Burns are a very specific type of injury and, particularly in the case of large and/or deep lesions, require highly specialized care. In the US, the number of patients seeking medical care for a burn injury seems to be stable at approximately 500,000 per year.1 Around 40,000 of these patients are hospitalized because of burn injuries, and 60% of those are treated in specialized burn centers.1
While small burns are the majority and usually not life threatening, larger burns, even partial-thickness ones, still pose a major threat when not treated properly. Small burns still may cause major morbidity, however, because the injury may be very painful and can lead to disfiguring outcomes such as hypertrophic scars, keloids, and contractures.2
This article gives a basic overview of burns and burn care and is not intended to discuss overall burn care in detail.
TYPES OF BURNS
Burns can be categorized as follows:3
- Scald injuries typically result in partial-thickness lesions when cooled quickly. The injury is caused by contact with a hot fluid such as hot tea or coffee.
- Flame injuries are caused by direct exposure to flames. House and car fires are common etiologies, and the burns usually are full-thickness.
- A flash burn may be caused by very short exposure to a burning gas or vapor. The lesion is often partial-thickness (unless, for instance clothing catches fire).
- Contact burns are caused by contact with a hot surface. In many cases, these injuries are not deep, although this depends on the temperature of the surface touched and the length of exposure. Major injuries may be caused by the combination of pressure and prolonged exposure to the heat source, as is the case in patients who, after an epileptic insult, remain in contact with a hot surface for a prolonged period.4,5 On a hot day, asphalt can cause a second-degree burn in less than a minute.6 Contact with hot coals, molten metal, and other high-temperature substances often leads to deep burns.
- Electrical burns are caused by contact with an electrical current or electricity strike. Electricity is converted to heat, leading to extensive and deep tissue necrosis that may initially be hidden to the naked eye. The amount of heat is proportional to the electrical resistance of the tissues and the amperage.7 Electric burns often rapidly lead to systemic complications such as acidosis or myoglobinuria and renal failure, and compartment syndrome.8
- A radiation injury is caused by exposure to heat radiation (in contrast to ionizing radiation). These injuries are usually first degree; a typical example of this type of injury is a sunburn.
Not all lesions that are commonly treated in burn centers are burns in a true sense. Patients with frostbite; chemical injuries; and diseases such as toxic epidermal necrolysis, epidermolysis bullosa, and necrotizing fasciitis nowadays are often treated in burn units because their systemic complications and required surgical interventions can be similar to those of thermal injuries.9–11
Most chemical agents damage the skin by producing a chemical reaction rather than a hyperthermic injury,12 and thus, chemical lesions are not burns in the literal sense. This type of injury may require special treatment copious irrigation with water is often a proper way to initiate treatment.13 Specific treatment depends on the type of chemical causing the injury; hydrogen fluoride, for example, enters the human body via where it contacts it and can penetrate skin, nails, mucosa, alimentary and respiratory tracts, and ocular surfaces,14 requiring treatment that focuses on the subcutaneous tissues and the (systemic) effects of absorption. Treatment may include compounds such as calcium gluconate gel or intra-arterial injections.15
Skin injuries caused by radiotherapy often also are called radiation burns.16 Because of their pathophysiology, these lesions should be considered ulcers (chronic wounds)17 rather than burns. Radiation injuries lead to changes in cytokine and metalloproteinase modulation and expression that are, indeed, much more similar to those seen in ulcerations.16,18–22
Morbidity and mortality of burn injuries are directly related to the size of the burn, whether an inhalation injury and/or other concomitant or preexisting diseases exist, and the general condition and age of the patient.23 Superficial but large burns, particularly in older adults and young children, are sometimes associated with a high level of morbidity and mortality.
Most wound measurements express the size of a lesion in cm2 (or in2). The size of a burn, however, is expressed as a percentage of the total body surface area (TBSA). The rule of nines is used to calculate a rough estimate of the burn size:24 the body is divided in areas of nine or multiples of 9%. Each leg and side of the trunk count for 18%, and the head and arms each count for 9%. The remaining 1% is reserved for the genitalia and the perineum.
In pediatric patients, these percentages are different: for example, in a neonate, the head counts for 18%. To determine the exact size of a burn, burn centers use much more specific charts based on the age of the patient;24 corrections on these charts are necessary for (morbidly) obese patients.25 An easy guideline is that the patient’s palm represents 0.5% TBSA.26 Still, without specific tools, accurate measurement of burn size is notoriously difficult for providers untrained in burn care.27
Sophisticated means for measuring TBSA are now available, using techniques such as three-dimensional computer modeling.28–30 While generally speaking the accuracy of these methods is excellent, they are not yet fully established and/or widely used.
CONCOMITANT INJURIES OR MORBIDITIES
Major burns (ie, those exceeding 20%–25% TBSA in adults) are associated with a number of complications. A rapidly occurring change in capillary permeability causes massive fluid transfer from the circulation into the interstitium, which, when untreated, quickly leads to hypovolemic shock. To avoid this, patients with large burns initially receive large I.V. volumes of fluid to sustain sufficient circulation. The type and amount of fluid are calculated using specific formulas.31,32 When capillary permeability has been restored, this fluid needs to be removed using forced diuresis.
The skin of an average-size male weighs in at around 20 pounds. Thus, a 50% TBSA full-thickness burn is associated with approximately 10 pounds of necrotic tissue. The amount of necrotic tissue and the reaction to heat exposure are directly responsible for systemic problems in large burns; this effect is known as burn disease.33
Infection and sepsis remain major risks34,35 and cannot always be avoided.36–38 A typical complication is systemic inflammatory response syndrome.39 This serious condition is related to organ dysfunction and failure and systemic inflammation.35,40 It is a subset of the cytokine storm, which is characterized by dysregulation of various cytokines.41 It is also closely related to sepsis, in which patients satisfy criteria for systemic inflammatory response syndrome and have a suspected or proven infection.41
A specific serious complication that may accompany flame burns in particular is inhalation injury. Essentially, the inhalation of toxic and/or hot gases and fumes causes damage to the tracheal and pulmonary system.42 This condition is associated with a high level of morbidity and mortality and often requires artificial ventilation.43–45
DEPTH OF BURNS
The depth classification of a burn is related to the anatomy of the skin (Figure 1). The basal membrane separates the epidermis from the dermis. The dermis contains epidermal structures such as sebaceous and sweat glands. Complete destruction of the epidermis and dermis renders re-epithelialization possible only from the wound edges. Re-epithelialization from the deeper, epidermal structures is possible, in principle, when these structures are still intact. Therefore, partial-thickness burns have a higher potential to heal spontaneously and without surgical intervention and do so more quickly than full-thickness burns.
