Childhood burns remain a major global health problem with disproportionate impact in low- and middle-income settings. Distinct pediatric anatomy and physiology (thinner dermis, higher body-surface-area–to–mass ratio, and immature thermoregulation) amplify risks of deeper injuries, hypovolemia, hypothermia, and infection. This narrative review synthesizes current evidence on epidemiology and etiologies, pathophysiology, clinical assessment, acute management, surgical/advanced interventions, rehabilitation, and prevention. Scalds predominate in children under five, with boys affected slightly more than girls; inhalation injury, delayed presentation, and limited burn-care resources drive morbidity and mortality. Accurate depth and total body surface area estimation, early airway protection when needed, and judicious, physiology-tailored fluid resuscitation are cornerstones of acute care. Multimodal analgesia, infection prevention, early enteral nutrition, and temperature control are essential supportive measures. Early excision and grafting, bioengineered skin substitutes, and negative-pressure wound therapy can accelerate closure and improve outcomes, while long-term rehabilitation (physiotherapy, scar modulation) and psychological support address functional and psychosocial sequelae. Sustained reductions in pediatric burn burden require comprehensive, context-specific prevention strategies—home safety, caregiver education, school/community programs, and policy-level interventions—integrated into child health systems.

• Pediatric burns; Epidemiology; Fluid resuscitation; Inhalation injury; Skin substitutes; Rehabilitation.

Dursun R, Aktar F (2025) Burns in Children: Epidemiology, Clinical Management and Prevention Strategies. Pediatr Child Health 13(4): 1361.

ABLS: Advanced Burn Life Support; ATLS: Advanced Trauma Life Support; ARDS: Acute Respiratory Distress Syndrome; CBT: Cognitive Behavioral Therapy; NPWT: Negative Pressure Wound Therapy; PRP: Platelet-Rich Plasma; SIRS: Systemic Inflammatory Response Syndrome; TBSA: Total Body Surface Area.

Burn injuries are among the leading causes of childhood morbidity and mortality worldwide, with the World Health Organization estimating over 180,000 burn-related deaths annually; children under 10 are disproportionately affected [1]. Compared with adults, children’s thinner dermis and higher body-surface-area–to–mass ratio predispose to deeper injuries and rapid fluid and heat loss, while immature immune and thermoregulatory systems increase risks of infection and hypothermia [2]. In addition to physical trauma, burns inflict substantial psychosocial burdens on children and families. This review summarizes contemporary evidence on pediatric burns epidemiology and etiology, pathophysiology, assessment, emergency management, surgical and advanced treatments,rehabilitation, and prevention to inform clinical practice and public health strategies.

The distribution and determinants of pediatric burns vary by region and socioeconomic context. Over 90% of severe burns occur in low- and middle-income countries, where household safety regulations and access to acute burn care are limited [1,3]. Mortality in high-income settings is typically <2% but remains 10-15% in under resourced regions due to delayed presentation and inadequate resuscitation [3]. Children under five constitute the majority of cases; boys are more frequently affected, likely reflecting behavioral and exposure factors, likely reflecting behavioral factors. In Turkey and comparable middle-income settings, scalds in domestic environments (kitchen, bathing areas) predominate [4]. Scalds are the leading etiology in toddlers, while flame burns increase with age; contact, electrical, and chemical burns are less common but may cause deep-tissue injury. Patterns such as sharp immersion lines or symmetric burns and discordant caregiver histories should raise concern for non-accidental injury [5].

Tissue damage severity depends on exposure temperature and duration. At approximately 60°C, irreversible protein denaturation occurs within seconds, leading to coagulative necrosis. Jackson’s classic model delineates three concentric zones: coagulation (irreversible necrosis), stasis (potentially salvageable), and hyperemia (reversible inflammation) [6]. Pediatric patients develop a pronounced systemic inflammatory response, capillary leak, and hypovolemia; within hours, a hypermetabolic state driven by catecholamines and cortisol elevates energy expenditure and promotes protein catabolism, impairing healing [7,8]. Immune dysfunction with barrier loss and altered innate responses increases susceptibility to colonization and invasive infection.

