Cutaneous Thermal Injury Research Articles

Complications and pitfalls of endovenous laser therapy for varicose veins of lower extremities.

Varicose veins of lower extremities are a common disorder affecting a significant proportion of adult population. Endovenous techniques have been used in clinical practice for more than 20 years for their radical treatment; of these, laser therapy is one of the most widely utilized options. However, this treatment modality, too, has its specific side effects and complications which can be divided into perioperative (difficult venous access, fiber or sheath damage, vasovagal reaction with a drop in blood pressure and bradycardia, cutaneous thermal injury), and postoperative (bruising and hematomas, exceptionally pain, superficial venous thrombosis (phlebitis) and fibrous cord formation or pigmentations). Paresthesias, infections, arteriovenous fistulas, deep venous thrombosis and pulmonary embolism are very rare. The introduction of new generators with higher wavelengths and fibers with radial emission of laser energy has substantially reduced the side effects and complications. Performing the surgery in the outpatient setting using tumescent local anesthesia and under perioperative ultrasound control is an essential condition of the procedure.

AB569, a Novel, Topical Bactericidal Gel Formulation, Kills Pseudomonas aeruginosa and Promotes Wound Healing in a Murine Model of Burn Wound Infection.

ABSTRACTCutaneous thermal injuries from burns/explosives are a major cause of morbidity and mortality and represent a monumental burden on our current health care system. Injury severity is predominantly due to potentially lethal sepsis caused by multidrug-resistant (MDR) bacteria such as Pseudomonas aeruginosa (MDR-PA). Thus, there is a critical need to develop novel and effective antimicrobials for the (i) prevention, (ii) treatment, and (iii) healing of such wounds that are complicated by MDR-P. aeruginosa and other bacterial infections. AB569 is a novel bactericidal tandem consisting of acidified NaNO2 (A-NO2–) and Na2-EDTA. Here, we first show that AB569 acts synergistically to kill all human burn wound strains of P. aeruginosa in vitro. This was found to be due, in part, to the generation of A-NO2–-mediated nitric oxide (NO) formation coupled with the metal chelating properties of Na2-EDTA. Using a murine scald burn wound model of P. aeruginosa infection, an AB569-Solosite gel formulation eradicated all bacteria. Futher, we also demonstrate enhanced AB569-mediated wound healing by not only accelerating wound contraction, but also by reducing levels of the proinflammatory cytokines interleukin-6 (IL-6) and IL-1β while increasing the levels of anti-inflammatory cytokine, IL-10, and granulocyte-colony-stimulating factor (G-CSF). We also observed better epidermal restoration in AB569-treated wounds. Taken together, we conclude that this study provides solid foundational evidence that AB569 can be used topically to treat highly problematic dermal insults, including wound, burn, blast, and likely, diabetic infections in civilian and military populations, and help relieve the economical burden that MDR organisms have on the global health care system.

Macroscopical and Biochemical differentiation between cutaneous thermal, scald, chemical and electrical burn injuries with forensic significance in rats

Burn is a cutaneous injury in the skin tissue that is caused by heat, freezing, chemical, electrical or radiation. This study was designed to differentiate between thermal cutaneous burn injury and other common cutaneous burn injuries. Twenty-five rats were divided randomly into five groups (n =5) as follows: control, thermal burned, scalding, chemical burned and electrical burned group. After five minutes from burn induction, rats were euthanized, and skin tissue was collected for biochemical assays. Each treated group has its unique macroscopic appearance. GST activity of skin tissue was significant decrease in all treated group. All groups showed significantly increase in MDA (LPO bio-indicator) level. while, MDA level was highest increase in chemical burn group. Also, pro-inflammatory cytokine (Il-6) level was increase in all groups. However, the highest IL-6 level was observed in electrical burn one. It could be concluded that different cutaneous burn injuries can differentiated from each other through their macroscopical examination. But the tested biochemical parameters did not exhibit a significance in differentiation between the selected types of the burns.

Cutaneous Thermal Injury Modulates Blood and Skin Metabolomes Differently in a Murine Model.

