Paguidian, Griffin John D.

BSN4A

Journal #1

Timely Treatment of Severe Maternal Hypertension and Reduction in Severe Maternal Morbidity

Highlights
• Antihypertensive treatment within 60 minutes of confirmed severe maternal hypertension is
associated with a significant reduction in severe maternal morbidity. Our study supports recent
ACOG and CMQCC guidelines.

• Women with severe hypertension who are at a higher risk of severe maternal morbidity cannot
necessarily be identified based on initial severity of blood pressures or their response to initial
treatment.

• Women with severe hypertension who develop severe maternal morbidity appear to have
hypertension that is more difficult to treat.

• Timely treatment of severe maternal hypertension with antihypertensive medications may be a

marker for good overall, more vigilant care.

Abstract
Objective

To determine if timely treatment within 60 minutes of confirmed diagnosis of severe maternal

hypertension with antihypertensive medications was associated with reduction in severe maternal
morbidity.

Study Design

Medical records of women with severe hypertension (at least two severe blood pressures, systolic
≥160mmHg and/or diastolic ≥110mmHg, within 60 minutes) were accessed for timing of severe
blood pressures, timing of treatment, and blood pressure response to treatment. Severe maternal
morbidity was confirmed by multidisciplinary case review. We compared the incidence of severe
maternal morbidity between women who received timely (within 60 minutes of diagnosis) vs. not-
timely treatment.

Results

Of 465 women with severe hypertension, 29 (6.2%) experienced severe maternal morbidity. Fifty-
six percent of women received timely treatment, of whom 1.9% had severe maternal morbidity,
compared with 6.4% of women who did not receive timely treatment (p=0.02). Timely treatment
was associated with a 72% reduction in relative risk of severe maternal morbidity (p=0.02). No
significant difference was seen in median pre-treatment systolic pressures (p=0.20) between the
groups.

Conclusion

Antihypertensive treatment within 60 minutes of confirmed diagnosis of severe hypertension was

associated with reduction in severe maternal morbidity. Our findings support current
Paguidian, Griffin John D.
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recommendations to treat all women with severe hypertension with antihypertensive medications
in a timely fashion.

Journal #2

Impact of Preeclampsia and Gestational Hypertension on Birth Weight by Gestational Age

Abstract

The predominant etiologic theory of preeclampsia is that reduced uteroplacental perfusion is the
unique pathogenic process in the development of preeclampsia. Decreased uteroplacental blood
flow would result in lower birth weights. To date, no study has assessed the effect of preeclampsia
on birth weight by gestational age. Thus, the authors conducted a retrospective cohort study based
on 97,270 pregnancies that resulted in delivery between 1991and 1996 at 35 hospitals in northern
and central Alberta, Canada. Differences in mean birth weight between women with preeclampsia
and normotensive women ranged from −547.5 g to 239.5 g for gestational age categories ranging
from ≤32 weeks to ≥42 weeks. The birth weights were statistically significantly lower among
mothers with preeclampsia who delivered at ≤37 weeks, with an average difference of –352.5 g.
However, the birth weights were not lower among preeclamptic mothers who delivered after 37
weeks (average difference of 49.0 g). In Alberta, 61.2% of preeclamptic patients gave birth after 37
weeks of gestation. The authors conclude that babies born to mothers with preeclampsia at term
have fetal growth similar to that of babies born to normotensive mothers. This finding does not
endorse the currently held theory that reduced uteroplacental perfusion is the unique
pathophysiologic process in preeclampsia.

Hypertensive disorders in pregnancy, especially preeclampsia, remain a major cause of maternal

and infant morbidity and mortality worldwide (1). Despite numerous basic, clinical, and
epidemiologic studies that have been conducted over the past half-century, knowledge of the
etiology and pathogenesis of preeclampsia remains elusive (2). Because the pathophysiology of
preeclampsia has not yet been elucidated, clinical trials have failed to demonstrate any effective
prevention or treatment strategies, apart from early delivery in cases where the disorder is severe
(2, 3).
Paguidian, Griffin John D.
BSN4A

A prevailing hypothesis regarding the pathogenesis of preeclampsia is the “ischemic model.”

Decreased uteroplacental perfusion is hypothesized to be the primary step and the point of
convergence of diverse pathogenic processes in the development of preeclampsia (4–6). It is
intuitive that reduced placental blood flow should result in decreased fetal growth, with an
increased risk of intrauterine growth restriction and low birth weight. However, epidemiologic
studies have not conclusively established an association between preeclampsia or gestational
hypertension and poor fetal growth (7).

