The following estimates were derived from sample and registry statistics compiled by ongoing national health care and fire casualty surveys, selected state health data systems, and the National Burn Repository (NBR) of the American Burn Association (ABA).
Burn Statistics. The American Burn Association states that roughly 450,000 patients receive hospital and emergency room treatment for burns each year.
Figure. Caring for a patient with severe burn injuries offers many challenges for critical care nurses. This article reviews various types of burns and what you need to know to provide initial resuscitative care for a patient if treatment in a designated burn center facility or burn ICU isn't possible.
Burn injuries are under-appreciated injuries that are associated with substantial morbidity and mortality. Burn injuries, particularly severe burns, are accompanied by an immune and inflammatory response, metabolic changes and distributive shock that can be challenging to manage and can lead to mult …
Burn injuries are a significant problem with more than 500,000 people seeking medical treatment, 40,000 resultant hospitalizations, and 4000 deaths per year in the United States. 1 The annual cost of treating these burns is estimated to be in excess of U.S. $ 1 billion, not including the indirect costs of disability and rehabilitation. 1 These statistics have driven a multitude of studies that ...
What Are the Classifications of Burns? 1 First-degree (superficial) burns#N#First-degree burns affect only the epidermis, or outer layer of skin. The burn site is red, painful, dry, and with no blisters. Mild sunburn is an example. Long-term tissue damage is rare and usually consists of an increase or decrease in the skin color. 2 Second-degree - (partial thickness) burns#N#Second-degree burns involve the epidermis and part of the dermis layer of skin. The burn site appears red, blistered, and may be swollen and painful. 3 Third-degree (full thickness) burns#N#Third-degree burns destroy the epidermis and dermis. Third-degree burns may also damage the underlying bones, muscles, and tendons. The burn site appears white or charred. There is no sensation in the area since the nerve endings are destroyed.
Third-degree burns destroy the epidermis and dermis. Third-degree burns may also damage the underlying bones, muscles, and tendons. The burn site appears white or charred. There is no sensation in the area since the nerve endings are destroyed.
Mild sunburn is an example. Long-term tissue damage is rare and usually consists of an increase or decrease in the skin color. Second-degree - (partial thickness) burns.
Burns affecting 10 percent of a child's body and those affecting 15 to 20 percent of an adult's body are considered to be major injuries and require hospitalization and extensive rehabilitation. Types Treatments.
Burn injuries are under-appreciated injuries that are associated with substantial morbidity and mortality. Burn injuries, particularly severe burns, are accompanied by an immune and inflammatory response, metabolic changes and distributive shock that can be challenging to manage and can lead to multiple organ failure. Of great importance is that the injury affects not only the physical health, but also the mental health and quality of life of the patient. Accordingly, patients with burn injury cannot be considered recovered when the wounds have healed; instead, burn injury leads to long-term profound alterations that must be addressed to optimize quality of life. Burn care providers are, therefore, faced with a plethora of challenges including acute and critical care management, long-term care and rehabilitation. The aim of this Primer is not only to give an overview and update about burn care, but also to raise awareness of the ongoing challenges and stigmata associated with burn injuries.
Burn injury usually results in a distributive shock38, an abnormal physiological state in which tissue perfusion and oxygen delivery is severely compromised owing to marked capillary leakage of fluid from the intravascular to interstitial space, that contributes to profound tissue oedema and fluid accumulation39,40. The marked capillary leakage can be attributed to oxidative stress that is characterized by increases in the levels of nitric oxide and inflammatory mediators, which damages the vascular endothelium. Burn injury also depresses cardiac function within a few hours of injury, lasting ~24–48 hours, via oxidative stress, the release of inflammatory mediators (such as IL-6 and tumour necrosis factor (TNF)) and cellular alterations (such as apoptosis and necrosis)32,34,39,41. The decrease in cardiac function and relative hypovolaemia, along with low blood flow caused by vasoconstriction, affects perfusion of tissues and organs (that is, distributive shock), including the lungs, liver and gastrointestinal tract — augmenting tissue and organ dysfunction and damage. The state of shock continues even if hypovolaemia is corrected38. Furthermore, the cardiovascular dysfunction can further exacerbate the systemic inflammatory response into a vicious cycle of accelerating organ dysfunction (summarized in ref.42).
Severe burns cause a complex pattern of responses that can last up to several years after the initial insult4. In general, immediately after the insult, an inflammatory response is triggered to promote the healing process5,6. However, in severe burns, this inflammatory process can be extensive and become uncontrolled, leading to an augmented inflammation that does not induce healing but rather causes a generalized catabolic state and delayed healing. This response is almost unique to burns and is referred to as the hypermetabolic response ; it is associated with catabolism, increased incidence of organ failure, infections and even death7.