As the field of metabolomics develops further, investigations of how the metabolome is affected following thermal injury may be helpful to inform diagnostics and guide treatments. In this study, changes to the metabolome were tested and validated in a murine burn injury model. After a 30% total body surface scald injury or sham procedure sera and skin biopsies were collected at 1, 2, 6, or 24 hr.Burn-specific changes in the metabolome were detected compared to sham animals. The sera metabolome exhibited a more rapid response to burn injury than that of the skin and it peaked more proximal to injury (6 vs 24 hr). Progression of metabolic response in the skin was less synchronous and showed a higher overlap of the significantly modified metabolites (SMMs) among tested time-points. Top affected pathways identified by SMMs of skin included inositol phosphate metabolism, ascorbate and alderate metabolism, caffeine metabolism, and the pentose phosphate pathway. Future research is warranted in human and larger animal models to further elucidate the role of metabolomic perturbations and the pathophysiology following burn injury.

Quantitative analysis of collagen and capillaries of 3.8-μm laser-induced cutaneous thermal injury and wound healing.

The biological effects of cutaneous thermal injury and wound healing after 3.8-μm laser radiation were investigated by observing the effects of different radiation doses on in vivo cutaneous tissue. A 3.8-μm laser with a radiation dose that changes from small (5.07) to large (15.74J/cm2) was used to irradiate mouse skin with the 2 × 4 grid array method. The healing progress of laser-injured spots, pathological morphology (H&E staining), and collagen structure changes (Sirius Red staining) were dynamically observed from one hour to 21days after laser radiation, and the capillary count and collagen content were quantitatively and comparatively analyzed. When the radiation doses were 5.07, 6.77, 8.21, and 9.42J/cm2, a white coagulation spot predominantly occurred, and when the radiation doses were 11.09 12.23, 14.13, 15.74J/cm2, a small injured spot predominantly occurred. One hour after radiation, the collagen structure was obviously damaged. Three to fourteen days after radiation, the hyperplasia and morphology of the collagen in the 5.07J/cm2 group were significantly better than those in the other dose groups. The number of capillaries in the 5.07J/cm2 and 6.77J/cm2 groups was significantly higher than that in the normal group (P < 0.01 or P < 0.05). Twenty-one days after radiation, only the collagen in the 5.07J/cm2 group was densely arranged, and it was basically close to the normal group level. The collagen content in the 5.07J/cm2 group was approximately 10.7%, but it was still lower than that in the normal group (with a collagen content of approximately 14.1%). The collagen in the other dose groups was diminished and had not returned to the normal group level. As the dose of the 3.8-μm laser increased, skin thermal injury gradually increased, the full-thickness skin increased, and the collagen content decreased, showing better dose-dependent and time-dependent effect relationships. The increase in capillaries in the early stage of laser radiation and the significant increase in collagen content in the middle and late stages of laser radiation were two important factors that promoted wound healing.

Quantitative and Qualitative Evaluation of Supercontinuum Laser‐Induced Cutaneous Thermal Injuries and Their Repair With OCT Images

