thyroid disease and pregnancy ppt
TRANSCRIPT
Sheila F. Perillo, MD
Thyroid Disease and Pregnancy
Thyroid disease is the second most common endocrine disease affecting women of reproductive age
a generic term referring to a clinical and biochemical state resulting in over-production of and exposure to thyroid hormone
Overt hyperthyroidism complicates approximately 2 in 1,000 pregnancies.
Thyrotoxicosis (thyroid storm)
Pregnant women with hyperthyroidism are at increased risk for:spontaneous pregnancy losscongestive heart failurethyroid stormpreterm birthPreeclampsiafetal growth restriction, and increased perinatal morbidity and mortality
the most common cause of thyrotoxicosis in pregnancy
An autoimmune condition characterized by production of thyroid-stimulating immunoglobulin (TSI) and thyroid-stimulating hormone binding inhibitory immunoglobulin (TBII)
facilitate the thyroid-stimulating hormone (TSH) receptor in the mediation of thyroid stimulation and inhibition
Grave's disease
Hyperthyroidism- thyrotoxicosis resulting from an abnormally functioning thyroid gland.
Thyroid storm- acute, severe exacerbation of hyperthyroidism
associated with hyperemesis gravidarumcan be due to high levels of human chorionic
gonadotropin (hCG) resulting from molar pregnancyhigh hCG levels TSH receptor stimulation and
temporary hypothyroidismrarely symptomatic treatment with antithyroxine drugs- not beneficial expectant managementnot associated with poor pregnancy outcomes
gestational transient thyrotoxicosis
Thyroxine (T4), the major secretory product of the thyroid gland, is converted in peripheral tissues to triiodothyronine (T3)
T3- biologically active form T4- secretion is under the direct control of pituitary
TSHT4 and T3 are transported in the peripheral circulation
bound to thyroxine-binding globulin (TBG), transthyretin (formerly called "prealbumin") and albumin.
Less than 0.05% of plasma T4, and less than 0.5% of plasma T3, are unbound and able to interact with target tissues
Impact of Pregnancy on Thyroid:
20 weeks' gestationreduced hepatic clearanceestrogen-induced change in the structure of TBG that
prolongs serum half-life
plasma TBG increases 2.5 folds 25% to 45% increase in serum total T4 (TT4) from a pregravid level of 5 to 12 mg to 9 to 16 mg
** Total T3 (TT3) increases by about 30% in the first trimester and by 50% to 65% later
Pregnancy increase in available protein transient change in free T4 (FT4) and free thyroxine index (FTI) in the first trimester (possibly related to an increase in hCG)
Increased concentrations of TSH stimulate restoration of the free serum T4 level, such that FT4 and FTI levels are generally maintained within the normal non-pregnant range
Increase in volumeEcho structure remains unchanged (Plasma iodide
levels decrease in pregnancy due to fetal use of iodide and increased maternal renal clearance)
15% to 18% increase in size of the thyroid glandenlargement usually resolves after delivery not associated with abnormal thyroid function tests
Ultrasound evaluation of the thyroid gland during pregnancy
Diagnostic Approach:
Mild hyperthyroidism:Fatigue increased appetiteVomitingPalpitationsTachycardiaheat intolerance, Increased urinary
frequency InsomniaEmotional instability
The suspicion increases if patient has TremorNervousnessfrequent stoolsexcessive sweatingbrisk reflexesmuscle weaknessgoiterHypertensionweight loss. Grave's ophthalmopathy (stare, lid
lag and retraction, exophthalmos) dermopathy (localized or pretibial
myxedema)
Untreated hyperthyroidism poses considerable maternal and fetal risks, including preterm delivery, severe preeclampsia, heart failure, and thyroid storm
- a hypermetabolic complication of hyperthyroidism:
hyperpyrexia (temperature >41ºC)cardiovascular compromise (tachycardia out of
proportion to the fever, dysrhythmia, cardiac failure)gastrointestinal upset (diarrhea)central nervous system changes (restlessness,
nervousness, changed mental status, confusion, and seizures).
Characteristics of Thyroid Storm:
Thyroid storm is a clinical diagnosis, and treatment should be initiated before confirmatory test results are available.