Birth weight is determined by both duration of gestation and rate of fetal growth. Preeclampsia
significantly increases the risk of iatrogenic preterm birth (delivery) for maternal indications. To
study the effect of preeclampsia and gestational hypertension on fetal growth, it is important to
compare the fetal growth of babies born to mothers with preeclampsia or gestational hypertension
with that of babies born to mothers without these conditions at the same gestational ages. To our
knowledge, no study to date has examined the impact of preeclampsia and gestational
hypertension on mean birth weight by gestational week, and no previous study has examined
whether the effect of preeclampsia or gestational hypertension on fetal growth differs according
to gestational age. Using an existing perinatal database, we conducted a study to assess the effect
of preeclampsia and gestational hypertension on fetal growth according to gestational age.

Results

The initial population in the database consisted of 97,270 women. Table 1 shows the
characteristics of the study population before exclusions. Overall, 8.2 percent of the women were
teenagers and 37.4 percent were over 30 years old; 40.5 percent were nulliparous, and 26.6
percent smoked during pregnancy. The incidences of gestational hypertension, preeclampsia, and
chronic hypertension were 3.9 percent, 1.7 percent, and 0.9 percent, respectively. The incidences
of preterm birth, low birth weight, and stillbirth were 9.0 percent, 6.9 percent, and 0.3 percent,
respectively.
Paguidian, Griffin John D.
BSN4A

Journal #3

Gestational Hypertension and Preeclampsia: Are They the Same Disease?

Preeclampsia, complicating 5% to 8% of pregnancies, has been traditionally defined by an elevated

blood pressure (over 140/90 mmHg on at least 2 occasions at least 6 hours apart) and proteinuria,
at or beyond 20 weeks’ gestation. In 2013, the American College of Obstetricians and
Gynecologists’ Task Force on Hypertension in Pregnancy recommended that the definition of PE
should be extended to include cases without evidence of proteinuria, provided that the
hypertension is accompanied by evidence of end-organ involvement. PE is associated with an
increased risk of adverse pregnancy outcome, including prematurity, placental abruption, and
intrauterine growth restriction.3 In contrast, gestational hypertension is defined by an elevated BP
at or beyond 20 weeks’ gestation in the absence of proteinuria, and is considered to be a transient
condition. The development of proteinuria later in pregnancy changes the final diagnosis to
preeclampsia. Otherwise, the final diagnosis is determined according to a re-evaluation of BP
recordings at approximately three months postpartum. For women who are then normotensive
(the most common scenario4), the final diagnosis is transient HTN of pregnancy. Persistence of
GHTN for more than three months postpartum is consistent with a diagnosis of chronic
hypertension.

Is gestational hypertension an independent clinical entity or a “pre-preeclampsia” state?

We will approach this question by comparing the epidemiologic, pathologic, pathogenetic, and
hemodynamic characteristics of GHTN and PE.6 Several observations indicate that GHTN and PE
have distinct epidemiologic features, including some differences in their underlying risk factors. In
a large Swedish population-based study, several factors were common to the two conditions,
whereas multiple pregnancy and diabetes mellitus were exclusively associated with PE.7 A
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secondary analysis of the WHO Antenatal Care Trial, involving almost 40 000 women, had similar
findings.8 While primiparity and maternal respiratory disease were associated only with PE,
antepartum hemorrhage (OR 1.4; 95% CI 1.1 to 1.7) and a history of large for gestational age
newborn (OR 1.7; 95% CI 1.3 to 2.2) were limited to women with GHTN.

Several studies have addressed the risk of recurrence of GHTN and PE in a subsequent pregnancy.
Overall, the risk of recurrence is higher in women with prior GHTN (20% to 47%) than in women
with prior PE (5% to 10%).9.,10. Furthermore, in a large retrospective study, women with prior GHTN
were more likely to experience GHTN (26%) than PE (6%) in a subsequent pregnancy, whereas
women with previous PE had a similar 6% risk of recurrence of either PE or GHTN.11

Only two studies comparing placental pathology in pregnancies complicated by GHTN versus PE
have been published, and both identified differences in placental pathology between the two
conditions. Correa et al.12found that GHTN and PE had some placental pathologic features in
common, but women with PE had placentas characterized by a higher number of syncytial knots
and by differences in the size and distribution of fibrin deposits. In a more recent retrospective
study of 150 women, placentas from women with PE were characterized by a trend towards higher
rates of decidual vasculopathy (47% vs. 33%; P=0.08) and villous infarction (50% vs.
38%; P=0.1),13 suggesting that placental ischemia is confined to PE.

