Thyroid storm

Thyroid storm is an exaggerated response to hyperthyroidism.

It is seen most frequently in Grave’s disease.

It is a rare condition and associated with a high (10-30%) mortality rate.

It is characterised by:

  1. A hypermetabolic state
  2. Increased sympathetic activity and circulating catecholamines
  3. Increased oxygen consumption

Thyroid storm is usually precipitated by another condition or insult

  • Infection
  • Vascular (MI/Stroke/PE)
  • Perioperative (thyroid surgery, non-thyroid surgery, anaesthesia)
  • Burns or trauma
  • Pregnancy

Diagnosis

TFTs are no different to those found in thyrotoxicosis.

As such, thyroid storm is a clinical diagnosis based on clinical features including:

  1. Pyrexia
  2. Profuse sweating
  3. Tachyarrhythmia
  4. Organ dysfunction

Management

The principles of treatment are based on experience rather than evidence.

These steps also applied to patients with severe hyperthyroidism who do not fully meet the criteria for thyroid storm.

The therapeutic regimen typically consists of multiple medications, each of which has a different mechanism of action. These should not be started without consultation with the endocrine team.

  1. A beta blocker to control the symptoms and signs induced by increased sympathetic drive
    1. Consider propranolol 60 to 80 mg orally every four to six hours, with appropriate adjustment for heart rate and blood pressure
  2. A thionamide to block new hormone synthesis
    1. Thionamides block de novo thyroid hormone synthesis within one to two hours after administration
    2. They have no effect on the release of preformed hormone from the thyroid gland
    3. Consider immediate treatment with PTU 200 mg every four hours
  3. An iodine solution to block the release of thyroid hormone
    1. e.g. Lugol’s iodine
    2. Iodine blocks the release of T4 and T3 from the thyroid gland within hours
    3. Administer iodine one hour after the first dose of thionamide is taken. This prevents the iodine from being used as substrate for new hormone synthesis in patients with toxic adenoma or toxic multinodular goiter (since the etiology of the thyrotoxicosis is frequently uncertain at the time of admission
  4. Glucocorticoids to reduce T4-to-T3 conversion, promote vasomotor stability, possibly reduce the autoimmune process in Graves’ disease, and possibly treat an associated relative adrenal insufficiency
  5. Bile acid sequestrants may also be of benefit in severe cases to decrease enterohepatic recycling of thyroid hormones
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