or classes of outcomes.

We assessed the methods used to blind outcome assessment as:

  • low, high or unclear risk of bias.

 

(4) Incomplete outcome data (checking for possible attrition bias through withdrawals, dropouts, protocol deviations)

We have described for each included study, and for each outcome or class of outcomes, the completeness of data including attrition and exclusions from the analysis. We have stated whether attrition and exclusions were reported, the numbers included in the analysis at each stage (compared with the total randomised participants), reasons for attrition or exclusion where reported, and whether missing data were balanced across groups or were related to outcomes. Where sufficient information was reported, or could be supplied by the trial authors, we re-included missing data in the analyses which we undertook.

We assessed methods as:

  • low risk of bias (e.g. no missing outcome data; missing outcome data balanced across groups; less than 2.5% of women were excluded from the analysis);
  • high risk of bias (e.g. numbers or reasons for missing data imbalanced across groups; "as treated" analysis done with substantial departure of intervention received from that assigned at randomisation);
  • unclear risk of bias.

 

(5) Selective reporting bias

We have described for each included study how we investigated the possibility of selective outcome reporting bias and what we found.

We assessed the methods as:

  • low risk of bias (where it was clear that all of the study’s pre-specified outcomes and all expected outcomes of interest to the review were reported);
  • high risk of bias (where not all of the study’s pre-specified outcomes were reported; one or more reported primary outcome(s) was(were) not pre-specified; outcomes of interest were reported incompletely and so cannot be used; study failed to include results of a key outcome that would have been expected to have been reported);
  • unclear risk of bias.

 

(6) Other sources of bias

We described for each included study any important concerns we had about other possible sources of bias.

We assessed whether each study was free of other problems that could put it at risk of bias:

  • low risk of other bias;
  • high risk of other bias;
  • unclear whether there is risk of other bias.

 

(7) Overall risk of bias

We made explicit judgments about whether studies were at high risk of bias, according to the criteria given in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). With reference to (1) to (6) above, we assessed the likely magnitude and direction of the bias and whether we considered it likely to impact on the findings.

 

Measures of treatment effect

 

Dichotomous data

For dichotomous data, we presented results as summary risk ratio with 95% confidence intervals.

 

Continuous data

No trials provided continuous data. In future updates, if continuous data are analysed, we will use the mean difference if outcomes are measured in the same way between trials. We will use the standardised mean difference to combine trials that measure the same outcome, but use different methods.

 

Unit of analysis issues

 

Cluster-randomised trials

In future updates, if identified and eligible for inclusion, we will include cluster-randomised trials in the analyses along with individually-randomised trials. We will adjust their sample sizes using the methods described in the Cochrane Handbook for Systematic Reviews of Interventions using an estimate of the intracluster correlation co-efficient (ICC) derived from the trial (if possible), from a similar trial or from a study of a similar population. If we use ICCs from other sources, we will report this and conduct sensitivity analyses to investigate the effect of variation in the ICC. If we identify both cluster-randomised trials and individually-randomised trials, we plan to synthesise the relevant information. We will consider it reasonable to combine the results from both if there is little heterogeneity between the study designs and the interaction between the effect of intervention and the choice of randomisation unit is considered to be unlikely. We will also acknowledge heterogeneity in the randomisation unit and perform a sensitivity analysis to investigate the effects of the randomisation unit.

 

Cross-over Trials

Cross-over trials were excluded from this review.

 

Other unit of analysis issues

None identified.

 

Dealing with missing data

For included studies, levels of attrition were noted.

For all outcomes, analyses were carried out, as far as possible on an intention-to-treat basis (i.e., we attempted to include all participants randomised to each group in the analyses). The denominator for each outcome in each trial was the number randomised minus any participants whose outcomes were known to be missing.

 

Assessment of heterogeneity

We assessed statistical heterogeneity in each meta-analysis using the T², I² and Chi² statistics. We regarded heterogeneity as substantial if the I² was greater than 50% and either the T² was greater than zero, or there was a low P value (< 0.10) in the Chi² test for heterogeneity.

 

Assessment of reporting biases

There were too few studies included and too few outcomes reported to assess the impact of potential reporting bias on outcomes. In future updates, if more studies are included, we will assess reporting biases.

If there are 10 or more studies in the meta-analysis, we will investigate reporting biases (such as publication bias) using funnel plots. We will assess funnel plot asymmetry visually.

 

Data synthesis

We carried out statistical analysis using the Review Manager software (RevMan 2012). We used fixed-effect inverse variance meta-analysis for combining data where trials examined the same intervention, and the trials’ populations and methods were judged sufficiently similar. Where we suspected clinical or methodological heterogeneity between studies sufficient to suggest that treatment effects may differ between trials, we used random-effects meta-analyses. The random-effects summary was treated as the average range of possible treatment effects. If the average treatment effect was not clinically meaningful, we did not combine trials.

If we used random-effects analyses, the results were presented as the average treatment effect with 95% confidence intervals, and the estimates of T² and I².

