KEMENTERIAN PENDIDIKAN DAN KEBUDAYAAN

UNIVERSITAS SRIWIJAYA

FAKULTAS KEDOKTERAN
UNIT PENDIDIKAN KEDOKTERAN (UPK)
Zona F. Gedung I Kampus Unsri Indralaya OI Sumatera Selatan, Indonesia Telp. 0711 580061
atau / or Jl. dr. Muh. Ali Komplek RSUP Palembang 30126, Indonesia, Telp. 0711 352342, Fax. 0711 373438,

Skenario B Blok 23 Tahun 2014

Learning Outcomes:
The graduated doctors capable of doing these following things:
1. Have the ability for anamnesis, general and obstetric physical examination of severe
preeclampsia/eclampsia and Graves disease to plan supporting examination as indicated,
such as routine blood and urine rutine, T3, T4,TSH and others.
2. Have the ability to conclude (diagnose) based on the data from physical and supporting
examination.
3. Have the ability to make a good obstetric medical record.
4. Have the ability to plan a management (treatment) based on competence.
5. Have the ability to plan follow up and evaluation and referal system.
6. Have the ability to make evidence based medicine-prognosis and give good explanation
(Informed Consent) about the case.
Learning Objectives:
At the end of this session, students should:
1. Understand the patophysiology of hypertension and Graves disease which may be
occured concomitantly in a pregnant woman.
2. Have the clinical skills to examine a pregnant woman who are suffering from
hypertension, and Graves disease and how to diagnose and manage it properly.
3. Known about symptoms and kind of seizure in a pregnant woman.
4. Have the ability to plan a management (treatment) emergency case in severe
preeclampsia and eclampsia.
5. Be able known complication severe preeclampsia/eclampsia and Graves disease based
on competence
6. Be able to prepare a plan for postnatal care. ( Family Planning & Rehabilitation )

Mrs. Mima, 38-year-old pregnant woman G4P3A0 39-weeks pregnancy, was brought by her
husband to the Puskesmas due to convulsion 2 hours ago. She has been complaining of headache
and visual disturbance for the last 2 days. According to her husband, she has been suffering from
Graves disease since 3 years ago, but was not well controlled.
In the examination findings:
Upon admission,
Height = 152 cm; Weight 65 kg;
BP: 180/110 mmHg. HR: 120 x/min, RR: 24 x/m.
Head and neck examination revealed exopthalmus and enlargement of thyroid gland.
Pretibial edema
Obstetric examination:
Outer examination: fundal height 32 cm, normal presentation.
FHR: 150 x/min.
Lab: Hb 11,2 g/dL; she had 2 + protein on urine, cylinder (-)
Term Clarification
1

G4P3A0
Convulsion
Exopthalmus
Graves Disease
Hypertension
Visual Disturbance
Pretibial edema
Headache.

Problem Identification
Mrs. Mima, 38-year-old pregnant woman G4P3A0 39 weeks pregnancy
She had suffered convulsion 2 hours ago.
She has been complaining of headache and visual disturbance for the last 2 days.
She has been suffering from Graves disease since 3 years ago, but were not well
controlled.
Physical exam: height: 152 cm, weight 65 kg, BP: 180/110 mmHg, HR: 120 x/min, RR:
24 x/m. Head and neck examination revealed exopthalmus and enlargement of thyroid
gland. Pretibial edema.
Obstetrics finding: fundal height 32 cm, normal presentations. FHR: 150 x /min.
Laboratory finding: Hb 11,2 g/dL. She had 2 + protein on urine, cylinder (-)
Problem Analysis
Anatomy & physiology of reproduction system & thyroid gland
Correlation between Graves disease and hypertension, preeclampia/eclampsia in
pregnancy.
Pathophysiology of convulsions, hypertension, exopthalmus, edema, proteinuria.
Diagnosis and management of eclampsia in pregnancy.
Diagnosis and management of Graves disease.
Additional examinations ( T3, T4, TSH)
Complications to mother and baby
Prognosis
Postnatal Management

