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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 xs 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 Increased sweating Tremors Palpitations Weight loss Hyperdefication Dyspnea Menstrual abnormalities

Signs
Goiter/thyroid burit Hyperkinesis Opthalmopathy Lid retraction/stare Lid lag Tremor Warm moist skin Hyperreflexia Tachycardia/arrhythmia 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 Iodine administration Ingestion of thyroid hormone Trauma MI PE Withdrawal of thyroid med 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 B-Blocker Guanethidine Reserpine 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 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

Prevent relases of hormone (after synthesis blockade intiated)

Prevent peripheral effects:

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 DTRs are characteristic neurologic findings See table below for more complete list

Hypothyroidism
Symptoms and Signs or Hypothyroidism (table 216-2)
Symptoms
Fatigue

Signs
Hoarseness

Weight Gain
Cold intolerance Depression Menstrual irregularities Constipation

Hypothermia
Periobital puffiness Delayed relaxation of ankle jerks Loss of outer third of eyebrow Cool, rough, dry skin

Joint Pain
Muscle cramps Infertility

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 ABGs

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

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