Thyroid Storm
Thyroid Storm
Thyroid Storm
Thyrotoxicosis and Thyroid Storm Harrison's Principles of Internal Medicine Perioperative management of the thyrotoxic patient
Bindu Nayak, MD, Kenneth Burman, MD, Endocrinol Metab Clin N Am 35(2006) 663-686
Roy W. Langley, MD, Henry B. Burch, MD, Endocrinol Metab Clin N Am 32 (2003) 519534
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Thyroid Storm
Exacerbation of hyperthyroidism Acute, life-threatening, hypermetabolic state Thyroid storm may be the initial presentation of thyrotoxicosis Less than 10% of hospitalized thyrotoxicosis Mortality: 20-30%
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Graves disease Solitary, multinodular goitor Hypersecretory thyroid carcinoma Axis related tumor Hyperthyroidism aggravated by iodine exposure (radiocontrast, Amiodarone)
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Systemic insults Discontinuation of antithyroid drug Pseudoephedrine, salicylate use Most common: infection
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Patients with thyroid storm have relatively higher levels of free thyroid hormones(THs) than patients with uncomplicated thyrotoxicosis, even though total TH levels may not be increased.
Adrenergic receptor activation is a hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of betaadrenergic receptors, thereby enhancing the effect of catecholamines.
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Another theory suggests a rapid rise of hormone levels as the pathogenic source. A drop in binding protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy. Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.
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Heat intolerance and diaphoresis are common in simple thyrotoxicosis -> hyperpyrexia in thyroid storm. Extremely high metabolism increases oxygen and energy consumption. Cardiac findings in thyrotoxicosis -> accelerated tachycardia, hypertension, high-output cardiac failure, and a propensity to develop cardiac arrhythmias.
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irritability and restlessness in thyrotoxicosis -> severe agitation, delirium, seizures, and coma. mild elevations of transaminases and simple enhancement of intestinal transport in thyrotoxicosis -> diarrhea, vomiting, jaundice, and abdominal pain
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37.2 37.7C
40C
A score of 45 or more is highly suggestive of thyroid storm; a score of 25 to 44 supports the diagnosis; and a score below 25 makes thyroid storm unlikely.
Adapted from Burch, HB, Wartofsky, L, Endocrinol Metab Clin North Am 1993; 22:263.
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The mortality rate due to cardiac failure, arrhythmia, or hyperthermia is as high as 30%, even with treatment.
Thyrotoxic crisis is usually precipitated by acute illness, surgery (especially on the thyroid), or radioiodine treatment of a patient with partially treated or untreated hyperthyroidism.
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Medications to halt the synthesis, release, and peripheral effects of thyroid hormone. Controlling adrenergic symptoms and systemic decompensation with supportive therapy
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Antiadrenergic agents
Reserpine Guanethidine
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Thionamides interfere with thyroperoxidasecatalyzed coupling, and inhibitory effect on thyroid follicular cell function and growth Thiouracil (propylthiouracil) v.s. imidazoles (methimazole, carbimazole) SE: abnormal taste, pruritus, urticaria, fever, arthralgia; agranulocytosis, hepatotoxicity, vasculitis
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Thionamides interfere with thyroperoxidasecatalyzed coupling, and inhibitory effect on thyroid follicular cell function and growth Thiouracil (propylthiouracil) v.s. imidazoles (methimazole, carbimazole) SE: abnormal taste, pruritus, urticaria, fever, arthralgia; agranulocytosis, hepatotoxicity, vasculitis
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Large doses of propylthiouracil (600mg loading dose and 200 to 300 mg every 6 h) orally or per rectum; stable iodide is given to block thyroid hormone synthesis via the Wolff-Chaikoff effect : saturated solution of potassium iodide (5 drops SSKI every 6 h), or ipodate or iopanoic acid (0.5 mg every 12 h), may be given orally. (Sodium iodide, 0.25 g intravenously
One hour after the first dose of propylthiouracil, every 6 h is an alternative but is not generally available.)
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Propranolol should also be given to reduce tachycardia and other adrenergic manifestations
(40 to 60 mg orally every 4 h; or 2 mg intravenously every 4 h).
Additional therapeutic measures include glucocorticoids (e.g., dexamethasone, 2 mg every 6 h), antibiotics if infection is present, cooling, oxygen, and intravenous fluids.
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Relative Indications
Symptomatic goiters Pregnancy Severe Graves ophthalmopathy Refractory thyroiditis Amiodarone related Nonremitting subacute thyroiditis Toxic adenoma Rapid control of symptoms required Aversion to antithyroidal drugs and radioablation therapy
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A combination of targets in the thyroid hormone synthetic, secretory and peripheral action pathways. Concurrent treatment to reverse any decompensation of normal homeostatic mechanisms
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Beta-adrenergic blockade Thionamide Oral cholecystographic agents Cortiosteroid Continue after operation?
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Keep regimen after resolution of thyrotoxicity Monitor thyroid hormones To render the patient as close as possible to clinical and biochemical euthyroidism
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High fever
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