Vascular biology studies have suggested that there is a contrasting pathophysiology between PE
and GHTN. Noori et al. compared endothelial dysfunction and angiogenic markers in women with
GHTN and PE.14 They followed 159 women from 10 weeks’ gestation to three months postpartum.
Flow-mediated dilatation (a sonographic measure of vascular endothelial function) was abnormal
only in those with PE; women with GHTN had flow-mediated dilatation that was similar to non-
hypertensive control subjects. Similarly, maternal blood levels of the anti-angiogenic markers sFlt1
and sEng were elevated only in women with PE.14 In concordance with these findings, Verlohren et
al. reported that the ratio of the anti-angiogenic marker sFlt1 to the pro-angiogenic marker PlGF
(sFlt1/PlGF) was significantly elevated in women with PE, but not in those with GHTN, again
suggesting that only PE is characterized by an anti-angiogenic milieu.15 Furthermore, in a
prospective study of 110 pregnant women, levels of endothelial microparticles (associated with
endothelial cell damage) were found to be significantly higher in women with PE but not
GHTN.16 Khalil et al. compared the effect of treatment with α-methyldopa on the levels of
angiogenic markers in women with GHTN and PE.17 They found that α-methyldopa treatment was
associated with a significant reduction (50%) in sFlt1 and sEng levels in women with PE, but not in
women with GHTN (whose levels were much lower). In a recent study, Sandrim et al. found
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differences in the polymorphism of vascular endothelial growth factor between women with GHTN
and women with PE, raising the possibility of differences in the genetic predisposition for
each.18 Another group found that the sensitivity of platelets to prostaglandin E1 was decreased only
in women with PE, suggesting that platelet activation is a characteristic specific to PE and not
GHTN.19 In a recent meta-analysis of the use of antiplatelet agents for the prevention of PE, it was
found that these agents decreased the risk of PE in either moderate- or high-risk women, while
such a beneficial effect in the prevention of GHTN was observed only among high-risk
women.20 Collectively, these findings suggest that endothelial dysfunction and an imbalance
between pro- and anti-angiogenic factors are characteristics specific for PE but not for GHTN.

Pathophysiologic changes are different in women with PE and those with GHTN, including
decreased maternal blood volume among the former.21 In addition, there is recent evidence that
non-invasive hemodynamic measures, such as changes in cardiac output and peripheral vascular
resistance, precede the onset of severe PE by several weeks in high-risk women.22., 23. Such a tool
may also be useful for predicting PE in the specific group of women with new onset of isolated
hypertension in pregnancy, since the detection of increased total peripheral resistance and
increased cardiac output in these cases may reflect the presence of early stage PE rather than
GTHN.

Another aspect to be considered is the long-term outcome following pregnancies complicated by

GTHN or PE. Most of the studies conducted to date have been focused on the long-term risks of
cardiovascular morbidity and mortality. Most of these studies have found that women with either
GHTN or PE are at increased risk of chronic hypertension, ischemic heart disease, cerebrovascular
disease, and venous thromboembolism, although the risk was higher for women with severe PE
than for women with GHTN.24., 25., 26., 27. One important limitation of many of these studies, most of
which are based on coding diagnoses, is that a considerable proportion of women with GTHN may
in fact have had undetected chronic hypertension.

In summary, it appears that there are significant differences between PE and GHTN with respect
to their epidemiologic, pathologic, pathogenetic, and hemodynamic characteristics. GHTN and PE
seem to be two distinct entities. Nevertheless, some pregnant women who initially present with
isolated HTN do progress to develop PE, reflected by subsequent development of proteinuria
and/or laboratory evidence of HELLP syndrome. How can these two apparently conflicting
observations be reconciled? One potential explanation is that women who present with isolated
HTN in pregnancy are a heterogeneous group, comprising some with an early stage of PE who
somehow delay the development of proteinuria, and others with GHTN, a distinct disorder
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BSN4A

representing a benign regulatory imbalance between systemic vascular tone and cardiac output
(Figure 2). This concept is supported by a recent study in which the levels of pro- and anti-
angiogenic markers in maternal blood were compared between three groups of patients: women
with GHTN, women who initially presented with isolated HTN but later developed PE, and women
who presented with PE.28 The group that presented with isolated HTN and progressed to PE had
sFlt/PlGF ratios and sEng levels that were similar to those in women with PE; both groups had
significantly higher levels than women who presented with isolated HTN but had a final diagnosis
of GHTN.27