 

Subgroup analysis and investigation of heterogeneity

If we identified substantial heterogeneity, we investigated it using the following subgroup analyses:

  • type of agent used to prevent postpartum hypertension (i.e., furosemide versus an antihypertensive);
  • treatment of mild-to-moderate versus severe postpartum hypertension.

The following outcomes were used in subgroup analyses:

  • maternal death;
  • maternal organ failure;
  • severe hypotension;
  • antihypertensive use in hospital;
  • and antihypertensive use at hospital discharge.

We assessed subgroup differences by interaction tests available within RevMan (RevMan 2012). We reported the results of subgroup analyses quoting the χ2 statistic and P value, and the interaction test I² value.

 

Sensitivity analysis

We planned to carry out sensitivity analyses to explore the effect of trial quality assessed by concealment of allocation, high attrition rates, or both, with poor quality studies being excluded from the analyses in order to assess whether this made any difference to the overall result. Poor quality was defined as studies being at high risk of bias for allocation concealment, or incomplete outcome data, or both.

 

Results

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms
 

Description of studies

See: Characteristics of included studies; Characteristics of excluded studies; Characteristics of ongoing studies.

 

Included studies

Nine trials were included.

See Characteristics of included studies.

 

Prevention of postpartum hypertension

Four trials studied (358 women) interventions for prevention of postpartum hypertension in women with antenatal pre-eclampsia (defined as pregnancy-induced hypertension with either proteinuria or adverse features such as haemolysis, elevated liver enzymes, low platelets syndrome). Women with pre-existing hypertension were excluded from one trial and those with chronic kidney disease from another.

Two trials (282 women) compared routine postnatal furosemide therapy (20 to 40 mg orally per day, for five to seven days) with either placebo or no therapy. In one trial (Ascarelli 2005), 20 mEq orally per day of supplemental potassium was administered, and in the other (Matthews 1997), intravenous magnesium sulphate was given if the woman was considered to be at 'high risk' of eclampsia. Neither trial reported mean and standard deviation (SD) of baseline blood pressure, but one trial (Matthews 1997) reported the change in blood pressure (BP) on days one, three and seven after delivery (i.e., -6.5 mmHg (furosemide) versus -3.5 (placebo) on day one, -10.6 (furosemide) versus -9.75 (placebo) on day three, and -11.5 (furosemide) versus -7.8 (placebo) on day seven). Follow-up ranged from day 10 postpartum (Ascarelli 2005) to six weeks postpartum (Matthews 1997).

A third trial (31 women) compared nifedipine capsules (10 mg orally every four hours for 48 hours) with placebo (Barton 1990). Women had mild hypertension at baseline, and at 18 to 24 hours following delivery, mean (±SD) diastolic BP was 93.9 ± 1.6 mmHg (nifedipine) versus 100.2 ± 2.6 (placebo). All women in this trial were on magnesium sulphate. Women were followed until hospital discharge.

A fourth trial (45 women) compared L-arginine (a nitric oxide donor) with placebo. Women had pre-eclampsia antenatally or postnatally and a mean pre-treatment BP of 169 ± 15mmHg systolic and 105 ± 8mmHg diastolic at a mean gestational age of 34.7 ± 4.0 weeks. Women received L-arginine before delivery and for three days postpartum; most women (30/45) were treated only postpartum. Women were followed to day three and day 10 postpartum.

No trials were identified that compared routine postpartum administration of one antihypertensive agent versus another.

 

Treatment of postpartum hypertension

No trials were identified that compared antihypertensive therapy with placebo/no therapy.

Five trials (480 women) studied treatment of postpartum hypertension by comparing different oral antihypertensive agents.

Women in these trials were hypertensive postpartum, but the nature of the hypertensive disorder was not well described, and included both women who were normotensive ante and intrapartum, and those who had severe antenatal pre-eclampsia. Diastolic BP was moderate to severe in nature. Approximately half of the women delivered their first child in the two trials that reported parity. Women with comorbid conditions were usually excluded, due to pre-existing hypertension (Griffis 1989; Walss Rodriguez 1991), renal disease (Fidler 1992; Walss Rodriguez 1991), hepatic dysfunction (Griffis 1989), need for intensive care (Walss Rodriguez 1991), or diabetes or multiple pregnancy (Fidler 1992). One trial reported a average gestational age at delivery which was at term [38.6 ± 1.26 (nifedipine sublingual) versus 37.6 ± 2.4 (hydralazine sublingual)] (Walss Rodriguez 1991). Another reported an average gestational age at delivery that was preterm [33.2 ± 4.1 (methyldopa) versus 33.5 ± 4.3 (nifedipine)] (Sayin 2005).