The location of a burn also may influence the depth of a burn because the thickness of the skin depends on the anatomical location on the body. Thicker skin can better resist a certain amount of thermal exposure: thus, a burn of the lower back, where the skin is thick, will be more superficial than the thin skin on the eyelids when exposed to the same amount of heat.
The depth of a burn is also related to the time of exposure and the temperature of the insulting mechanism. Therefore, as mentioned, contact burns are mostly superficial because the exposure time is very short. Scalding, on the other hand, rapidly leads to deep burns. Exposure to water with a temperature of 55° C for 25 seconds results in deep dermal or full-thickness burns, whereas a 2-second exposure to water at 65° C causes a similar injury.46 Further, because of the much higher thermal capacity of water, a scald usually is deeper than a grease burn, despite the (often much) higher temperature of the grease.
Depth per se is not directly related to the level of morbidity or mortality (in contrast to size of the burn injury), but it determines whether surgical intervention is necessary.
A burn wound is an active wound with a particular physiology;47 burns initially diagnosed as superficial partial-thickness burns have been known to deepen after a few days, known as conversion or secondary deepening.48–50 On a cellular level, inadequate tissue perfusion, free radical damage, and systemic alterations in the cytokine milieu of patients47–51 are part of the underlying etiology. These phenomena are the result of a number of events in and surrounding the wound such as impaired wound perfusion, infection, tissue desiccation, edema, a circumferential eschar, metabolic derangements, and older age.52 Whatever the exact mechanisms, choosing the appropriate dressing plays an important role in the prevention of conversion in partial-thickness burns, although some burns may still convert.53
Most sunburns are typical examples of a first-degree burn. The epidermis is not breached, but the lesion is painful and looks red because of the inflammatory response. Desquamation may occur after a couple of days. Small first-degree burns do not require any specific treatment; although many dressings have a formal indication for first-degree burns, the patient may benefit from the application of a soothing cream or ointment and some form of pain treatment instead.
Superficial Partial-Thickness Burns
In superficial second-degree burns, the epidermis is destroyed, and the lesion exposes superficial parts of the dermis. Blisters may or may not occur. The skin is hypersensitive to the touch, and the lesion is moist and pink in color underneath the blisters (Figure 2A). Capillary refill is almost immediate. Given appropriate treatment, this type of burn will heal with minimal scarring within 10 to 14 days.
Deep Partial-Thickness Burns
In deep second-degree burns, the deep dermis is exposed because both the epidermis and the superficial dermis are destroyed. Visually, the lesion may mimic a superficial partial-thickness injury or a full-thickness injury. Capillary refill is slow or may not occur at all (Figure 3A). The amount of pain varies.
The exact depth of this type of burn may be very difficult to determine visually. Laser Doppler flowmetry (LDF) may assist in establishing a more accurate diagnosis. Because most deep-seated epidermal structures are destroyed, healing from deep structures is limited: healing may take significantly longer, and (late) surgical intervention may be warranted.
In these burns, the wound surface is usually dry to the touch and leather-like. The color of the burn depends on the acting agent (Figure 4): a full-thickness scald is usually white, whereas a flame burn is often black because of the soot. The lesions are generally not painful, because the whole dermis and epidermis, including the nerve endings, have been destroyed. In most cases, excision and grafting are warranted.
In these burns, the entire skin is destroyed, and substantial thermal damage is evident in subcutaneous and deeper tissues. Extensive carbonization may be present in flame burns. This type of burn is also seen in patients exposed to a combination of prolonged pressure and a hot surface. Major reconstruction efforts with or without amputation are often necessary.
For a provider to make an accurate depth diagnosis, patient history is important, as is the mechanism of injury and the physical aspects of the burn. If, for example, the patient history indicates immediate cooling after a flash burn, chances are that the burn is not very deep, whereas exposure to flames will virtually always result in a full-thickness burn. If the patient history is not congruent with the injury, providers should suspect abuse, particularly when the patient is a young child; they should notify authorities and ensure the safety of the patient.
Even experienced burn physicians and nurses can misjudge the initial depth of a burn.54 The level of skin blanching can help establish proper depth diagnosis because slow or absent refill indicates a deep lesion. Another method to assist in this determination is the pinprick test, in which the injured area is very gently probed with a sharp needle tip, and the patient self-assesses the intensity of his/her pain. Serious pain indicates a superficial burn. Minimal or no pain indicates a deep dermal or full-thickness burn.
Ultrasound also can be used to assess depth, but results may not be significantly different from clinical judgment,55 although newer devices with higher levels of discrimination are currently being tested. Dyes such as fluorescein have been evaluated and can help make a distinction between nonnecrotic and necrotic tissue56 but are not commonly used.
In experimental and clinical research, LDF was proven to provide a reliable depth diagnosis.57,58 In general, LDF devices have become smaller, faster, and easier to use, making the technique more practical59 and allowing for quick, accurate, and rapid diagnosis over large surfaces.58–61 Even more sophisticated techniques, such as the use of laser speckle contrast, are currently being investigated for the analysis of burn depth.62
FIRST AID AND GUIDELINES FOR REFERRAL
The simple measures that comprise initial care are essentially identical whether or not a patient is referred to a burn center.3
- For thermal and chemical injuries, immediate cooling is important because tissue temperatures greater than 45° C will exacerbate local injury.63 Dissipating heat is the first step. Running tap water for a minimum of 10 minutes over the injury site helps reduce the initial pain,64–66 decreases wound edema,67 and decreases the risk of secondary deepening.50,67 Water also helps to dilute any chemical agent; however, depending on the agent, additional measures may be necessary. Too much cooling carries the risk of hypothermia; patients, particularly children, should not be immersed in ice water.
