A slender young male appears anxious sitting on the couch as you approach. He is awake and alert, acknowledging your presence by looking at you and saying, “Hey.” The dispatch information sent to you was for a 24-year-old male with a “racing heart.” Beginning your assessment, you feel warm skin and a rapid, irregular pulse. The patient confirms his chief complaint is a racing heart, and he feels hot and dizzy.
He adamantly denies drug use and tells you this has never happened to him before. He says he caught a “bug” and has had a sore throat for several days along with feeling hot all the time. He reports having no energy for the past week and has been experiencing frequent diarrhea. He attributes all his symptoms to his recent illness. Today, however, his racing heart and dizziness have him concerned.
Your physical exam reveals a healthy appearing young male. He’s anxious but responding appropriately. His skin is hot to the touch and breath sounds are clear. His pulse rate is weak and irregular at a rate of 160 beats per min. His blood pressure is 96/68 and respirations are 20 per minute. The pulse oximetry is 98% on room air and the capnogram has a good waveform with an end-tidal carbon dioxide reading of 28 mmHg.
The cardiac monitor shows rapid atrial fibrillation. Your partner establishes an IV while you continue your physical exam. A blood glucose evaluation reads 210 mg/dL. He denies a diabetic history. The patient’s anterior neck is tender to palpation, and you notice a red spider-like mark on the patient’s cheek. He denies recent trauma. The patient denies chest pain or shortness of breath but remains aware of his rapid heart rate. He agrees that being transported for evaluation is a good idea.
During transport, you administer a fluid bolus of 250 mL with a change in blood pressure to 100/70. The patient remains anxious and requests a window be opened because he’s so hot. The patient is delivered to the emergency department with no further changes. You let the receiving physician know you’re slightly perplexed about the patient’s presentation. The physician tells you she has a good idea but will run some tests and let you know.
Following up with the emergency physician later that day, you learn that the patient’s symptoms were secondary to hyperthyroidism, most likely triggered by a viral infection. The thyroid gland is located below the larynx, anterior to and on each side of the trachea. It secretes thyroxine commonly known as T4 and triodothyronine more commonly referred to as T3.
T4 is the most prevalent hormone secreted from the thyroid and almost all of the T4 is then converted to T3 in the body. Thyroid secretion is regulated primarily by thyroid-stimulating hormone (TSH) also known as thyrotropin, which is released by the anterior pituitary gland. As the levels of T3 decrease, there’s an increase of TSH. This causes an increase in secretion of T4 and T3. As T3 levels increase either by direct thyroid secretion or from conversion from T4, TSH levels decrease. These hormones are intimately involved in metabolism. A decrease in thyroid function (hypothyroidism) can cause a decrease in metabolic rate up to 50%. An increase in thyroid function (hyperthyroidism) can increase metabolic rate more than 60%.1
The patient in this case had hyperthyroidism, which is an elevation of circulating thyroid hormone. Specific diagnoses, such as thyrotoxicosis or thyroid storm, are subjective. Most of these patients have a history of Graves’s disease, which is chronic hyperthyroidism. It may be more plausible just to identify patients as being symptomatic secondary to elevated thyroid hormones.
A virus is a common cause of acute hyperthyroidism. Hyperthyroidism presents with general signs of increased metabolism, including weight loss and heat intolerance. In addition, acute hyperthyroidism can cause anxiety, abdominal pain, increased defecation and diarrhea, palpitations and such arrhythmias as atrial fibrillation and dyspnea, and double vision and neck tenderness. Hyperthyroidism can also cause an increase in blood glucose levels and spider angiomas, which are red spider web-like areas on the skin. Severe presentations are rare, accounting for less than 10% of hyperthyroid cases.2 When severe cases present, patients can have acute heart failure and be comatose. These cases can be referred to as thyroid storms.
Prehospital care is mostly supportive. Consider other causes of the patient’s symptoms, such as myocardial infarction and toxic ingestions. Support the patient’s blood pressure with fluid or cardiac rhythm management. In the case of extreme anxiety, the administration of a benzodiazepine is appropriate. Beta blockers can be administered to relieve the effects of the elevated thyroid levels. Long-term care will be focused on the cause of the hyperthyroidism. Although not a common call for EMS, it’s important to remember the role of the thyroid gland and include alterations in thyroid function as part of our differential.
1. Guyton A: Textbook of Medical Physiology. WB Saunders: 2000.
2. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 2006;35(4)663–686.