Morning Report: 10/9/2014 - The Original Kings of County

Thanks to Dr. Brown for presenting today’s Morning Report!

Case presentation:

46 y/o F with no sig PMH presented to ED with chief complaint of vomiting and weakness. HR 132, RR 20, Temp 99.6, BP 185/75, and O2 100% on RA. Not too much history, kind of delirious. PE remarkable for well appearing in mild agitation. MMM, nml S1S2, Bibasilar rales, abd soft NTND.

Thyroid Storm

Thyroid storm is an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones.

Epidemiology: Incidence increases with age, may affect as many as 2% of older women.

3-5 times more common in females

Adult mortality approaches 90% if untreated, 20% if diagnosed and treated early.

Although thyroid storm can develop in patients with long-standing untreated hyperthyroidism (Graves’ disease, toxic multinodular goiter, solitary toxic adenoma), it is often precipitated by an acute event such as:

thyroid or non-thyroidal surgery, anesthesia
trauma, especially to thyroid gland
infection, sepsis
acute iodine load
parturition
withdrawal of antithyroid medications
DKA
Drugs (anticholinergics, adrenergics, salicylates, NSAIDS, iodinated contrast agents)

***Clinical diagnosis: usually an exaggeration of the usual symptoms of hyperthyroidism. No specific laboratory test to confirm.

Severe hyper-metabolism involving multiple organ systems:

Cardiac: tachycardia, HTN with wide pulse pressure, high-output cardiac failure, arrhythmias
Neuro: severe agitation, delirium, seizures and coma
GI: diarrhea, vomiting, jaundice, abdominal pain

There is no universally accepted criteria or validated clinical tools for diagnosing thyroid storm.

In 1993, Burch and Wartofsky introduced a scoring system

> 45 is highly suggestive
25-44 is suggestive of impending storm

scoring system is likely sensitive, but not specific
degree of hyperthyroidism (suppressed TSH and elevated T3 and free T4) is not a criterion for diagnosing thyroid storm

Other nonspecific laboratory findings:

hyperglycemia: secondary to catecholamine-induced inhibition of insulin release and increased glycogenolysis
hypercalcemia: hemoconcentration and enhanced bone resorption
abnormal LFTs
leukocytosis or leukopenia

Treatment:

supportive therapy and recognition/treatment of any precipitating factors.

dextrose solutions are preferred to cope with high metabolic demand

for fever, tylenol is preferred over ASA (which may increase serum free T4 and T3 concentrations by interfering with their protein binding). also cooling blankets

Medications:

Propranol: control the symptoms and signs induced by increased adrenergic tone
- IV: 0.5 to 1mg over 10 minutes followed by 1-2mg over 10 minutes every few hours
- PO: 60-80mg every 4-6 hours.
- ***esmolol is an alternative regimen that permits rapid titration of the drug.
Thionamides: block new hormone synthesis withing 1-2 hours after administration. No effect on release of preformed hormone from the thyroid gland
- PTU (200mg Q4h): recommended for the acute treatment of life-threatening thyroid storm.
  - Blocks T4 conversion to T3 and may reduce serum T3 concentrations more rapidly than methimazole
  - preferred because of its early onset of action., however boxed warning emphasizes risk for severe liver injury.

reserve for first trimester of pregnancy of patients allergic to methimazole.

Methimazole (20mg Q4-6h): has a longer duration of action and is less hepatotoxic.
- transition to methimazole once leave ICU
*** If unable to tolerate a thionamide (agranulocytosis, hepatotoxicity, allergy), thyroidecomy is treatment of choice. Treat with propranalol, glucocorticoids, and iodine preoperatively.
- Do not delay surgery for more than 8-10 days because of “escape from Wolff-Chaikoff” effect.
  - large doses of exogenous iodine inhibit the organification of iodine in the thyroid gland, however the effect is transient. The iodide transport system is able to adapt to higher concenctrations of iodine, allowing thyroid hormone synthesis to proceed, with potential exacerbation of thyrotoxicosis.

Iodine solution: Blocks the release of thyroid hormone from the gland within hourse
- Delay administering for at least 1 hour after thionamide administration to prevent the iodine from being used as substrate for new hormone synthesis
- Potassium iodide-iodine (Lugol’s) solution: 10 drops TID
- Saturated Solution of Potassium Iodide (SSKI): 5 drops QID
An iodinated radiocontrast agent: Inhibits the peripheral conversion of T4 to T3: not available in the U.S. anymore
Glucocorticoids: reduce T4 to T3 conversion, promotes vasomotor stability, and possibly treat an associated relative adrenal insufficiency.
- Hydrocortisone: 100mg q8h

References:

http://emedicine.medscape.com/article/925147

http://www.uptodate.com/contents/thyroid-storm

The views expressed on this blog are the author's own and do not reflect the views of their employer. Please read our full disclaimer here. Any references to clinical cases refer to patients treated at a virtual hospital, Janus General Hospital.

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Jay Khadpe MD

Editor in Chief of "The Original Kings of County" Assistant Professor of Emergency Medicine Assistant Residency Director SUNY Downstate / Kings County Hospital