Various studies support the suggestion that the gut, being the major source of bacteria and bacterial products, also plays an important part in pathogenesis after burn injury68,69. Previous studies have shown an increase in intestinal bacterial growth after burn injury, resulting from diminished gut immunity, hypoperfusion and gut dysmotility70. Furthermore, an increase in intestinal permeability (due to hypoperfusion and subsequent tissue inflammation and damage) has also been documented in patients and in animals within a few hours of burn injury70–72and enables the gut bacteria to enter extra-intestinal sites such as mesenteric lymph nodes, liver and lungs. Indeed, increased bacterial translocation has been noted within the first few days after burn injury70–72. However, this process becomes recurrent when the burn injury is followed by additional triggers that lead to gut hypoperfusion, such as peri-operative haemorrhagic shock and infectious complications. The microbial communities in faecal samples from patients with burn injury have been shown to be different from those observed in faecal samples from healthy controls73,74. Specifically, the faecal microbial communities of controls were dominated by the Bacteroidaceae, Lachnospiraceae, and Ruminococcaceae families. The faecal samples from patients with burn injuries exhibited a marked decrease in the relative abundance of these three families, but also demonstrated sharp increases in the relative abundance of the Enterobacteriaceae, a finding that has been replicated in mice74. Furthermore, results obtained using in situ hybridization suggest large populations of Enterobacteriaceae in close proximity to the villi in the small intestine of mice receiving burn injury74. This observation provides further evidence that intestinal bacteria and their products (such as endotoxin) can cross the intestinal epithelial barrier into the systemic or lymphatic circulation and contribute to the pathology after burn injury. Changes in the microbial community or diversity have been implicated in the development of many diseases including allergies, obesity, inflammatory bowel disease and many infectious diseases75–80. However, a more systematic approach is needed to better appreciate the role of gut-derived bacteria or the microbiome in pathogenesis after burn injury.
Tissue injury following severe burns results in release of endogenous damage-associated molecular patterns (DAMPs) such as mitochondrial DNA263and double-stranded RNA (dsRNA), which along with exogenous pathogen-associated molecular pattern molecules (PAMPs) such as lipopolysaccharides (LPS) and peptidoglycans, can induce vascular leak, an inflammatory response and metabolic changes. Vascular leak and transfer of intravascular fluid to third spaces leads to tissue oedema and further injury. The inflammatory response can result in immunosuppression and ineffective response to bacterial invasion. Metabolic changes include increased muscle protein degradation, insulin resistance and increased cardiac load. The culmination of these events is often systemic inflammatory response syndrome (SIRS), an inflammatory state affecting the whole body, which can lead to multiple organ failure, and ultimately, death. MHC, major histocompatibility complex; PGE2, prostaglandin E2; TNF, tumour necrosis factor. Adapted from ref.264, Springer Nature Limited.
Immediately after injury, the burn wound can be divided into three zones: the zone of coagulation ( with the most damage in the central portion); the zone of stasis or zone of ischaemia (characterized by decreased perfusion that is potentially salvageable); and the zone of hyperaemia (the outermost region of the wound characterized by increased inflammatory vasodilation). The degree of cellular injury varies depending on the zone of injury and spans the spectrum from immediate cellular autophagy within the first 24 hours following injury, delayed-onset apoptosis ~24–48 hours after the burn injury and the presence of reversible oxidative stress. The natural healing of these wounds involves dynamic and overlapping phases (Fig. 2) that include an inflammatory phase, which is initiated by neutrophils and monocytes homing to the injury site via localized vasodilation.
The American Burn Association (ABA) National Burn Repository 2019 reports that, overall, flame burns are still the majority of injuries in the USA (41%) , with scalds second at 31%1. Chemical (3.5%) and electrical burn injuries (3.6%) occur much less commonly1. Burns in children <5 years of age tend to be scald injuries, with increasing flame-related burns as age increases28. Around the world, burns in the elderly population are increasing, and are predominantly flame-related. However, scald injuries are increasing substantially as well29. Finally, depending on the environment, burn injuries are more frequent in some vulnerable populations, such as those with epilepsy30.
Burn injuries are under-appreciated injuries that are associated with substantial morbidity and mortality. Burn injuries, particularly severe burns, are accompanied by an immune and inflammatory response, metabolic changes and distributive shock that can be challenging to manage and can lead to multiple organ failure. Of great importance is that the injury affects not only the physical health, but also the mental health and quality of life of the patient. Accordingly, patients with burn injury cannot be considered recovered when the wounds have healed; instead, burn injury leads to long-term profound alterations that must be addressed to optimize quality of life. Burn care providers are, therefore, faced with a plethora of challenges including acute and critical care management, long-term care and rehabilitation. The aim of this Primer is not only to give an overview and update about burn care, but also to raise awareness of the ongoing challenges and stigmata associated with burn injuries.
