Transcript SVT Peg - Latest Publications | An

Case Presentation
Dr Mahmoud Abu Esleih
L.J. a 38 year old female patient was
admitted to Thabet Hospital of Tulkarem
on 19.5 2009 with Palpitation and Tremor.
The patient is pregnant (32 wks) LMP
1.10.2008.
The patient is known to have attacks of
palpitation since 2003, which were more
frequent during her pregnancies. Since
then she was diagnosed to have
thyrotoxicosis.
Propranolol and PTU were prescribed. She
was maintained on them since 2003.
In the ER she was tachycardic >180 bpm.
Monitor showed narrow complex
tachycardia 190 bpm.
Carotid Massage was tried three times by a
colleague but there was no response.
She was given Verapamil 2 doses IV but
there was no response.
The patient was hemodynamically stable.
BP 110/60, there was no dizziness, no
sweating. She was given Adenosine 6 mg
but there was no response. Another
carotid massage was done with relief of
SVT.
The patient has 2 sons and daughters. One
son died with Marfan syndrome because
of Aortic Arch Dissection which was
operated twice.
PMH was negative except for a previous CS
and abortion and curettage.
Hb 11.9 g, WBC 10800, PLT 284000, BUN 15,
creatinine 0.6, RBS 103, Na 140, K 4.7,
TSH 0.54, FT3 2.25, FT4 0.95.
The second day the patient was stable and
was discharged in good general condition
on Propranolol and PTU.
After 1 mo she attended the Outpatient
Clinic with good general condition and no
palpitation with normal thyroid function.
On 8.7.2009 the patient was admitted to the
hospital with Labour Pain. Abd US
showed single viable fetus. She
underwent CS with good outcome. The
second day after CS the patient developed
an attack of SVT for which she was given
Amiodarone 300 mg.
TSH for the baby was 2.73 and was repeated
after 1 mo and was 2.4
What to discuss?
Physiologic Changes in pregnancy?
How frequent is SVT in pregnancy?
Effect of pregnancy on SVT and vice versa.
Management of SVT in Pregnancy
How safe are non pharmacological therapeutic
procedures on the fetus?
How safe are antiarrhythmics on the fetus?
How common is thyrotoxicosis in pregnancy?
Diagnosis of thyrotoxicosis in pregnancy?
Management of thyrotoxicosis in Pregnancy.
Safety of ATD in Pregnancy.
Effect of thyrotoxicosis on the fetus
Effect of therapy on the fetus
BP decreases
The resting HR also increases
about 10 beats per minute
Cardiac Arrhythmias in Pregnancy
Cardiac diseases complicate 1% to
4% of pregnancies in women without
preexisting cardiac abnormalities.
Serious cardiac arrhythmias are uncommon
in pregnancy.
Effect of Pregnancy on SVT
Pregnancy may predispose to and
exacerbate symptoms of PSVT. Several
case reports and a retrospective study of
60 patients with documented SVT showed
pregnancy to be associated with both an
increased risk, and an exacerbation of
symptoms.
Clearly, both mother and fetus are at
risk when SVT occurs during
pregnancy. There are no maternal
deaths as a result of arrhythmia
reported. There is minimal information
on morbidity associated with SVT in
pregnancy.
However, emergency CS is often a
consequence, increasing maternal risk
and if pre-term, increasing fetal risk.
A cardiac lesion may
predispose to SVT.
Congenital heart disease
such as Ebstein’s anomaly.
Treatment of SVT in pregnancy may also affect the fetus
Carotid massage
Facial ice immersion
Direct current electrical shock has been used at all
stages in pregnancy without significant complication
The amount of current reaching the fetus is
thought to be negligible. However, transient
fetal dysrhythmia has been described.
Sanchez–Diaz et al. reported 20 cases in
which electrical cardioversion was used
on an emergency basis during pregnancy.
All of the patients were successfully
cardioverted, and no immediate adverse
effects were reported.
Ueland et al. reviewed 15 cases of electrical
cardioversion use in pregnancy. The
cardioversion was successful in 13 of the
15 cases, using energy levels of 50 to 300
joules. One fetus developed a nonreactive
heart rate tracing after cardioversion and
emergency CS was subsequently
performed for suspected fetal distress,
which in fact was not present.