Background and ObjectivesLaser‐induced thermal injuries are a heavily researched topic in laser medicine and biomedicine. To explore the quantitative biological effects of laser‐induced injury repair, we propose an optical imaging‐based in vivo evaluation method and discuss the injury effect and repair characteristics of skin tissue.Study Design/Materials and MethodsA supercontinumm laser (spectrum width ranged from 400 to 2400 nm) was used to irradiate live mice. The radiation doses were set as 32.85, 65.69, 98.4, and 197.08 J/cm2. Laser‐induced cutaneous thermal injuries were observed and measured after laser radiation. Optical coherence tomography (OCT) was used to image the injured spots. The optical attenuation coefficient (OAC) was computed using a Fourier‐domain algorithm. Three‐dimensional (3D) visualizations of the injured spots in the OCT images were constructed to qualitatively demonstrate the degree of the thermal injury at different times. The corresponding pathological changes of the skin injuries were observed dynamically.ResultsUnder increasing radiation doses, the injured spots, which ranged in degree from mild to severe, appeared accordingly. The mean OAC value of normal skin was 1.15 ± 0.01 mm−1. The mean values of the OAC maps in the region of interests (ROIs) were 0.88 ± 0.05, 0.91 ± 0.02, 0.93 ± 0.04, and 0.98 ± 0.08 mm−1 at each of the four radiation levels, respectively. Additionally, the 3D OCT visualization showed a directed view of the injured spots and the healing process and was used as a qualitative evaluation method. The OCT images and pathological results showed that the damage tended to vary across all groups, but this trend tended to weaken as the radiation dose increased.ConclusionOptical imaging provides an in vivo noninvasive and real‐time evaluation method to comprehensively quantify supercontinuum laser‐induced thermal injuries and wound healing. The OACs and 3D visualizations of the OCT cubic data enable the areas of the direct injured spots to be measured and the inner structure to be viewed. The results obtained with these techniques indicate that the skin injuries are aggravated and tissue repair trends weaken as the radiation doses increase. This method would have a potential application for laser‐medicine and laser‐biological effects in the future. Lasers Surg. Med. © 2020 Wiley Periodicals LLC

Standards in Biologic Lesions: Cutaneous Thermal Injury and Inhalation Injury Working Group 2018 Meeting Proceedings.

On August 27 and 28, 2018, the American Burn Association, in conjunction with Underwriters Laboratories, convened a group of experts on burn and inhalation injury in Washington, DC. The goal of the meeting was to identify and discuss the existing knowledge, data, and modeling gaps related to understanding cutaneous thermal injury and inhalation injury due to exposure from a fire environment, and in addition, address two more areas proposed by the American Burn Association Research Committee that are critical to burn care but may have current translational research gaps (inflammatory response and hypermetabolic response). Representatives from the Underwriters Laboratories Firefighter Safety Research Institute and the Bureau of Alcohol, Tobacco, Firearms and Explosives Fire Research Laboratory presented the state of the science in their fields, highlighting areas that required further investigation and guidance from the burn community. Four areas were discussed by the full 24 participant group and in smaller groups: Basic and Translational Understanding of Inhalation Injury, Thermal Contact and Resulting Injury, Systemic Inflammatory Response and Resuscitation, and Hypermetabolic Response and Healing. A primary finding was the need for validating historic models to develop a set of reliable data on contact time and temperature and resulting injury. The working groups identified common areas of focus across each subtopic, including gaining an understanding of individual response to injury that would allow for precision medicine approaches. Predisposed phenotype in response to insult, the effects of age and sex, and the role of microbiomes could all be studied by employing multi-omic (systems biology) approaches.

Management of combined massive burn and blast injury: A 20-year experience

IntroductionBlast injuries are complex types of physical trauma resulting from direct or indirect exposure to an explosion, which can be divided into four classes: primary, secondary, tertiary, and quaternary. Primary blast injury results in damage, principally, in gas-containing organs such as the lungs (blast lung injury, BLI). BLI is defined as radiological and clinical evidence of acute lung injury occurring within 12h of exposure to an explosion and not due to secondary or tertiary injury. BLI often combines with cutaneous thermal injury, a type of quaternary blast injury, either in terrorist bomb attacks or in civilian accidental explosions. This report summarizes our experience in the management of combined massive burn and BLI at a Shanghai Burn Center in China. MethodsA retrospective observational analysis of clinical data was performed for massive burn patients with or without BLI during a 20-year interval. Patient characteristics, causes of injury, clinical parameters, management, and outcomes were recorded and evaluated. ResultsA total of 151 patients (120 males and 31 females) with severe burn injury (≥50% TBSA) treated at the Burn Center of Changhai Hospital in Shanghai between July 1997 and June 2017 were enrolled in this study. Their mean age was 38.6±17.8 (3–75) years. Among them, 28 patients had combined BLI and burn injury and 39 patients had no BLI or smoke inhalation injury (non-BLI-SII). No significant difference was observed in the burn area or full-thickness burn area between the two groups. The lowest PaO2/fraction of inspired oxygen (FiO2) ratio during the first 24h in BLI patients was significantly lower than that in non-BLI-SII patients. Exudative changes were observed by X-ray radiography in all BLI patients but not in non-BLI-SII patients within 6h after injury. A significantly higher proportion of colloids were used for fluid resuscitation in BLI patients than that in non-BLI-SII patients. A higher proportion and longer time of mechanical ventilation were needed for BLI patients than those for non-BLI-SII patients, and a higher proportion of patients received sedative agents in the BLI group than those in the non-BLI-SII group. The first escharectomy was performed relatively later in BLI patients than in non-BLI-SII patients because of more time taken by BLI patients to recover from lung injury. The length of ICU and hospital stay in BLI patients was significantly longer than that in non-BLI-SII patients. No significant difference in the overall mortality was detected between these two groups. ConclusionIt is a formidable challenge for clinicians to diagnose and manage massive burn patients combined with BLI. A comprehensive treatment approach is strongly recommended, including fluid resuscitation, airway management, mechanical ventilation, and surgical treatment. Given the high mortality of massive burn patients combined with BLI even in a recognized burn center, more prospective studies are encouraged to assess more effective strategies for the treatment of such patients.