- Rings may act as a tourniquet and have to be removed.
- Wounds may be gently cleaned using a soap with neutral pH. Some providers prefer chlorhexidine gluconate soap because of its antimicrobial effect against regular skin flora.68
- Tar and asphalt burns should be cooled first. If the causative agents stick to the skin, peeling them away may do additional mechanical harm to the skin; the use of a solvent is preferred.69
- Most chemical lesions may benefit from rinsing with water to dilute the agent. As previously stated, for many chemical agents, first aid is specific,13,70–75 so providers must identify the chemical that caused the injury.
- Prior to transportation, clothing may be carefully removed; it may be stuck to the wound. Providers should use a nonadherent dressing to cover the burned areas. Silver sulfadiazine (SSD) or other creams should not be used if the patient is referred, because the cream will need to be removed upon arrival in the burn center to assess the wound aspect and size, and this can be painful. The creams, particularly SSD, may also change the visual aspect of the burn by creating a so-called “pseudo-eschar.”76 Further, many over-the-counter “burn creams” are contaminated within a relatively short time after opening their container.
- In larger burns, I.V. fluids are indicated prior to patient transport to a burn center if transportation is expected to take more than 60 minutes: this is necessary to provide circulatory volume support. Several resuscitation guidelines and regimens are used. Among them, the administration of lactated Ringer’s solution, infused at 2 to 4 mL/kg per percent TBSA per 24 hours,77 is one of the standards, but consult with the burn center in case a different regimen is preferred. If possible, I.V. access should not penetrate through burned skin and should be achieved using larger veins (central lines are preferable in patients with extensive burns).
- Opioids may be used as pain medication but may only be given intravenously; avoid other methods of administration because the pattern of uptake is unpredictable.
- If providers suspect an inhalation injury, 100% humidified oxygen should be administered during transportation. However, providers should first consult with the burn center to which the patient will be transported about possible intubation prior to putting the patient in the ambulance or helicopter. Inhalation injury should be suspected in patients with a cough, facial burns, or soot in the mouth or nostrils and/or when the patient is hoarse or wheezing.
- Headache, nausea, confusion, and vomiting are symptoms of carbon monoxide poisoning.78 Admission for observation with humidified 100% oxygen, attentive pulmonary toilet, bronchodilators as needed, and prophylactic endotracheal intubation as indicated are the mainstays of treatment. Consult with the burn center to which the patient is referred.79
- Escharotomies may be needed in patients with circumferential deep burns that may restrict respiratory excursion of the chest, circulation into the limbs, and/or postburn intra-abdominal hypertension.80–82 Consult guidelines from a burn center before performing an escharotomy.
The American Burn Association has several helpful criteria for referral, including any burns that involve sensitive areas such as the face or major joints.83 These can be viewed at http://ameriburn.org/wp-content/uploads/2017/05/burncenterreferralcriteria.pdf.
Some providers prefer patients with acute respiratory distress syndrome to be transported in a prone position, whereas others prefer a sitting position during transportation;84 still others prefer transportation in a semisitting position, particularly when patients are intubated.85 Before transporting a patient to a burn center, the center should be contacted to discuss general and specific treatment, transport methods, and necessary interventions.
Mortality in burn care has dropped significantly during recent decades. Nowadays, survival of patients with full-thickness burns of more than 95% TBSA is not uncommon.86,87 This may be attributed to better understanding of the physiology of burn disease and systemic responses, better prevention and management of complications, and more aggressive surgical approaches.
Smaller, partial-thickness burns that are fresh can easily be treated outside of a burn clinic with proper dressings. The dressing chosen should have a number of properties, including (but not limited to) keeping the wound moist, providing protection from infection, and reducing pain.88,89 Ideally, dressing changes should be limited because these interventions may be painful and may damage the healing wound.
In the past, global surveys have shown that SSD was the most commonly and frequently used antimicrobial agent for the management of burns, including small partial-thickness burns;90,91 this is probably still the case. There are a number of reasons, however, why this may not be justified for fresh, small, partial-thickness burns, including
- pseudoeschar, which makes judging burn depth difficult,76
- the need for frequent changes,92
- the potential for developing leukopenia,93 and
- frequently observed delayed wound healing.94
Gauze dressings are also commonly used and associated with delayed healing, increased infection rates for burns and donor sites, and an increase in pain when compared with modern biologic and occlusive dressings.90,94–102 Many proven dressings are available. If burns are fresh and small, the use of medicated creams is usually not necessary. Most importantly, if a burn is not healed within 10 to 14 postburn days, the initial depth diagnosis may have been incorrect, or conversion may have occurred (Figures 3A-C). The patient should be referred to a burn specialist because prolonged healing may lead to the formation of serious scars. This article does not recommend specific dressings; however, clinicians are encouraged to find information on properly tested materials with good outcomes from the published medical literature.
Full-thickness burns virtually always require excision and grafting, which should be performed by a specialist. Early excision is preferred103–105 because it reduces a number of complications associated with necrosis. Several techniques can be used to close the resulting open wound, including straightforward autografting, with or without meshing and with or with an overlay of allograft in widely meshed autografts.106–109 Other closure techniques can be used but are beyond the scope of this article. If excision and grafting are not possible because of serious comorbidities or additional extensive, nonthermal trauma, this in itself may be a reason for referral.
The remodeling phase of wound healing involves reorganization of the extracellular matrix and is initiated after re-epithelialization is complete. The process may go awry, however, as the result of many biochemical processes that are involved in “improper” wound healing, among them a deregulation of a number of inflammatory mediators.110,111 These mediators play a major role in the development of scarring complications110 via a state of continuous and histologically localized inflammation,112 which macroscopically results in hypertrophic scarring and the formation of contractures and/or keloids.
