THYROTOXICOSIS MEDICAL MANAGEMENT2. RADIOACTIVE I131 :MOA: > Destroys functioning thyroid cells > Inhibits their ability to replicateDose: 180-370 MBq (5-10mCi) orally (Dep. on goitre size)• 4-6 weeks to be effective (long lag period)• -blockers control symptoms in lag period.• Severe cases: Carbimazole within 48 hrs of I131
THYROTOXICOSIS MEDICAL MANAGEMENT3. Role of -blockers: ONLY SYMPTOMATIC RELIEF (within 12-24 h) Propronolol: 160 mg/day Nadolol: 40-80 mg/dayT3 toxicosis : I131(555-110Mbq), Hemithyroidectomy
THYROTOXICOSIS MANAGEMENT OF ATRIAL FIBRILLATION• Generally control of serum T4 causes a return to sinus rhythm.• Drugs provide symptomatic relief. • Ventricular Rate responds little to Digoxin. • Good response to addition of - blockers. • CARDIOVERSION to revert to sinus rhythm. (Only after TSH/T4 ) • Anti coagulation with Warfarin / Aspirin.
SUBCLINICAL HYPOTHYROIDISM Defined as:“Biochemical evidence of thyroid hormonedeficiency in patients who have few or no apparentclinical features of hypothyroidism.” Previously called: Mild hypothyroidism Early thyroid failure Preclinical hypothyroidism Decreased thyroid reserve
SUBCLINICAL HYPOTHYROIDISM Associated with risk of cardiac, neuropsychiatric and dyslipidemic abnormalities. Risk of neonatal hypothyroidism if encountered in pregnancy. Risk of progression to overt hypothyroidism is high when TSH is elevated and Anti TPO Ab+
SUBCLINICAL HYPOTHYROIDISM Recent guidelines do not recommend routine treatment when TSH levels are < 10 mU/L. (Har 18th ed, Pg 2922) Confirm sustained elevation of TSH over a 3 month period prior to initiating therapy. Start with low dose of 25-50ug/day with the goal of normalising TSH.
23/F, Primi Gravida, no past history of thyroiddisease.TFT during ANC (12 weeks GA) revealed anormal T3, T4 but raised TSH 6.4uIU/ml.No treatment done, at term (36 weeks) herTSH increased to 8.2 uIU/ml (T3, T4 Normal).8 months postpartum:T3: <10ng/dlT4: <0.30 ug/dlTSH: >150.00 uIU/ml
THYROIDFUNCTION INPREGNANCY- An Enigma in its own right!
FACTORS ALTERING THYROID FUNCTION Transient increase in hCG during first trimester stimulates TSH-R Estrogen induced rise in TBG during Trimester I sustained throughout pregnancy Alterations in immune system expression of an underlying thyroid disease Increased thyroid hormone metabolism by placenta Increased urinary excretion of iodide high risk of deficiency in women taking <50ug of iodide/day
The hCG phenomenon Rise in hCG in first trimester is accompanied by a reciprocal fall in TSH that persists upto the middle of pregnancy. Weak binding of hCG, which is present at very high levels to the TSH-R hCG induced changes in thyroid function can result in: Transient gestational hyperthyroidism Hyperemesis gravidarum Rarely warrants use of antithyroid drugs
HYPOTHYROIDISM - PREGNANCY Maternal hypothyroidism occurs in 2-3% of women of child-bearing age. All pregnant women & those planning pregnancy (esp with family history) must be screened for hypothyroisism in first & third trimester. Most pregnant women with primary hypothyroidism require an additional 25-50ug increase to their dose. Subclinical hypothyroidism must be treated TSH Target to treat in pregnacy: 2.5-3.0uIU/ml
HYPERTHYROIDISM - PREGNANCY Rare Pregnancy has an attenuating influence on hyperthyroidism due to associated immunosuppression Medical therapy is the trt of choice
HYPERTHYROIDISM - PREGNANCY PTU or Carbimazole? Both cross placenta, can cause low T4 and high TSH in fetus Maternal T4 flux across placenta is highly variable PTU > 200mg / Carbimazole >15mg is undesirable (esp in III trim) Serum free T4 should be maintained in upper limit of normal and no attempt at normalisation must be made.
HYPERTHYROIDISM - PREGNANCY In most cases maintainence dose must be 200mg PTU or less in early pregnancy. PTU preferred to methimazole due to risk of fetal aplasia cutis with the latter. Emerging reports of a “carbimazole embryopathy” have made PTU the drug of choice. (LeBeau et al. Thy dis dur preg. Endo Clin North Am 2006;35:117-136, vii)
65/M, admitted with c/o severe abdominalpain and vomintings. High grade fever+.On examination, RIF tenderness + withGuarding and rigidiity +.Patient was taken up or emergencylaparotomy for perforated appendix.Post op case kept in SICU, Thyroid profilerevealed:T3: 43 ng/dl (low)T4: 8.7 ug/dl (normal)TSH: 3.8 uIU/ml (normal)
SICKEUTHYROIDSYNDROME- To treat or not to treat?
SICK EUTHYROID SYNDROME Abnormalities of circulating TSH or thyroid hormone levels as a consequence of any acute, severe illness. Major cause of these hormonal changes is the release of cytokines such as IL-6. Unless a thyroid disorder is strongly suspected, the routine testing of thyroid function should be avoided in acutely ill patients.
SICK EUTHYROID SYNDROME (SES) Most common hormone pattern in SES: Low T3 (total & free) Normal T4 Normal TSH Magnitude of fall in T3 correlates with the severity of the illness. Decreased peripheral conversion of T4 T3. leading to increased rT3 (more due to decreased clearance rather than increased production). Low T3 also seen in fasting. (Decreased catabolism)
SICK EUTHYROID SYNDROME (SES) Very sick patients exhibit a fall in total T4 as well (low T4 syndrome). Poor prognosis Fall in T4 is due to altered binding to TBG. (Normal unbound fraction) TSH may range from <0.1 to >20 mIU/L. These alterations maybe due to IL-12 and IL-18.
SICK EUTHYROID SYNDROME (SES) Acute liver failure: Initial rise in total T3 and T4 (but not unbound hormone), due to TBG release. Levels become subnormal with progression to liver failure. Acute psychiatric states (5-30%): Transient increase in total & unbound T4 Normal T3, Low, normal or high TSH HIV: Early disease T3, T4 rise, TSH normal. T3 falls with progression to AIDS. Renal disease: Low T3, normal rT3 (NOT increased rT3) due to increased rT3 uptake by liver.
SICK EUTHYROID SYNDROME (SES) Based on history, severity of patient state, thyroid hormone assays (including rT3) Diagnosis is frequently presumptive Treatment is controversial. Most of the abnormalities recover with recovery from the acute crisis. Monitor TFT during recovery. No need of hormonal replacement unless clinical evidence of hypothyroidism + or low T4 levels.