Hyperthyroidism and Thyroid Storm

Tintinalli Chapter 21512/15/05

Prepared by Trent W. SmithLecture 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 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

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

HyperthyroidismSymptoms Signs

Weaknes Goiter/thyroid burit

Fatigue Hyperkinesis

Heat intolerance Opthalmopathy

Nervousness Lid retraction/stare

Increased sweating Lid lag

Tremors Tremor

Palpitations Warm moist skin

Weight loss Hyperreflexia

Hyperdefication Tachycardia/arrhythmia

Dyspnea Systolic hypertension

Menstrual abnormalities 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 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

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 Trauma

DKA MI

CVA PE

Surgery Withdrawal of thyroid med

Iodine administration Palpation of thyroid gland

Ingestion of thyroid hormone

Unknown etiology (20-25%)

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 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

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 21512/15/05

Prepared by Trent W. SmithLecture 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 Signs

Fatigue Hoarseness

Weight Gain Hypothermia

Cold intolerance Periobital puffiness

Depression Delayed relaxation of ankle jerks

Menstrual irregularities Loss of outer third of eyebrow

Constipation Cool, rough, dry skin

Joint Pain Nonpitting edema

Muscle cramps Bracycardia

Infertility 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

• 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

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