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J. E. Marcus et al.
screening strategy for early diagnosis and treatment. Clin Infect Dis. 2016;63(10):1312–7.
29. Erol S, Altoparlak U, Akcay MN, Celebi F, Parlak M.Changes of microbial flora and wound colonization in burned patients. Burns. 2004;30(4):357–61.
30. Manson WL, Pernot PC, Fidler V, Sauer EW, Klasen HJ. Colonization of burns and the duration of hospital stay of severely burned patients. J Hosp Infect. 1992;22(1):55–63.
31. Murray PM, Finegold SM.Anaerobes in burn-wound infections. Rev Infect Dis. 1984;6(Suppl 1):S184–6.
32. Dokter J, Brusselaers N, Hendriks WD, Boxma H.Bacteriological cultures on admission of the burn patient: to do or not to do, that's the question. Burns. 2016;42(2):421–7.
33. Park HS, Pham C, Paul E, Padiglione A, Lo C, Cleland H.Early pathogenic colonisers of acute burn wounds: a retrospective review. Burns. 2017;43(8):1757–65.
34. Lesseva M, Girgitzova BP, Bojadjiev C. Beta-haemolytic streptococcal infections in burned patients. Burns. 1994;20(5):422–5.
35. Sheridan RL, Weber JM, Pasternack MS, Tompkins RG. Antibiotic prophylaxis for group A streptococcal burn wound infection is not necessary. J Trauma. 2001;51(2):352–5.
36. Pangli H, Papp A.The relation between positive screening results and MRSA infections in burn patients. Burns. 2019;45(7):1585–92.
3 7. Altoparlak U, Erol S, Akcay MN, Celebi F, Kadanali A. The
time-related changes of antimicrobial resistance patterns and predominant bacterial profiles of burn wounds and body flora of burned patients. Burns. 2004;30(7):660–4.
38. Keen EF 3rd, Robinson BJ, Hospenthal DR, Aldous WK, Wolf SE, Chung KK, etal. Prevalence of multidrug-resistant organisms recovered at a military burn center. Burns. 2010;36(6):819–25.
39. Azzopardi EA, Azzopardi E, Camilleri L, Villapalos J, Boyce DE, Dziewulski P, et al. Gram negative wound infection in hospitalised adult burn patients—systematic review and metanalysis. PloS One. 2014;9(4):e95042.
40. Barlam TF, Cosgrove SE, Abbo LM, MacDougall C, Schuetz AN, Septimus EJ, etal. Implementing an antibiotic stewardship program: guidelines by the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America. Clin Infect Dis. 2016;62(10):e51–77.
41. Maurel V, Denis B, Camby M, Jeanne M, Cornesse A, Glavnik B, etal. Outcome and characteristics of invasive fungal infections
Chapter 9. Burn Wound Infection
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in critically ill burn patients: A multicenter retrospective study. Mycoses. 2020;63(6):535–42.
42. Cochran A, Morris SE, Edelman LS, Saffle JR.Systemic Candida infection in burn patients: a case-control study of management patterns and outcomes. Surg Infect (Larchmt). 2002;3(4):367–74.
43. Ballard J, Edelman L, Saffle J, Sheridan R, Kagan R, Bracco D, etal. Positive fungal cultures in burn patients: a multicenter review. J Burn Care Res. 2008;29(1):213–21.
44. Devauchelle P, Jeanne M, Fréalle E. Mucormycosis in burn patients. J Fungi (Basel, Switzerland). 2019;5(1)
45. Kiley JL, Chung KK, Blyth DM. Viral infections in burns. Surg Infect (Larchmt). 2020;
46. Dai T, Huang YY, Sharma SK, Hashmi JT, Kurup DB, Hamblin MR. Topical antimicrobials for burn wound infections. Recent Pat Antiinfect Drug Discov. 2010;5(2):124–51.
4 7. Lansdown AB. Silver. I: its antibacterial properties and
mechanism of action. J Wound Care. 2002;11(4):125–30.
48. Stefanides MM Sr, Copeland CE, Kominos SD, Yee RB. In vitro penetration of topical antiseptics through eschar of burn patients. Ann Surg. 1976;183(4):358–64.
49. Storm-Versloot MN, Vos CG, Ubbink DT, Vermeulen H.Topical silver for preventing wound infection. Cochrane Database Syst Rev. 2010;(3):Cd006478.
50. Wasiak J, Cleland H, Campbell F, Spinks A. Dressings for superficial and partial thickness burns. Cochrane Database Syst Rev. 2013;2013(3):Cd002106.