Other signs of thyrotoxicosis in any patient with postpartum congestive heart failure: tachycardiasevere hypertension central nervous system (CNS) features, such as coma
after cesarean section or seizures suggestive of eclampsia
Delay in diagnosis increase the risk of maternal mortality
Patients without classic symptoms
Thyroid storm is usually seen in patients with poorly controlled hyperthyroidism complicated by additional physiologic stressors, such as infection, surgery, thromboembolism, preeclampsia, and parturition
Laboratory Tests: CBC (Leukocytosis)
Thyroid function test results are consistent with hyperthyroidism (elevated FT4/FT3 and depressed TSH) but they may not always correlate with the severity of the thyroid storm
Baseline electrolyte (occasionally hypercalcemia)
Glucose Renal Liver function testing (elevated
hepatic enzymes)
Coagulation studies
CT or MRI of the brain (unconscious patients, signs of focal CNS signs)
blood, uterine and wound cultures (as appropriate)
chest x-ray 12-lead electrocardiogram
(ECG) and continuous cardiac monitoring
Pulse oximetry blood gas analysis
Thyroid storm is a clinical diagnosis based on severe signs of thyrotoxicosis:significant hyperpyrexia (>103ºF or >41ºC)
neuropsychiatric symptoms Tachycardia with a pulse rate exceeding 140 beats/min congestive heart failure Gastrointestinal symptoms (nausea and vomiting)
accompanied by liver compromise
Management of thyroid Storm
Obstetric intensive care unit (ICU)/ ICU that has continuous fetal monitoring and can handle an emergent delivery
Therapy is designed to:Reduce the synthesis and release of thyroid hormoneRemove thyroid hormone from the circulation and
increase the concentration of TBGBlock the peripheral conversion of T4 to T3Block the peripheral actions of thyroid hormoneTreat the complications of thyroid storm and provide
supportIdentify and treat potential precipitating conditions
Management of Thyroid Storm:
Supportive adjunctive care for the patient in thyroid storm are:IV fluids and electrolytesCardiac monitoringConsideration of pulmonary artery catheterization (central
hemodynamic monitoring to guide beta-blocker therapy during hyperdynamic cardiac failure)
Cooling measures: blanket, sponge bath, acetaminophen, avoid salicylates (risk of increased T4). Acetaminophen is the drug of choice
Oxygen therapy (consider arterial line to follow serial blood gases)
Nasogastric tube
Management of Thyroid Storm
Reduce synthesis of thyroid hormones:Thionamides : propylthiouracil (PTU) Methimazole)
inhibit iodination of tyrosine -- leading to reduce synthesis of thyroid hormones and block peripheral conversion of T4 to T3 can reduce the T3 concentration by 75%
Medications:
Iodide (Lugol's iodine, SSKI (Strong Solution of Potassium Iodide), sodium iodide, orografin, or lithium carbonate)
inhibit proteolysis of thyroglobulin block the release of stored hormone
**Because one of the side effects is an initial increase in production of thyroid hormone, it is therefore very important to start PTU before you give iodides
Glucocorticoids
block release of stored hormone (as do iodides), and peripheral conversion of T4 to T3 (as do thionamides)
They may also bolster adrenal function, and prevent adrenal insufficiency
PTU orally or via nasogastric tube, 300-800 mg loading dose followed by 150-300 mg every 6 hours
One hour after instituting PTU give: Sodium iodide, 500 mg every 8-12 hours or oral Lugol's solution, 30-60 drops daily in divided doses.
Iodides may be discontinued after initial improvement
Give adrenal glucocorticoids (Hydrocortisone, 100 mg IV every 8 hour, or Prednisone, 60 mg PO every day, or
Dexamethasone, 8 mg PO every day)
Glucocorticoids may be discontinued after initial improvement
Dosage/ Management:
Beta-blocker agents -- Propranolol can be used to control autonomic symptoms (especially
tachycardia)
Some effect on inhibition of peripheral conversion of T4 to T3, but will not alter thyroid hormone release nor prevent thyroid storm.