Depth categories superficial, superficial partial thickness, deep partial-thickness, and full-thickness guide prognosis and management; fourth-degree burns involve underlying fascia, muscle, or bone [9,10]. Accurate total body surface area (TBSA) estimation is critical and best achieved with the age-adjusted Lund and Browder chart in children; the palmar method (~1% TBSA) aids in small burns. Inhalation injury (10–20% of pediatric burns) markedly increases morbidity and mortality; suspicious features include enclosed-space fire, facial burns, singed nasal hairs, carbonaceous sputum, hoarseness, or hypoxemia. Fiberoptic bronchoscopy confirms diagnosis and grades injury; early airway protection is prudent when edema progression is likely [11]. Non-accidental injury should be considered when distribution patterns or histories are inconsistent [5].

Initial care follows ATLS/ABLS priorities. (A) Airway: anticipate edema in facial burns and enclosed-space exposures; consider early endotracheal intubation. (B) Breathing: administer 100% humidified oxygen; evaluate carboxyhemoglobin; consider bronchodilators. (C) Circulation: obtain IV/IO access through unburned skin; begin pediatric-tailored fluids. (D) Disability: assess neurologic status. (E) Exposure/Environment: remove burned clothing, prevent hypothermia [12]. Fluid resuscitation may start with a modified Parkland approach (3–4 mL × kg × %TBSA in 24 h), giving half in the first 8 h; incorporate maintenance dextrose in children <20 kg; target urine output ~1 mL/kg/h and avoid over-resuscitation (‘fluid creep’) [13]. Multimodal analgesia (paracetamol/NSAIDs; titrated IV morphine for severe pain; ketamine or nitrous oxide for procedures) plus non-pharmacologic techniques (parental presence, distraction) is recommended [14]. Early wound cooling with running water for 20 minutes (within 3 h), gentle cleansing, judicious blister management, and moisture retentive dressings (e.g., silver-impregnated foams) support re-epithelialization. Prophylactic systemic antibiotics are discouraged; topical antimicrobials and strict asepsis are central. Early closure reduces sepsis risk; common pathogens include Pseudomonas aeruginosa, Staphylococcus aureus, and Acinetobacter spp [15].

Early excision of devitalized tissue with split-thickness autografting within 3–5 days can reduce infection, length of stay, and mortality [16,17]. When donor sites are limited, temporary coverage (allograft, xenograft) or bioengineered options (e.g., Integra®, Biobrane®, cultured epithelial autografts) assist closure and optimize functional and cosmetic outcomes in children [18]. Negative pressure wound therapy enhances graft take and decreases edema and bioburden [19]. Long-term, contracture prevention hinges on early physiotherapy and scar modulation; refractory deformities often require Z-plasty, local/regional flaps, or tissue expansion [20]. Emerging modalities—including stem cell–augmented constructs, platelet-rich plasma, growth factor matrices, and fractional lasers—show promise for scar quality and pigmentation [21].

Infections and sepsis remain leading causes of adverse outcomes; rigorous wound care and early closure are protective [22]. Persistent hypermetabolism necessitates high-calorie, high-protein nutrition with micronutrient support; early enteral feeding maintains gut integrity [7]. Rehabilitation begins once hemodynamically stable and continues throughout growth: range-of-motion exercises, splinting, pressure garments, silicone therapy, and scar massage mitigate hypertrophy and contracture [23]. Psychological sequelae anxiety, depression, PTSD, sleep disturbances are common and warrant early assessment, family-centred counselling, CBT, and school reintegration planning [24].

Most pediatric burns are preventable. Home safety (thermostatic mixing valves, stove guards, safe storage of hot liquids and chemicals) and caregiver education on supervision and evidence-based first aid (20-minute cool running water; avoid ice, toothpaste, or butter) can markedly reduce incidence and severity [25]. School- and community-based programs, coupled with policy measures (housing codes, flammable material regulation, emergency response systems), are pillars of sustainable prevention [26,27]. Integrating burn prevention into child health platforms and national injury strategies is essential [1].

Most pediatric burns are preventable. Home safety (thermostatic mixing valves, stove guards, safe storage of hot liquids and chemicals) and caregiver education on supervision and evidence-based first aid (20-minute cool running water; avoid ice, toothpaste, or butter) can markedly reduce incidence and severity [25]. School- and community-based programs, coupled with policy measures (housing codes, flammable material regulation, emergency response systems), are pillars of sustainable prevention [26,27]. Integrating burn prevention into child health platforms and national injury strategies is essential [1].

