Mechanism and Management of Scald Burns

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A 3-year-old boy was brought to the emergency room by his mother. She reported that the child, reaching above his head, accidentally pulled a cup of hot coffee onto himself from the countertop (Figure 1). The burn was cleansed with a 5% chlorhexidine solution. The fragile blisters were debrided, and the wound was dressed with Xeroform and Bacitracin ointment, along with a protective dressing. The wound healed within 3 weeks.

Figure 1. Blisters are found on the anterior and medial aspect of the leg. The burn is tender with good capillary refill. The wound was completely healed within 3 weeks. 

A scald is a thermal injury resulting from exposure to hot fluid. The vulnerability of children to such injuries can be attributed to their thinner dermis and a higher proportion of body surface area exposed to scalding agents compared with adults. The rate of heat transfer from a liquid to the skin depends on the temperature gradient between the applied heat source and the skin, the thickness of the skin, and its thermal conductivity. It can be calculated from the formula:¹

Where:

Q  = Heat transfer per unit time

K  = Thermal conductivity of skin

L  = Skin thickness

T₁ = Temperature of the heat source

T₂ = Tissue surface temperature

Time-temperature thresholds have been used to set water safety standards, predict burn severity, and provide forensic evidence. Pioneering studies by Henriques and Moritz investigating porcine and human subjects revealed that tissue injury becomes apparent at temperatures exceeding 44°C, leading to a logarithmic increase in tissue destruction (Figure 2; Table 1).² Human skin, being hydrophilic, possesses high specific heat and low thermal conductivity, resulting in slow overheating and cooling processes. Consequently, thermal damage continues after the burning agent is removed. 

Hot water spills, however, seldom exceed 5 seconds during which the temperature gradient near the surface of the skin is steep but decreases rapidly with tissue depth. Therefore, the thickness of tissue injured is small with respect to the surface area. The temperature threshold necessary to cause a severe burn in spills was found to be 85°C,³ which corresponds to the temperature of a freshly brewed cup of coffee. It should be noted that time-temperature relationships have not been established for burns in children. When extrapolating adult data to children and infants, the accuracy is influenced by skin properties such as thickness, fragility, and consistency. It has therefore been recommended that, for safety, standards for hot water using existing adult burn data be revised downward by 3ºC to 4ºC.⁴

Figure 2. Time-surface temperature thresholds at which cutaneous burning occurs. An exposure of approximately 44°C requires 6 hours before irreversible damage is sustained at the basal level of the skin. A deep second- or third-degree scald requires exposure of 60°C for 5 seconds or 70°C for 1 second. Adapted from Moritz AR, Henriques FC. Studies of thermal injury: ii. the relative importance of time and surface temperature in the causation of cutaneous burns. Am J Pathol. 1947;23(5):695-720.

Table 1. Time and temperature relationship for deep burns in human skin. Adapted from Moritz AR, Henriques FC. Studies of thermal injury: ii. the relative importance of time and surface temperature in the causation of cutaneous burns. Am J Pathol. 1947;23(5):695-720. 

Acetaminophen and nonsteroidal anti-inflammatory agents provide effective analgesia in small superficial burns. Combinations of an opiate with a benzodiazepine are used for larger burns and procedural pain. Alternatively, Ketamine has proved successful for painful procedures.⁵ Small wounds have minimal risk of infection, and treatment focuses on providing a moist environment for epithelialization. Gentle cleansing with soap and water removes slough, while contaminated or infected wounds may need pressurized irrigation to remove biofilm. 

Common dressings for small burns include porous meshed gauze (Adaptic), petroleum-impregnated gauze (Tulle gras), or 3% bismuth tribromophenate (Xeroform). These are often coated with bacitracin, Neosporin, or Polymyxin B, although there is no consensus on the benefit of topical antibiotics. Alternatively, polyurethane foam or alginate dressings can be used. A gauze bandage secured with loosely knitted stretch fabric or a cohesive bandage protects the dressing. Patients are monitored twice weekly, or more frequently if pain or signs of infection increase.⁶ After epithelialization, the application of moisturizing cream is recommended. 