Synthesis
Hypertension in Pregnancy
Definition
Hypertension in pregnancy is defined as a systolic blood pressure of 140 mmHg and/or a
diastolic blood pressure of 90 mmHg. The significance of any blood pressure measurement is
related to the gestation of the pregnancy and, in general terms, the earlier in pregnancy
hypertension occurs the more likely it is to be chronic hypertension.
Chronic hypertension
(CHT) describes all hypertension that exists pre-pregnancy. The majority of women in this group
have essential hypertension, though many will be diagnosed for the first time in pregnancy.
Renal hypertension can complicate renal disease of any underlying pathology. Its presence
increases maternal and perinatal morbidity and mortality though its management is as for other
causes. The increased morbidity is usually related to the underlying renal pathology and it is
concern for the maternal kidneys that usually precipitates delivery if problems arise.
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Mild preeclampsia
Mild preeclampsia is specific syndrome in pregnancy with decreased perfusion of organs caused
by vasospasm and activity of endothelial cell
a. Blood presure 140/90 mmHg - < 160/110 mmHg.
b. Proteinuria: 300mg/ 24 hours with urine output, or dipstick: +1.
c. Local edema.

a.
b.
c.
d.
e.
f.
g.
h.
i.
j.
a.

Severe preeclampsia
Severe preeclampsia is a complication in pregnancy women with sign hypertension 160/110
mmHg or higher and there is proteinuria, edema and in 20 weeks gestasional age or more. Sign
and simptom severe preeclampsia:
Proteinuria: 5g with urine output for 24 hours, or dipstick: +4.
Oligouria: urine production < 400-500 ml/24 jam.
Increased creatinin serum.
Edema pulmonal and cyanosis.
Epigastrium pain and abdominal upper right pain
Disturbance of visus.
Disturbance of hepar function: increased alanine or aspartate amino transferase
Hemolisys microangiopatic.
Trombositopenia < 100.000/ml
Sindroma HELLP
Classification of severe preeclampsia
Severe preeclampsia without impending eclampsia
b. Severe preeclampsia with impending eclampsia, symptoms of impending eclampsia:
headache, disturbance of visus, nausea and vomitus, epigastrium pain, upper right
abdominal pain.
Management for severe preeclampsia
1. Medicine for complication of severe preeclampsia
2. Plan about the pregnancy depend age of gestational age: expectative and active
Other causes of hypertension in pregnancy are:
Phaeochromocytoma: rare but maternal mortality is 50%
Coarctation of the aorta: high maternal mortality
Cushings syndrome: can be difficult to diagnose as features can be mimicked by normal
pregnancy; associated with a high fetal loss
Conns syndrome: hypertension is associated with hypokalaemia
Chronic Hypertension versus Pregnancy Induced Hypertension (PIH)
In the first trimester of pregnancy the marked vasodilatation and drop in vascular
resistance sees blood pressure fall in both normotensive and hypertensive women, (the drop
being greater in the CHT group). As such hypertension may not be seen until the third or late in
the second trimester. CHT can therefore only be diagnosed with reference to non-pregnant BP
readings and this requires either prenatal BPs or more commonly detailed postnatal follow-up.
Pharmacological management of CHT and PIH is identical and as a general rule if hypertension
is present before 20 weeks CHT is more likely. Women with CHT tend to be older, heavier and
of higher parity.
COMPLICATIONS
Superimposed Pre-eclampsia
CHT is a major risk factor for pre-eclampsia. The signs of superimposed pre-eclampsia are
similar in this group but blood pressures (BP) will be higher or the BP picture will be difficult to
interpret, due to CHT treatment with antihypertensives. In women with CHT the development of
proteinuria is diagnostic of pre-eclampsia and is almost universally associated with fetal growth
restriction. Another very predictive feature of pre-eclampsia in CHT is a high urate (uric acid). If
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pre-eclampsia does not develop then women with CHT can expect a relatively uncomplicated
pregnancy and outcome.
Fetal Growth Restriction
Even in the absence of other features of pre-eclampsia fetal growth restriction is more common
in women with CHT. The underlying aetiology is usually poor placentation. Routine assessment
of fetal growth with ultrasound scan (USS) from 28 weeks is commonplace.
Placental Abruption
Placental abruption is a rare but serious complication affecting 1% of CHT pregnancies. It is
unlikely that antihypertensive treatment would reduce this risk, but women should be advised of
the risk and encouraged to stop smoking.
Severe Hypertension
Episodes of acute hypertension can occur in this group of women, who may stop medication
when they conceive despite medical advice. The acute management is as for hypertension
associated with severe pre-eclampsia and then oral therapy can be recommenced.
Hyperthyroidism in Pregnancy
Overview
Hyperthyroidism complicates approximately 12 in 1000 pregnancies. The overwhelming
cause of hyperthyroidism during pregnancy is Graves disease or autoimmune thyrotoxicosis.
Pregnant women with hyperthyroidism are at increased risk for congestive heart failure, thyroid
storm, preterm labor, preeclampsia, fetal growth restriction, and perinatal mortality. Treatment of
hyperthyroid women to achieve adequate metabolic control will result in improved pregnancy
outcomes. However, overtreatment may result in maternal or fetal hypothyroidism. Gestational
transient thyrotoxicosis (GTT) is 10 times more prevalent than Graves disease and may be
caused by the elevated hCG values typically observed with hyperemesis gravidarum. Subclinical
hyperthyroidism effects 1.7% of pregnant women and has only recently been introduced into
clinical practice because of the development of extremely sensitive serum TSH assays.
Subclinical hyperthyroidism is not associated with any adverse maternal pregnancy outcomes.
Treatment of the latter two clinical entities has not been shown to be beneficial.
Graves disease is an organ-specific autoimmune process whereby thyroid-stimulating
autoantibodies attach to and activate TSH receptors. Other less common causes include toxic
multinodular goiter, subacute thyroiditis, adenoma, or iodine-induced thyrotoxicosis. Thyrotropin
receptor activation by hCG, which has some cross-reactivity with TSH, explains the biochemical
and occasional clinical findings of thyrotoxicosis in women with hyperemesis gravidarum and
gestational trophoblastic decrease.
Presentation
As with hypothyroidism, clinical features of hyperthyroidism can be easily confused with
physiologic symptoms of pregnancy. Suggestive complaints or findings include nervousness,
heat intolerance, palpitations, goiter, failure to gain weight or weight loss, and exophthalmos.
GTT usually occurs in women with hyperemesis gravidarum. Subclinical hyperthyroidism
defined as a serum TSH concentration below the statistically defined lower limit of normal with
a serum concentration of fT4 within the reference range, is typically identified in asymptomatic
women.
Complications
Thyrotoxicosis increases the risk of miscarriage. Diagnosis of thyrotoxicosis may be
difficult because some of the symptoms and signs are mimicked by normal pregnancy. Serum
investigations are necessary. Graves disease (GD) tends to improve in pregnancy, and may remit
completely during the second half of pregnancy. Fetal or neonatal thyrotoxicosis affects 210%
of Graves disease pregnancies. This can cause a small for dates baby, premature labour and
intrauterine death or neonatal death. It is also associated withcraniostenosis.
Overtreatment of maternal thyrotoxicosis will cause fetal hypothyroidism and goitre. If
ultrasound scans show a fetal goitre the differential diagnosis is fetal hypothyroidism or fetal
thyrotoxicosis. This is an indication for cordocentesis to measure fetal TSH and fT42.
4