51. Cooper ML, Boyce ST, Hansbrough JF, Foreman TJ, Frank DH. Cytotoxicity to cultured human keratinocytes of topical antimicrobial agents. J Surg Res. 1990;48(3):190–5.
52. Cartotto R. Topical antimicrobial agents for pediatric burns. Burns Trauma. 2017;5:33.
53. Burke JF, Bondoc CC, Morris PJ.Metabolic effects of topical silver nitrate therapy in burns covering more than fifteen percent of the body surface. Ann N Y Acad Sci. 1968;150(3):674–80.
54. Glasser JS, Guymon CH, Mende K, Wolf SE, Hospenthal DR, Murray CK. Activity of topical antimicrobial agents against multidrug-resistant bacteria recovered from burn patients. Burns. 2010;36(8):1172–84.
55. White MG, Asch MJ. Acid-base effects of topical mafenide acetate in the burned patient. N Engl J Med. 1971;284(23):1281–6.
56. Rode H, Hanslo D, de Wet PM, Millar AJ, Cywes S.Efficacy of mupirocin in methicillin-resistant Staphylococcus aureus
230
J. E. Marcus et al.
burn wound infection. Antimicrob Agents Chemother. 1989;33(8):1358–61.
5 7. Strock LL, Lee MM, Rutan RL, Desai MH, Robson MC,
Herndon DN, et al. Topical Bactroban (mupirocin): efficacy in treating burn wounds infected with methicillin-resistant staphylococci. J Burn Care Rehabil. 1990;11(5):454–9.
58. Jaspers ME, Breederveld RS, Tuinebreijer WE, Diederen BM.The evaluation of nasal mupirocin to prevent Staphylococcus aureus burn wound colonization in routine clinical practice. Burns. 2014;40(8):1570–4.
59. Barsoumian A, Sanchez CJ, Mende K, Tully CC, Beckius ML, Akers KS, etal. In vitro toxicity and activity of Dakin's solution, mafenide acetate, and amphotericin B on filamentous fungi and human cells. J Orthop Trauma. 2013;27(8):428–36.
60. Barret JP, Ramzy PI, Heggers JP, Villareal C, Herndon DN, Desai MH. Topical nystatin powder in severe burns: a new treatment for angioinvasive fungal infections refractory to other topical and systemic agents. Burns. 1999;25(6):505–8.
61. Ergün O, Celik A, Ergün G, Ozok G. Prophylactic antibiotic use in pediatric burn units. Eur J Pediatr Surg = Zeitschrift fur Kinderchirurgie. 2004;14(6):422–6.
62. Kiser TH, Hoody DW, Obritsch MD, Wegzyn CO, Bauling PC, Fish DN.Levofloxacin pharmacokinetics and pharmacodynamics in patients with severe burn injury. Antimicrob Agents Chemother. 2006;50(6):1937–45.
63. Conil JM, Georges B, Breden A, Segonds C, Lavit M, Seguin T, etal. Increased amikacin dosage requirements in burn patients receiving a once-daily regimen. Int J Antimicrob Agents. 2006;28(3):226–30.
64. Stone HH, Cuzzell JZ, Kolb LD, Moskowitz MS, McGowan JE Jr. Aspergillus infection of the burn wound. J Trauma. 1979;19(10):765–7.
65. Rodriguez CJ, Tribble DR, Murray CK, Jessie EM, Khan M etal. Invasive fungal infection in war wounds. Joint Trauma Service Clinical Practice Guidelines; 2016.
66. Lachiewicz AM, Hauck CG, Weber DJ, Cairns BA, van Duin D.Bacterial infections after burn injuries: impact of multidrug resistance. Clin Infect Dis. 2017;65(12):2130–6.
6 7. McManus AT, Mason AD Jr, McManus WF, Pruitt BA Jr. A
decade of reduced gram-negative infections and mortality associated with improved isolation of burned patients. Arch Surg (Chicago, Ill : 1960, 1994;129(12):1306–9.
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68. Mayhall CG, Lamb VA, Gayle WE Jr, Haynes BW Jr. Enterobacter cloacae septicemia in a burn center: epidemiology and control of an outbreak. J Infect Dis. 1979;139(2):166–71.
69. Embil JM, McLeod JA, Al-Barrak AM, Thompson GM, Aoki FY, Witwicki EJ, et al. An outbreak of methicillin resistant Staphylococcus aureus on a burn unit: potential role of contaminated hydrotherapy equipment. Burns. 2001;27(7):681–8.