Hypertrophic scars are red, inflamed, raised scars. They can be seriously debilitating and negatively impact patient quality of life because they may limit movement, can be painful, and are virtually always pruritic.113 If scarring is visible or extensive, the psychological burden of being considered “ugly” and “scary” by society is important to note.114
Hypertrophic scarring is virtually certain to occur in burns that have taken a long time to heal spontaneously.115 Scarring is also genetically determined: dark-skinned patients have a significantly higher risk of serious scarring.2,116 Scarring also depends on other factors, such as the location of the wound. A sternotomy incision, for example, frequently results in a hypertrophic scar.117
During initial healing, not much can be done to prevent hypertrophic scarring. However, using dressings and techniques that are proven to reduce time to healing may indirectly reduce the incidence of these scars.115 In patients who have a history of scarring, providers should take measures that lower the chance of hypertrophic scars, such as the use of (customized) pressure garments118–121 with or without silicon sheeting as a contact layer on the wound.122–124
If a scar has developed, consider corticosteroid injections.125,126 Other therapies are being developed, among them different types of lasers127,128 and promising pharmacologic agents.129 In a recent report, the use of 2,940-nm wavelength Er:YAG as a treatment for hypertrophic scarring was shown to lead to a high patient satisfaction with the outcome.130
However, treatment of hypertrophic scars is often not satisfactory, and visible scars may remain, although they will become flatter and less inflamed over time. Surgical scar revision may be necessary, particularly when scar formation leads to contractures.131–133
Keloid formation is different from hypertrophic scarring, physiologically as well as macroscopically: a typical keloid extends beyond the borders of the original wound and has a cauliflower-type appearance.134–136 Prevention and treatment of keloids are even more difficult than those of hypertrophic scarring137–141 and are beyond the scope of this article.
Contractures typically occur over joints, in the neck, and on the female breast and may lead to severe morbidity, requiring surgical reconstruction.142–144 Preventive measures include splinting and physiotherapy, but success is not guaranteed; often, secondary reconstructive surgery may be needed.
A Marjolin ulcer may develop in a burn scar, particularly when part of the original lesion is not healing. These ulcers, commonly basal cell carcinomas, should be treated as a regular skin malignancy but are not always recognized as such.145–148
Other, non–skin-related postburn complications are not uncommon, such as heterotopic ossifications in periarticular tissue,149 but are beyond the scope of this article.
SKIN DONOR SITES
Skin donor sites can be full- or partial-thickness and located virtually anywhere in the body.150–152 Full-thickness donor sites are not common in primary burn management: the donor site itself must be covered with epithelium unless it is very small and can be primarily closed. Partial-thickness donor sites still contain deep-seated epithelial remnants, from which skin can regrow. A re-epithelialized donor site may be reharvested a number of times, although the quality of the skin diminishes over time.
In extensive burns, the scalp is often used because the site re-epithelializes rapidly and thus can be reharvested quickly and often,150 although the use of this site in children with dark skin was recently shown to lead to a relatively high number of complications.153 The skin quality of a donor site should resemble the skin of the recipient site as much as possible.
Donor sites themselves can cause considerable morbidity, primarily because they are very painful.154–158 They may also present healing difficulties,152 particularly in older adult patients with frail skin and in patients with large burns. In large burns, when no other locations are available, donor sites may also be surrounded by burned areas and thus become more prone to infection and present difficulty in dressing the wound.
Donor sites bleed profusely. Different hemostatic materials (eg, epinephrine and thrombin dressings) are often used in combination with, or prior to application of, a cover dressing. While superficial donor sites usually heal without serious scarring, some patients do develop hypertrophic scars.
Many different types of dressings are used to treat donor sites.90 The same criteria apply for these dressings as those for partial-thickness burns.88,89 Choose materials that help provide hemostasis and provide pain reduction and rapid healing to reduce short- and long-term morbidity.
The treatment of serious burns, donor sites, and related injuries and diseases should happen in a burn center. In these centers, interprofessional teams are dedicated to burn care, and their knowledge of the latest and most effective treatment options often leads to relatively satisfying results. Further, the physical structure of a burn center is specialized and may include advantages such as advanced temperature control to heat up patient rooms during dressing changes and a hierarchic treatment of air pressure using patient room entry locks.159,160
However, the large majority of patients with burns suffer from lesions that do not necessitate this high level of care. These lesions can be successfully treated outside in a general hospital or an outpatient clinic, provided that wound management is conducted in line with evidence-based burn care guidelines and with proper materials and techniques. Guidelines for referral83 should be followed, and if a burn has not healed within 10 to 14 days, the patient should be referred to a specialist.
- Immediate cooling with running tap water for about 10 minutes is the best first aid.
- Superficial burns may become deeper secondarily; therefore, burns that take longer than 2 weeks to heal should be referred to a specialist, because they may very well have to be excised and grafted.
- Full-thickness burns, unless they are very small, should be excised and grafted unless there are specific contraindications.
- Particularly with flame burns, always be aware of the possibility of an inhalation injury and/or carbon monoxide poisoning.
- Short-term acceptable cosmetic outcome (ie, immediately after reepithelialization) does not guarantee patient satisfaction with long-term scars.
1. American Burn Association. Burn Incidence Fact Sheet. 2016. http://ameriburn.org/who-we-are/media/burn-incidence-fact-sheet
. Last accessed October 16, 2018.
2. Rockwell WB, Cohen IK, Ehrlich HP. Keloids and hypertrophic scars: a comprehensive review. Plast Reconstr Surg 1989;84(5):827-37.
3. Treadwell T, Hermans MHE. An introduction to wounds. In: Microbiology of Wounds. 1st ed. Percival S, Cutting K, eds. Boca Raton, FL: CRC Press; 2010.
4. DeToledo JC, Lowe MR. Microwave oven injuries in patients with complex partial seizures. Epilepsy Behav 2004;5(5):772-4.
5. Josty IC, Mason WT, Dickson WA. Burn wound management in patients with epilepsy: adopting a multidisciplinary approach. J Wound Care
6. Harrington WZ, Strohschein BL, Reedy D, et al. Pavement temperature and burns
: streets of fire. Ann Emerg Med 1995;26(5):563-8.