Five trials compared one oral antihypertensive agent with another. In three trials, methyldopa was compared with either timolol (Fidler 1992), hydralazine (Griffis 1989), or nifedipine (oral) (Sayin 2005). In two trials, hydralazine (parenteral) was compared with either nifedipine (sublingual) (Walss Rodriguez 1991) or labetalol (iv) (Vigil-De Gracia 2007). Follow-up appeared to occur until hospital discharge (Griffis 1989; Sayin 2005; Vigil-De Gracia 2007; Walss Rodriguez 1991) or until two to six weeks postpartum (Fidler 1992).

 

Excluded studies

Twenty trials were excluded based on: applying a surgical intervention (i.e., endometrial curettage), incomplete information about clinical outcomes, failure to report outcomes among women treated only postpartum, or the absence of abstractable data on clinical outcomes. See Characteristics of excluded studies.

 

Risk of bias in included studies

All included trials were small, with a median sample size of 45 women (range 18 to 264). The quality of the trials was poor. No trials reported the potential co-intervention of non-steroidal anti-inflammatory drug (NSAID) use for postnatal analgesia.

See Figure 1 and Figure 2 for summaries of 'Risk of bias' assessment.

 FigureFigure 1. 'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.
 FigureFigure 2. 'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.

 

Allocation

Four trials described a random component in the sequence generation process. Four trials described adequate concealment of allocation.

 

Blinding

Three of the nine trials reported outcome assessment blinding and most outcomes included data from only one trial.

 

Incomplete outcome data

There was adequate follow-up (less than 2.5% loss to follow-up) in all but one trial.

 

Selective reporting

Only two trials were deemed to be at low risk of bias for selective reporting. The risk of bias was unclear for five of the nine trials; they were published prior to the year 2000 and, as such, did not have published study protocols with which to compare reported outcomes in the manuscripts. One trial did not describe all pre-specified outcomes and another did not report all outcomes according to randomised group.

 

Other potential sources of bias

No other sources of bias were identified.

 

Effects of interventions

Nine trials are included.

 

(A) Routine postnatal antihypertensive therapy in women with antenatal pre-eclampsia, in order to prevent postpartum hypertension

Four trials (358 women) compared routine antihypertensive therapy (furosemide, nifedipine capsules, or L-arginine) with an approach that dictated antihypertensive treatment only for severely elevated blood pressure postpartum. There are insufficient data for any conclusions about the possible benefits and harms of these management strategies.

There were no maternal deaths ( Analysis 1.1), serious maternal morbidity ( Analysis 1.2), or severe maternal hypotension reported ( Analysis 1.3) but the data are limited and not consistent with either benefit or risk.

With use of routine postnatal furosemide, there was a strong trend for a decrease in the need for additional antihypertensive therapy (for blood pressure 150 systolic or 100 diastolic, or higher) on the postnatal wards (risk ratio (RR) 0.74, 95% confidence interval (CI) 0.55 to 1.00; one trial, N = 264 women) ( Analysis 1.5). The direction of effect was the same for antihypertensive therapy at hospital discharge but the results were not statistically significant (RR 0.81, 95% CI 0.59 to 1.12; two trials, N = 282 women) ( Analysis 1.6.1). The mean number of medical attendances during hospitalisation did not differ between the furosemide (14.9 attendances) and control (18.0 attendances) groups in one trial (Matthews 1997); however, statistical comparisons were not possible because standard deviations were not reported. Mean postnatal hospital stay did not appear to differ in one trial (7.3 versus 7.6 days) but SD were not reported (Matthews 1997).

The trial of routine nifedipine capsules reported no significant difference in the occurrence of severe hypertension treatment between groups, but data were not provided (Barton 1990). The trial of L-arginine versus placebo did not find a between-group difference in severe hypertension (or use of antihypertensive therapy on day three postpartum).

None of the 31 women in the nifedipine versus placebo trial changed drugs due to side-effects ( Analysis 1.7).

No differences between subgroups were observed ( Analysis 1.6).

None of the aforementioned trials reported: whether or not women used NSAIDs for postpartum analgesia, the incidence of adverse drug reactions, or the incidence of breastfeeding.

 

(B) Antihypertensive therapy for women with postpartum hypertension

No trials were located that compared antihypertensive with placebo or no therapy for mild-to-moderate postpartum hypertension, of any type.

For treatment of mild-moderate postpartum hypertension, three trials (189 women) compared timolol, hydralazine (oral), or nifedipine (oral) with methyldopa. Magnesium sulphate therapy was administered for 12 hours postpartum in one trial (Griffis 1989). There were no maternal deaths ( Analysis 2.1). The need for additional antihypertensive therapy did not differ between the groups (average RR 0.92, 95% CI 0.20 to 4.20; three trials, 189 women; heterogeneity: Tau² = 0.75; Chi² = 2.09, df = 1 (P = 0.15); I² = 52%); however, the trials were more different in their effects than could be expected by chance alone ( Analysis 2.3). The need to change drugs due to side-effects was infrequent ( Analysis 2.4).

