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I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK.  I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature. 

Monday, October 30, 2017

Thyroid Storm

Thyroid hormone exists in two forms: thyroxine and triiodothyronine. The ratio of thyroxine to triiodothyronine released in the blood is about 20:1 and peripherally, thyroxine is converted to the active triiodothyronine (T3), which is three to four times more potent than thyroxine.

Basic Terminologies
  • Primary hyperthyroidism is caused by the excess production of thyroid hormones from the thyroid glands. 
  • Secondary hyperthyroidism is caused by the excess production of thyroid-releasing hormones (Hypothalamus) or thyroid-stimulating hormones (Pituitary).

  • Hyperthyroidism refers to excess circulating hormone resulting only from thyroid gland hyper function. Most commonly cause by Graves' Disease. 
  • Thyrotoxicosis refers to excess circulating thyroid hormone originating from any cause. 
  • Thyroid storm is an extreme manifestation of thyrotoxicosis. It presents as an acute life-threatening hypermetabolic state caused either by excessive release of thyroid hormones or due to altered peripheral response to thyroid hormone following a precipitating event. 

Causes of Hyperthyroidism
  • Graves' Disease
  • Toxic Goitre
  • Thyroiditis (Viral, Radiation)
  • Hashimoto's
  • Secondary (Pituitary or Hypothalamus related)
  • Thyrotoxicosis Factitia
  • Drug Induced (Amiodarone, Interleukin 2)
  • Metastatic (Struma Ovarii)
  • Hydatidiform Mole

Precipitants of Thyroid Storm
  • Trauma
  • Heat related Illness
  • Recreational Drug Use
  • Psychosis
  • Stress
  • Infection
  • Iodinated Contrasts
  • ACS
  • DKA/HHS
  • Thyroxine Overdose
Consider thyroid Strom in any patient presenting with fear, tachycardia and altered mental status. Use Burch-Wartofsky scale to gauge your suspicion and diagnosis. 





Management
Following the order of treatment is of utmost importance here. Inhibition of thyroid gland synthesis of new thyroid hormone with a thionamide (Methimazole or PTU) must be initiated before iodine therapy.


1. Supportive care 
  • ABC
  • Cardiac Monitor and IV accsess.
  • Fluids, Maintenance of Electrolytes and Glucose. Cooling for hyperthermia. 
  • Add antibiotics as infection is a known precipitant and hard to distinguish in ED
  • Consider Cholestyramine to decrease the reabsorption of thyroid hormone from the enterohepatic circulation. In thyrotoxicosis, there is increased enterohepatic circulation of thyroid hormone. 

2. Inhibition of new hormone synthesis
Thionamides: Methimazole or PropylThioUracil. Thionamides decrease the synthesis of new hormone production. 

Methimazole: 40 to 100 milligrams PO as loading dose then 20 milligrams q4h


Propylthiouracil: Load with 600 to 1000 mg PO followed by 200 to 250 milligrams every 4 hours. PTU is hepatotoxic but in addition to decreasing the synthesis of new hormone production, it also blocks the peripheral conversion of thyroxine to triiodothyronine. 


Use PTU in first trimester and Methimazole in second and third trimester. 

 3. Inhibition of thyroid hormone release
Potassium iodide can be given to stop thyroid hormone release. PTU or Methimazole must be started first and Iodine therapy should be given at least 1 hour later. Iodine therapy blocks the release of pressured hormone. Start with 8 to 10 drops initially. 


Iodine-containing solutions should not be given to patients with iodine overload or iodine-induced hyperthyroidism or amiodarone-induced thyrotoxicosis. Lithium or potassium perchlorate should be used instead. 

 4. Peripheral β-adrenergic receptor blockade

Propranolol can be given IV in slow 1- to 2-milligram boluses q5-10min. Orally, propranolol therapy usually begins at 20 to 120 milligrams per dose.

 5. Preventing peripheral conversion of thyroxine to triiodothyronine 
The peripheral conversion of thyroxine to triiodothyronine is blocked by propylthiouracil, propranolol, and glucocorticoid. Glucocorticoids are essential in treatment since blockade produced by propylthiouracil and propranolol is not significant. . Glucocorticoid also treat underlying relative adrenal insufficiency. 

6. Find and treat the precipitation event (Sepsis, DKA, ACS)
7. Definitive Treatment - Radioactive Iodine or Surgery 



Other potential considerations:
  • Direct removal of thyroid hormone with plasma exchange
  • Use of Potassium Perchlorate in Amiodarone induced thyrotoxicosis: Potassium perchlorate  interferes with the production of new hormones 
  • Lithium: Used in cases of hypersensitivity to iodine. Lithium inhibits thyroid hormone release from thyroid gland. Typical dosing in thyroid storm is 300 milligrams every 8 hours. Monitor levels to avoid toxicity. 
  • Peripheral beta blockade: Reserpine or Guanethidine can be used, if there is a contraindication for BB use. These agents do not block beta receptors and interfere with catecholamine function (by depleting stores and blocking release)

Take Home:
  • Consider Thyroid Strom in any patient presenting with fever, tachycardia and Altered Mental Status.
  • PTU or Methimazole must be started first and Iodine therapy should be given at least 1 hour later.
  • Manage with beta blockers, PTU/Methimazole, Steroids and Potassium iodide
  • Identify and treat the precipitation cause 

Further Reading
Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic








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