7. Sances A Jr, Myklebust JB, Larson SJ, et al. Experimental electrical injury studies. J Trauma 1981;21(8):589-97.
8. Cancio LC, Jimenez-Reyna JF, Barillo DJ, et al. One hundred ninety-five cases of high-voltage electric injury. J Burn Care
9. Arnoldo BD, Purdue GF, Tchorz K, et al. A case report of phaeohyphomycosis caused by Cladophialophora bantiana treated in a burn unit. J Burn Care
10. Barillo DJ, McManus AT, Cancio LC, et al. Burn center
management of necrotizing fasciitis. J Burn Care
11. Redman DP, Friedman B, Law E, et al. Experience with necrotizing fasciitis at a burn care
center. South Med J 2003;96(9):868-70.
12. Edlich RF, Farinholt HM, Winters KL, et al. Modern concepts of treatment and prevention of chemical injuries. J Long Term Eff Med Implants 2005;15(3):303-18.
13. Leonard LG, Scheulen JJ, Munster AM. Chemical burns
: effect of prompt first aid. J Trauma 1982;22(5):420-3.
14. Wang X, Zhang Y, Ni L, et al. A review of treatment strategies for hydrofluoric acid burns
: current status and future prospects. Burns
15. Dunn BJ, MacKinnon MA, Knowlden NF, et al. Hydrofluoric acid dermal burns
. An assessment of treatment efficacy using an experimental pig model. J Occup Med 1992;34(9):902-9.
16. Berger ME, Hurtado R, Dunlap J, et al. Accidental radiation injury to the hand: anatomical and physiological considerations. Health Phys 1997;72(3):343-8.
17. Lorette G, Machet L. Radiation-induced skin toxicities: prevention, treatment [in French]. Cancer Radiother 2001;5 Suppl 1:116s-20s.
18. Muller K, Meineke V. Radiation-induced alterations in cytokine production by skin cells. Exp Hematol 2007;35(4 Suppl 1):96-104.
19. Saarialho-Kere U, Kerkela E, Jeskanen L, et al. Accumulation of matrilysin (MMP-7) and macrophage metalloelastase (MMP-12) in actinic damage. J Invest Dermatol 1999;113(4):664-72.
20. Beetz A, Messer G, Oppel T, et al. Induction of interleukin 6 by ionizing radiation in a human epithelial cell line: control by corticosteroids. Int J Radiat Biol 1997;72(1):33-43.
21. Lefaix JL, Daburon F. Diagnosis of acute localized irradiation lesions
: review of the French experimental experience. Health Phys 1998;75(4):375-84.
22. Vozenin-Brotons MC, Gault N, Sivan V, et al. Histopathological and cellular studies of a case of cutaneous radiation syndrome after accidental chronic exposure to a cesium source. Radiat Res 1999;152(3):332-7.
23. Herndon DN. Total Burn Care
. 2nd ed. New York, NY: Saunders; 2002.
24. Lund CC, Browder NC. The estimate of area of burns
. Surg Gynecol Obstet 1944;79:352-8.
25. Borhani-Khomani K, Partoft S, Holmgaard R. Assessment of burn size in obese adults; a literature review. J Plast Surg Hand Surg 2017;51(6):375-80.
26. Sheridan RL, Petras L, Basha G, et al. Planimetry study of the percent of body surface represented by the hand and palm: sizing irregular burns
is more accurately done with the palm. J Burn Care
27. McCulloh C, Nordin A, Talbot LJ, et al. Accuracy of prehospital care providers in determining total body surface area
burned in severe pediatric thermal injury. J Burn Care
28. Benjamin NC, Wurzer P, Voigt CD, et al. Using a 3D tool to document and determine graft loss: a mini-review and case report. Burns
29. Cheah AKW, Kangkorn T, Tan EH, et al. The validation study on a three-dimensional burn estimation smart-phone application: accurate, free and fast? Burns
30. Rashaan ZM, Euser AM, van Zuijlen PPM, et al. Three-dimensional imaging is a novel and reliable technique to measure total body surface area
31. Daigeler A, Kapalschinski N, Lehnhardt M. Therapy of burns
[in German]. Chirurg 2015;86(4):389-401.
32. Aoki K, Yoshino A, Yoh K, et al. A comparison of Ringer’s lactate and acetate solutions and resuscitative effects on splanchnic dysoxia in patients with extensive burns
33. Mitra B, Fitzgerald M, Wasiak J, et al. The Alfred pre-hospital fluid formula for major burns
34. Deitch EA, Bridges RM, Dobke M, et al. Burn wound sepsis may be promoted by a failure of local antibacterial host defenses. Ann Surg 1987;206(3):340-8.
35. Allgower M, Stadtler K, Schoenenberger GA. Burn sepsis and burn toxin. Ann R Coll Surg Engl 1974;55(5):226-35.
36. Devrim I, Kara A, Duzgol M, et al. Burn-associated bloodstream infections in pediatric burn patients: time distribution of etiologic agents. Burns
37. Issler-Fisher AC, Fakin RM, Fisher OM, et al. Microbiological findings in burn patients treated in a general versus a designated intensive care unit: effect on length of stay. Burns
38. Trouve C, Blot S, Hayette MP, et al. Epidemiology and reporting of candidaemia in Belgium: a multi-centre study. Eur J Clin Microbiol Infect Dis 2017;36(4):649-55.
39. Jeschke MG, Mlcak RP, Finnerty CC, et al. Burn size determines the inflammatory and hypermetabolic response. Crit Care 2007;11(4):R90.
40. Rosenthal SR. Burn toxin and its competition. Burns
Incl Therm Inj 1982;8(3):215-9.
41. Chong DL, Sriskandan S. Pro-inflammatory mechanisms in sepsis. Contrib Microbiol 2011;17:86-107.
42. Enkhbaatar P, Traber DL. Pathophysiology of acute lung injury in combined burn and smoke inhalation injury. Clin Sci (Lond) 2004;107(2):137-43.
43. Smith DL, Cairns BA, Ramadan F, et al. Effect of inhalation injury, burn size, and age on mortality: a study of 1447 consecutive burn patients. J Trauma 1994;37(4):655-9.