Spinal cord motor neuron plasticity accompanies second-degree burn injury and chronic pain.

Burn injuries and associated complications present a major public health challenge. Many burn patients develop clinically intractable complications, including pain and other sensory disorders. Recent evidence has shown that dendritic spine neuropathology in spinal cord sensory and motor neurons accompanies central nervous system (CNS) or peripheral nervous system (PNS) trauma and disease. However, no research has investigated similar dendritic spine neuropathologies following a cutaneous thermal burn injury. In this retrospective investigation, we analyzed dendritic spine morphology and localization in alpha‐motor neurons innervating a burn‐injured area of the body (hind paw). To identify a molecular regulator of these dendritic spine changes, we further profiled motor neuron dendritic spines in adult mice treated with romidepsin, a clinically approved Pak1‐inhibitor, or vehicle control at two postburn time points: Day 6 immediately after treatment, or Day 10 following drug withdrawal. In control treated mice, we observed an overall increase in dendritic spine density, including structurally mature spines with mushroom‐shaped morphology. Pak1‐inhibitor treatment reduced injury‐induced changes to similar levels observed in animals without burn injury. The effectiveness of the Pak1‐inhibitor was durable, since normalized dendritic spine profiles remained as long as 4 days despite drug withdrawal. This study is the first report of evidence demonstrating that a second‐degree burn injury significantly affects motor neuron structure within the spinal cord. Furthermore, our results support the opportunity to study dendritic spine dysgenesis as a novel avenue to clarify the complexities of neurological disease following traumatic injury.

Inhalation Injury: Unmet Clinical Needs and Future Research.

Pulmonary and systemic insults from inhalation injury can complicate the care of burn patients and contribute to significant morbidity and mortality. However, recent progress in diagnosis and treatment of inhalation injury has not kept pace with the care of cutaneous thermal injury. There are many challenges unique to inhalation injury that have slowed advancement, including deficiencies in our understanding of its pathophysiology, the relative difficulty and subjectivity of bronchoscopic diagnosis, the lack of diagnostic biomarkers, the necessarily urgent manner in which decisions are made about intubation, and the lack of universal recommendations for the application of mucolytics, anticoagulants, bronchodilators, modified ventilator strategies, and other measures. This review represents a summary of critical shortcomings in our understanding and management of inhalation injury identified by the American Burn Association's working group on Cutaneous Thermal Injury and Inhalation Injury in 2018. It addresses our current understanding of the diagnosis, pathophysiology, and treatment of inhalation injury and highlights topics in need of additional research, including 1) airway repair mechanisms; 2) the airway microbiome in health and after injury; and 3) candidate biomarkers of inhalation injury.

