Approach to hypothyroidism: Clinical sciences

Hypothyroidism refers to low thyroid hormone levels, which leads to a reduction of the basal metabolic rate. Patients with hypothyroidism present with a wide spectrum of signs and symptoms which can range from subclinical disease to a life-threatening condition called myxedema coma.

The diagnostic workup for hypothyroidism mainly involves checking thyroid-stimulating hormone, or TSH level, and free thyroxine, or free T4 level, to determine the cause of hypothyroidism.

Now, if your patient presents with chief concerns suggesting hypothyroidism, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a clinical pearl to keep in mind! If your patient presents with hypothermia, bradycardia, hypoventilation, and lethargy, you should suspect myxedema coma, which is a severe, life-threatening form of hypothyroidism.

Myxedema coma typically occurs later in patients with long-standing hypothyroidism. Treatment consists of supportive care, which in some patients means ventilatory or circulatory support, as well as corticosteroids, and thyroid hormone and electrolyte replacement. Any underlying precipitant such as an infection or heart failure should be identified and treated as well.

Alright, now that we're done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones.

First, obtain a focused history and physical examination. Your patient will likely report symptoms suggesting a low basal metabolic rate and sympathetic activity, including atigue, weight gain, and cold intolerance. In addition, constipation is common, and patients may develop depression, hair loss, and even menstrual abnormalities.

On the flip side, physical exam findings include cardiovascular manifestations, such as bradycardia and diastolic hypertension; as well as CNS findings, primarily delayed relaxation of deep tendon reflexes. Next, your patient can have dry skin, fragile hair, and sometimes even non-pitting peripheral edema, often referred to as myxedema.

Myxedema occurs due to the accumulation of mucopolysaccharides, also called glycosaminoglycans, in the dermis, which binds to water molecules, resulting in edema.

Finally, in some individuals, you might detect a palpable goiter!

At this point, you should consider hypothyroidism, so your next step is to order a TSH and free T4.

Normal TSH and free T4 reflects euthyroidism, which means the thyroid works properly, so you should consider alternative diagnoses.

Now here’s a clinical pearl to keep in mind! Some patients with a severe acute illness, like acute myocardial infarction, can have labs suggesting abnormal thyroid function in the absence of thyroid disease.

One common example is euthyroid sick syndrome, also called nonthyroidal illness. In this case, TSH and free T4 levels could be low or normal, and T3 levels are low due to reduced peripheral conversion of T4 to T3. Since euthyroid sick syndrome isn't an actual thyroid disorder, there's no need for thyroid hormone replacement. Instead, treatment should focus on addressing the underlying condition. That’s why, ideally, hypothyroidism assessment should be performed in the absence of acute illness!

However, if TSH high, or even just mildly elevated, and free T4 is normal...

you can diagnose subclinical hypothyroidism.

Keep in mind that these individuals are typically asymptomatic, so the diagnosis is based on abnormal lab findings.

Alright, now let’s go back and take a look at TSH and free T4 levels.

If TSH is high and the free T4 is low, you can diagnose primary hypothyroidism.

Next, order anti-thyroid peroxidase and anti-thyroglobulin antibodies. If either are present, you can diagnose Hashimoto thyroiditis.

Keep in mind that patients with Hashimoto thyroiditis often experience an initial hyperthyroid phase, which is when the damaged thyroid tissue releases tons of preformed thyroid hormones. And then, as the thyroid continues to atrophy over time, patients typically progress to develop chronic hypothyroidism.