44. Barrow RE, Spies M, Barrow LN, et al. Influence of demographics and inhalation injury on burn mortality in children. Burns
45. Jones SW, Williams FN, Cairns BA, et al. Inhalation injury: pathophysiology, diagnosis, and treatment. Clin Plast Surg 2017;44(3):505-11.
46. Artz C, Moncrief J, Pruitt BA Jr, eds. The Body’s Response to Heat. New York, NY: Saunders; 1979.
47. Singh V, Devgan L, Bhat S, et al. The pathogenesis of burn wound conversion. Ann Plast Surg 2007;59(1):109-15.
48. Saranto JR, Rubayi S, Zawacki BE. Blisters, cooling, antithromboxanes, and healing in experimental zone-of-stasis burns
. J Trauma 1983;23(10):927-33.
49. Zawacki BE. The natural history of reversible burn injury. Surg Gynecol Obstet 1974;139(6):867-72.
50. Zawacki BE. Reversal of capillary stasis and prevention of necrosis in burns
. Ann Surg 1974;180(1):98-102.
51. Kaufman T, Neuman RA, Weinberg A. Is postburn dermal ischaemia enhanced by oxygen free radicals? Burns
52. Schmauss D, Rezaeian F, Finck T, et al. Treatment of secondary burn wound progression in contact burns
—a systematic review of experimental approaches. J Burn Care
53. Hermans MHE. Treatment of burns
with occlusive dressings: some pathophysiological and quality of life aspects. Burns
54. Goverman J, Bittner EA, Friedstat JS, et al. Discrepancy in initial pediatric burn estimates and its impact on fluid resuscitation. J Burn Care
55. Wachtel TL, Leopold GR, Frank HA, et al. B-mode ultrasonic echo determination of depth of thermal injury. Burns
Incl Therm Inj 1986;12(6):432-7.
56. Black KS, Hewitt CW, Miller DM, et al. Burn depth evaluation with fluorometry: is it really definitive? J Burn Care
57. Park DH, Hwang JW, Jang KS, et al. Use of laser Doppler flowmetry for estimation of the depth of burns
. Plast Reconstr Surg 1998;101(6):1516-23.
58. Holland AJ, Martin HC, Cass DT. Laser Doppler imaging prediction of burn wound outcome in children. Burns
59. Hemington-Gorse SJ. A comparison of laser Doppler imaging with other measurement techniques to assess burn depth. J Wound Care
60. Mileski WJ, Atiles L, Purdue G, et al. Serial measurements increase the accuracy of laser Doppler assessment of burn wounds. J Burn Care
61. Riordan CL, McDonough M, Davidson JM, et al. Noncontact laser Doppler imaging in burn depth analysis of the extremities. J Burn Care
62. Mirdell R, Farnebo S, Sjoberg F, et al. Accuracy of laser speckle contrast imaging in the assessment of pediatric scald wounds. Burns
63. Moritz AR, Henriques FC. Studies of thermal injury: II. The relative importance of time and surface area in the causation of cutaneous burns
. Am J Pathol 1947;23:695-720.
64. King TC, Zimmerman JM. First-aid cooling of the fresh burn. Surg Gynecol Obstet 1965;120:1271-3.
65. King TC, Zimmerman JM. Optimum temperatures for postburn cooling. Arch Surg 1965;91(4):656-7.
66. King TC, Zimmerman JM, Price PB. Effect of immediate short-term cooling on extensive burns
. Surg Forum 1962;13:487-8.
67. Demling RH, Mazess RB, Wolberg W. The effect of immediate and delayed cold immersion on burn edema formation and resorption. J Trauma 1979;19(1):56-60.
68. Demling RH. Burns
. N Engl J Med 1985;313(22):1389-98.
69. Stratta RJ, Saffle JR, Kravitz M, et al. Management of tar and asphalt injuries. Am J Surg 1983;146(6):766-9.
70. Hermans MHE, Vloemans AFPM. A patient with a subungual burn caused by hydrofluoric acid [in Dutch]. Ned Tijdschr Geneeskd 1985;129(52):2510-1.
71. Eldad A, Chaouat M, Weinberg A, et al. Phosphorous pentachloride chemical burn—a slowly healing injury. Burns
72. Eldad A, Simon GA. The phosphorous burn—a preliminary comparative experimental study of various forms of treatment. Burns
73. Iverson RE, Laub DR. Hydrofluoric acid burn therapy. Surg Forum 1970;21:517-9.
74. Murao M. Studies on the treatment of hydrofluoric acid burn. Bull Osaka Med Coll 1989;35(1-2):39-48.
75. Mangion SM, Beulke SH, Braitberg G. Hydrofluoric acid burn from a household rust remover. Med J Aust 2001;175(5):270-1.
76. Monafo WW, Ayvazian VH. Topical therapy. Surg Clin North Am 1978;58(6):1157-71.
77. American Burn Association. Advanced Life Support Providers Manual. Chicago, IL: American Burn Association; 1994.
78. Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med 1988;17(12):1316-20.
79. Otterness K, Ahn C. Emergency department management of smoke inhalation injury in adults. Emerg Med Pract 2018;20(3):1-24.
80. Pegg SP. Escharotomy in burns
. Ann Acad Med Singapore 1992;21(5):682-4.
81. Tsoutsos D, Rodopoulou S, Keramidas E, et al. Early escharotomy as a measure to reduce intraabdominal hypertension in full-thickness burns
of the thoracic and abdominal area. World J Surg 2003;27(12):1323-8.
82. Wong L, Spence RJ. Escharotomy and fasciotomy of the burned upper extremity. Hand Clin 2000;16(2):165-74, vii.
83. American Burn Association. Burn Center Referral
Criteria. 2017. http://ameriburn.org/wp-content/uploads/2017/05/burncenterreferralcriteria.pdf
. Last accessed October 16, 2018.
84. Oto B, Orosco RI, Panter E, et al. Prone positioning of the burn patient with acute respiratory distress syndrome: a review of the evidence and practical considerations. J Burn Care
85. Nederlandse Brandwonden Stichting. Wat zijn brandwonden? 2018. https://brandwondenstichting.nl/brandwonden
. Last accessed October 16, 2018.
