From Medscape
SAN DIEGO — Myxedema coma, a rare but potentially fatal form of decompensated hypothyroidism, can be identified according to key clinical signs and successfully treated in most patients with 500 µg of intravenous levothyroxine (L-thyroxine), according to a new study.
Myxedema (Getty Images)

A first important step toward improving diagnosis of the syndrome, however, would be to assign it a more appropriate name, specifically “severely decompensated hypothyroidism” (SDH), asserted coinvestigator Dr Caroline T Nguyen, (Keck School of Medicine, University of Southern California, Los Angeles).
” ‘Myxedema coma’ is a misnomer, because most patients who present initially with this syndrome often do not have myxedema or coma,” Dr Nguyen said.
“Rather, the term ‘severely decompensated hypothyroidism’ is more accurate and descriptive of this syndrome, and our thinking of it in this manner may lead to earlier diagnosis and initiation of treatment,” she said.
Even with treatment, mortality rates from myxedema coma can be as high as 25% to 60%, yet, due to its rarity, reports on effective diagnosis and treatment in the literature are limited mainly to single case reports and small case series.
Altered Mental Status Most Helpful Clinical Parameter
In presenting her data on the case series of 47 patients and 50 episodes — said to be the largest case series to date — at the recent 2014 Annual Meeting of the American Thyroid Association, Dr Nguyen said she and her colleagues identified four key clinical signs of the syndrome. They include:
Hypothyroidism as determined by clinical exam, history, or biochemical findings.
A precipitating event, such as an infection, that takes a patient from a compensated to decompensated state.
Hypothermia or defective thermoregulation, whether absolute or relative. “For example, a septic patient with a normal temperature,” Dr Nguyen said.
An altered mental status. “This can range from disorientation to coma, and in our experience, altered mental status has been the most helpful clinical parameter to distinguish between the compensated and decompensated hypothyroid patient.”
Patients had a median free-T4 value of 0.39 ng/L, and median thyroid stimulating hormone (TSH), which was available for 38 patients with primary hypothyroidism, was 69.28 mIU/mL.
Patients were treated with 500 µg IV of L-thyroxine, with additional treatments including hydrocortisone and supportive care.
“The goal [the L-thyroxine therapy] is to partially reverse the hypothyroid state, enabling the patient to effectively adapt to the precipitating event that led to decompensation,” Dr Nguyen said.
“The dose is designed to restore the total body thyroxine pool.”
The average time from presentation to treatment with L-thyroxine was 27.3 hours.
From the time of treatment with L-thyroxine, 56% of patients showed improvements in mental status within 24 hours, 18% improved within 48 hours, and 6% improved in a week or less. In 16% of cases, the time to improvement was unknown.
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