For treatment of severe postpartum hypertension, two trials (120 women) compared intravenous hydralazine with either sublingual nifedipine (Walss Rodriguez 1991) or intravenous labetalol (Vigil-De Gracia 2007). Magnesium sulphate therapy was given for 24 hours postpartum in one trial (Vigil-De Gracia 2007). There were no maternal deaths and no reported maternal hypotension (Vigil-De Gracia 2007) ( Analysis 2.1) ( Analysis 2.2). The need for additional antihypertensive therapy did not differ between groups (average RR 0.58, 95% CI 0.04 to 9.07; two trials, 120 women; heterogeneity: Tau² = 2.24; Chi² = 2.21, df = 1 (P = 0.14); I² = 55%), but the trials were not consistent in their effects ( Analysis 2.3). The need to change drugs due to side-effects was not reported.

No differences between subgroups were observed ( Analysis 2.3).

None of these trials reported whether or not women used NSAIDs for postpartum analgesia.

 

Discussion

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

From the few trials that focused on the prevention or management of postpartum hypertension, there are insufficient data for any reliable conclusions to be drawn about the relative benefits and risks of different management strategies.

 

Prevention of postpartum hypertension

For women with antenatal hypertension, even that of pre-eclampsia, there is a strong trend towards reduced use of antihypertensive therapy in hospital with use of routine postnatal furosemide (with routine potassium supplementation). It is unclear whether there may be other potential benefits (e.g., reduced antihypertensive use at hospital discharge and/or length of maternal hospital stay) or potential harms (e.g., on breastfeeding).

 

Treatment of postpartum hypertension

For women with manifest postpartum hypertension (whether or not they were hypertensive before delivery), there are no data that inform whether or not mild-to-moderate hypertension should be treated, and if so, whether or not one agent is preferable to another. Certainly, two of the agents studied (timolol and methyldopa) are not in common usage postpartum. Regardless of the approach taken, the currently evaluated antihypertensive therapies appear to be associated with few women changing drugs due to maternal side-effects.

 

Authors' conclusions

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

 

Implications for practice

For women with pre-eclampsia, postnatal furosemide may decrease the need for postnatal antihypertensive therapy in hospital, but more data are needed on substantive outcomes before this practice can be recommended. There are no reliable data to guide management of women who are hypertensive postpartum. Any antihypertensive agent used should be based on a clinician's familiarity with the drug. Given that peak postpartum blood pressure occurs on days three to six postpartum, clinicians should be aware that peaks may occur after hospital discharge and, therefore, may be missed unless close follow up is ensured.

 
Implications for research

Future trials of prevention of postpartum hypertension or treatment of mild-moderate postpartum hypertension should randomise women to an antihypertensive medication versus placebo, before comparing one antihypertensive agent with another. All trials should include information about use of non-steroidal anti-inflammatories after delivery, and examine the following relevant clinical endpoints: severe maternal hypertension, breastfeeding, hospital length of stay, and maternal satisfaction with care.

 

Acknowledgements

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

We would like to thank Susan Sadeghi for her work as an author on previous versions of this review.

 

Data and analyses

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms
Download statistical data

 
Comparison 1. Routine postnatal oral antihypertensive therapy for prevention of postpartum hypertension

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 Maternal death2295Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    1.1 Furosemide versus placebo/no therapy
1264Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    1.2 Routine antihypertensive versus placebo
131Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 2 Maternal organ failure1264Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    2.1 Furosemide versus placebo/no therapy
1264Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 3 Severe hypotension131Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    3.1 Routine antihypertensive versus placebo
131Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 4 Severe hypertension145Risk Ratio (M-H, Fixed, 95% CI)0.91 [0.60, 1.39]

    4.1 L-arginine vs. placebo
145Risk Ratio (M-H, Fixed, 95% CI)0.91 [0.60, 1.39]

 5 Postnatal antihypertensive use in hospital1264Risk Ratio (M-H, Fixed, 95% CI)0.74 [0.55, 1.00]

    5.1 Furosemide versus placebo/no therapy
1264Risk Ratio (M-H, Fixed, 95% CI)0.74 [0.55, 1.00]

 6 Postnatal antihypertensive use at hospital DISCHARGE3325Risk Ratio (M-H, Fixed, 95% CI)0.79 [0.58, 1.08]

    6.1 Furosemide vs. placebo/no therapy
2282Risk Ratio (M-H, Fixed, 95% CI)0.81 [0.59, 1.12]

    6.2 L-arginine vs. placebo
143Risk Ratio (M-H, Fixed, 95% CI)0.64 [0.21, 1.94]

 7 Medication changed secondary to maternal side-effects131Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    7.1 Routine antihypertensive versus placebo
131Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 
Comparison 2. Oral antihypertensive therapy for treatment of postpartum hypertension

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 Maternal death2106Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    1.1 Antihypertensive agent versus another for mild-moderate postpartum hypertension
2106Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 2 Maternal hypotension182Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

    2.1 Antihypertensive agent versus another for severe postpartum hypertension
182Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 3 Need for additional antihypertensive therapy5309Risk Ratio (M-H, Random, 95% CI)0.70 [0.25, 1.96]