86. Herndon DN, Gore D, Cole M, et al. Determinants of mortality in pediatric patients with greater than 70% full-thickness total body surface area
thermal injury treated by early total excision and grafting. J Trauma 1987;27(2):208-12.
87. Herndon DN, LeMaster J, Beard S, et al. The quality of life after major thermal injury in children: an analysis of 12 survivors with greater than or equal to 80% total body, 70% third-degree burns
. J Trauma 1986;26(7):609-19.
88. Broussard KC, Powers JG. Wound dressings: selecting the most appropriate type. Am J Clin Dermatol 2013;14(6):449-59.
89. Selig HF, Lumenta DB, Giretzlehner M, et al. The properties of an “ideal” burn wound dressing—what do we need in daily clinical practice? Results of a worldwide online survey among burn care
90. Hermans MH. Results of an internet survey on the treatment of partial thickness burns
, full thickness burns
, and donor sites. J Burn Care
91. Hermans MHE. Results of a survey on the use of different treatment options for partial and full thickness burns
92. Fox CL Jr.. Silver sulfadiazine for control of burn wound infections. Int Surg 1975;60(5):275-7.
93. Fraser GL, Beaulieu JT. Leukopenia secondary to sulfadiazine silver. JAMA 1979;241(18):1928-9.
94. Wasiak J, Cleland H, Campbell F, et al. Dressings for superficial and partial thickness burns
. Cochrane Database Syst Rev 2013(3):CD002106.
95. Ang E, Lee ST, Gan CS, et al. Pain control in a randomized, controlled, clinical trial comparing moist exposed burn ointment and conventional methods in patients with partial-thickness burns
. J Burn Care
96. Ang ES, Lee ST, Gan CS, et al. The role of alternative therapy in the management of partial thickness burns
of the face—experience with the use of moist exposed burn ointment (MEBO) compared with silver sulphadiazine. Ann Acad Med Singapore 2000;29(1):7-10.
97. Chatterjee DS. A controlled comparative study of the use of porcine xenograft in the treatment of partial thickness skin loss in an occupational health centre. Curr Med Res Opin 1978;5(9):726-33.
98. Hermans MHE, Hutchinson JJ. Advantages of Occlusive Dressings. London: Springer Verlag; 1990.
99. Platt AJ, Phipps A, Judkins K. A comparative study of silicone net dressing and paraffin gauze dressing in skin-grafted sites. Burns
100. Vloemans AF, Hermans MH, van der Wal MB, et al. Optimal treatment of partial thickness burns
in children: a systematic review. Burns
101. Wasiak J, Cleland H. Burns
: dressings. BMJ Clin Evid 2015;2015.
102. Wyatt D, McGowan DN, Najarian MP. Comparison of a hydrocolloid dressing and silver sulfadiazine cream in the outpatient management of second-degree burns
. J Trauma 1990;30(7):857-65.
103. Alsbjorn BF. Towards early excision and extended grafting of excessive burns
. Dan Med Bull 1991;38(4):328-37.
104. Hermans RP. De techniek van de behandeling van brandwonden. Leiden: Staphleu’s wetenschappelijke uitgeversmaatschappy; 1968.
105. MacMillan B. Early excision. J Trauma 1967;7:75-81.
106. Chua AWC, Khoo YC, Truong TTH, et al. From skin allograft coverage to allograft-micrograft sandwich method: a retrospective review of severe burn patients who received conjunctive application of cultured epithelial autografts. Burns
107. Kreis RW, Mackie DP, Hermans RR, et al. Expansion techniques for skin grafts: comparison between mesh and Meek island (sandwich-) grafts. Burns
1994;20 Suppl 1:S39-42.
108. Kreis RW, Mackie DP, Vloemans AW, et al. Widely expanded postage stamp skin grafts using a modified Meek technique in combination with an allograft overlay. Burns
109. Kreis RW, Vloemans AF, Hoekstra MJ, et al. The use of non-viable glycerol-preserved cadaver skin combined with widely expanded autografts in the treatment of extensive third-degree burns
. J Trauma 1989;29(1):51-4.
110. Castagnoli C, Stella M, Berthod C, et al. TNF production and hypertrophic scarring. Cell Immunol 1993;147(1):51-63.
111. Niessen FB, Andriessen MP, Schalkwijk J, et al. Keratinocyte-derived growth factors play a role in the formation of hypertrophic scars. J Pathol 2001;194(2):207-16.
112. Ogawa R. Keloid and hypertrophic scars are the result of chronic inflammation in the reticular dermis. Int J Mol Sci 2017;18(3).
113. Zurada JM, Kriegel D, Davis IC. Topical treatments for hypertrophic scars. J Am Acad Dermatol 2006;55(6):1024-31.
114. Bock O, Schmid-Ott G, Malewski P, et al. Quality of life of patients with keloid and hypertrophic scarring. Arch Dermatol Res 2006;297(10):433-8.
115. Deitch EA, Wheelahan TM, Rose MP, et al. Hypertrophic burn scars: analysis of variables. J Trauma 1983;23(10):895-8.
116. Worley CA. The wound healing process: part III—the finale. Dermatol Nurs 2004;16(3):274, 95.
117. Lista FR, Thomson HG. The fate of sternotomy scars in children. Plast Reconstr Surg 1988;81(1):35-9.
118. Roques C. Pressure therapy to treat burn scars. Wound Repair Regen 2002;10(2):122-5.
119. Rochet JM, Zaoui A. Burn scars: rehabilitation and skin care [in French]. Rev Prat 2002;52(20):2258-63.
120. Puzey G. The use of pressure garments on hypertrophic scars. J Tissue Viability 2002;12(1):11-5.
121. Jordan RB, Daher J, Wasil K. Splints and scar management for acute and reconstructive burn care
. Clin Plast Surg 2000;27(1):71-85.
122. Ayhan M, Gorgu M, Silistreli KO, et al. Silastic sheet integrated polymethylmetacrylate splint in addition to surgery for commissure contractures complicated with hypertrophic scar. Acta Chir Plast 2004;46(4):132-5.
