Thyroid Storm

Pathophysiology

• Only 1-2% of patients with hyperthyroidism will progress to thyroid storm. Most patients with thyroid storm have previous symptoms of uncomplicated hyperthyroidism for an average duration of 6-8 mo.
• Thyrotoxicosis + an acute precipitant leads to thyroid storm.
• The exact mechanisms underlying the shift from thyrotoxicosis to thyroid storm are unclear. It is more than simply excess hormone production, as thyrotoxicosis cannot be distinguished from thyroid storm on the basis of hormone levels. An acute precipitant is usually the catalyst for converting thyrotoxicosis to thyroid storm.
• The etiology of thyroid storm includes all the etiologies of thyrotoxicosis. Grave’s disease represents 85% of all thyrotoxicosis. Other etiologies include: toxic diffuse goiter, toxic multinodular goiter, thyroiditis, metastatic follicular carcinoma, struma ovarii, or medications (thyroid hormone, amiodarone, IV contrast).
• Common precipitants include infection (most common, especially pulmonary), ischemia (cardiac, CNS, mesenteric), trauma, surgery (especially thyroid), burns, or medications (thyroid hormone, radioactive iodine, contrast dye).
• Historically, the mortality of untreated thyroid storm approached 100%, but this is now decreasing.

Diagnosis and Evaluation

Signs and Symptoms

• Constitutional symptoms including weight loss, anorexia, weakness, nervousness, heat intolerance, and fever are common.
• Cardiovascular symptoms include palpitations, dyspnea, chest pain, tachycardia, widened pulse pressure, CHF (high output), arrhythmias (PVCs/PACs/A-fib/A-flutter), or shock in severe cases, hypercalcemia.
• CNS symptoms of tremor and restlessness are common. Altered mental status ranging from confusion to psychosis and coma distinguish thyroid storm from severe thyrotoxicosis.
• GI symptoms of diarrhea, abdominal pain, jaundice, and tender hepatomegaly (due to cardiac congestion) may be present.
• Musculoskeletal symptoms may include proximal muscle weakness (thyrotoxic myopathy). Laboratories/Studies
• Thyroid function studies demonstrate a low TSH, elevated Total T4, and Free T4. There are no pathognomonic values, and these studies are often not available during the emergency department time course.
• Complete blood count may demonstrate an anemia of chronic disease and leftward shift of WBCs. The peripheral white count may be elevated from thyroid storm or from precipitating illness.
• Mild azotemia from dehydration may be present.
• Mild hyperglycemia secondary to a hypermetabolic state is common, hypernatremia.
• LFT elevation (liver congestion secondary to high-output CHF) is occasionally found.
• EKG demonstrates sinus tachycardia, PVCs, PACs, A-fib, A-flutter or evidence of concurrent or precipitating ischemia.
• CXR may demonstrate CHF, cardiomegaly, or pulmonary infiltrates suggestive of concurrent disease or precipitating illnesses.
• Head CT scan to rule out other causes of altered mental status may be indicated.
• Other studies are indicated as needed in order to diagnose precipitating/concurrent illness.

ED Management

The treatment of thyroid storm can be divided into three components:

1. supportive care,
2. anti-thyroid therapy, and
3. treatment of acute precipitant and coexisting disease.

Supportive Care

• Fluid replacement is given as needed to compensate for dehydration from insensible and GI losses.
• Supplemental oxygen is indicated for the increased oxygen demand.
• Fever control with cooling measures and acetominophen is indicated. Avoid aspirin as it displaces T4 from thyroglobulin.
• Glucocorticoid replacement is often needed. Plasma cortisol levels are low in thyroid storm. Steroids have been reported to increase survival in doses equivalent to 300 mg of hydrocortisone. Dexamethasone is preferred; added benefit of decreasing peripheral conversion of T3 to T4.

Anti-Thyroid Therapy

• Medications are used to block the peripheral effects of thyroid hormone, to block the synthesis and release of thyroid hormone, and to block the peripheral conversion of thyroid hormone to its active state.
• Block peripheral effects: â-blocking agents inhibit the end-organ effects of thyroid hormone. They have become the cornerstones of thyroid storm management, reducing both morbidity and mortality. Propranalol is the B-blocking agent of choice, as it also helps to block peripheral conversion of T4 to T3. The standard dose of propranalol is 1-2 mg titrated to tachycardia q 10-15 min to a maximum dose of 10 mg. High-output cardiac failure in thyroid storm will benefit from â-blockade, but a-blockers may worsen CHF among patients with preexisting heart failure.
• Block synthesis: Propylthiouricil (PTU) 150-300 mg orally or per NG tube every 6 h inhibits thyroid peroxidase. PTU produces a more rapid effect than methimazole (within 1 h) and has the added advantage of decreasing peripheral conversion of Free T4 to T3.
• Block release: Iodides (potassium iodide, sodium iodide, Lugol’s solution) block release of T4 from the thyroid, but must be given 1-2 h after PTU in order to block the uptake of iodides for synthesis of thyroid hormone. Options include
  1. SSKI: 5-10 gtts po q 12 h or
  2. Lugol’s solution: 30 gtts po q 12 h or
  3. sodium iodide: 1 g IV.
• Block peripheral conversion: Peripheral conversion of T4 accounts for 85% of circulating T3, a more physiologically active form. Dexamethasone, PTU, and propranalol all play a role in blocking peripheral conversion.
• The treatment of thyroid storm necessitates the management of any underlying precipitant.
• The patient in thyroid storm requires ICU admission.

Special Considerations

Apathetic Thyrotoxicosis

• Apathetic thyrotoxicosis is thyrotoxicosis without the usual hyperkinetic manifestations. It is a difficult diagnosis to make. The clinical picture is dominated by cardiac manifestations and altered mental status. CHF and A-fib are common. It is usually seen in the elderly with toxic multinodular goiter. These patients probably have an attenuated response to thyroid hormone and, therefore, do not display the typical symptoms.