    3.1 Antihypertensive agent versus another for mild-moderate postpartum hypertension
3189Risk Ratio (M-H, Random, 95% CI)0.92 [0.20, 4.20]

    3.2 Antihypertensive agent versus another for severe postpartum hypertension
2120Risk Ratio (M-H, Random, 95% CI)0.58 [0.04, 9.07]

 4 Medication changed secondary to maternal side-effects2106Risk Ratio (M-H, Fixed, 95% CI)0.5 [0.05, 5.30]

    4.1 Antihypertensive agent versus another for mild-moderate postpartum hypertension
2106Risk Ratio (M-H, Fixed, 95% CI)0.5 [0.05, 5.30]

   4.2 Antihypertensive therapy for severe postpartum hypertension
00Risk Ratio (M-H, Fixed, 95% CI)0.0 [0.0, 0.0]

 

Appendices

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms
 

Appendix 1. Search strategy for PubMed

PubMed (2002-2009) (Search carried out by authors):

(pregnancy complications (MeSH) OR pregnancy (MeSH) AND (hypertension) AND (postpartum OR postnatal OR puerperal OR puerperium)

 

Appendix 2. Search strategy used in previous version of the review

MEDLINE (1966 to May 2003) and EMBASE (1980 to January 2003) (Search carried out by authors):

("pregnancy complications" OR "pregnancy") AND ("hypertension") AND ("postpartum" OR "postnatal" OR "puerperal" OR "puerperium"

 

Appendix 3. Methods used in previous versions of this review

 

Selection of studies

Two review authors independently assessed for inclusion all the potential studies we identified as a result of the search strategy. We resolved any disagreement through discussion, or, if required, we consulted a third person.

 

Data extraction and management

We designed a form to extract data. For eligible studies, at least two review authors (S Sadeghi and LA Magee (LAM), or LAM and P von Dadelszen) extracted the data using the agreed form. We resolved discrepancies through discussion or, if required, we consulted a third person. Data were entered into Review Manager (RevMan 2008) software and checked for accuracy.

When information regarding any of the above was unclear, we attempted to contact authors of the original reports to provide further details.

 

Assessment of risk of bias in included studies

Two review authors independently assessed risk of bias for each study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2008). Any disagreement was resolved by discussion or by involving a third assessor.

 

(1) Sequence generation (checking for possible selection bias)

We have described for each included study, the method used to generate the allocation sequence in sufficient detail to allow an assessment of whether it should have produced comparable groups.

We assessed the method as:

  • adequate (any truly random process, e.g., random number table; computer random number generator);
  • inadequate (any non-random process, e.g., odd or even date of birth; hospital or clinic record number); or
  • unclear.

 

(2) Allocation concealment (checking for possible selection bias)

We have described for each included study the method used to conceal the allocation sequence in sufficient detail and determine whether intervention allocation could have been foreseen in advance, or during recruitment, or changed after assignment.

We assessed the methods as:

  • adequate (e.g., telephone or central randomisation; consecutively numbered sealed opaque envelopes);
  • inadequate (open random allocation; unsealed or non-opaque envelopes, alternation; date of birth);
  • unclear.

 

(3) Blinding (checking for possible performance bias)

We have described for each included study the methods used, if any, to blind study participants and personnel from knowledge of which intervention a participant received. Studies were judged at low risk of bias if they were blinded, or we judged that the lack of blinding could not have affected the results. Blinding was assessed separately for different outcomes or classes of outcomes.

We assessed the methods as:

  • adequate, inadequate or unclear for participants;
  • adequate, inadequate or unclear for personnel;
  • adequate, inadequate or unclear for outcome assessors.

 

(4) Incomplete outcome data (checking for possible attrition bias through withdrawals, dropouts, protocol deviations)

We have described for each included study, and for each outcome or class of outcomes, the completeness of data including attrition and exclusions from the analysis. We have stated whether attrition and exclusions were reported, the numbers included in the analysis at each stage (compared with the total randomised participants), reasons for attrition or exclusion where reported, and whether missing data were balanced across groups or were related to outcomes. Where sufficient information was reported, or could be supplied by the trial authors, we re-included missing data in the analyses which we undertook.

We assessed methods as:

  • adequate (i.e., less than 2.5% of women were excluded from the analysis);
  • inadequate; or
  • unclear.

 

(5) Selective reporting bias

We have described for each included study how we investigated the possibility of selective outcome reporting bias and what we found.

We assessed the methods as:

  • adequate (where it was clear that all of the study’s pre-specified outcomes and all expected outcomes of interest to the review were reported);
  • inadequate (where not all of the study’s pre-specified outcomes were reported; one or more reported primary outcome(s) was(were) not pre-specified; outcomes of interest were reported incompletely and so cannot be used; study failed to include results of a key outcome that would have been expected to have been reported); or
  • unclear.

 

(6) Other sources of bias

We described for each included study any important concerns we had about other possible sources of bias.