Diagnosis
In women with a depressed serum TSH level (<0.4 mIU/L), clinical hyperthyroidism is
confirmed by an elevation in fT4 (>1.8 ng/dL) concentration. As is true for the diagnosis of
hypothyroidism, one must consider the impact of pregnancy on TSH and possibly fT4 (Table
22.1). Rarely, hyperthyroidism is caused by abnormally high serum triiodothyronine values (T3
thyrotoxicosis). In women with depressed TSH yet normal fT4, evaluation of fT3 or free T3
index may explain a patients hypermetabolic symptoms. Also, evaluation of TSH receptor
antibodies may be helpful in evaluation of women with Graves disease to identify those at risk
for delivery of an infant with fetal or neonatal hyperthyroidism.
Management and Treatment
Thyrotoxicosis during pregnancy can nearly always be controlled by thioamide drugs and
treatment has been associated with improved pregnancy outcomes. Some clinicians prefer
propylthiouracil because it inhibits peripheral conversion of T4 to T3 and it crosses the placenta
less readily than methimazole. Methimazole used in early pregnancy has also been associated
with esophageal and choanal atresia as well as aplasia cutis. Transient leukopenia occurs in
approximately 10% of women treated with thioamides, but this does not require cessation of
therapy. In approximately 0.2%, agranulocytosis develops suddenly, is not dose related, and,
because of its acute onset, serial leukocyte counts during therapy are not helpful. Rather, if fever
or sore throat develops, patients should be instructed to discontinue medication immediately and
report for a complete blood count. The dose of propylthiouracil is empirical, and the American
Thyroid Association recommends an initial daily dose of 100 600 mg for propylthiouracil or
1040 mg for methimazole.
Women with overt hyperthyroidism diagnosed during pregnancy may require a higher
initial dose between 300 and 450 mg/day. The starting daily dose of methimazole is 2040 mg.
The goal of therapy is clinical euthyroidism with free thyroxine in the upper range of normal.
The median time to normalization of thyroid function tests is 68 weeks, but TSH levels may
remain suppressed beyond normalization of fT4. Once euthyroidism is achieved, serial
measurement of TSH and fT4 during each trimester is recommended.
There is currently no convincing evidence that subclinical hyperthyroidism should be
treated in nonpregnant individuals. In fact, it should be considered contraindicated during
pregnancy because maternal antithyroid drugs cross the placenta and may cause fetal thyroid
suppression. There are other alternatives for treatment of overt hyperthyroidism which are rarely
undertaken during pregnancy. For example, although thyroidectomy is typically reserved for
treatment outside of pregnancy, pregnant women who cannot adhere to medical therapy or in
whom therapy is toxic may benefit from surgical management . Ablative radioactive iodine is
contraindicated in pregnancy as it can cause fetal thyroid destruction.