If an ICD is deemed necessary for the mother’s
survival, the procedure can be considered.
Radiofrequency ablation generally requires
the use of large amounts of fluoroscopy,
far more than would be required for
implantation of an ICD, for instance.
Therefore, this procedure should virtually
never be performed during pregnancy
with the exception of a life-threatening
arrhythmia.
A case report showed no adverse effects in
the fetus following an ICD discharge.
The major concern during treatment of SVT during pregnancy
is the potential for adverse effects on the fetus, as all
commonly used antiarrhythmic drugs cross the placental
barrier to some extent.
All antiarrhythmic drugs should be regarded as potentially toxic to the fetus
and should be avoided if possible, especially during the first trimester
Thyrotoxicosis in pregnancy
Thyroid abnormalities affect 5-15% of
pregnant women & 4-8% of post partum
women. Hyperthyroidism occurs in 0.2%
of pregnancies
Thyroid disease has adverse effects on
maternal health, the course of pregnancy, and
development of the fetus
Up to 60% of women with hyperemesis
gravidarum have a subnormal TSH and
nearly 50% have an elevated free T4
concentration
Causes of Hyperthyroidism
Grave’s disease
HCG related thyrotoxicosis
Toxic adenoma
Toxic multinodular goitre
Thyroiditis
In some women, the THX precedes
the pregnancy. In others, THX
begins during pregnancy, usually in
the first trimester or early in the
second. Relapses of THX also
occur during pregnancy in women
who were in remission before
becoming pregnant.
Figure 2 Most frequent symptoms and signs of hyperthyroidism
Because nonspecific symptoms of hyperthyroidism such as tachycardia,
warm moistVita
skin,
tremor,
andwith
systolic
murmur
be mimicked
by normal
R et al.
(2008) A patient
stress-related
onset andmay
exacerbations
of Graves disease
Nat Clinof
Pract
Endocrinol
Metab doi:10.1038/ncpendmet1006
pregnancy, the presence
classic
thyroid
ophthalmopathy, a significant
goiter, or pretibial myxedema may point to a diagnosis of true GD. A careful
PE should be performed in all patients
Diagnosis of hyperthyroidism
Patients suspected of having
hyperthyroidism require measurement of
serum TSH, T4, T3 levels, and thyroid
receptor antibodies. However,
interpretation of TFTs must be made in
relation to the hCG-mediated decrease in
serum TSH levels and the increase in TBG
concentrations that occur during
pregnancy.
Pregnant woman with GD
Thyroid stimulating
antibodies are present
and cross freely the
placenta.
50 percent higher than normal
If the diagnosis is not established by
these tests, the wisest course is
continued observation.
Adverse effects of maternal
hyperthyroidism: pregnancy outcome
The risk of complications for both mother
and fetus is related to the duration and
control of maternal hyperthyroidism. Fetal
and neonatal risks of maternal
hyperthyroid disease are related to the
disease itself and/or to the medical
treatment of the disease.
Maternal complications:
- Miscarriage
- Infection
- Preeclampsia
- Preterm delivery
- Congestive heart failure
- Thyroid storm
- Placental abruption
Fetal and neonatal
complications:
- Prematurity
- Small size for gestational age
- Intrauterine fetal death
- Toxemia
- Fetal or neonatal THX,
including accelerated bone
maturation, goiter, and hydrops
THERAPEUTIC OPTIONS
In managing hyperthyroidism during
pregnancy, it should be remembered
that two patients are being treated:
the mother and the fetus. A balance
must be made in optimizing
treatment for one without impinging
on the other.
If a subnormal serum TSH concentration is
detected during gestation, hyperthyroidism
must be distinguished from both normal
physiology during pregnancy and HG
because of the adverse effects of overt
hyperthyroidism on the mother and fetus.
Differentiation of GD from gestational THX
is supported by evidence of autoimmunity,
a goiter, and presence of TSH receptor
antibodies (TRAb).
For overt hyperthyroidism due to GD or
hyper-functioning thyroid nodules, ATD
therapy should be either initiated (for
those with new diagnoses) or adjusted
(for those with a prior history) to maintain
the maternal thyroid hormone levels for
free T4 in the upper nonpregnant
reference range.
Antithyroid drugs
Thionamide (PTU) drugs are
considered first-line therapy.
