TFTs are abnormal in 70% of hospitalized patients [Arch Intern Med 150: 1249, 1990] and up to 90% of ICU patients [Crit Care Med 22: 1603, 1994]. In most (but not all) cases, these lab abnormalities represent an adaptive response to non-thyroidal illness and are not a sign of thyroid disease.
Evaluation of Thyroid Function
TSH and free T4 are a good screening combination. Normal TSH is 0.5 – 3.5 mU/L. Note that as the lower end of normal is so low, only an elevated TSH is interpretable (a low TSH could actually be ~ 0.5). Also remember that in patients taking dopamine or high-dose glucocorticoids, TSH release may be suppressed and the lab values can be normal even if the patient is hypothyroid.
T3 is the active form of thyroid hormone, is peripherally converted, and is not an accurate indicator of thyroid function. Serum T3 levels can be normal in as many as 30% of hypothyroid patients. Total T4 is also not recommended as it is dependent on both the protein bound (ex. TBG) T4 and free T4.
Usually cased by Graves, autoimmune disease, or chronic amiodarone therapy. Manifestations include sinus tach, A-fib, tremor, obtundation, agitation (or lethargy in the elderly), and thyroid storm (agitation, fever, hyperdynamic shock). Immediate management should include beta-blockers followed by methimazole 10 – 30 mg qday (works faster than propylthiouracil and causes less agranulocytosis [NEJM 330: 1731, 1994]). In severe cases, iodide can be added to therapy with PTU, either orally as Lugoll’s solution or peripherally as NaI. If the patient is allergic to iodide, use lithium instead. Thyroid storm requires the above measures, but often requires aggressive volume infusion as well, and sometimes steroid replacement (300 mg hydrocortisone to start) because these patients will often be relatively adrenally insufficient. ALWAYS try to determine and treat the precipitating event.
Hypothyroid disease is uncommon in hospitalized patients. May cause effusions (pericardial and pleural), hyponatremia, muscle myopathy, elevated creatinine, hypothermia, dermal infiltration, or depressed consciousness. Pericardial effusion is the most common cardiovascular manifestation, develops in ~ 30% of cases, and is the most common cause of enlarged cardiac silhouette in hypothyroid patients.
Advanced cases may lead to myxedema coma, but frank coma is rare [Crit Care Clin 7: 43, 1991]. The edema in myxedema is due to dermal infiltration of proteins and not due to interstial fluid edema. Treat hypothyroid patients with L-thyroxine (T4) 50 – 200 µg PO qday, starting with 50 µg and working up in 50 µg increments every 3-4 weeks. Keep increasing the dose until TSH normalizes (90% of patients will do so with < 200 µg). In severe cases, IV replacement is recommended at least initially, because of the risk of impaired gastric motility in these patients – one recommended IV regimen is 250 µg in day 1, then 100 µg on day 2, then 50 µg on each day afterwards [Crit Care Clin 7: 43, 1991]. There is no data to show that giving T3 is beneficial to T4 (L-thyroxine). In cases of myxedema coma, also give hydrocortisone 100 mg q8h in the event of coexisting adrenal insufficiency – also give steroids pre-op as these patients’ adrenals have atrophied subsequent to hypothyroidism.