CURRICULUM VITAE

Dr. Muhammad Yusuf.,SpOG

Staf Obstetri Ginekologi
RSDS/FK UNAIR

Hp. 08121674373
email. dr.muhyusuf@gmail.com

• Fk Unair
• PPDS I FK Unair / RSDS
• PPDS II FK Unair / RSDS
• Divisi Obginsos FK Unair /
RSDS
Recent Update in Preeclampsia
and Postpartum hemorrhage
management
Muhammad Yusuf
Causes are known, Cure is available,
Services are Used, Staff is skillful :

So, why still so many pregnant women die ?

(Questions that staff should ask to achieve better health outcomes)

Mohammad Afzal Mahmood

 Survey Demografi Kesehatan
Indonesia 2015
Angka Kematian Ibu (AKI) di Indonesia masih tinggi, yaitu
359 per 100.000 kelahiran hidup
Jawa Timur, tahun 2016 sebesar 91 per 100.000 kelahiran
hidup
Angka Kematian Bayi (AKB) juga masih tinggi di Indonesia.
Pada tahun 2015, angkanya adalah 25,3 per 1000 kelahiran
hidup
Prevalensi Anemia pada ibu hamil 37,1% (Riskesdas 2013).
Batasan WHO < 20%
3 besar penyebab kematian Ibu (Dirjen Kesmas, 2016) :
1. Perdarahan (30,3%)
2. HT kehamilan (27,1 %)
3. Infeksi (7,3%)
Preeclampsia Management
• Preeclampsia is a multi-system progressive disorder
characterized by the new onset of hypertension and
proteinuria, or hypertension and end-organ dysfunction with or
without proteinuria, in the last half of pregnancy or
postpartum.
• The disorder is caused by placental and maternal vascular
dysfunction and always resolves after delivery.
• Although most affected pregnancies deliver at term or near
term with good maternal and fetal outcomes, these
pregnancies are at increased risk for maternal and/or fetal
mortality or serious morbidity.
• Women with preeclampsia are at increased risk for future
cardiovascular disease.
PREVALENCE — In a systematic review, 4.6 percent (95%
CI 2.7-8.2) of pregnancies worldwide were complicated by
preeclampsia.
Variations in prevalence reflect, at least in part, differences in
the maternal age distribution and proportion of nulliparous
pregnant women among populations.
The prevalence of preeclampsia in the United States is
approximately 3.4 percent, but 1.5-fold to 2-fold higher in
first pregnancies.
Preeclampsia is less prevalent before 34 weeks of gestation.
In one population-based study, the prevalence before and
after 34 weeks was 0.3 and 2.7 percent, respectively.
RISK FACTORS —
• A past history of preeclampsia increases the risk of developing preeclampsia in a subsequent
pregnancy eightfold compared with women without this history (relative risk [RR] 8.4, 95% CI
7.1-9.9).



●  First pregnancy (nulliparity) (RR 2.1, 95% CI 1.9-2.4).




●  A family history of preeclampsia in a first-degree relative (RR 2.90, 95% CI 1.70-4.93).




● Prior pregnancy complications – fetal growth restriction (RR 1.4, 95% CI 0.6-3.0), abruption (RR
2.0, 95% CI 1.4-2.7), or stillbirth (RR 2.4, 95% CI 1.7-3.4).



●  Pre-existing medical conditions :




• Pregestational diabetes (RR 3.7, 95% CI 3.1-4.3).


• Chronic hypertension (RR 5.1, 95% CI 4.0-6.5).

• Systemic lupus erythematosus (RR 1.8, 95% CI 1.5-2.1).

• Antiphospholipid syndrome (RR 2.8, 95% CI 1.8-4.3).

• Body mass index >25 (RR 2.1, 95% CI 2.0-2.2) and body mass index (BMI) >30 (RR 2.8, 95%
CI 2.6-3.1). 

• Chronic kidney disease (CKD) (RR 1.8, 95% CI 1.5-2.1).

● Multifetal pregnancy (RR 2.9, RR 2.6-3.1).