The response of muscle progenitor cells to cutaneous thermal injury

BackgroundSevere burn results in a systemic response that leads to significant muscle wasting. It is believed that this rapid loss in muscle mass occurs due to increased protein degradation combined with reduced protein synthesis. Alterations in the microenvironment of muscle progenitor cells may partially account for this pathology. The aim of this study was to ascertain the response of muscle progenitor cells following thermal injury in mice and to enlighten the cellular cascades that contribute to the muscle wasting.MethodsC57BL/6 mice received a 20% total body surface area (TBSA) thermal injury. Gastrocnemius muscle was harvested at days 2, 7, and 14 following injury for protein and histological analysis.ResultsWe observed a decrease in myofiber cross-sectional area at 2 days post-burn. This muscle atrophy was compensated for by an increase in myofiber cross-sectional area at 7 and 14 days post-burn. Myeloperoxidase (MPO)-positive cells (neutrophils) increased significantly at 2 days. Moreover, through Western blot analysis of two key mediators of the proteolytic pathway, we show there is an increase in Murf1 and NF-κB 2 days post-burn. MPO-positive cells were also positive for NF-κB, suggesting that neutrophils attain NF-κB activity in the muscle. Unlike inflammatory and proteolytic pathways, the number of Pax7-positive muscle progenitor cells decreased significantly 2 days post-burn. This was followed by a recovery in the number of Pax7-positive cells at 7 and 14 days, suggesting proliferation of muscle progenitors that accompanied regrowth.ConclusionOur data show a biphasic response in the muscles of mice exposed to burn injury, with phenotypic characteristics of muscle atrophy at 2 days while compensation was observed later with a change in Pax7-positive muscle progenitor cells. Targeting muscle progenitors may be of therapeutic benefit in muscle wasting observed after burn injury.

Cutaneous Thermal Injury Increases Vascular Permeability of Rat Mesenteric Venules by a Reactive Oxidant‐Dependent Mechanism

BackgroundFollowing major burns, edema develops in systemic organs and contributes to the development of remote organ dysfunction. The underlying mechanisms responsible for microvascular inflammation in this setting are not yet fully known. The purpose of our study was to determine if thermal injury to the skin of rats would increase vascular permeability in the mesenteric microcirculation, and if the mechanism involved generation of reactive oxidants.MethodsIntravital microscopy was used to examine mesenteric venules of anesthetized rats. FITC‐albumin was used to determine a vascular permeability index (VPI) based on the ratio of extravascular to intravascular fluorescence. Thermal injury was induced by exposing skin of animals to steam for 1 min (~40% of body surface area). Control animals were not exposed to steam. Vehicle or the antioxidant lipoic acid (2 mg/kg bolus, 0.5 mg/kg/h) was administered i.v. to animals after steam injury.ResultsVPI significantly increased after burn (0.39±0.13 at 30 min vs 0.61±0.08 at 4 h, p&lt;0.05, n=5), but not in non‐burned animals (0.08±0.09 at 30 min vs 0.12±0.03 at 4 h, n=5). These values for VPI were significantly different at these times in burned and non‐burned animals (p&lt;0.05). Lipoic acid significantly attenuated VPI in burn animals (0.20±0.06 at 30 min and 0.23±0.05 at 4 h, n=5) compared to vehicle‐treated burn animals (p&lt;0.05).ConclusionsThermal injury to the skin of rats increased vascular permeability in the mesenteric microcirculation of rats. Lipoic acid attenuated this increase which supports a role for increased generation of reactive oxidants in this mechanism.Support or Funding InformationDepartment of Surgery Research Funds

Cutaneous Thermal Injury Increases Leukocyte Adherence in Rat Mesenteric Venules by a Reactive Oxidant‐Dependent Mechanism

Background The inflammatory response following major burns is known to cause remote organ dysfunction, although the underlying mechanisms are not yet known. Purpose: Our goal was to determine if thermal injury to the skin of rats would promote microvascular inflammation in the mesenteric microcirculation, and if the mechanism involved generation of reactive oxidants. Methods Intravital microscopy was used to assess mast cell degranulation and leukocyte adherence in mesenteric venules of anesthetized rats. Thermal injury was induced by exposing skin on the back of animals to steam for 30 sec or 1 min. The area of injury was ~ 20 or 40% of the total body surface area. Control animals were not exposed to steam. Results: Leukocyte adherence significantly increased during 5 h after burn, but not in control animals. Mast cell degranulation was not increased by burns, and the antioxidant lipoic acid significantly attenuated leukocyte adherence in burned rats. Conclusions Thermal injury to the skin of rats resulted in microvascular inflammation in the mesenteric microcirculation of rats by a mechanism dependent on generation of reactive oxidants.