We assessed whether each study was free of other problems that could put it at risk of bias:

  • yes;
  • no; or
  • unclear.

 

(7) Overall risk of bias

We made explicit judgments about whether studies were at high risk of bias, according to the criteria given in the Handbook (Higgins 2008). With reference to (1) to (6) above, we assessed the likely magnitude and direction of the bias and whether we considered it likely to impact on the findings.

 

Measures of treatment effect

 

Dichotomous data

For dichotomous data, we presented results as summary risk ratio with 95% confidence intervals.

 

Continuous data

We had no continuous data.

 

Dealing with missing data

For included studies, levels of attrition were noted.

For all outcomes, analyses carried out, as far as possible, were on an intention-to-treat basis (i.e., we attempted to include all participants randomised to each group in the analyses). The denominator for each outcome in each trial was the number randomised minus any participants whose outcomes were known to be missing.

 

Assessment of heterogeneity

We used the I2 statistic to measure heterogeneity among the trials in each analysis. If we identified substantial heterogeneity (i.e., I2 greater than 50%), we explored it by pre-specified subgroup analysis.

 

Assessment of reporting biases

 

Assessment of reporting biases

There were too few studies included and too few outcomes reported to assess the impact of potential reporting bias on outcomes.

 

Data synthesis

 

Data synthesis

We carried out statistical analysis using the Review Manager software (RevMan 2008). We used fixed-effect inverse variance meta-analysis for combining data where trials examined the same intervention, and the trials’ populations and methods were judged sufficiently similar. Where we suspected clinical or methodological heterogeneity between studies sufficient to suggest that treatment effects may differ between trials, we used random-effects meta-analyses.

If substantial heterogeneity was identified in a fixed-effect meta-analysis, this was noted and the analysis repeated using a random-effects method.

 

Subgroup analysis and investigation of heterogeneity

We planned to carry out the following subgroup analyses:

  • type of agent used to prevent postpartum hypertension (i.e., furosemide versus an antihypertensive);
  • treatment of mild to moderate versus severe postpartum hypertension.

The following outcomes were used in the subgroup analyses: maternal death, maternal organ failure, severe hypotension, antihypertensive use in hospital, and antihypertensive use at hospital discharge.

For fixed-effect meta-analyses, we conducted planned subgroup analyses classifying whole trials by interaction tests as described by Deeks 2001. For random-effects meta-analyses, we assessed differences between subgroups by inspection of the subgroups’ confidence intervals; non-overlapping confidence intervals indicated a statistically significant difference in treatment effect between the subgroups.

 

What's new

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

Last assessed as up-to-date: 12 February 2013.


DateEventDescription

12 February 2013New search has been performedSearch updated. Incorporated new data from one trial (Hladunewich 2006), and revised the results and discussion, accordingly.

Excluded one trial (Jia 2007). Methods updated.

12 February 2013New citation required but conclusions have not changedIncorporated data from one trial.



 

History

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

Protocol first published: Issue 3, 2003
Review first published: Issue 1, 2005


DateEventDescription

1 June 2009New search has been performedIncorporated new data (Ascarelli 2005), included two new studies (Sayin 2005; Vigil-De Gracia 2007), reviewed background, results, and discussion.

Excluded six studies (Adarsh 2006; Alkan 2006; Ehrenberg 2006; Gomez 2005; Hennessy 2007; Livingston 2003), added one to Studies awaiting classification (Hladunewich 2006a) and one to Ongoing studies (Aina-Mumuney 2006).

20 September 2008AmendedConverted to new review format.

4 November 2004New search has been performedSearch updated on 31 March 2004.

We have updated the references in the Background since the protocol was first published.



 

Contributions of authors

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

For this update, Dr L Magee conducted the updated literature search and data entry. Data entry was double-checked by P von Dadelszen. All review authors revised the review for publication.

 

Declarations of interest

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

Peter von Dadelszen is a paid consultant to Alere International, and receives grant funding from the Bill & Melinda Gates Foundation and CIHR. These activities are unrelated to this review.

 

Sources of support

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms
 

Internal sources

  • BC Research Institute for Children's and Women's Health, Canada.
    Laura Magee has received Establishment Grants from both the MSFHR and the BC Research Institute for Children's and Women's Health.

 

External sources

  • Michael Smith Foundation for Health Research (MSFHR), Canada.
    L Magee received salary support from the Michael Smith Foundation for Health Research (MSFHR). She has received Establishment Grants from both the MSFHR and the BC Research Institute for Children's and Women's Health.

 

Differences between protocol and review

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Results
  6. Discussion
  7. Authors' conclusions
  8. Acknowledgements
  9. Data and analyses
  10. Appendices
  11. What's new
  12. History
  13. Contributions of authors
  14. Declarations of interest
  15. Sources of support
  16. Differences between protocol and review
  17. Index terms

Methods for data collection and analysis were updated for the 2013 update. A number of outcomes not prespecified in the protocol have been highlighted.

