Tormenta Tiroidea

Thyroid Storm

Intervention in thyroid storm requires a three-step treatment approach.
First, treat the peripheral effects of the hyperthyroidism.
Second, prevent further synthesis of thyroid hormone with antithyroid medications.
And third, prevent further release of thyroid hormone. (See Table 7.)


1. First, treat the peripheral effects of the hyperthyroidism.

β-blockingagents reduce the systemic effects of excess thyroid hormone. If the patient shows cardiovascular stability and has mild symptoms, such as mild tachycardia and tremor, an oral β-blocking
agent can be chosen. If the patient has a more dramatic presentation, such as signs of cardiovascular instability, chest pain, or altered mental status, intravenous β-blocking are required. Based on case reports,initial stabilization with short-acting β-blocking agents that are titrated to effect is the preferred method of treatment. Although the use of propanolol for b-blockade has been related to bad outcomes, it does have the physiologic advantage of decreasing peripheral conversion of T4 to T3 that other b-blocking agents have not been demonstrated to possess.
The fever related to thyroid storm andunderlying infection contributes to tachycardia. This can worsen cardiovascular dynamics, and it complicates the physician’s assessment of the patient’s volume status. Antipyretics are indicated to treat fever. Acetaminophen is the antipyretic of choice. Textbooks recommend avoiding aspirin, as it increases free T3 and T4 concentrations because of protein binding. Although aspirin overdose has beenlinked to thyroid storm, there is little research on the clinical effect of therapeutic doses of aspirin.

The patient has pulmonary edema usually in the setting of volume depletion. For this reason, diuretics should be avoided. The patient needs increased intravascular volume. Diuretics would reduce intravascular volume, possibly precipitating a hypotensive event.
The inciting event in highoutput heart failure is tachycardia. To improve hemodynamics, the heart
rate must be slowed to allow increased cardiac filling time. b-blockade of the heart will slow the heart
and allow the appropriate filling time. The decision to use b-blockers can be difficult in a patient who
has pulmonary edema and hypovolemia and may have underlying cardiac hypomotility. A continuous
infusion of ashort-acting b-blocker is preferred for this reason. The starting dose and decision to use
a loading bolus is controversial.

Ventilation with noninvasive positive airway pressure can facilitate the redistribution of pulmonary edema without the use of diuretics. It is difficult to balance pulmonary edema and fluid replacement.

Judicious replacement of fluid while monitoring the patient’s responseto fluid with invasive monitoring, frequent physical examination, and bedside ultrasonography is the best approach.

2. Second, prevent further synthesis of thyroid hormone with antithyroid medications.
Thioureas, propylthiouracil (PTU), and methimazole block the synthesis of thyroid hormone in the thyroid. PTU is the only thioureas approved for use in pregnancy. PTU is loaded in a dosage of600 to 1000 mg orally, then 200 to 300 mg orally every 4 to 6 h for a total of 1200 mg per day (pediatric dosage 5-7 mg/kg per day divided q8). The methimazole dosage is 20 mg orally or rectally every 4 h (pediatric dosage 0.4-0.7 mg/kg per day divided q8 to q24). There is no parenteral dose of thioureas. PTU is the less expensive thiourea and has the added therapeutic benefit of inhibiting theconversion of inactive T4 to physiologically active T3 in the serum.
Corticosteroids also block the peripheral conversion of T4 to T3. Dexamethasone is the most effective
corticosteroid, administered in a dosage of 2 mg IV every 6 h. An alternative is hydrocortisone 100 mg
IV every 8 h.51 Dexamethasone offers the advantage of not affecting subsequent adrenal testing. There is no significant...