SUMMARY
The contemporary evidence suggests that GHTN and PE are distinct entities with different clinical
characteristics. Therefore, women who present with isolated HTN in pregnancy are a
heterogeneous group. Most of these women have true GHTN, but between 10% and 50% of
women with isolated HTN will subsequently develop PE later in pregnancy. The proportion of
women in the latter group (at risk of developing PE) is higher in women with lower gestational age
at diagnosis, elevated systolic BP and serum uric acid levels at presentation, abnormal uterine
artery Doppler velocimetry, elevated serum levels of anti-angiogenic markers such as sFlt-1, and
reduced levels of the pro-angiogenic placental growth factor. Those who eventually progress to PE
do so within a period of one to five weeks from the time of diagnosis with isolated HTN, and this
lag period is inversely related to gestational age at the time of diagnosis with GHTN. Those women
who have GHTN and do not progress to PE still have an increased risk for pregnancy complications,
a risk that is proportional to the severity of GHTN. Although the recent recommendations regarding
the definition of PE (i.e., that PE should also include cases without proteinuria if the hypertension
is associated with end-organ involvement) may shed more light on the question at the centre of
the current review, we believe that this is unlikely to be the case because most women with
hypertension and significant end-organ disease have likely been given a diagnosis of PE even before
these new recommendations.

The practical implications of these findings are that women who present with isolated HTN in
pregnancy should be evaluated for the risk of progression to PE, with those at highest risk being
offered education about the symptoms and signs of PE and then monitored more closely. In the
absence of risk factors for the development of PE, women can be reassured that they most likely
have GHTN and consequently the risk of adverse maternal–infant outcomes is low.
Paguidian, Griffin John D.
BSN4A

Reflection on Journal #1

In the first journal, it discussed there all about the fast and quick treatment for hypertension. It
really is effective if treatment for hypertension was given at hand when it occurs. If so given, it is
effective immediately, then I have learned that if given that fast, it could save a lot of mothers
that’s experiencing gestational hypertension, it could also reduce the risks of other morbidities for
the baby too. There have been lots and lots or mortality about gestational hypertension, these
methods can reduce those rates and save many lives. As one of the student nurses, I can help in
the clinical setting by encouraging the mothers to have complete pre-natal check ups to reduce
possible morbidities.

Reflection on Journal #2

On what I have learned about maternal and child back when I was in second year college, is that if
a baby inside the mother is not receiving enough blood supply, the function of the systems and
meeting the needs of the baby may not be complete, hence may affect the growth of the child,
such as having low birth weight or in general the baby might be small, which can be caused by
having maternal hypertension, and other vices such as smoking and being an alcoholic and also
stress, which can later on cause vasoconstriction within the blood vessels of the mother, therefore
lowering the blood supply to the baby. As a student nurse, I can help in the clinical setting by
informing the mother, providing health teaching that they should stop any vices and putting on too
much stress on their bodies, because it may cause the baby any insufficiency and cause a lot more
of morbidities.

Reflection on Journal #3

On the 3rd journal, it is being compared the difference between pre eclampsia and gestational
hypertension. But as a nurse, I do know that they both have distinct differences. We do know that
pre eclampsia is a pregnancy which includes hypertension and damages to other organ system
most often the liver and the kidneys. Gestational hypertension is also known as Pregnancy Induced
Hypertension or PIH, it’s a normal process where the mother develops hypertension due to high
blood supply demand of the baby, and also the heart supplies both the mother and the baby of
blood.
Paguidian, Griffin John D.
BSN4A

Predisposing factor Precipitating Factors

Hereditary Pathophysiology Hypertension Pregnancy
Primigravida Diet

Increase cardiac output

Interrupts the action Injures endothelial

of prostaglandin cells

Decrease Increase
prostacyclin thromboxane

Vascular spasm Increase blood flow

Heart is force to pump

Vasoconstriction

Decrease blood flow

Increase blood Lack of nutrients distribution

pressure into the placenta
Paguidian, Griffin John D. Journal
BSN-IVA