  • Maternal end-organ failure (any).
  • Use of non-steroidal anti-inflammatories (NSAIDs) for postpartum analgesia.
  • Maternal side-effects to antihypertensive medication.
  • Severe maternal hypotension.

* Indicates the major publication for the study

References

References to studies included in this review

  1. Top of page
  2. AbstractRésumé
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Differences between protocol and review
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
Ascarelli 2005 {published data only}
  • Ascarelli M, Johnson V, McCreary H, May WL, Martin JN Jr. Adjunctive postpartum treatment of preeclampsia with furosemide. Obstetrics & Gynecology 1999;180(1 Pt 2):S18.
  • Ascarelli MH, Johnson V, McCreary H, Cushman J, May WL, Martin Jr JN. Postpartum preeclampsia management with furosemide: a randomized clinical trial. Obstetrics & Gynecology 2005;105:29-33.
Barton 1990 {published data only}
  • Barton JR, Hiett AK, Conover WB. The use of nifedipine during the postpartum period in patients with severe preeclampsia. Proceedings of 10th Annual Meeting of Society of Perinatal Obstetricians; 1990 Jan 23-27; Houston, Texas, USA. 1990:307.
  • Barton JR, Hiett AK, Conover WB. The use of nifedipine during the postpartum period in patients with severe pre-eclampsia. American Journal of Obstetrics and Gynecology 1990;162:788-92.
Fidler 1992 {published data only}
  • Fidler J, Smith V, de Swiet M. A randomized study comparing timolol and methyldopa in hospital treatment of puerperal hypertension. British Journal of Obstetrics and Gynaecology 1982;89:1031-4.
Griffis 1989 {published data only}
  • Griffis KR Jr, Martin JN Jr, Palmer SM, Martin RW, Morrison JC. Utilization of hydralazine or alpha-methyldopa for the management of early puerperal hypertension. American Journal of Perinatology 1989;6:437-41.
  • Martin JN, Griffis KR, Martin RW, Hess LW, Morrison JC. Early puerperal hypertension management: hydralazine vs methyldopa. 6th International Congress of the International Society for the Study of Hypertension in Pregnancy; 1988 May 22-26; Montreal Quebec, Canada. 1988:197.
Hladunewich 2006 {published data only}
  • Hladunewich MA, Derby GC, Lafayette RA, Blouch KL, Druzin ML, Myers BD. Effect of L-arginine therapy on the glomerular injury of preeclampsia: a randomized controlled trial. Obstetrics & Gynecology 2006;107(4):886-95.
Matthews 1997 {published data only}
  • Matthews G, Gornall R, Saunders N. A randomized placebo trial of loop diuretics in moderate/severe pre-eclampsia, following delivery. Journal of Obstetrics and Gynaecology 1997;17(1):30-2.
Sayin 2005 {published data only}
  • Sayin NC, Altundag G, Varol FG. Efficacy of alpha-methyldopa and nifedipine in the treatment of postpartum hypertension [Postpartum hipertansiyon tedavisinde alfametildopa ve nifedipinin etkinligi]. Journal of the Turkish German Gynecology Association 2005;6(2):118-22.
Vigil-De Gracia 2007 {published data only}
  • Vigil-De Gracia P, Ruiz E, Lopez JC, de Jaramillo IA, Vega-Maleck JC, Pinzon J. Management of severe hypertension in the postpartum period with intravenous hydralazine or labetalol: a randomized clinical trial. Hypertension in Pregnancy 2007;26(2):163-71.
Walss Rodriguez 1991 {published data only}
  • Walss Rodriguez RJ, Villarreal Ordaz F. Severe pre-eclampsia management during puerperium. Comparative study between sublingual nifedipine and hydralazine [Manejo de preeclampsia severa en el puerperio]. Ginecologia y Obstetricia de Mexico 1991;59:207-10.