70. Davison PG, Loiselle FB, Nickerson D. Survey on current hydrotherapy use among North American burn centers. J Burn Care Res. 2010;31(3):393–9.
71. Popp JA, Layon AJ, Nappo R, Richards WT, Mozingo DW.Hospital-acquired infections and thermally injured patients: chlorhexidine gluconate baths work. Am J Infect Control. 2014;42(2):129–32.
72. Thompson JT, Meredith JW, Molnar JA. The effect of burn nursing units on burn wound infections. J Burn Care Rehabil. 2002;23(4):281–6.
Chapter 10
Pediatric Burns
EricS.Ruff, NikhilR.Shah, RamonL.Zapata-Sirvent, andJongO.Lee
Introduction
Pediatric burns are a leading cause of injury and mortality both in the United States and abroad. Each day, over 300 children ages 0–19 are treated in emergency departments for burn-
E. S. Ruff (*) Department of Plastic and Reconstructive Surgery, University of Texas Medical Branch, Galveston, TX, USA e-mail: esruff@utmb.edu; razapata@utmb.edu
N. R. Shah Department of Surgery, University of Texas Medical Branch, Galveston, TX, USA e-mail: nikshah@utmb.edu
R. L. Zapata-Sirvent Department of Plastic and Reconstructive Surgery, University of Texas Medical Branch, Galveston, TX, USA
Shriners Children’s Texas, Galveston, TX, USA e-mail: esruff@utmb.edu; razapata@utmb.edu
J. O. Lee Department of Surgery, University of Texas Medical Branch, Galveston, TX, USA
Shriners Children’s Texas, Galveston, TX, USA e-mail: jolee@utmb.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 J. O. Lee (ed.), Essential Burn Care for Non-Burn Specialists,
https://doi.org/10.1007/978-3-031-28898-2_10
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related injuries [1]. Recent studies, however, have shown that ED visits for pediatric burns have been decreasing, suggesting that care for less severe burns may be taking place in outpa­tient settings such as urgent care or primary care offices [2].
The type of burn injury is often related to the child’s age and developmental stage. In the toddler age group, scald burns from hot liquids or grease predominate, as well as con­tact burns from stoves or grills. Younger children tend to suf­fer thermal burns from lighters or matches, while older children and teens are more likely to sustain flame burns from risk-taking activities such as use of flammable sub­stances or fireworks [3]. Chemical burns and high-voltage (>1000 volts) electrical injuries may also be encountered in the pediatric population. Fire and flame-induced burns account for the majority of fatalities, whereas death due to scald burns are exceedingly rare. Risk factors for mortality in burned children are larger total body surface area (TBSA) burn, inhalation injury, multiorgan failure, age less than 4years old, and non-accidental burn [4].
Notably, 16–20% of children admitted with burns are victims of abuse, which significantly increases mortality, though possibly due to concomitant injuries [3]. This should be consid­ered when there is a delay in presentation or the history of the burn does not match the pattern of the injury. Anatomic loca­tion of the burn is an unreliable factor in differentiating non­accidental and accidental burns, however burns on both lower extremities convey a three times greater likelihood of being an abusive injury [5]. There are also patient- and parent- specific risk factors one should consider when there is suspicion of child abuse. Patient-specific risk factors include children with behavioral problems, chronic conditions, and disabilities. Parent-specific risk factors include unplanned pregnancies, single-parent household, mental illness, partner violence, and substance abuse. Obtaining collateral information from social workers can be beneficial; however, physicians do not need to definitively diagnose abuse but rather have reasonable cause to suspect it in order to report it to child protective services.
Emergency care of each pediatric burn patient requires an individualized care plan. Consideration must be given to the mechanism and size of the burn, age-specific relationship
Chapter 10. Pediatric Burns
between body surface area and body weight when calculating fluid replacement, and physiological differences between children and adults. A critical understanding of these vari­ables is essential to improving both short- and long-term outcomes in this population.
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Pathophysiology
Patients suffering less than 15% TBSA burns generally have minimal systemic manifestations. Larger burns have the potential to cause overwhelming inflammatory states, espe­cially in the pediatric patient [6]. Pathogenesis has been found to be largely multifactorial.
Breakdown of the integumentary barrier leads to large evaporative losses. This, in tandem with intravascular deple­tion from impaired function of capillary tight junctions, leads to devastating hypovolemic shock [4, 7]. The pediatric popu­lation has lower circulating volumes and can decompensate rapidly after such insults [8]. Burn injury also induces an overwhelming vasoplegic state. This is attributed to an array of endogenous substances, including nitric oxide, histamine, and reactive oxygen species [9]. The resulting distributive shock further reduces tissue perfusion.