In vivo laser cartilage reshaping with carbon dioxide spray cooling in a rabbit ear model: a pilot study.

Similar to conventional cryogen spray cooling, carbon dioxide (CO2) spray may be used in combination with laser cartilage reshaping (LCR) to produce cartilage shape change while minimizing cutaneous thermal injury. Recent ex vivo evaluation of LCR with CO2 cooling in a rabbit model has identified a promising initial parameter space for in vivo safety and efficacy evaluation. This pilot study aimed to evaluate shape change and cutaneous injury following LCR with CO2 cooling in 5 live rabbits. The midportion of live rabbit ears were irradiated with a 1.45 µm wavelength diode laser (12 J/cm(2)) with simultaneous CO2 spray cooling (85 millisecond duration, 4 alternating heating/cooling cycles per site, 5 to 6 irradiation sites per row for 3 rows per ear). Experimental and control ears (no LCR) were splinted in the flexed position for 30 days following exposure. A total of 5 ears each were allocated to the experimental and control groups. Shape change was observed in all irradiated ears (mean 70 ± 3°), which was statistically different from control (mean 37 ± 11°, P = 0.009). No significant thermal cutaneous injury was observed, with preservation of the full thickness of skin, microvasculature, and adnexal structures. Confocal microscopy and histology demonstrated an intact and viable chondrocyte population surrounding irradiated sites. LCR with CO2 spray cooling can produce clinically significant shape change in the rabbit auricle while minimizing thermal cutaneous and cartilaginous injury and frostbite. This pilot study lends support for the potential use of CO2 spray as an adjunct to existing thermal-based cartilage reshaping modalities. An in vivo systematic evaluation of optimal laser dosimetry and cooling parameters is required.

Epidermal Aquaporin-3 Expression Is Increased in the Burn Wound after a Cutaneous Thermal Injury

Matthews, Jamil MD; Sebastian, Raul MD; Fillmore, Parker MD; Price, Leigh Ann MD; Sidhaye, Ramana MD; Milner, Stephen DDS, MD, FACS Author Information

Cutaneous Thermal Injury Increases Leukocyte Adherence in Rat Mesenteric Venules by a Reactive Oxidant-Dependent Mechanism

Cutaneous Thermal Injury Increases Leukocyte Adherence in Rat Mesenteric Venules by a Reactive Oxidant-Dependent Mechanism

Cutaneous thermal injury increases leukocyte adherence in rat mesenteric venules by a mast cell‐independent mechanism (678.15)

Background: The inflammatory response following major burns is known to cause remote organ dysfunction, although the underlying mechanisms are not yet known. Purpose: Our goal was to determine if thermal injury to the skin of rats would promote microvascular inflammation in the mesenteric microcirculation, and if the mechanism involved degranulation of mast cells. Methods: Intravital microscopy was used to assess mast cell degranulation and leukocyte adherence in mesenteric venules of anesthetized rats. Thermal injury was induced by exposing skin on the back of animals to steam for 1 min. The area of injury was ~ 40% of the total surface area. Control animals were not exposed to steam. Results: Leukocyte adherence significantly increased during 5 h after burn, but not in control animals. Mast cell degranulation was not increased by burns, and the mast cell stabilizer cromolyn did not attenuate leukocyte adherence in burned rats. Conclusions: Thermal injury to the skin of rats resulted in microvascular inflammation in the mesenteric microcirculation of rats by a mechanism independent of mast cell activation.