Use with caution: it has a tendency to increase pulmonary diastolic pressure, and cardiac failure is a frequent presentation of thyroid storm
Reserved for heart rates of 120 beats per minute or higher
Propranolol, labetalol, and esmolol
Medications to control maternal tachycardia
Propranolol,1-2 mg/min IV or dose sufficient to slow heart rate to 90 bpm; or 20-80 mg PO or via nasogastric tube every 4-6 hourly
Esmolol, a short-acting beta-acting antagonist given IV with a loading dose of 250 to 500 µg/kg of body weight followed by a continuous infusion at 50 to 100 µg/kg/min
Echocardiogram and/or pulmonary artery catheter to help guide management, especially in cardiac failure
If patient has severe bronchospasm -- give 1-5 mg reserpine every 4-6 hours or 1 mg/kg orally of guanethidine every 12 hours.
Dosages:
Heart failure due to cardiomyopathy from excessive thyroxine in women with uncontrolled hyperthyroidism is more common in pregnant womenSame treatment as that of thyroid stormMedical emergencyGive phenobarbital to control restlessness
Phenobarbital: 30 to 60 mg orally every 6-8 hours as needed
Plasmapheresis or peritoneal dialysis to remove circulating thyroid hormone reserved for patients who do not respond to conventional
therapySubtotal thyroidectomy (during second-trimester
pregnancy) or radioactive iodine (postpartum)for unsuccessful conventional therapy
Most asymptomatic women should have a TSH and free T4 performed approximately 6 weeks postpartum
PTU and methimazole are excreted in breast milkPTU is largely protein bound and does not seem to pose
a significant risk to the breastfed infant Methimazole has been found in breastfed infants of
treated women in amounts sufficient to cause thyroid dysfunctionat low doses (10-20 mg/d) it does not seem to pose a major risk
to the nursing infant
Postpartum Care:
PTUfirst-line treatment for Grave's disease in pregnancy due
to lower risks of teratogenicity than methimazole.It crosses the human placenta and associated with fetal
hypothyroidism Cordocentesis is sometimes recommended to test fetal
thyroid functiondoes not readily crosses membranes milk concentrations are quite low
Teratogenic effects of Antithyroid Medications:
Methimazole (Thiamazole, Mercazole, Tapazole): Second-line treatment of Grave's diseasecrosses the human placenta and can induce fetal goiter
and even cretinism in a dose-dependent fashioncommonly associated with fetal anomalies such as
aplasia cutis, esophageal atresia, and choanal atresiaLong-term follow-up studies of exposed children:
no deleterious effects on their thyroid function or physical and intellectual development with doses up to 20 mg/d
excreted in breast milk
The American College of Obstetricians and Gynecologists (ACOG) recommends treatment for women with a systolic blood pressure higher than 170 mmHg and/or diastolic blood pressure above 109 mmHg
There is no consensus whether lesser degrees of hypertension require treatment during pregnancy because antihypertensive therapy improves only the maternal, not the fetal, outcome in women with mild to moderate chronic hypertension
Radioactive iodine (iodine-131; I-131): contraindicated in pregnant womencost-effective, safe, and reliable treatment for
hyperthyroidism in non-pregnant women ACOG recommendation: women should avoid pregnancy
for 4-6 months following treatmentDetrimental effects on the thyroid of the developing
fetus as a result of I-131 treatment for thyrotoxicosis of the mother in the first trimester of pregnancy are reported.
Breast-feeding should be avoided for at least 120 days after treatment
Thyroid storma life-threatening condition, requiring early recognition and aggressive
therapy in an intensive care unit setting.
During gestation, women with hyperthyroidism should have their thyroid function checked every 3-4 weeks.
Grave's disease represents the most common cause of maternal hyperthyroidism during pregnancy
Only 0.2% of gestations are complicated by thyroid storm and more than 90% of cases are caused by Grave's disease
Increased production of thyroid hormone occurs when autoantibodies
(thyroid-stimulating antibody [TSAb] -- formerly known as LATS [long-acting thyroid stimulator]) against TSH receptors -- acts as TSH agonists.
Summary
Thyroid Storm: Critical Care In ObstetricsWHEC Practice Bulletin and Clinical Management
Guidelines for healthcare providers. Educational grant provided by Women's Health and Education Center (WHEC).
Published: 2 June 2010