● Advanced maternal age (maternal age ≥35 RR 1.2, 95% CI 1.2-2.0 and ≥40 RR 1.5, 95% CI
1.2-2.0).
Screening for traditional risk factors for
preeclampsia is of value at the first prenatal
visit to identify women at high risk of
developing the disease, as these women are
offered low-dose aspirin + calcium therapy to
reduce their risk of developing the disease.
• Despite advances in detection and management,
preeclampsia/eclampsia remains a common cause of
maternal morbidity and death.
• Eclampsia occurs in 2 to 3 percent of women with
severe features of preeclampsia not receiving anti-
seizure. 0.6 percent of women with preeclampsia
without severe features (previously referred to as
“mild” preeclampsia)
• In developing countries, however, the incidence varies
widely: from 6 to 157 cases per 10,000 deliveries.
• Women at highest risk of developing
eclampsia are nonwhite, nulliparous, and from
lower socioeconomic backgrounds.
• The peak incidence is in adolescence and the
early twenties but is also increased in women
over age 35.
Loading dose – of magnesium sulfate 6 g
intravenously over 15 to 20 minutes. This dose
quickly and consistently achieves a therapeutic
level. Loading doses of 4 to 6 g intravenously are
commonly used 


Maintenance dose – of magnesium sulfate 2 g/

hour as a continuous intravenous infusion to
women with good renal function. Maintenance
doses of 1 to 3 g/hour are commonly used. 

A clear threshold magnesium concentration
for insuring the prevention of seizures has not
been established, but a range of 4.8 to 8.4
mg/dL (1.9 to 3.5 mmol/L) is recommended if
serum levels are checked because of
recurrent seizures or concerns about toxicity.
The dose should be adjusted according to the
clinical response of individual patients.


Management of persistent seizures — Recurrent
seizures in patients on maintenance magnesium
sulfate therapy can be treated with an additional
bolus of 2 g magnesium sulfate over 5 to 10
minutes, with frequent monitoring for signs of
magnesium toxicity (eg, loss of patellar reflex,
respirations <12 per minute). If two such boluses do
not control seizures, then other drugs should be
given. Diazepam or lorazepam is a common choice.
• The definitive treatment of preeclampsia is delivery,
which is always beneficial for the mother. As long as the
gravida remains undelivered, she is at increased risk of
complications such as seizures, placental abruption,
thrombocytopenia, cerebral hemorrhage, pulmonary
edema, liver hemorrhage, and acute kidney injury.
• The risk of these complications subsides in the hours
after delivery since preeclampsia resolves after delivery
and long-term sequelae are rare.
Although the fetus is at increased risk of
intrauterine growth restriction and stillbirth in
the preeclamptic environment, conservative
management, including antihypertensive
therapy, may be pursued in selected cases to
gain fetal maturity.
• Do not prescribe antihypertensive therapy for
mild hypertension in the context of
preeclampsia, which we define as blood
pressures consistently less than 150/100
mmHg.
• We initiate antihypertensive therapy in adult
women at systolic pressures ≥150 mmHg or
diastolic blood pressures ≥100 mmHg.
• Intravenous labetalol or hydralazine as first-line
agents for acute therapy of severe
hypertension. 


• A 2014 systematic review suggested that oral

nifedipine is an acceptable alternative to
parenteral labetalol or hydralazine for severe
hypertension.
• Nifedipine (30 mg sustained release tablet)
and nicardipine are other options. 

• (ACOG) recommends treatment of persistent chronic
hypertension when systolic pressure is ≥160 mmHg or
diastolic pressure is ≥105 mmHg and suggests avoiding
antihypertensive therapy in women with blood pressures
below this level and no evidence of end-organ damage.
They suggest labetalol, nifedipine, or methyldopa as
first-line therapy. They also suggest avoiding
angiotensin- converting enzyme inhibitors, angiotensin
receptor blockers, renin inhibitors, and mineralocorticoid
receptor antagonists. The goal of management is
maintenance of blood pressures between 120/80 and
160/105 mmHg.
SUMMARY AND RECOMMENDATIONS 


●   The four major hypertensive disorders related to pregnancy are

preeclampsia, chronic hypertension, preeclampsia superimposed upon
chronic hypertension, and gestational hypertension. 


● Major risk factors for development of preeclampsia include past history of

preeclampsia, nulliparity, pregestational diabetes, chronic hypertension,
obesity, family history of preeclampsia, and multiple gestation.



●  The diagnosis of preeclampsia is based on the new onset of hypertension

and proteinuria or end-organ dysfunction with or without proteinuria after 20
weeks of gestation in a previously normotensive woman. 


● At the first prenatal visit, we evaluate pregnant women for traditional risk
factors for preeclampsia to identify those at high risk for developing the
disease. These women are offered low-dose aspirin therapy in the second
and third trimesters to reduce their risk of developing preeclampsia.
SUMMARY AND RECOMMENDATIONS
● The definitive treatment of preeclampsia is delivery to prevent development of
maternal or fetal complications from disease progression. Timing of delivery is based
upon gestational age, the severity of preeclampsia, and maternal and fetal condition.
● Preeclampsia with features of severe disease is generally regarded as an indication for
delivery, regardless of gestational age, given the high risk of serious maternal morbidity.



