Slow Release Iodine Dressings in Large Burns: Thyroid Impact & Outcomes

Introduction: Iodine containing dressings comprise contraindications for patients with thyroid disfunction. Further, precautions for surface areas greater than labeled limits for single and cumulative applications are provided. However, immediate release/high dose iodine products (povidone/tincture) are the basis for these precautions. Limited data exists for slower releasing/lower dose modern iodophors.    High TBSA burns are known metabolic crises resulting in hypermetabolic states. The acute thyroidal response is reported as a predictable drop in hormone marked by inconsistent TSH levels over time. Patient criticality, pharmacotherapy and thyroid function are all identified as potential sources of variability. Do low dose/slow release modern iodophors contribute to thyroid function changes in large burns? Methods: A retrospective series is reported with large TBSA burns treated with a modern lower dose, slow release iodophor foam dressing. The patient clinical outcomes and thyroid function profiles were assessed in comparison with untreated controls. Results: Only (3) of (8) patients, recorded TSH levels above normal; however, these elevated values were either prior to iodine exposure or decreasing during exposure. Further, these TSH levels were not outside of published values for similar sized untreated burn wounds. Even at very high exposures (required for such large burns – averaging 19 fold greater than labeled limits) including patients with Hashimoto’s disease, no patient demonstrated clear correlations with the topical SR iodine treatment and thyroid changes. Discussion: No impact on thyroid function testing (TFT) could be linked to the slow-release/low dose iodine dressing, even at exceptionally high surface areas that far exceed labeled precautions. Specifically, when elevated TSH levels were present, the frequency of elevation was independent of iodine dressing treatment periods and in perfect alignment with untreated patients with similar burn TBSA’s. This is especially encouraging, as burn units need more treatment options, and this intervention may have proved life saving for several of these critically ill patents. Independent of iodine, a clear link with severe burns to TFT changes is supported by this study. In fact, the data indicate that routine TFT may be warranted, which is further supported given that so many pharmaceuticals employed during burn care are also known to impact the thyroid, as noted in patient one (1). Interestingly, a true mapping of TFT over the full course of healing appears lacking in the literature. For a more comprehensive view of the dynamic thyroid impact for severe burns, future study might include repetitive TFT over the full course of care and serum iodine levels. References:1. Porter C, Tompkins RG, Finnerty CC, Sidossis LS, Suman OE and Herndon DN. The Metabolic Stress Response to Burn Trauma: Current Understanding and Therapies. Lancet 2016: 388(10052):1417-1426. 2. Vaughan GM and Pruitt BA. The Metabolic Thyroid Function in Critical Illness and Burn Injury. Seminars in Nephrology 1993: 13(4):359-370. 3. Becker RA, Wilmore DW, Goodwin CW, Zitzka CA, Wartofsky L, Burman KD, Mason AD, and Pruitt BA. Free T4, Free T3, and Reverse T3 in Critically Ill, Thermally Injured Patients. J of Trauma 1980: 20(9):713-721.