A 2-year-old girl was found with an empty bottle of levothyroxine and blue coloring around her mouth. Forty tablets of 150-μg levothyroxine tablets were missing. Her 6-hour postingestion total thyroxine (T4) level was 68.1 μg/dL (normal range: 5–12 μg/dL), and her total triiodothyronine (T3) level was 472 ng/dL (normal range: 40–130 ng/dL). Serum levels of thyrotropin, T3, and T4 were then checked on days 3, 5, 7, and 10. On postingestion day 5, the child presented for follow-up with hyperthermia, vomiting, irritability, and increased lethargy. She was referred to the emergency department, where a heart rate of 220 beats per minute, a blood pressure of 130/80 mm Hg, and a temperature of 101°F were recorded. She also had multiple episodes of diarrhea. The patient was treated with oral propranolol (0.8 mg/kg) every 6 hours, intravenous normal saline, and ibuprofen; all her vital signs improved. Serial T3, T4, and thyrotropin serum levels were measured. Her total T3 levels were >800, 798, 445, 446, and 98 ng/dL on days 3, 5, 6, 9, and 13, respectively. Total T4 measurement was repeated on day 13, and the concentration was found to be 11.9 μg/dL. Her thyrotropin levels remained undetectable throughout the course of treatment. The patient was discharged from the hospital after a 4-day PICU stay, in good condition, on oral propranolol 0.8 mg/kg every 8 hours. Propranolol administration was discontinued 8 days after initiation with no further tachycardia, hypertension, or hyperthermia. The child tolerated the recommended regimen.
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August 2010
Case Reports|
August 01 2010
Thyroid Storm After Pediatric Levothyroxine Ingestion
Nima Majlesi, DO;
aEmergency Department, Staten Island University Hospital, Staten Island, New York;
Address correspondence to Nima Majlesi, DO, Emergency Department, Staten Island University Hospital, 475 Seaview Ave, Staten Island, NY 10305. E-mail: nima.majlesi@gmail.com
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Howard A. Greller, MD;
Howard A. Greller, MD
bEmergency Department/Division of Medical Toxicology, North Shore University Hospital, Manhasset, New York; and
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Michael A. McGuigan, MD;
Michael A. McGuigan, MD
cLong Island Regional Poison and Drug Information Center, Mineola, New York
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Tom Caraccio, PhD;
Tom Caraccio, PhD
cLong Island Regional Poison and Drug Information Center, Mineola, New York
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Mark K. Su, MD;
Mark K. Su, MD
bEmergency Department/Division of Medical Toxicology, North Shore University Hospital, Manhasset, New York; and
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Gar M. Chan, MD
Gar M. Chan, MD
bEmergency Department/Division of Medical Toxicology, North Shore University Hospital, Manhasset, New York; and
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Address correspondence to Nima Majlesi, DO, Emergency Department, Staten Island University Hospital, 475 Seaview Ave, Staten Island, NY 10305. E-mail: nima.majlesi@gmail.com
FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.
Pediatrics (2010) 126 (2): e470–e473.
Article history
Accepted:
April 12 2010
Citation
Nima Majlesi, Howard A. Greller, Michael A. McGuigan, Tom Caraccio, Mark K. Su, Gar M. Chan; Thyroid Storm After Pediatric Levothyroxine Ingestion. Pediatrics August 2010; 126 (2): e470–e473. 10.1542/peds.2009-2138
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After reading the case report by Majlesi et al (1) in the August 2010 issue of Pediatrics and based on my own experience with the case of a 32- month-old girl (2) with the third largest ingestion of levothyroxine (15mg), for her size reported (3) and one of the, if not the highest serum level of thyroxine (281ug/dL), and the review of the medical literature, I feel there a number of very important issues that need to be brought up. Acute involuntary ingestion of levothyroxine remains a non-fatal and relatively benign condition. Nonetheless, after the required gastrointestinal decontamination, very close monitoring of the patient is of the utmost importance in order to provide conservative treatment (propanolol, prednisone, etc) as soon as the patient becomes symptomatic, avoiding in this way the development of a thyroid storm, as was the case in our patient. We disagree with Majlesi et al’s suggestion “…the use of T3 serum concentration as a marker of exposure of clinical consequence…”, because there is a very well known lack of close correlation between the amount of levothyroxine ingested and the time of onset and severity of the symptoms as well as the serum concentrations of both T4 and T3. In fact, in a number of cases, including mine, the symptoms appear or get worse well after the serum T3 levels have decreased considerably. This lack of correlation could be explained as suggested by May et al (4) because the levothyroxine symptoms probably reflect the tissue T3 levels, which lag behind the serum T3 levels. As for the possible indication for use of antithyroid medications, this is easily dismissed because their main effect is to block the synthesis of thyroid hormones, effect which is voided because massive doses of levothyroxine suppresses the thyroid gland and their effect on blocking the peripheral conversion of T4 to T3 is very minor and is not present in methimazole but only in propylthiouracil, the use of which has recently been discouraged in children due to its association with liver damage-related fatalities. Finally, I have been unable to find the “new understanding of the consequences of these ingestions and new concepts regarding management and diagnostic testing” purported by the authors.
(1) Majlesi N, Greller HA, McGuigan MA, et al: Thyroid Storm After Pediatric Levothyroxine Ingestion. Pediatrics.2010; 126; e470-e473. (2) Pardo JM: Acute Levothyroxine Overdose in a Young Child. International Pediatrics. 1989; 4(3): 283-284. (3) Tenenbeim M, Dean H. Benign course after massive ingestion of levothyroxine, abstracted. Vet Hum Toxicol. 1981;23 (supp 1):37 (4) May MD, Mintz PD, Lowry P, et al.: Plasmapheresis in thyroxine overdose: a case report. J Toxicol Clin Toxicol. 1983;20:517-20.
Conflict of Interest:
None declared