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also referred to as thyrotoxic crisis, is an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones in individuals with thyrotoxicosis. One major sign of thyroid storm that differentiates it from ordinary hyperthyroidism is a marked elevation of body temperature, which may be as high as 105-106 F (40.5-41.1 C). Thyroid storm is unusual, but is a life-threatening emergency when it does occur. People experiencing symptoms of thyroid storm should be promptly taken to an emergency department.

Infection Abrupt withdrawal of anti-thyroid medications Recent surgery to the thyroid Radioactive iodine treatment (RAI) of the thyroid Excessive palpation of the thyroid gland Overdose of thyroid hormone Pregnancy and labor Severe emotional stress Heart attack in patients with hyperthyroidism Destruction of thyroid tissue by tumors

Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed: Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, although total TH levels may not be increased. Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines. The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines. However, it does not explain why beta-blockers fail to decrease TH levels in thyrotoxicosis.

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 catecholamine-like substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.

GENERAL SYMPTOMS Fever that consistently exceeds 38.5C Profuse sweating Poor feeding and weight loss Respiratory distress Fatigue (more common in older adolescents) GI SYMPTOMS Nausea and vomiting Diarrhea Abdominal pain Jaundice
CARDIOVASCULAR SIGNS Hypertension with wide pulse pressure Hypotension in later stages with shock Tachycardia disproportionate to fever Signs of high-output heart failure Cardiac arrhythmia (Supraventricular arrhythmias are more common, [eg, atrial flutter and fibrillation], but ventricular tachycardia may also occur.) NEUROLOGIC SIGNS Agitation and confusion Anxiety Altered behavior Hyperreflexia and transient pyramidal signs Tremors, seizures Coma Goiter

Usual findings include elevated triiodothyronine (T3), thyroxine (T4) and free T4 levels; increased T3 resin uptake; suppressed thyroid-stimulating hormone (TSH) levels; and an elevated 24hour iodine uptake. TSH levels are not suppressed in the rare instances of excess TSH secretion. CBC count: CBC count reveals mild leukocytosis, with a shift to the left. Liver function tests (LFTs): LFTs commonly reveal nonspecific abnormalities such as elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatinine kinase, alkaline phosphatase, and serum bilirubin. ABG and urinalysis: Measurement of blood gas and electrolyte levels and urinalysis testing may be performed to assess and monitor short-term management.

Chest radiography - may reveal cardiac enlargement due to congestive heart failure. Radiography may also reveal pulmonary edema caused by heart failure and/or evidence of pulmonary infection. CT scanning: Head CT scanning may be necessary to exclude other neurologic conditions if diagnosis is uncertain after the initial stabilization of a patient who presents with altered mental status.

Other Tests
ECG is useful in monitoring for cardiac arrhythmias. Atrial fibrillation is the most common cardiac arrhythmia associated with thyroid storm. Other arrhythmias such as atrial flutter and, less commonly, ventricular tachycardia may also occur.

PROPYLTHIOURACIL (PTU, Propyl-Thyracil) preferred because of its early onset of action and capacity to inhibit peripheral conversion of T4 to T3. Used until the patient is euthyroid treatment of choice during pregnancy

Nursing management:
1. Monitor cardiac parameters. 2. Watch for rash, nausea, vomiting, agranulocytosis, and lupus syndrome. 3. Observe for conversion to hypothyroidism. 4. Must be given by mouth.

Hydrocortisone (Solu-Cortef) Hydrocortisone provides mineralocorticoid activity

and glucocorticoid effects and may help ameliorate decreased adrenal reserve. It reduces the conversion of T4 to T3. prescribed to treat shock or adrenal insufficiency

Propanolol (Inderal)
DOC most widely used in this group; is a nonselective betaadrenergic antagonist. Decreases heart rate, myocardial contractility, BP, and myocardial oxygen demand. Often the only adjunctive drug needed to control thyroid storm symptoms.

Esmolol (Breyibloc)

Beta 1specific antagonist with a short duration of action. a short-acting selective beta 1-antagonist, has been used successfully in children

Potassium iodide, saturated solution (Pima, SSKI, Thyro-Block)

This agent is used to inhibit TH release from the thyroid gland. One mL of SSKI contains 1 g of potassium iodide or 750 mg of iodide (ie, approximately 50 mg iodide/drop and 15 drops per mL). Because of the viscosity, SSKI comes as 15 drops per mL rather than the usual 20 drops per mL.

Strong iodine (Lugol Solution)

Contains 100 mg potassium iodide and 50 mg iodine; provided 8 mg iodide/drop, 20 drops per ml. Iodinated radiographic contrast dyes that contain ipodate (Oragrafin) or iopanoic acid (Telepaque) have also been used and effectively prevent conversion of T4 to T3.

Patients with Graves disease who need urgent treatment of hyperthyroidism but have absolute contraindications to thioamides may be managed acutely with beta-blockers, iodine preparations, and glucocorticoids as described. Subsequently, thyroidectomy may be performed after about 7 days of iodine administration. Iodine reduces the vascularity of the gland and the risk for thyroid storm.

Assess patients LOC and ability to maintain a patent airway. Assess oxygen status via pulse oximetry. Assess cardiac status frequently, noting heart rate and rhythm. Auscultate heart sounds such as S3 or decreased or muffled heart sounds, indicative of heart failure. Watch for chest pain or dyspnea suggesting possible myocardial ischemia. Maintain MAP at 70 mm Hg because MAP les than this can interfere with renal and cerebral perfusion. Administer IV fluid replacements therapy as ordered. Monitor the patients fluid status closely for possible overload. IV fluids containing dextrose are administered to replace liver glycogen stores that have been decreased in the hyperthyroid patient.

Administer antithyroid agents as ordered. When administering PTU, monitor CBC results periodically to detect leukopenia, thrombocytopenia and agranulocytosis. Anticipate administering dexamethasone, as ordered to help suppress T3 and T4 conversion and also to replace cortisol being rapidly metabolized because of the patients hypermetabolic state. Assess the patient for signs and symptoms of hyperglycemia, and monitor blood glucose closely. During antithyroid therapy, watch for symptoms of hypothyroidism, such as weakness, fatigue, sensitivity to cold, weight gain, decreasing LOC and bradycardia.