Management of Ocular Conditions in the Burn Unit: Thermal and Chemical Burns and Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis Amy Lin, MD,* Neha Patel, MD,* David Yoo, MD,* Sheri DeMartelaere, MD,† Charles Bouchard, MD* Patients in burn intensive care units suffer from potentially life-threatening conditions in- cluding thermal or chemical burns and Stevens-Johnson syndrome/toxic epidermal necroly- sis. There is often involvement of the ocular surface or adnexal structures which may be present at the time of hospital admission or may develop later in the hospital course. This article will describe the types of ocular burns, the mechanisms and manifestations of Stevens-Johnson syndrome/toxic epidermal necrolysis, the circumstances that may influence outcome, and acute and long-term treatment strategies, including new and evolving options. (J Burn Care Res 2011;32:547–560) Patients hospitalized in burn intensive care units have a variety of conditions resulting from different types and mechanisms of burns. There may also be widespread inflammation and sloughing of the epi- dermal and mucosal surfaces, as in Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN). Optimal care typically involves a multidisciplinary approach, including ophthalmologists involved in the daily management of their ocular problems. THERMAL AND CHEMICAL BURNS Mechanisms Ocular thermal injuries usually occur from exposure to direct flame, scalding liquid, blast injury, and handheld sources of heat such as cigarettes and curling irons. 1,2 At one tertiary care burn unit, 59% of all thermal burn patients were a result of flame injury, and 24% resulted from hot liquids. 1 Periorbital burns are the most com- mon ocular injury and account for 48% of cases. 1 Direct thermal injury to the globe is less common than perior- bital injury because of the simultaneous blinking reflex and Bell’s phenomenon (eyes rolling upward) which protect the ocular surface. The severity of thermal burns is related to the duration and extent of exposure as well as the nature of the causative agent. High temperatures induce inflammation and stromal protease expression that can lead to corneal melting if severe. Oil-based liq- uids are more adherent and cause deeper thermal inju- ries than water-based liquids. 3 Molten metal particles, if lodged in the eye, can cause continued contact with heat, leading to more severe damage. Similarly, chemical injuries, such as those caused by acid and alkaline agents, can cause extensive damage leading to visual impairment by causing widespread inflammation, scarring, melting, and necrosis of the ocular structures. 4–6 Partial or total corneal stem cell deficiency may also result. These cases require ocular surface reconstruction with corneal stem cell trans- plantation and systemic immunosuppression. Acids cause coagulation necrosis, forming an eschar which reduces further tissue penetration. 7 The hydrogen ion alters surface pH, while its associated anion dena- tures proteins, which subsequently coagulate to- gether to form a barrier. 2 However, strong acids, such as hydrofluoric acid, may penetrate as readily as alka- line agents and have the same spectrum of injury (see Figure, Supplemental Digital Content 1, showing a 43-year-old man after self-inflicted sulfuric acid injury with resultant full-thickness lid necrosis of all eyelids From the *Loyola University Medical Center, Maywood, Illinois; and †Brooke Army Medical Center, San Antonio, Texas. Address correspondence to Amy Lin, MD, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153. Supplemental digital content is available for this article. Direct URL citation appears in the printed text and is provided in the HTML and PDF versions of this article on the journal’s Web site (www.burncareresearch.com). Copyright © 2011 by the American Burn Association. 1559-047X/2011 DOI: 10.1097/BCR.0b013e31822b0f29 547