Finally, the notion of post-burn cardiomyopathy has become increasingly prevalent, particularly in the initial 24–48h period [10]. This is believed to be cytokine-mediated; interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 have been found to be markedly elevated in children following ther­mal injury [11, 12]. Although reportedly reversible, cardiac depression poses diagnostic and resuscitative challenges [13]. Expeditious patient evaluation and intervention are crucial to systematically address all etiologies of burn shock.
Initial Evaluation
If feasible, a targeted history from a parent, caretaker, or witness should be taken to ascertain details about the burn occurrence, environment, and inciting events. Etiology of
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accidental versus non-accidental trauma should be further investigated as well. The time of presentation may be distant from the time of injury which should warrant alteration of resuscitation strategies. Patients presenting more than four hours after injury without appropriate explanation should raise concern for possible child abuse [14]. Nonetheless, all major burn patients are assumed to be trauma patients and must be evaluated in the same systematic approach.
As such, the airway and breathing take precedence. Supplemental oxygen should be applied if there is suspicion for inhalation injury, particularly after a house or building fire, during which prolonged smoke exposure is common. Physical examination may demonstrate significant facial burns, singed nasal hair or eyebrows, or carbonaceous soot in the oropharynx. Arterial blood gas and carboxyhemoglobin levels may assist in decision-making as pulse oximetry read­ings are typically normal in patients with carbon monoxide poisoning [15]. Warning signs that may indicate impending respiratory failure include tachypnea, stridor, and hoarseness, and should prompt emergent intubation [4].
Children with burns involving a large TBSA (>20%) or younger than two years old also necessitate a low threshold for intubation [3, 4, 16]. Younger children have considerably smaller airway diameters, thus even minimal edema from large volume fluid resuscitation may induce life-threatening obstruction. If ventilation becomes difficult or airway pres­sures increase in the setting of circumferential thorax burns, escharotomies may be indicated to restore adequate chest expansion.
Circulation is often challenging to assess in a severely burned patient. Palpation of distal pulses, assessment of capil­lary refill, and blood pressure monitoring should be attempted if possible; however, invasive monitoring may be necessary. In the infantile and younger pediatric population, a femoral arterial line is likely easier to secure. Of note, inability to appreciate extremity pulses in the setting of circumferential eschar may also indicate need for escharotomy.
Chapter 10. Pediatric Burns
Following evaluation of the trauma “ABCs,” the secondary survey should ensue. Efficient “head to toe” evaluation is performed to identify additional traumatic injury. Those involved in explosive or electrical burns are at high risk for associated intracranial, intraabdominal, or orthopedic inju­ries. However, the inability of the neonatal or infant patient to convey and localize pain greatly limits early identification of these injuries. Thus it may be necessary to obtain full body radiographic and tomographic imaging following stabilization.
Clothing and coverings should be removed to expose all burn wounds. This step often occurs earlier during initial evaluation if the patient suffered chemical burns, as any resi­due retained on clothing could inflict further caustic injury [4]. The reflexive tendency to apply ice should be avoided. Clean sheets and blankets should be applied in order to maintain normothermia. External warming devices and room temperature manipulation may be required in the pediatric population, as they inherently have lower muscle and soft tis­sue mass. Desired ambient and core body temperatures range from 30 to 35°C and 36 to 38°C, respectively [17].
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Extent ofInjury
Only wounds that are partial- and full-thickness are accounted for when assessing extent of injury, especially if planning for surface area-based resuscitation. Clinical evaluation of wound depth is estimated to be accurate 60–75% of the time in the general population, however this may be even lower in children. Having thinner dermis, children’s burn injury often requires 24–48h to evolve; serial wound examinations may help delineate true depth [18, 19]. It is important to note that burns may often be mixed-thickness, however the deepest component is generally identified at the center. This is due to vessel thrombosis at the periphery, causing a centripetal pat­tern of injury.
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F . Lund and Browder chart for estimation of burn size in pediatric patient
The standard “Rule of Nines” cannot be readily applied to patients younger than 15years of age due to a significantly higher surface area to body weight ratio. This skewed ratio manifests because of children’s large cranial surface area compared to extremities [18, 19]. As such, Lund and Browder chart can be used, in order to rapidly assess extent of injury [20] (Fig.10.1). For non-confluent regions, the patient’s pal­mar surface with fingers adducted may approximate 1% of body surface area [21].