Interview with Dr. Jonathan LoPresti
In last month’s column, we discussed myxedema coma. This month we will cover the other cardinal thyroid emergency – thyroid storm. Our expert for this segment is Dr. Jonathan LoPresti, a senior endocrinologist and thyroid researcher at LA County/USC Medical Center. Our interview on thyroid emergencies was one of the most interesting that I have done for EM:RAP’s audio edition – really worth a listen.
Dr. LoPresti has a knack for making sense of thyroid emergencies. You’ll remember from last month that he used the term “decompensated hypothyroidism” instead of myxedema coma. He explained that patients who are hypothyroid, and thus have a decreased metabolic rate, conserve heat by being in a constant state of vasoconstriction. That is why they feel cool to the touch. So when these patients, who are dependent on chronic vasoconstriction to maintain their body temperature suddenly become vasodilated in response to an infection, its like the bottom is pulled out from underneath them. They are now decompensated.
Thyroid storm can be understood in exactly the same way – just in reverse. Patients with hyperthyroidism walk around every day in a state of vasodilatation. They are dependent on vasodilatation to get rid of the excess heat that they generate in their hypermetabolic state. Patients with thyroid storm are decompensated – no longer able to vasodilate sufficiently, their core temperature begins to rise. This occurs in response to any number of stressors that result in a release of catecholamines, to which the hyperthyroid patients are uniquely sensitive.
The diagnosis of thyroid storm is made on the basis of the following: characteristic clinical features, such as sweating, tremor, hyperreflexia and supraventricular tachycardias, elevated temperature, and some precipitating event, such as infection, surgery or trauma. Lastly, in order to make the formal diagnosis of storm, the patient must also have some degree of altered mental status, but this may be rather subtle and subjective.
The diagnosis is even more difficult in the elderly because they have a less dramatic response to the hyperthyroid state. Interestingly, even though the diagnosis is easier to make in younger people, thyroid storm is more dangerous for them because of their greater capacity to respond to the inappropriately high thyroid activity. This is something that seems quite counterintuitive to most EPs, but it makes sense when you think about it.
Because infection is such a common trigger of a decompensated hyperthyroid state, you should draw blood and urine cultures and initiate empiric antibiotic treatment when the diagnosis of storm is being entertained. To help confirm the diagnosis, a TSH and T4 should be sufficient. Other laboratory abnormalities that are typical include a mild normocytic anemia, low platelets, and hypocalcemia. White blood cell counts are typically, and misleadingly, low.
The thing that scares most EPs is pulling the trigger on thyroid-specific treatment, especially before results of thyroid laboratory studies are available. These patients are critically ill and we worry that treatment of the hyperthyroid state might blunt their ability to compensate for shock. Just like in decompensated hypothyroidism, the critical message here is that when in doubt, the EP should treat. If left untreated, thyroid storm is fatal. If you are wrong, a few doses of anti-thyroid medication is unlikely to harm the euthyroid patient.
Treatment consists of a three-pronged approach: lowering thyroid hormone levels, treating the symptoms, and cooling measures. Treatment should begin with an anti-thyroid medication such as propylthiouracil (Dr. LoPresti recommends 100-150 mg every 8 hours) or methimazole, followed an hour later by ten drops of potassium iodide. A glucocorticoid will further lower thyroid hormone activity, and Dr. LoPresti recommends using dexamethasone 4mg IV every 6 hours.
Although patients may be in cardiogenic shock, treatment with beta-blockers and cautious fluid administration is nonetheless indicated. Remember that thyroid storm patients are generally hypovolemic and need to have their “tank” replenished. Moreover, beta-blockers are necessary to decrease the heart rate and promote diastolic filing. The fear that many EPs have of beta–blockers in this scenario is well justified and based on the fact that you can “overdo” it by giving too much propanolol (e.g. an initial dose of 7.5 or 10 mg IV) – excessive doses may worsen the situation. A few milligrams (e.g. 3-5 mg) is usually all that is necessary. If propanolol is given in small increments of 1 mg every few minutes, it can be safely titrated to the patient’s vital signs. Dr. LoPresti recommends aiming for a heart rate of about 90-100 bpm. If the vital signs begin to deteriorate then further doses should be withheld.
Two things to avoid – excessive diuresis and aggressive cooling measures. Dr. LoPresti cautions that both can precipitate or worsen the decompensated hyperthyroid state by causing vasoconstriction. With respect to their temperature, it will correct naturally with the treatment of hyperthyroidism. At LA County-USC, a small dose of IV meperidine and chlorpromazine is often used to decrease shivering (which may actually increase temperature) and will assist in gently allowing the temperature to correct.
Dr. Swadron is an Associate Professor of Clinical Emergency Medicine at the Keck School of Medicine of the University of Southern California. He partners with Dr. Mel Herbert to bring you EM:RAP (Emergency Medicine: Reviews and Perspectives), the monthly audio program that can be found at http://www.EMRAP.org)