Hyperthyroidism and Thyroid Storm

1. Hyperthyroidism and Thyroid Storm Tintinalli Chapter 215 12/15/05 Prepared by Trent W. Smith Lecture by Dr. Klien MD

2. Normal Thyroid State • Synthesis and release of thyroid hormone is controlled by TSH relaesed form the anterior pituitary • TSH is controlled by the release of thyroid releasing hormone (TRH) from the hypothalmus and a negative feedback loop to the pituitary • Thyroid hormone production s dependent on adequate adequate iodine intake

3. Normal Thyroid State • Thyroid hormone is reversible bound to various proteins including thyronine-binding globulin (TBG) • Free unbound portions are biologically active • T4 is the predominant circulating hormone • T4 is deiodinated to t3 • T3 is biologically more active than T4 but has a shorter half-life

4. Hyperthyroidism • Occurs in in all ages • Uncommon under the age of 15 • 10 x’s more common in women (1/10,000) • Graves disease is the most common etiology • 80% of cases in the U.S. • Common in the 3rd and 4th decades • Caused by autoimmune thyroid-stimulating antibodies • Associated with diffuse goiter, opthalmopathy, and local dermopathy

5. Hyperthyroidism • Toxic multinodular and toxic nodular goiters are the next most common etiologies • Usually occurs in older populations • Commonly with previous history of goiter • Often with milder symptoms of thyrotoxicosis

6. Hyperthyroidism • Amiodarone-induced thyrotoxicosis (AIT) • Amiodarone is iodine rich and may cause both hyper and hypothyroidism • Difficult to treat because of incomplete understanding of mechanism • Two major forms exists • Type 1 occurs with a normal thyroid • Type 2 occurs with a abnormal thyroid • Tx. Varies based on the the type

7. Hyperthyroidism • Hyperthyroidism resembles a state of increased adrenergic activity despite a normal or low serum cortisol level • Classic complaints include heat intolerance, palpitations, weight loss, sweating, nervousness, and fatigue

8. Hyperthyroidism

9. Hyperthyroidism • Confirmed by thyroid function test • Elevated free T4 and Low TSH • In some cases of graves disease T4 may be normal and TSH decreased but the patient appears thyrotoxic • T3 level should be done to rule out T3 toxicosis • Hypothyroidism secondary to pituitary adenoma will have elevated TSH levels

10. Hyperthyroidism • Treatment • Palliative treatment of mild hyperthyroidism is accomplished using B-blockers • Most commonly used is propanolol • Treatment of Graves diseases include long-term use of antithyroid medications, radioactive iodine, or subtotal thyroidectomy • Type I AIT is treated with methimazole and potassium perchlorate • Type II AIT is treated with glucocorticoids

11. Hyperthyroidism • Treatment cont. • Toxic multinodular goiter and solitary adenomas may be treated with radioiodine therapy • Thryoiditis is usually self limited and therapy is rarely needed

12. Thyroid Storm • A life threatening hypremetabolic state due to hyperthyroidism • Mortality rate is high (10-75%) despite treatment • Usually occurs as a result of previously unrecognized or poorly treated hyperthyroidism • Thyroid hormone levels do not help to differentiate between uncomplicated hyperthyroidism and thyroid storm

13. Thyroid Storm • Preciptatnts of Thyroid Storm (tabel 215-4)

14. Thyroid Storm • Clinical features • The most common signs are fever, tachycardia out of proportion to the fever, altered mental status, and diaphoresis • Clues include a history of hyperthyroidism, exophthalmoses, widened pulse pressure and a palpable goiter • Patients may present with signs of CHF

15. Thyroid Storm • Clinical features cont. • Common GI symptoms include diarrhea and hyperdefication • Apathetic thyrotoxicosis is a distinct presentation seen in the elderly • Characteristic symptoms include lethargy, slowed mentation, and apathetic facies • Goiter, weight loss , and proximal muscle weakness also present

16. Thyroid Storm • Diagnosis • Thyroid storm is a clinical diagnosis based upon suspicion and treated empirically • Lab work is non specific and may include Leukocytosis, hyperglycemia, elevated transaminase and elevated bilirubin