For burns greater than 20% of the total body surface area or those clinically infected or contaminated, antimicrobial agents are essential. Silver sulfadiazine (SSD) cream has bactericidal activity against gram-positive and gram-negative organisms, as well as Pseudomonas and yeasts. However, SSD can impair epithelialization and create a pseudoeschar that interferes with burn depth assessment. To prevent disruption of newly formed epithelium and minimize discomfort associated with frequent dressing changes, Biobrane, which integrates collagen peptides into a knitted nylon fabric, can be retained for 10 to 14 days until reepithelialization occurs. Silver-impregnated agents, such as nanocrystalline dressings, or hydrocolloid or hydrofiber silver dressings, can be left undisturbed for 5 to 7 days. Alternatively, biological dressings, such as allograft, xenograft, and amnion can create a moist and comfortable environment for wound healing. 

Blisters are attributed to early inflammatory changes due to increased capillary permeability and accumulation of edema fluid between the epidermis and dermis. The management of blisters remains controversial. Advocates for blister preservation emphasize its role as a barrier to infection while creating a moist environment that favors epidermal cell migration. The presence of Interleukin-6, transforming growth factor-alpha, and calmodulin in blister fluid has been found to exert mitogenic effects, stimulating keratinocyte growth.⁷ Blister fluid also contains angiogenic precursor cells CD14, which mobilize from the bone marrow following burn injuries, attract chemokines, participate in neovascularization, and differentiate into functional endothelial cells.⁸ Moreover, the increased expression of chemokine CXCL12 in human burn blister fluid, a potent chemoattractant for immature hematopoietic stem cells and endothelial progenitor cells, supports the role of blister fluid in angiogenesis.⁹ Collectively, these studies indicate removing blisters may compromise wound circulation. It should be stated, however, that once blisters spontaneously rupture, they should be debrided to reduce the risk of infection.

Conversely, proponents of blister fluid evacuation argue that these interventions prevent injury progression by eliminating inflammatory mediators. Prostaglandins, thromboxanes, leukotrienes, and oxygen-free radicals can impair the already fragile microcirculation of the wound bed and convert the zone of stasis into necrotic tissue. While wound desiccation may contribute to conversion, contemporary dressings can help retain wound moisture. Blister fluid may also compromise local defense mechanisms, as it has been shown to inhibit phagocytosis and opsonization of Pseudomonas aeruginosa.¹⁰ Debridement may increase local innate systems since defensins were found to be absent in burn blister fluid.¹¹

In clinical practice, small blisters (<6 mm) unlikely to rupture or impede tissue healing are best left undisturbed. Similarly, thick-walled blisters on the palms and soles of the feet should be preserved due to the discomfort associated with removal. Debridement is advisable for large fragile blisters (Figure 1) to prevent rupture, improve patient comfort, and assess the wound bed.¹²

The scald depicted in Figure 1 on the child’s leg was an accidental injury, as supported by the history and corresponding burn pattern. The child’s ability to independently reach the countertop and the absence of other injuries further align with this explanation. Scalds in toddlers and infants caused by hot drinks typically affect the face, shoulder, upper arms, and trunk but can affect the lower extremities. These burns exhibit variable depth and leave an irregular pattern characterized by splash marks. Conversely, forced immersion is indicated by the absence of splash marks, sharply defined wound margins, uniform burned depth, flexor sparing, and stocking and glove burn patterns. Symmetrical injuries are also observed (Figure 3).¹³ Suspicion should also be raised where the caregiver was absent at the time of injury, the parent denies the burn, the narrative changes over time, the child claims self-infliction, or there is a history of previous burns or injuries to other siblings. The child may also appear unusually passive and may show signs of neglect such as lack of cleanliness, malnutrition, or poor dentition, and there are older burns or other injuries.¹⁴ Any case raising suspicion for non-accidental injury should be reported to the appropriate child-protection agency.

Figure 3. Non-accidental injury. (A) A 2-year-old girl’s upper extremity was forcibly held in a sink of hot water. Immersion is suggested by a distinct line of demarcation around the child’s arm. (B) Examination of this 3-year-old girl revealed symmetrical burns to both cheeks. The mother explained that the child accidentally fell against a radiator. Subsequent investigation proved the injuries were caused by contact of the face with an iron.