Storm’s a Comin’: A Review of Thyrotoxicosis and Thyroid Storm
THE CASE
A 30-year-old female with past medical history notable for substance use disorder, multiple psychiatric comorbidities, and cyclic vomiting syndrome presents to the emergency department with periumbilical pain, nausea, and multiple episodes of vomiting for the past 2 days. On arrival she is anxious, agitated, and demonstrates mood lability (alternating between laughing, crying, and screaming). Her physical exam is notable for tachycardia with a heart rate of approximately 100 bpm, warm moist skin, proptosis, and an absence of abdominal tenderness on palpation. She had previously presented for similar symptoms which improved with the use of haloperidol. She endorsed that her symptoms at the present time were similar to her prior presentations. Accordingly, the decision was made to engage in symptomatic treatment with provision of IV fluid as well as a dose of intravenous haloperidol. On reevaluation she was noted to be more tachycardic (see Figure 1) and her nausea persisted.
DIAGNOSIS AND DISCUSSION
A broad metabolic and toxicological evaluation (including CT imaging of the abdomen/pelvis) was pursued. Imaging was without evidence of acute pathology. Diagnostic lab work was notable for a thyroid panel consistent with thyrotoxicosis--TSH level 0.005 uIU/mL, free thyroxine level of 6 ng/dL, and free triiodothyronine level of 1218 pg/dL). A Burch-Wartofsky Point Scale (BWPS) was calculated and the patient’s score of 50 was highly suggestive of thyroid storm. Endocrinology was consulted and treatment for thyroid storm was initiated.
Thyrotoxicosis and Thyroid Storm
Thyrotoxicosis is a clinical syndrome which results from elevated levels of circulating thyroid hormone (1,3). Thyrotoxicosis has a multitude of causes (refer to Table 1) and can result in a vast number of clinical manifestations (refer to Table 2). Thyroid storm is an overt hypermetabolic state which represents the most severe form of thyrotoxicosis (2). While exceptionally rare (occurring at a rate of 0.13/100,000), thyroid storm remains an important clinical entity as it can lead to multiorgan failure and death (1,4,5). What is perhaps most challenging about thyroid storm is its propensity to present with nonspecific manifestations, which oftentimes mimic other clinical conditions (refer to Table 3).
Diagnostic Evaluation of Presumed Thyroid Storm
Thyroid storm can represent the initial presentation of unrecognized thyrotoxicosis. However, thyroid storm can also arise in patients with underlying thyrotoxicosis who experience a new physiologic stress. Common precipitants of thyroid storm include infection, recent surgery or traumatic injury, metabolic derangements (such as diabetic ketoacidosis or hypoglycemia), myocardial infarction, stroke, and pulmonary embolism. Additional considerations include medication-induced thyroid storm (amiodarone initiation, alpha-interferon, interleukin-2), nonadherence with anti-thyroid regimen, and surreptitious use of thyroid hormone. The key to diagnosing thyrotoxicosis and thyroid storm is maintaining a broad differential. As such, consider initiating a broad metabolic evaluation in suspected cases including creatine kinase, cortisol, thyroid-stimulating hormone, total/free thyroxine (T4), total/free triiodothyronine (T3). If the resultant diagnostic evaluation shows biochemical evidence of thyrotoxicosis, the Burch-Wartofsky Point Scale (BWPS) is then used to determine the likelihood of thyroid storm (1,2). If the BWPS score is greater than 45 points, consult endocrinology and initiate treatment for thyroid storm (refer to Figure 2).
TAKE-AWAYS:
Maintain a high index of suspicion for thyroid storm because it has physical manifestations which mimic other common complaints.
Use the Burch-Wartofsky Point Scale (BWPS) to risk stratify thyrotoxicosis.
Use beta-blockade for tachycardia.
Use propylthiouracil (PTU) and methimazole (MMI) to reduce synthesis of T3 and T4.
Use Iodine 1 hour after PTU or MMI to slow the release of thyroid hormones.
Consider hydrocortisone for treatment of concomitant adrenal insufficiency.
AUTHOR: Alexander Dayton, MD is a 3rd year Emergency Medicine Resident at Brown University
FACULTY REVIEWER: Amy Matson, MD is an Assistant Professor of Emergency Medicine and Clinician Educator at Brown/Rhode Island Hospital
References
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