Management of Toxic Multinodular Goiter
The next step is to treat with antithyroid medications (methimazole or propylthiazole) to control the hyperthyroidism, followed by definitive therapy with radioactive iodine ablation or thyroidectomy. 1, 2
Understanding the Clinical Picture
Your patient has toxic multinodular goiter (also called Plummer's disease), characterized by:
- Low TSH with normal T3/T4 indicates subclinical hyperthyroidism progressing toward overt disease 1
- Multiple areas of increased uptake on radioiodine scan represent autonomously functioning nodules that produce thyroid hormone independent of TSH control 1, 2
- Areas of suppressed uptake represent normal thyroid tissue that has been shut down by the autonomous nodules 1
This pattern is pathognomonic for toxic multinodular goiter and distinguishes it from Graves' disease (which shows diffuse homogeneous uptake) and thyroiditis (which shows globally decreased uptake) 1, 2.
Immediate Management Algorithm
Step 1: Initiate Medical Therapy
- Start methimazole as first-line antithyroid medication to control thyroid hormone production from the autonomous nodules 3
- Consider beta-blockers (preferably non-selective with alpha-blocking capacity) for symptomatic control of palpitations, tremor, or anxiety 3
- The goal is to normalize thyroid hormone levels before definitive treatment 1
Step 2: Plan Definitive Treatment
Once euthyroid on medical therapy, proceed with one of two definitive options:
- Radioactive iodine (I-131) ablation is typically preferred for elderly patients or those with surgical contraindications 2, 4
- Thyroidectomy is preferred for younger patients, those with compressive symptoms, or when malignancy cannot be excluded 1
Critical Monitoring Requirements
- Recheck TSH and free T4 every 4-6 weeks during antithyroid medication titration 3
- Monitor for progression to overt hyperthyroidism (elevated T3/T4 with suppressed TSH), which increases risk for atrial fibrillation and cardiac complications 5
- Watch for cardiac arrhythmias, especially atrial fibrillation, which occurs more frequently with TSH suppression in patients over 45 years 5
Why This Differs from Other Causes of Hyperthyroidism
- Graves' disease would show diffuse homogeneous uptake throughout the gland, not patchy areas 1, 2
- Thyroiditis would show globally decreased uptake (not increased), as the inflamed gland cannot trap iodine 3, 1
- Resistance to thyroid hormone would show elevated (not low) TSH despite high thyroid hormones 6
Common Pitfalls to Avoid
- Do not assume the patient is euthyroid based solely on normal T3/T4—the low TSH indicates the pituitary is already sensing excess thyroid hormone, and progression to overt disease is likely 1, 4
- Do not delay treatment waiting for symptoms to develop, as subclinical hyperthyroidism increases cardiovascular risk, particularly atrial fibrillation and bone loss 5
- Do not confuse this with non-thyroidal illness syndrome, which would show low T3 with elevated reverse T3 and normal/low TSH in the context of acute illness 7
- Never start thyroid hormone replacement in this scenario—these patients are hyperthyroid (or becoming so), not hypothyroid 5
Long-term Considerations After Definitive Treatment
- Following radioactive iodine ablation, monitor for late hypothyroidism, which develops in most patients and requires lifelong levothyroxine replacement 4
- TSH may remain suppressed for months after treatment even as the patient becomes hypothyroid, so monitor free T4 levels in addition to TSH 4
- Patients who undergo thyroidectomy will require immediate levothyroxine replacement at approximately 1.6 mcg/kg/day 5