References to studies excluded from this review

  1. Top of page
  2. AbstractRésumé
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Differences between protocol and review
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
Adarsh 2006 {published data only}
  • Adarsh B, Reena P, Nimmi C, Singh SK. In search of accelerated recovery from eclampsia. Journal of Obstetrics and Gynaecology of India 2006;56(5):402-5.
Alkan 2006 {published data only}
  • Alkan A, Tugrul S, Oral O, Uslu H, Kose D, Catakli FT. Effects of postpartum uterine curettage on maternal well-being in severe preeclamptic patients. Clinical and Experimental Obstetrics and Gynecology 2006;33(1):55-8.
Barrilleaux 2003 {published data only}
  • Barrilleaux PS, Martin JM Jr, Klauser C, Bufkin L, May W. Adjunctive intravenous dexamethasone in patiens with severe preeclampsia not complicated by HELLP syndrome. American Journal of Obstetrics and Gynecology 2003;189(6):S94.
Belfort 1988 {published data only}
Ehrenberg 2006 {published data only}
  • Ehrenberg H, Mercer B. Abbreviated post-partum magnesium sulfate therapy for women with mild preeclampsia [abstract]. American Journal of Obstetrics and Gynecology 2004;191(6 Suppl 1):S73.
  • Ehrenberg HM, Mercer BM. Abbreviated postpartum magnesium sulfate therapy for women with mild preeclampsia: a randomized controlled trial. Obstetrics & Gynecology 2006;108(4):833-8.
Garden 1982 {published data only}
  • Garden A, Davey DA, Dommisse J. Intravenous labetalol and intravenous dihydralazine in severe hypertension in pregnancy. Clinical and Experimental Hypertension 1982;B1:371-83.
Gomez 2005 {published data only}
  • Gomez LM, De la Vega GA, Ludmir J, Padilla L, Angulo D. Immediate postpartum curettage accelerates clinical recovery in severe preeclampsia [abstract]. Obstetrics & Gynecology 2005;105(4 Suppl):111S.
Hennessy 2007 {published data only}
Jia 2007 {published data only}
  • Jia JP, Wu YX, Xie GH. Clinical observation on treatment of albuminuria in patients with pregnancy-induced hypertension syndrome in puerperium by xiaobai decoction. Chinese Journal of Integrated Traditional and Western Medicine 2007;27(7):644-6.
Keiseb 2002 {published data only}
  • Keiseb J, Moodley J, Connolly C. Comparison of the efficacy of continuous furosemide and low-dose dopamine infusion in preeclampsia/eclampsia related oliguria in the immediate postpartum period. Hypertension in Pregnancy 2002;21(3):225-34.
Livingston 2003 {published data only}
Mabie 1987 {published data only}
  • Mabie WC, Gonzalez AR, Sibai BM, Amon E. A comparative trial of labetalol and hydralazine in the acute management of severe hypertension complicating pregnancy. Obstetrics & Gynecology 1987;70:328-33.
  • Mabie WC, Gonzalez-Ruiz A, Amon E, Sibai BM. A comparative trial of labetalol and hydralazine for acute management of severe hypertension complicating pregnancy. 5th International Congress for the International Society for the Study of Hypertension in Pregnancy; 1986 July 7-10; Nottingham, UK. 1986:91.
Magann 1993 {published data only}
  • Magann EF, Martin JN, Isaacs JD, Perry KG, Martin RW, Meydrech EF. Immediate postpartum curettage: accelerated recovery from preeclampsia. American Journal of Obstetrics and Gynecology 1993;168:320.
  • Magann EF, Martin JN, Isaacs JD, Perry KG, Martin RW, Meydrech EF. Immediate postpartum curettage: accelerated recovery from severe preeclampsia. Obstetrics & Gynecology 1993;81:502-6.
Magann 1994 {published data only}
  • Magann EF, Bass JD, Chauhan SP, Perry KG, Morrison JC, Martin JN. Accelerated recovery from severe preeclampsia: uterine curettage versus nifedipine. Journal of the Society for Gynecological Investigation 1994;1(3):210-4.
Mantel 1997 {published data only}
Marsoni 1985 {published data only}
Montenegro 1985 {published data only}
  • Montenegro R, Knuppel RA, Shah D, O'Brien WF. The effect of serotonergic blockade in postpartum preeclamptic patients. American Journal of Obstetrics and Gynecology 1985;153:130-4.
Morrison 1993 {published data only}
  • Morrison JC. Curettage for severe pregnancy-induced hypertension. Personal communication.
Vermillion 1999 {published data only}
  • Scardo J, Vermillion S, Newman R, Chauhan S, Brost B. Randomized double-blinded hemodynamic study of oral nifedipine and iv labetalol in hypertensive urgencies of pregnancy. American Journal of Obstetrics and Gynecology 1999;180:S18.
  • Scardo JA, Vermillion ST, Newman RB, Chauhan SP, Hogg BB. A randomized, double-blind, hemodynamic evaluation of nifedipine and labetalol in preeclamptic hypertensive emergencies. American Journal of Obstetrics and Gynecology 1999;181(4):862-6.
  • Vermillion S, Scardo J, Newman R, Chauhan S. A prospective randomized double blind trial of oral nifedipine and intravenous labetalol in hypertensive emergencies. American Journal of Obstetrics and Gynecology 1999;180:S14.
  • Vermillion ST, Scardo JA, Newman RB, Chauhan SP. A randomized, double-blind trial of oral nifedipine and intravenous labetalol in hypertensive emergencies of pregnancy. American Journal of Obstetrics and Gynecology 1999;181(4):858-61.
Weiner 1984 {published data only}
  • Weiner CP, Socol ML, Vaisrub N. Control of preeclamptic hypertension by ketanserin, a new serotonin receptor antagonist. American Journal of Obstetrics and Gynecology 1984;149:496-500.

Additional references

  1. Top of page
  2. AbstractRésumé
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Differences between protocol and review
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
Abalos 2007
Ascarelli 1999
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Atterbury 1996
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Bayliss 2002
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Beardmore 2002
Bond 1989
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Bowler 2002
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Castro 1994
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Duley 2002
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