Iodine pleurodesis—a word of caution†

Abstract

We read with interest the article by Mohsen et al .[ 1] and the associated editorial by Astoul [2] concerning a randomized trial comparing povidone–iodine and talc poudrage pleurodesis for malignant pleural effusions. In their conclusion, intra-pleural iodine was found to have a good safety profile except for the occasional report of visual loss after local application. Nevertheless, we would like to share with the readers our experience of another hidden danger of iodine. Iodine was first discovered by a Frenchman Bernard Courtois in 1811 while processing seaweed washed up on the coast of Normandy for the production of gunpowder during the Napoleonic Wars. Since then, it has become indispensible as a nutritional supplement, disinfectant and medical radiological isotope. In our unit, povidone–iodine is widely used as a surgical skin disinfectant and for management of infected surgical wounds. We were first alerted of the potential danger when we encountered a dialysis-dependent renal failure patient with clinical manifestation of systemic iodine toxicity after irrigation of infected mediastinal wound with povidone–iodine solution [3]. Subsequently, we conducted a prospective study on systemic iodine absorption following a single application of povidone– iodine to the sternal wound prior to closure in patients undergoing routine cardiac surgery [4]. In a cohort of 40 patients, we found an average 3-fold increase in post-operative serum iodine levels in all patients compared with pre-operative baseline. Furthermore, the difference was significantly greater in patients with impaired renal function when compared with normal renal function, 4.3 versus 2.2 mol/l, respectively (p= 0.03). The iodine toxicity manifested as post-operative delirium in four patients with serum iodine levels ranging from 7.39 to 15.13 mol/l. One patient had visual hallucinations lasting for 48 h, and three patients had cognitive impairment which lasted for 36 h. Iodine clearance in humans is solely dependent on renal excretion which is directly related to the glomerular filtration rate. Therefore, individuals with renal impairment have prolonged iodine excretion, making them more susceptible to iodine toxicity. Previously, lethal cases have been reported when serum iodine levels reached above 553 mol/l, and even at lower serum levels between 32 and 55 mol/l, patients can develop reversible altered mental status and seizures [5, 6]. Our data suggested that a single application of povidone–iodine to subcutaneous tissue can cause a significant increase in post-operative serum iodine levels and possible altered mental status in susceptible individuals. Interestingly, Mohsen et al .[ 1] proposed that patients with malignant pleural effusion might have impaired pleural absorption and hence lower the chance of systemic iodine toxicity. Future studies on povidone–iodine pleurodesis should measure serum iodine levels in order to ascertain the degree of pleural iodine absorption. At exactly 200 years following the discovery of iodine, our experience serves as a poignant reminder that significant iodine absorption and toxicity can occur when povidone–iodine is used within body cavities, particularly in those with renal impairment. The quest for the Holy Grail must continue!