123. Van den Kerchhove E, Boeckx W, Kochuyt A. Silicone patches as a supplement for pressure therapy to control hypertrophic scarring. J Burn Care
124. Kavanagh GM, Page P, Hanna MM. Silicone gel treatment of extensive hypertrophic scarring following toxic epidermal necrolysis. Br J Dermatol 1994;130(4):540-1.
125. Haedersdal M, Poulsen T, Wulf HC. Laser induced wounds and scarring modified by antiinflammatory drugs: a murine model. Lasers Surg Med 1993;13(1):55-61.
126. Beldon P. Management of scarring. J Wound Care
127. Lupton JR, Alster TS. Laser scar revision. Dermatol Clin 2002;20(1):55-65.
128. Liew SH, Murison M, Dickson WA. Prophylactic treatment of deep dermal burn scar to prevent hypertrophic scarring using the pulsed dye laser: a preliminary study. Ann Plast Surg 2002;49(5):472-5.
129. Xiang J, Wang XQ, Qing C, et al. The influence of dermal template on the expressions of signal transduction protein Smad 3 and transforming growth factor beta1 and its receptor during wound healing process in patients with deep burns
[in Chinese]. Zhonghua Shao Shang Za Zhi 2005;21(1):52-4.
130. Madni TD, Nakonezny PA, Imran JB, et al. Patient satisfaction after fractional ablation of burn scar with 2940nm wavelength erbium-YAG laser. Burns
131. Suliman MT. Experience with the seven flap-plasty for the release of burns
132. Deb R, Giessler GA, Przybilski M, et al. Secondary plastic surgical reconstruction in severely burned patients [in German]. Chirurg 2004;75(6):588-98.
133. Lu KH, Guo SZ, Ai YF, et al. Management of severe postburn scar contracture in the lower extremities [in Chinese]. Zhonghua Shao Shang Za Zhi 2004;20(2):69-71.
134. Selezneva LG. Keloid scars after burns
. Acta Chir Plast 1976;18(2):106-11.
135. Iudenich VV, Pal’tsyn AA, Zalugovskii OG. Electron microscopic and autoradiographic study of keloid scars [in Russian]. Arkh Patol 1982;44(1):44-9.
136. Bang RL, Dashti H. Keloid and hypertrophic scars: trace element alteration. Nutrition 1995;11(5 Suppl):527-31.
137. Morison WL. Oral treatment of keloid. Med J Aust 1968;1(10):412-3.
138. Donati L, Taidelli Palmizi GA. Treatment of hypertrophic and keloid cicatrices with thiomucase [in Italian]. Minerva Chir 1975;30(6):326-33.
139. Tammelleo AD. Suit for post-operative scar: keloid or burn? Regan Rep Nurs Law 1996;37(4):4.
140. Ahlering PA. Topical silastic gel sheeting for treating and controlling hypertrophic and keloid scars: case study. Dermatol Nurs 1995;7(5):295-7, 322.
141. Sizov VM. The diagnosis and treatment of hypertrophic and keloid scars [in Russian]. Klin Khir 1994(9):41-3.
142. El-Otiefy MA, Darwish AM. Post-burn breast deformity: various corrective techniques. Ann Burns
Fire Disasters 2011;24(1):42-5.
143. Mody NB, Bankar SS, Patil A. Post burn contracture neck: clinical profile and management. J Clin Diagn Res 2014;8(10):NC12-7.
144. Sabapathy SR, Bajantri B, Bharathi RR. Management of post burn hand deformities. Indian J Plast Surg 2010;43(Suppl):S72-9.
145. Iqbal FM, Sinha Y, Jaffe W. Marjolin’s ulcer: a rare entity with a call for early diagnosis. BMJ Case Rep 2015;2015.
146. Karasoy Yesilada A, Zeynep Sevim K, Ozgur Sucu D, et al. Marjolin ulcer: clinical experience with 34 patients over 15 years. J Cutan Med Surg 2013;17(6):404-9.
147. Oruc M, Kankaya Y, Sungur N, et al. Clinicopathological evaluation of Marjolin ulcers over two decades. Kaohsiung J Med Sci 2017;33(7):327-33.
148. Phillips TJ, Salman SM, Bhawan J, et al. Burn scar carcinoma. Diagnosis and management. Dermatol Surg 1998;24(5):561-5.
149. Siemers F, Lohmeyer JA, Machens HG, et al. Heterotopic ossifications: a severe complication following extensive burn injury [in German]. Handchir Mikrochir Plast Chir 2007;39(5):360-3.
150. Barret JP, Dziewulski P, Wolf SE, et al. Outcome of scalp donor sites in 450 consecutive pediatric burn patients. Plast Reconstr Surg 1999;103(4):1139-42.
151. Desai MH, Herndon DN, Rutan RL, et al. An unusual donor site, a lifesaver in extensive burns
. J Burn Care
152. Smith DJ Jr, Thomson PD, Garner WL, et al. Donor site repair. Am J Surg 1994;167(1A):49S-51S.
153. van Niekerk G, Adams S, Rode H. Scalp as a donor site in children: is it really the best option? Burns
154. Madden MR, Nolan E, Finkelstein JL, et al. Comparison of an occlusive and a semi-occlusive dressing and the effect of the wound exudate upon keratinocyte proliferation. J Trauma 1989;29(7):924-30; discussion 30-1.
155. Zapata-Sirvent R, Hansbrough JF, Carroll W, et al. Comparison of Biobrane and Scarlet Red dressings for treatment of donor site wounds. Arch Surg 1985;120(6):743-5.
156. Innes ME, Umraw N, Fish JS, et al. The use of silver coated dressings on donor site wounds: a prospective, controlled matched pair study. Burns
157. Hansbrough W. Nursing care of donor site wounds. J Burn Care
Rehabil 1995;16(3 Pt 1):337-9; discussion 39-40.
158. Hyland WT. A painless donor-site dressing. Plast Reconstr Surg 1982;69(4):703-4.
159. Jennings RG. Design of a burn treatment unit. J Clin Eng 1981;6(2):133-6.
160. Wachtel TL, Hartford CE, Hughes JA. Building a balanced scorecard for a burn center