Several studies have shown no significant
correlation between daily maternal ATD
dose and fetal thyroid status. Elevation in
serum TSH concentration can still be
found in newborns of 23% of mothers
taking low-dose PTU (100 mg daily or
less) and 15% of those taking low-dose
MMI (10 mg daily or less).
Until recently, it was recommended that
ATD doses be individualized such that
maternal serum FT4 levels were in the
upper third of or just above the normal
nonpregnant reference range.
Teratogenicity
No prospective studies to establish causality.
Multiple case reports have associated MMI
with two types of congenital anomalies:
choanal or esophageal atresia, and aplasia
cutis (Incidence 0.03%).
These malformations can occur as part of an
‘embryopathy’ that also includes
developmental delay, hearing loss, and
dysmorphic facial features.
No case reports of aplasia cutis and only rare
anecdotal reports of embryopathies associated with
PTU ingestion.
Propranolol
A useful treatment for hyperthyroid
symptoms and preparation for
thyroidectomy is BB, specifically with
propranolol; however, continued
propranolol use in pregnancy has been
associated with fetal growth retardation.
Iodide
Iodide has not been recommended in the
treatment of hyperthyroidism during
pregnancy because of its association with
neonatal goiter and hypothyroidism when
given in conjunction with thionamides.
Previously treated Grave’s disease
May escape detection but the fetus is at risk
because thyroid stimulating antibodies cross
the placenta and cause fetal THX.
Fetal THX may present with fetal tachycardia,
IUGR, goitre, cardiomegaly, premature fusion
of the cranial sutures
Measure antibodies early in pregnancy & at 30
weeks.
Treat fetus by giving PTU
Complications of treatment
PTU & CMZ are both safe for use in
pregnancy & both cross the placenta
PTU & CMZ in high doses used in
conjunction with T4 can cause fetal
hypothyroidism
Rare but potentially lethal agranulocytosis
caused by PTU
Surgery
Owing to obstetric and fetal risks, surgery
is not regarded as first-line therapy, but
might be considered if necessary for the
mother’s health.
First trimester
spontaneous abortions
Second trimester
Preoperative preparation includes ATD therapy
(if not contraindicated), short-term use of
iodides, and BB. THX should be controlled as
best as possible to lower the risk of thyroid
storm.
Surgery is reserved for patients who meet 1
of the following criteria:
- High doses of ATDs (PTU > 300 mg, MMI >
20 mg) are required.
- Clinical hyperthyroidism cannot be
controlled.
- Fetal hypothyroidism occurs at the dosage
needed for maternal control.
- The patient cannot tolerate ATDs (severe
adverse reaction).
- The patient is noncompliant.
- Malignancy is suspected.
Radioactive iodine
Administration of radioactive iodine for
diagnostic or therapeutic purposes is
contraindicated in pregnancy and
lactation. After 10–12 weeks of gestation,
once the fetal thyroid has the ability to
concentrate iodine, congenital
hypothyroidism can occur.
Gestational Thyrotoxicosis
A small percentage of pregnant women (2
percent in one survey) have transient THX
during the latter part of the first trimester
of pregnancy. As a group, they have few
symptoms and signs of THX and no
thyroid enlargement, but some have
nausea, vomiting, and weight loss.
The THX usually subsides in 4 to 8 weeks
as CG secretion declines from its peak at
10 to 12 weeks of pregnancy.
Postpartum Thyroiditis
PPT occurs in 1 to 6 percent of postpartum
women of whom about half have THX.
Thyrotoxicosis may occur in the first several months
after delivery. Three forms of PPT are recognized:
- New development of Graves' hyperthyroidism.
- Recurrence of Graves' hyperthyroidism.
- THX occurs as part of the syndrome of PPT. -
PPT is a clinically heterogeneous disorder; some women have only transient THX, others have
transient THX followed by transient hypothyroidism,
and still others have only transient hypothyroidism.
Schematic diagram of the course of subacute
thyroiditis, painless (silent) thyroiditis, and
postpartum thyroiditis.
An annual TSH level should be performed in
these women.
Fetal thyroid dysfunction
If the mother is not treated, there is an
increase in congenital anomalies and
increased fetal loss resulting from
spontaneous abortion and premature
delivery. These are probably direct effects
of maternal THX, as they do not occur in
mothers who receive ATD.
