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Explore a detailed case study of a pregnant patient with SVT, discussing physiological changes, frequency, and management of SVT during pregnancy, along with the impact of thyrotoxicosis on the fetus.
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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 Serious cardiac arrhythmias are uncommon in pregnancy. Cardiac diseases complicate 1% to 4% of pregnancies in women without preexisting cardiac abnormalities.
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 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
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.
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 Maternal complications: - Miscarriage - Infection - Preeclampsia - Preterm delivery - Congestive heart failure - Thyroid storm - Placental abruption
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.