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.
Dr Mahmoud Abu Esleih
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.
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 has 2 sons and daughters. One son died with Marfan syndrome because of Aortic Arch Dissection which was operated twice.
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.
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
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?
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
The resting HR also increases
about 10 beats per minute
Serious cardiac arrhythmias are uncommon in pregnancy.
Cardiac diseases complicate 1% to 4% of pregnancies in women without preexisting cardiac abnormalities.
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.
A cardiac lesion may predispose to SVT. Congenital heart disease such as Ebstein’s anomaly.
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.
If an ICD is deemed necessary for the mother’s survival, the procedure can be considered.
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
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
HCG related thyrotoxicosis
Toxic multinodular goitre
Figure 2 Most frequent symptoms and signs of hyperthyroidism
Because nonspecific symptoms of hyperthyroidism such as tachycardia, warm moist skin, tremor, and systolic murmur may be mimicked by normal pregnancy, the presence of 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
Vita R et al. (2008) A patient with stress-related onset and exacerbations of Graves disease Nat Clin Pract Endocrinol Metab doi:10.1038/ncpendmet1006
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.
Thyroid stimulating antibodies are present
and cross freely the placenta.
If the diagnosis is not established by these tests, the wisest course is continued observation.
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.
- Small size for gestational age
- Intrauterine fetal death
- Fetal or neonatal THX, including accelerated bone maturation, goiter, and hydrops
- Preterm delivery
- Congestive heart failure
- Thyroid storm
- Placental abruption
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.
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).
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.
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 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.
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
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
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
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.
- 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.
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.
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.
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.
Schematic diagram of the course of subacute thyroiditis, painless (silent) thyroiditis, and postpartum thyroiditis.
An annual TSH level should be performed in these women.
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.
- Fetal tachycardia (fetal heart rate >160 bpm)
- Intrauterine growth restriction
- Fetal goiter
- Advanced Bone age
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
FTD is treated with adjustment of maternal ATD therapy.
Fetal hypothyroidism may require intra-amniotic administration of T4.
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.
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.
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%.
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:
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
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
Surgery may be required in some instances. PTU, propranolol, and iodides may be used for preoperative preparation.
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.
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