Suggestive findings:
- Fetal tachycardia (fetal heart rate >160 bpm)
- Intrauterine growth restriction
- Fetal goiter
- Hydrops
- Advanced Bone age
- Craniosynostosis
- CHF
Diagnosis and
screening
Fetal diagnosis requires umbilical cord sampling to
differentiate hyperthyroidism from hypothyroidism.
In women with a past or current history of autoimmune
thyroid disease, thyroid antibody values should be
checked at the end of the first pregnancy. For those with
positive results for TR–stimulating antibodies or those
taking ATDs, fetal US should be performed at least
monthly after 20 weeks of gestation.
Diagnosis of FTD is challenging
Causes of FTD
Treatment of FTD
The risk of fetal or
neonatal thyrotoxicosis
is related to the
mother's level of TR–
stimulating antibodies.
Fetal or neonatal
hypothyroidism may
also be due to
maternal use of ATDs.
FTD is treated with
adjustment of
maternal ATD
therapy.
Fetal hypothyroidism
may require intraamniotic
administration of T4.
Neonatal thyroid dysfunction
Neonatal THX due to persistence of
maternal TRAbs occurs in about 1% of
babies born to mothers with either active
or previously treated GD and lasts for up
to 3 months. Multiple studies have
attempted to predict neonatal thyroid
status using maternal antibody levels.
Baby of mother with Grave’s
disease in pregnancy
All newborns of mothers with GD should be
evaluated for thyroid dysfunction and treated
if necessary.
Cord blood should be reserved at
delivery for measurement of neonatal
serum TSH and either total T4 or FT4
levels.
It has also been suggested that a
hyperthyroid fetal environment might
cause central congenital hypothyroidism.
The incidence of central congenital
hypothyroidism in these cases has been
found to be about 0.9%.
Screening
Although the benefits of universal
screening for hypothyroidism may not be
justified by current evidence, we
recommend case finding among the
following groups of women at high risk
for thyroid dysfunction:
1. Women with a history of hyperthyroid or
hypothyroid disease, PPT, or thyroid
lobectomy
2. Women with a FH of thyroid disease
3. Women with a goiter
4. Women with thyroid antibodies
5. Women with symptoms or clinical signs
suggestive of thyroid Dysfunction,
including anemia, elevated cholesterol,
and hyponatremia
6. Women with type I DM
7. Women with other autoimmune disorders
8. Women with infertility should have
screening with TSH as part of their
infertility work-up.
9. Women with prior therapeutic head or
neck irradiation.
10. Women with a prior history of
miscarriage or preterm delivery
Targeting ATD treatment to maintain maternal
serum free T4 levels at the upper limit of the
nonpregnant T4 range usually protects the
fetus from hypothyroidism. Close following of
maternal T4 and TSH levels, assay of TRAb,
and fetal US including the thyroid are
recommended for guiding therapy and fetal
blood sampling is rarely needed.
Fetal hyperthyroidism does not occur during
pregnancies in which TRAb levels are normal
and ATD is not administered.
Surgery may be required in some instances.
PTU, propranolol, and iodides may be used
for preoperative preparation.
Fetal
TRAb (either TSH receptor-stimulating or -binding
antibodies) freely cross the placenta and can
stimulate the fetal thyroid. These antibodies should
be measured before pregnancy or by the end of the
second trimester in mothers with current Graves’
disease, with a history of GD and treatment with
131I or thyroidectomy, or with a previous neonate
with GD. Women who have a negative TRAb and do
not require ATD have a very low risk of fetal or
neonatal thyroid dysfunction.
In women with elevated TRAb or in women
treated with ATD, fetal US should be
performed to look for evidence of fetal thyroid
dysfunction that could include IUGR,
hydrops, presence of goiter, or cardiac
failure.
Umbilical blood sampling should be considered
only if the diagnosis of fetal thyroid disease is
not reasonably certain from the clinical data
and if the information gained would change
the treatment.
The fetal thyroid begins concentrating iodine at 10–12
wk gestation and is under control of fetal pituitary TSH
by approximately 20 wk gestation. Fetal serum levels of
TSH, TBG, free T4, and free T3 increase throughout
gestation, reaching mean adult levels at approximately
36 wk. TSH does not cross the placenta