Effect of Lidocaine on Reducing Injury in a Rat Electrical Burn Model Erol Benlier, MD,* Sevgi Eskiocak, MD,Þ Fulya Oz Puyan, MD,þ Emel Yurdakul Sikar, MD,§ Huseyin Kandulu, MD,|| Imran Kurt Omurlu, MD,¶ Husamettin Top, MD,* and Ahmet Cemal Aygit, MD# Abstract: Electrical injuries induce progressive tissue loss. We evaluated the effect of lidocaine on tissue necrosis after electrical burn injuries. Forty-two male Wistar albino rats (250Y300 g) were divided into 3 groups [Group A (n = 6), control group without an electrical burn injury; and Groups B (n = 18) and C (n = 18), electrical burn injury groups without and with lidocaine therapy, respectively]. Three separate analyses were performed at different time points on 6 of 18 rats from Groups B and C at each time point. Electrical burns were induced by applying 220 V AC between the left upper and right lower ex- tremities for 10 seconds. Myeloperoxidase and malondialdehyde levels were measured in skin and muscle biopsy specimens after the first hour, fresh and dry weight differences in the amputated extremities were calculated after 24 hours, and live and necrotic tissue areas were measured at 7 days after burn injury. We found that lidocaine reduced edema, the number of neutrophils, and neutrophil damage in tissues. We conclude that lidocaine decreased the amount of necrotic tissue caused by electric injury. Key Words: electric burns, lidocaine, neutrophils, myeloperoxidase, rats (Ann Plast Surg 2012;69: 152Y156) E lectrical burn injuries have become frequent with the common use of electrical energy. Electrical injuries were previously defined as a pathological event related to an increase in tissue temperature. How- ever, unforeseen electrical current pathways, variable tissue resistance, progressive tissue loss, the extent of multisystem involvement, and in- creasing neurological deficit risks in subsequent months are all char- acteristics of electrical injuries. Therefore, electrical burns should be evaluated differently than thermal burns. 1Y3 Because of the complexity of injuries in patients with electrical burn trauma, there are still many unanswered questions and insuffi- cient knowledge regarding the underlying physiological and patho- logical mechanisms. An electrical burn injury cannot be fully explained by 1 physiological mechanism, and various mechanisms have been suggested. 1,2,4,5 The pathophysiological mechanisms of electrical burn injuries should be well understood to improve medical treatment and intervention. Many clinical and experimental studies have been conducted to un- derstand the pathology of the neutrophil-endothelial interaction after electrical injuries. 3Y6 In addition to an increase in tissue temperature, electric current induces tissue necrosis by obstructing and coagulating small vessels. 5,6 When high voltage passes through the body, it causes neural injury, vasospasm, vascular thrombosis, and myonecrosis. 6 In- creases in arachidonic acid and thromboxane metabolism products are detected in deeper skin layers, which appear undamaged. The throm- boxane level also increases in the superficial layers of the skin and normal skin becomes necrotic. 4 The activation of neutrophils increases free oxygen radical levels during the early phase of a thermal burn. Several enzymes released from neutrophils play important roles in microvascular injury. Free oxygen radicals are one reason for progressive tissue loss and distant organ injury. 1,6 The neutrophil-endothelial interaction after injury has been re- ported as an inducer of edema during early periods after direct thermal injury because of the local release of inflammatory mediators. 1,2,4 Edema beneath the skin caused by an electrical injury increases perfusion pressure inside the muscle fascia causing compartment syndrome. Compartment syndrome is the elevation of interstitial pressure in a closed fascial compartment that leads to ischemia-related progressive functional loss in nerves and muscles. The local anesthetic lidocaine inhibits the release and synthesis of inflammatory mediators such as leukotriene B 4 , interleukin 1>, and histamine. Lidocaine increases adhesion, migration, and collection of neutrophils, which may depress the activity and release of macro- phages. Vascular and antithrombotic effects of lidocaine have also been reported. 1,6,7 Lidocaine reduces tissue edema by decreasing vascular permeability and albumin extravasation. 8 Therefore, lidocaine therapy can be easily converted to clinical use based on its edema reducing potential, particularly for electrical burn injuries with progressive tis- sue loss caused by edematous changes such as myonecrosis in com- partment syndrome. The aim of this study was to evaluate the effect of lidocaine on tissue necrosis in a rat experimental electrical burn injury model. MATERIAL AND METHODS This experimental animal study was performed at the Trakya University Faculty of Medicine, experimental animal laboratory. This study was approved by the Trakya University Ethics Committee and conducted in accordance with the Animal Rights Committee Universal Report (Ref num; 086, September 9, 2004). Experimental Protocol Forty-two male Wistar albino rats (weight, 250Y300 g) were used. Throughout the study, animals were cared for by veterinarians and were under standard laboratory conditions. Forty-two rats were divided into 3 main groups. Group A was the control group and contained 6 rats without electrical burn injury. Groups B (n = 18) and C (n = 18) were electrical burn injury groups without and with lidocaine therapy, respectively. Three separate analyses were performed at different time points on 6 of 18 rats from Groups B and C. Groups B and C were divided into 3 subgroups to separately evaluate biochemical and BURN SURGERY AND RESEARCH 152 www.annalsplasticsurgery.com Annals of Plastic Surgery & Volume 69, Number 2, August 2012 Received August 5, 2011, and accepted for publication, after revision, April 2, 2012. From the Departments of *Plastic Reconstructive and Aesthetic Surgery, †Biochemistry, and ‡Pathology, Trakya University Faculty of Medicine, Edirne; §Afyonkarahisar Kocatepe State Hospital, Afyonkarahisar; ||Bilecik State Hospital, Bilecik; ¶Department of Biostatistics, Adnan Menderes University Faculty of Medicine, Aydın; and #Bagcilar Research and Education Hospital, Istanbul, Turkey. Presented at the 30th National Congress of Turkish Plastic, Reconstructive and Aesthetic Surgery (E-076, p: 316, Antalya, Turkey, 15Y19 October, 2008); and at the 6th Congress of The Balkan Association of Plastic, Reconstructive and Aesthetic Surgery (no. 115, pp. 105Y106, Ohrid, Macedonia, June 4Y7, 2009). Conflicts of interest and sources of funding: Supported by Trakya University Scientific Research Project no. 642. Reprints: Erol Benlier, MD, Department of Plastic Reconstructive and Aesthetic Surgery, Trakya University Faculty of Medicine, 22030 Edirne, Turkey. E-mail: drebenlier@hotmail.com. Copyright * 2012 by Lippincott Williams & Wilkins ISSN: 0148-7043/12/6902-0152 DOI: 10.1097/SAP.0b013e3182586b2a Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.