● Antihypertensive therapy is indicated for treatment of severe hypertension (defined as

systolic blood pressure ≥160 mmHg and diastolic blood pressure ≥110 mmHg) to prevent
stroke ; it does not prevent eclampsia. Antihypertensive therapy to control mild
hypertension does not alter the course of preeclampsia or diminish perinatal morbidity or
mortality, and should be avoided in most patients. 


●   For women with preeclampsia without features of severe disease, we suggest

conservative management with delivery when the pregnancy has reached 37 weeks of
gestation.


●   For women with a viable fetus and preeclampsia <34 weeks of gestation, we
recommend a course of antenatal glucocorticoids (betamethasone) (Grade 1A). Use of
steroids at 34 to 36 weeks is controversial.
SUMMARY AND RECOMMENDATIONS —
• When hypertension is diagnosed in a pregnant woman, the major issues
are establishing a diagnosis, deciding the blood pressure at which
treatment should be initiated and the target blood pressure, and avoiding
drugs that may adversely affect the fetus.
• Treatment of severe hypertension has a well-established maternal benefit
of reduction in stroke risk, but there is no proven maternal or fetal benefit
from treatment of mild to moderate hypertension over the relatively short
duration of a full-term pregnancy. In addition, lowering maternal blood
pressure excessively may be associated with decreased placental
perfusion, and exposure of the fetus to potentially harmful effects of
medications.
• Angiotensin converting enzyme inhibitors, angiotensin II receptor
blockers, and direct renin inhibitors are contraindicated at all stages of
pregnancy.
Postpartum Hemorrhage
Management
Postpartum hemorrhage (PPH) is an obstetric emergency. It is
one of the top five causes of maternal mortality in both high and
low per capita income countries, although the absolute risk of
death from PPH is much lower in high-income countries. Timely
diagnosis, appropriate resources, and appropriate management
are critical for preventing death.
The incidence of PPH varies widely, depending upon the criteria
used to diagnose the disorder. A reasonable estimate is 1 to 5
percent of deliveries.
Women with risk factors for PPH should be identified and
counseled as appropriate for their level of risk and gestational
age.
In 2017, (ACOG) revised their definition of PPH
from the classic one (≥500 mL after vaginal
birth or ≥1000 mL after cesarean delivery) to (1)
cumulative blood loss ≥1000 mL or (2) bleeding
associated with signs/symptoms of
hypovolemia within 24 hours of the birth
process regardless of delivery route in order to
reduce the number of women inappropriately
labeled with this diagnosis.
B-Lynch suture - UpToDate 09/02/18 09.04

© 2018 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Anterior uterine wall with B-Lynch suture in place and

an enlarged drawing (box) of lower uterine segment
with B-Lynch suture in place

A large Mayo needle with #2 chromic catgut is used to enter and exit the
uterine cavity at A and B. The suture is looped over the fundus and then
reenters the uterine cavity posteriorly at C, which is directly below B. The
suture should be pulled very tight at this point. It then enters the posterior
wall of the uterine cavity at D, is looped back over the fundus, and anchored
by entering the anterior lateral lower uterine segment at E and crossing
through the uterine cavity to exit at F. The free ends at A and F are tied
down securely to compress the uterus.

Adapted from: Ferguson JE, Bourgeois JF, Underwood PB. B-LYNCH SUTURE FOR
POSTPARTUM HEMORRHAGE. Obstetrics & Gynecology 2000; 95(Supp 6):1020.

Graphic 71907 Version 2.0

https://www.uptodate.com/contents/image?imageKey=OBGYN%2F719…12&search=postpartum%20hemorrhage&rank=4~150&source=see_link Page 1 of 1
SUMMARY AND RECOMMENDATIONS
● Primary PPH occurs in the first 24 hours after delivery (also called early
PPH), and secondary PPH occurs 24 hours to 12 weeks after delivery (also
called late or delayed PPH).


● The most common causes of PPH are atony (which may be related to
placental disorders), trauma, and acquired or congenital coagulation defects.



●   Routine prophylactic use of uterotonic drugs, such as oxytocin, reduces

the risk of PPH by 50 percent in the overall obstetric population.



●   We treat patients with mild to moderate postpartum anemia with an oral

rather than a parenteral iron preparation. Oral treatment is more convenient,
cheaper, and not associated with severe side effects. Severe anemia may
require transfusion.


● Women with a prior PPH have as much as a 15 percent risk of recurrence

in a subsequent pregnancy.
Terima Kasih
Case Study