Pediatric burns demand age-specific, multidisciplinary care across the continuum: accurate assessment, airway and fluid management, infection control, nutrition, early closure, rehabilitation, and psychosocial support. Advances in bioengineered coverage and reconstructive strategies are improving survival and quality of life, but the greatest population-level gains will come from prevention embedded in homes, schools, and policy. Coordinated clinical, educational, and public health action can dramatically reduce the burden of preventable burn injuries in children.

We thank our clinical and nursing colleagues for their dedication to pediatric burn care.

1. World Health Organization. Burns: key facts. Geneva: WHO; 2023.
2. Jeschke MG, Herndon DN, Finnerty CC. Pediatric burn injury: current management and future directions. Burns. 2020; 46: 1-10.
3. Forjuoh SN. Pediatric burns in developing countries: epidemiology and prevention. Burns. 2020; 46: 528-537.
4. Yasti AC, ?ahin ?, Aksu B. Epidemiology of pediatric burns in Turkey: a multicenter analysis. Ulus Travma Acil Cerrahi Derg. 2021; 27: 159- 165.
5. Kemp AM, Maguire SA, Nuttall D. Non-accidental burns in children: a systematic review. Arch Dis Child. 2020; 105: 45-54.
6. Jackson DM. The diagnosis of the depth of burning. Br J Surg. 1953; 40: 588-596.
7. Williams FN, Branski LK, Herndon DN. Metabolic and inflammatory responses after pediatric burns: implications for clinical care. J Burn Care Res. 2021; 42: 168-176.
8. Leung L, Wiseman SM, Joffe AR. Pediatric burn injury and systemic inflammatory response: mechanisms and management. Pediatr Crit Care Med. 2020; 21: 421-430.
9. Hettiaratchy S, Papini R. Initial management of a major burn: II—assessment and resuscitation. BMJ. 2004; 329: 101-103.
10. Jaskille AD, Shupp JW, Jordan MH, Jeng JC. Critical review of burn depth assessment techniques: implications for pediatric care. Burns. 2020; 46: 225-235.
11. Sheridan RL, McTigue KM, Tompkins RG. Diagnosis and management of inhalation injury in children. J Burn Care Res. 2018; 39: 12-19.
12. Herndon DN. Total burn care. 5th ed. Elsevier; 2020.
13. Pham TN, Cancio LC, Gibran NS. American Burn Association practiceguidelines on fluid resuscitation. J Burn Care Res. 2020; 41: 113-127.
14. Miller K, Rodger D, Lloyd O. Pain management in pediatric burns: evidence-based review. Paediatr Anaesth. 2021; 31: 403-412.
15. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. 2020; 33: e00078-19.
16. Janzekovic Z. A new concept in the early excision and immediate grafting of burns. J Trauma. 1970; 10: 1103-1108.
17. Sheridan RL, Tompkins RG, Burke JF. Pediatric burn surgery. N Engl J Med. 2012; 367: 2341-2349.
18. Boyce ST, Lal S. Tissue engineering of skin and regenerative medicine approaches to pediatric burn care. Pediatr Surg Int. 2020; 36: 549- 559.
19. Molnar JA, DeFranzo AJ, Hadaegh A. Application of negative pressure wound therapy in pediatric burns. Ann Plast Surg. 2014; 73: 21-28.
20. Schouten HJ, Nieuwenhuis MK, Niemeijer AS. Surgical management of pediatric post-burn contractures. Burns. 2012; 38: 556-562.
21. Supp DM, Boyce ST, Swope VB. Advances in regenerative medicine for burn wound repair. Burns Trauma. 2019; 7: 1-15.
22. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. 2006; 19: 403-434.
23. Parry IS. Multidisciplinary rehabilitation following pediatric burns. J Burn Care Res. 2018; 39: 708-716.
24. Patterson DR. Psychological issues in pediatric burn patients. Burns. 2010; 36: 479-485.
25. Cuttle L. First aid treatment of burn injuries. Wound Repair Regen. 2008; 16: 436-447.
26. Forjuoh SN. Burns in low- and middle-income countries: a review of descriptive epidemiology, risk factors, treatment, and prevention. Burns. 2006; 32: 529-537.
27. Mock C, Peck M, Peden M, Krug E. A WHO plan for burn prevention and care. Geneva: World Health Organization; 2008.