17. Thyroid Storm • Treatment • Initial stabilization includes airway protection, oxygenation, fluids and cardiac monitoring • Treatment can then be divided into 5 areas: • General supportive care • Inhibition of thyroid hormone synthesis • Retardation of thyroid hormone release • Blockade of peripheral thyroid hormone effects • Identification and treatment of precipitating events

18. Thyroid Storm • Drug Treatment of Thyroid Storm(table 216-6) • Decrease de novo synthesis: • Porpythiouracil 600-1000mg PO initially, followed by 200-250 mg q 4 hrs • Methimazole 40 mg PO initial dose, then 25 mg PO q6h • Prevent relases of hormone (after synthesis blockade intiated) • Iodine Iaponoric acid (Telepaque) 1 gm IV q8h for the first 24 h, then 500 mg bid or Potassium iodide (SSKI) 5 drops PO q6h or Lugol solution 8-10 drops PO q6h • Lithuim 800-1200 mg PO every day • Prevent peripheral effects: • B-Blocker Propanolol (IV) titrate 1-2 mg q 5min prn (may need 240-480mg PO q day) or Esmolol (IV) 500 mcg/kg IV bolus, then 50-200 mcg/kg per min maintenance • Guanethidine 30-40 mg PO q 6 h • Reserpine 2.5-5 mg IM q4-6h • Other consideration: • Corticosteroids Hydrocortisone 100 mg IV q 8 h or dexamethosone 2 mg IV q 6 hr • Antipyretics Cooling blanket acteaminophen 650 mg PO q 4-6h

19. Thyroid Storm • Treatment cont • Propranolol has the additional effects or blocking perpheral conversion of T4-T3 • Avoid Salicylates because it may displace T4 from TBG • If the patient continues to deteriorate despite appropriate therapy circulating thyroid hormone may be removed by plasma transfusion, plasmapheresis, charchoal plasmaperfusion • Remember you must not administer iodine until the synthetic pathway has been blocked

20. Thyroid Storm • Disposition • Admit to the ICU

21. Hypothyroidism and Myxedeam Coma Tintinalli Chapter 215 12/15/05 Prepared by Trent W. Smith Lecture by Dr. Klien MD

22. Hypothyroidism • Occurs when there is insufficient hormone production or secretion • Occurs more frequently in women (0.6 to 5.9 %) • The most common etiologies are • Primary thyroid failure due to autoimmune diseases (Hashimoto thyroiditis is the most common) • Idiopathic causes • Ablative therapy • Iodine deficiency • May be transient • Pathophysiology is unclear but may be viral in nature

23. Hypothyroidism • Etiologies of Hypothyroidism • Primary • Autoimmune etiologies • Hashimotos is the most common • Idopathic • Post ablation (surgical, radioiodine) • Post external radiation • Thryoiditis (subacute, silent, postpartum) • Postpartum thyroiditis occurs within 3-6 months and occurs in 2- 16 % of women • Self limited etiologies, often prededed by hyperthroid phase • Infiltrative disease (lymphoma, sarcoid, amyloidosis, Tuberculosis • Congenital

24. Hypothyroidism • Etiologies of Hypothyroidism • Post Partum • Occurs 3-6 months post partum and occurs in 2-16% of women • Secondary (pituitary) • Neoplasm • Infiltrative Dz. • Hemorrhage • Tertiary (hypothalamic) • Neoplasm • Infiltrative Dz.

25. Hypothyroidism Etiologies of Hypothyroidism • Drugs • Amiodarone • Occurs in 1-32% of patients • Most likely due to the large amount of iodine released in the metabolism of the drug which inhibits thyroid hormone synthesis, release, and conversion of T4 to T3 • Lithium • Acts similarly to iodine and inhibit thyroid hormone release • Iodine (in patients with pre-existing autoimmune disease) • Antithyroid medication

26. Hypothyroidism • Clinical Features • The typical symptoms of hypothyroidism include fatigue, weakness, cold intolerance, constipation, weight gain, and deepening of voice. • Cautaneous signs include dry, scaly, yellow skin, non-pitting, waxy edema of the face and extremities (myxedema): and thinning eyebrows

27. Hypothyroidism • Clinical Features cont. • Cardiac findings include bradycardia, enlarged heart, and low-voltage electrocardiogram • Paresthesia, ataxia, and prolongation or DTR’s are characteristic neurologic findings • See table below for more complete list

