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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