Hyperthyroidism and Thyroid Storm

Hyperthyroidism and Thyroid Storm Tintinalli Chapter 215 12/15/05 Prepared by Trent W. Smith Lecture by Dr. Klien MD 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 Normal Thyroid State • Thyroid hormone is reversible bound to various proteins including thyroninebinding 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 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 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 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 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 Hyperthyroidism Symptoms Weaknes Fatigue Heat intolerance Nervousness Signs Goiter/thyroid burit Hyperkinesis Opthalmopathy Lid retraction/stare Increased sweating Tremors Palpitations Weight loss Hyperdefication Lid lag Tremor Warm moist skin Hyperreflexia Tachycardia/arrhythmia Dyspnea Menstrual abnormalities Systolic hypertension Widened pulse pressure 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 Hyperthyroidism • Treatment – Palliative treatment of mild hyperthyroidism is accomplished using B-blockers • Most commonly used is propanolol – Treatment of Graves diseases include longterm 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 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 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 Thyroid Storm • Preciptatnts of Thyroid Storm (tabel 215-4) Infection DKA CVA Surgery Trauma MI PE Withdrawal of thyroid med Iodine administration Ingestion of thyroid hormone Palpation of thyroid gland Unknown etiology (2025%) 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 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 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 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 Thyroid Storm • Drug Treatment of Thyroid Storm (table 216-6) – Decrease de novo synthesis: • Porpythiouracil • Methimazole • Iodine • Lithuim 600-1000mg PO initially, followed by 200-250 mg q 4 hrs 40 mg PO initial dose, then 25 mg PO q6h 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 800-1200 mg PO every day – Prevent relases of hormone (after synthesis blockade intiated) – Prevent peripheral effects: • B-Blocker • Guanethidine • Reserpine 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 30-40 mg PO q 6 h 2.5-5 mg IM q4-6h Hydrocortisone 100 mg IV q 8 h or dexamethosone 2 mg IV q 6 hr Cooling blanket acteaminophen 650 mg PO q 4-6h • Other consideration: • Corticosteroids • Antipyretics 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 Thyroid Storm • Disposition – Admit to the ICU Hypothyroidism and Myxedeam Coma Tintinalli Chapter 215 12/15/05 Prepared by Trent W. Smith Lecture by Dr. Klien MD 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 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 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. 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 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 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 Hypothyroidism • Symptoms and Signs or Hypothyroidism (table 216-2) Symptoms Fatigue Weight Gain Cold intolerance Depression Signs Hoarseness Hypothermia Periobital puffiness Delayed relaxation of ankle jerks Menstrual irregularities Constipation Joint Pain Muscle cramps Infertility Loss of outer third of eyebrow Cool, rough, dry skin Nonpitting edema Bracycardia Peripheral Neuropathy 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 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 Myxedema • Precipitating events include – – – – – – Infection CHF Trauma CVA Exposure to cold Drugs • Sedatives • Lithium • Amiodarone 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 Myxedema • Diagnosis – Must have high clinical suspicion – Commonly has Hx. Of hypothyroidism – Delcine in function is usually insidious in onset Myxedema • Diagnosis cont – Laboratory evaluation may reveal • • • • • • • Anemia Hyponatremia Hypoglycemia ↑ Transaminases ↑ CPK ↑ LDH ↓Po2 and ↑PCo2 on ABG’s Myxedema • Diagnosis cont. – EKG may reveal • • • • Sinus Bradycardia Prolonged QT interval Low voltage Flattened or inverted T waves 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 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 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 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 Hydrocortisone: 100 mg IV q8h Prevent additional loss Passive external rewarming Gentle fluid restriction for dilutional hyponatremia Hypertonic saline for severe hyponatremia Dextrose-containing IV fluids Monitoring Glucocorticoid Hypothermia Electrolyte correction Hypoglycemia Aggressive treatment of presipitating causes Admit patient to a monitored setting Myxedema • Disposition – Admit to appropiately monitored bed Questions • 1. Hyperthyroidism is Characterized by which of the following – A. Fatigue – B. Palpitations – C. Weight Loss – D. Heat intolerance – E. All the above • 2. The most common etiology of hyperthyroidism is – A. Toxic Multinodular – B. Graves – C. Toxic Nodular – D. Amiodarone induces • 3. Typical Feature of Hyperthyroidism include – A. Fatigue – B. Weakness – C. Constipation – E. Cold Intolerance – F. All the above • 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