28. Hypothyroidism • Symptoms and Signs or Hypothyroidism (table 216-2)

29. Hypothyroidism • Treatment • Most patient with uncomplicated symptomatic Hypothyroidism may be referred to the primary physician for further evaluation and initiation of treatment • If hypothyroidism is due to a secondary etiology initiation of thyroid hormone therapy may exacerbate preexisting adrenal insufficiency

30. Myxedema • Myxedema is a rare life threatening decompensation of hypothyroidism • Usually in individuals with long-standing hypothyroidism • Most often seen in the winter months • More common in elderly women with underdiagnosed or undertreated hypothyroidism

31. Myxedema • Precipitating events include • Infection • CHF • Trauma • CVA • Exposure to cold • Drugs • Sedatives • Lithium • Amiodarone

32. Myxedema • In addition to the clinical features of hypothyroidism patients may present with • Hypothermia • Altered metal status • Coma, delusions, and psychosis (myxedema maddness) • Hyponatremia • Dilutional secondary to decreased free-water clearance • Hypoglycemia • Secondary to impaired gluconeogenesis • Hypotension • Bradycardia • Respiratory Failure • Secondary to decreased strength of respiratory muscle • Hypercapnia and hypoxia is common

33. Myxedema • Diagnosis • Must have high clinical suspicion • Commonly has Hx. Of hypothyroidism • Delcine in function is usually insidious in onset

34. Myxedema • Diagnosis cont • Laboratory evaluation may reveal • Anemia • Hyponatremia • Hypoglycemia • ↑ Transaminases • ↑ CPK • ↑ LDH • ↓Po2 and ↑PCo2 on ABG’s

35. Myxedema • Diagnosis cont. • EKG may reveal • Sinus Bradycardia • Prolonged QT interval • Low voltage • Flattened or inverted T waves

36. Myxedema • Treatment (see table 216-5 below) • No prospective studies on optimal therapy have been done thus treatment recommendations are not uniform • Airway stabilization with adequate oxygenation and ventilation or vital • Cardiovascular status must be monitored closely • Hypothermic patients should be gradually rewarmed with gentle passive external rewarming • Hypotension from reversal of hypothermic vasoconstriction should be avoided

37. Myxedema • Treatment cont. • Hyponatremia typically responds to fluid restrictions. Severe cases may require hypertonic saline with lasixs • Vasopressors are usually ineffective and should only be used in severe hypotension • Lovothyroxine 300-500 mcg slow IVP followed by 50-100 mcg daily

38. Myxedema • Treatment cont. • L-triiodothyronine 25 mcg IV or orally q 8 h is a alternative • This dose should be halved in patients with cardiovascular disease • Hydrocortisone 100 mg IV q 8 hours should be given • Send baseline cortisol level to lab if possible • Precipitating causes should be sought and treated

39. Myxedema • Treatment of Myxedema Coma (table 216-5) • Recognition • Supportive therapy including ventilatory support • Thyroid replacement • Lovothyroxine 300-500 mcg slow IVP followed by 50-100 mcg daily or • T3 25 mcg IV or PO q 8 hrs • Glucocorticoid • Hydrocortisone: 100 mg IV q8h • Hypothermia • Prevent additional loss • Passive external rewarming • Electrolyte correction • Gentle fluid restriction for dilutional hyponatremia • Hypertonic saline for severe hyponatremia • Hypoglycemia • Dextrose-containing IV fluids • Monitoring • Aggressive treatment of presipitating causes • Admit patient to a monitored setting

40. Myxedema • Disposition • Admit to appropiately monitored bed

41. Questions • 1. Hyperthyroidism is Characterized by which of the following • A. Fatigue • B. Palpitations • C. Weight Loss • D. Heat intolerance • E. All the above

42. 2. The most common etiology of hyperthyroidism is • A. Toxic Multinodular • B. Graves • C. Toxic Nodular • D. Amiodarone induces

43. 3. Typical Feature of Hyperthyroidism include • A. Fatigue • B. Weakness • C. Constipation • E. Cold Intolerance • F. All the above

44. 4. T or F Hyperthyroidism is more common in women • 5. T or F Hypothyroidism is more common in women • 6. T or F Mild hyperthyroidism may be treated with B-blockers • Answers 1. E 2. B 3. F 4.T 5.T 6.T