REFERENCES:
1. Queenan JT, Spong CY, Lockwood CJ (eds). Management of High-Risk Pregnancy An
Evidence-Based Approach, Blackwell Publishing, 5th ed, Victoria, 2007.
2. S. E. Robson and J. Waugh (eds). Medical Disorders in Pregnancy: A Manual for
Midwives, Blackwell Publishing. 1st ed, Iowa, 2008.

KEMENTERIAN PENDIDIKAN DAN KEBUDAYAAN

UNIVERSITAS SRIWIJAYA

FAKULTAS KEDOKTERAN
UNIT PENDIDIKAN KEDOKTERAN (UPK)
Zona F. Gedung I Kampus Unsri Indralaya OI Sumatera Selatan, Indonesia Telp. 0711 580061

atau / or Jl. dr. Muh. Ali Komplek RSUP Palembang 30126, Indonesia, Telp. 0711 352342, Fax. 0711 373438,

Skenario B Blok 23 Tahun 2014

Mrs. Mima, 38-year-old pregnant woman G4P3A0 39-weeks pregnancy, was brought by her husband to
the Puskesmas due to convulsion 2 hours ago. She has been complaining of headache and visual
disturbance for the last 2 days. According to her husband, she has been suffering from Graves disease
since 3 years ago, but was not well controlled.
In the examination findings:
Upon admission,
Height = 152 cm; Weight 65 kg;
BP: 180/110 mmHg. HR: 120 x/min, RR: 24 x/m.
Head and neck examination revealed exopthalmus and enlargement of thyroid gland.
Pretibial edema
Obstetric examination:
Outer examination: fundal height 32 cm, normal presentation.
FHR: 150 x/min.
Lab: Hb 11,2 g/dL; she had 2 + protein on urine, cylinder (-)

KEMENTERIAN PENDIDIKAN DAN KEBUDAYAAN

UNIVERSITAS SRIWIJAYA

FAKULTAS KEDOKTERAN
UNIT PENDIDIKAN KEDOKTERAN (UPK)
Zona F. Gedung I Kampus Unsri Indralaya OI Sumatera Selatan, Indonesia Telp. 0711 580061
atau / or Jl. dr. Muh. Ali Komplek RSUP Palembang 30126, Indonesia, Telp. 0711 352342, Fax. 0711 373438,

Skenario B Blok 23 Tahun 2014

Mrs. Mima, 38-year-old pregnant woman G4P3A0 39-weeks pregnancy, was brought by her husband to
the Puskesmas due to convulsion 2 hours ago. She has been complaining of headache and visual
disturbance for the last 2 days. According to her husband, she has been suffering from Graves disease
since 3 years ago, but was not well controlled.
In the examination findings:
Upon admission,
Height = 152 cm; Weight 65 kg;
BP: 180/110 mmHg. HR: 120 x/min, RR: 24 x/m.
Head and neck examination revealed exopthalmus and enlargement of thyroid gland.
Pretibial edema
Obstetric examination:
Outer examination: fundal height 32 cm, normal presentation.
FHR: 150 x/min.
Lab: Hb 11,2 g/dL; she had 2 + protein on urine, cylinder (-)