Role of endogenous TRPV1 agonists in a postburn pain model of partial-thickness injury

Oxidized linoleic acid metabolites (OLAMs) are a class of endogenous transient receptor potential vanilloid 1 (TRPV1) channel agonists released on exposure of tissue to transient noxious temperatures. These lipid compounds also contribute to inflammatory and heat allodynia. Because persistent pain after a burn injury represents a significant clinical challenge for treatment, we developed an in vivo rat model of partial-thickness cutaneous thermal injury and examined whether TRPV1 and specific OLAM metabolites play a role in mediating postburn pain injury. This peripheral model of burn injury had marked thermal allodynia peaking at 24h after thermal injury, with allodynia being maintained for up to 7d. Immunohistochemical characterization of tissue taken from injury sites revealed an increase in leukocyte/macrophage infiltration that was colocalized with TRPV1-positive fibers. Using this peripheral thermal injury model, we found that pharmacological blockade of peripheral TRPV1 receptors reduced thermal allodynia by about 98%. Moreover, there was a significant increase in OLAM levels compared to naive controls in hind paw skin biopsies. Additional studies of the metabolism of [C14]-linoleic acid in skin biopsies revealed the role of the cytochrome P450 (CYP) system in mediating the metabolism of linoleic acid after thermal injury. Finally, we demonstrated that direct inhibition of OLAMs using OLAM antibodies and indirect inhibition using the CYP inhibitor ketoconazole significantly reduced postburn thermal allodynia. Collectively, these findings point to a novel role of the OLAMs and CYP-related enzymes in generating postburn allodynia via activation of peripheral TRPV1.

Ex vivo investigations of laser auricular cartilage reshaping with carbon dioxide spray cooling in a rabbit model

Laser cartilage reshaping (LCR) with cryogen spray cooling is a promising modality for producing cartilage shape change while reducing cutaneous thermal injury. However, LCR in thicker tissues, such as auricular cartilage, requires higher laser power, thus increasing cooling requirements. To eliminate the risks of freeze injury characteristic of high cryogen spray pulse rates, a carbon dioxide (CO2) spray, which evaporates rapidly from the skin, has been proposed as the cooling medium. This study aims to identify parameter sets which produce clinically significant reshaping while producing minimal skin thermal injury in LCR with CO2 spray cooling in ex vivo rabbit auricular cartilage. Excised whole rabbit ears were mechanically deformed around a cylindrical jig and irradiated with a 1.45-μm wavelength diode laser (fluence 12-14 J/cm(2) per pulse, four to six pulse cycles per irradiation site, five to six irradiation sites per row for four rows on each sample) with concomitant application of CO2 spray (pulse duration 33-85 ms) to the skin surface. Bend angle measurements were performed before and after irradiation, and the change quantified. Surface temperature distributions were measured during irradiation/cooling. Maximum skin surface temperature ranged between 49.0 to 97.6 °C following four heating/cooling cycles. Significant reshaping was achieved with all laser dosimetry values with a 50-70 °C difference noted between controls (no cooling) and irradiated ears. Increasing cooling pulse duration yielded progressively improved gross skin protection during irradiation. CO2 spray cooling may potentially serve as an alternative to traditional cryogen spray cooling in LCR and may be the preferred cooling medium for thicker tissues. Future studies evaluating preclinical efficacy in an in vivo rabbit model are in progress.

Propagation of cutaneous thermal injury: A mathematical model

Cutaneous burn wounds represent a significant public health problem with 500,000 patients per year in the USA seeking medical attention. Immediately after skin burn injury, the volume of the wound burn expands due to a cascade of chemical reactions, including lipid peroxidation chain reactions. Such expansion threatens life and is therefore highly clinically significant. Based on these chemical reactions, the present paper develops for the first time a three-dimensional mathematical model to quantify the propagation of tissue damage within 12 hours post initial burn. We use the model to investigate the effect of supplemental antioxidant vitamin E for intercepting propagation. We show, for example, that if tissue levels of vitamin E tocotrienol are increased, postburn, by five times then this would slow down the lipid peroxide propagation by at least 50%. We chose the alpha-tocotrienol form of vitamin E as it is a potent inhibitor of 12-lipoxygenase, which is known to propagate oxidative lipid damage. Our model is formulated in terms of differential equations, and sensitivity analysis is performed on the parameters to ensure the robustness of the results.