Burn injury usually results in a distributive shock38, an abnormal physiological state in which tissue perfusion and oxygen delivery is severely compromised owing to marked capillary leakage of fluid from the intravascular to interstitial space, that contributes to profound tissue oedema and fluid accumulation39,40. The marked capillary leakage can be attributed to oxidative stress that is characterized by increases in the levels of nitric oxide and inflammatory mediators, which damages the vascular endothelium. Burn injury also depresses cardiac function within a few hours of injury, lasting ~24–48 hours, via oxidative stress, the release of inflammatory mediators (such as IL-6 and tumour necrosis factor (TNF)) and cellular alterations (such as apoptosis and necrosis)32,34,39,41. The decrease in cardiac function and relative hypovolaemia, along with low blood flow caused by vasoconstriction, affects perfusion of tissues and organs (that is, distributive shock), including the lungs, liver and gastrointestinal tract — augmenting tissue and organ dysfunction and damage. The state of shock continues even if hypovolaemia is corrected38. Furthermore, the cardiovascular dysfunction can further exacerbate the systemic inflammatory response into a vicious cycle of accelerating organ dysfunction (summarized in ref.42).
Severe burns cause a complex pattern of responses that can last up to several years after the initial insult4. In general, immediately after the insult, an inflammatory response is triggered to promote the healing process5,6. However, in severe burns, this inflammatory process can be extensive and become uncontrolled, leading to an augmented inflammation that does not induce healing but rather causes a generalized catabolic state and delayed healing. This response is almost unique to burns and is referred to as the hypermetabolic response ; it is associated with catabolism, increased incidence of organ failure, infections and even death7.
Various studies support the suggestion that the gut, being the major source of bacteria and bacterial products, also plays an important part in pathogenesis after burn injury68,69. Previous studies have shown an increase in intestinal bacterial growth after burn injury, resulting from diminished gut immunity, hypoperfusion and gut dysmotility70. Furthermore, an increase in intestinal permeability (due to hypoperfusion and subsequent tissue inflammation and damage) has also been documented in patients and in animals within a few hours of burn injury70–72and enables the gut bacteria to enter extra-intestinal sites such as mesenteric lymph nodes, liver and lungs. Indeed, increased bacterial translocation has been noted within the first few days after burn injury70–72. However, this process becomes recurrent when the burn injury is followed by additional triggers that lead to gut hypoperfusion, such as peri-operative haemorrhagic shock and infectious complications. The microbial communities in faecal samples from patients with burn injury have been shown to be different from those observed in faecal samples from healthy controls73,74. Specifically, the faecal microbial communities of controls were dominated by the Bacteroidaceae, Lachnospiraceae, and Ruminococcaceae families. The faecal samples from patients with burn injuries exhibited a marked decrease in the relative abundance of these three families, but also demonstrated sharp increases in the relative abundance of the Enterobacteriaceae, a finding that has been replicated in mice74. Furthermore, results obtained using in situ hybridization suggest large populations of Enterobacteriaceae in close proximity to the villi in the small intestine of mice receiving burn injury74. This observation provides further evidence that intestinal bacteria and their products (such as endotoxin) can cross the intestinal epithelial barrier into the systemic or lymphatic circulation and contribute to the pathology after burn injury. Changes in the microbial community or diversity have been implicated in the development of many diseases including allergies, obesity, inflammatory bowel disease and many infectious diseases75–80. However, a more systematic approach is needed to better appreciate the role of gut-derived bacteria or the microbiome in pathogenesis after burn injury.
Tissue injury following severe burns results in release of endogenous damage-associated molecular patterns (DAMPs) such as mitochondrial DNA263and double-stranded RNA (dsRNA), which along with exogenous pathogen-associated molecular pattern molecules (PAMPs) such as lipopolysaccharides (LPS) and peptidoglycans, can induce vascular leak, an inflammatory response and metabolic changes. Vascular leak and transfer of intravascular fluid to third spaces leads to tissue oedema and further injury. The inflammatory response can result in immunosuppression and ineffective response to bacterial invasion. Metabolic changes include increased muscle protein degradation, insulin resistance and increased cardiac load. The culmination of these events is often systemic inflammatory response syndrome (SIRS), an inflammatory state affecting the whole body, which can lead to multiple organ failure, and ultimately, death. MHC, major histocompatibility complex; PGE2, prostaglandin E2; TNF, tumour necrosis factor. Adapted from ref.264, Springer Nature Limited.
Immediately after injury, the burn wound can be divided into three zones: the zone of coagulation ( with the most damage in the central portion); the zone of stasis or zone of ischaemia (characterized by decreased perfusion that is potentially salvageable); and the zone of hyperaemia (the outermost region of the wound characterized by increased inflammatory vasodilation). The degree of cellular injury varies depending on the zone of injury and spans the spectrum from immediate cellular autophagy within the first 24 hours following injury, delayed-onset apoptosis ~24–48 hours after the burn injury and the presence of reversible oxidative stress. The natural healing of these wounds involves dynamic and overlapping phases (Fig. 2) that include an inflammatory phase, which is initiated by neutrophils and monocytes homing to the injury site via localized vasodilation.
The American Burn Association (ABA) National Burn Repository 2019 reports that, overall, flame burns are still the majority of injuries in the USA (41%) , with scalds second at 31%1. Chemical (3.5%) and electrical burn injuries (3.6%) occur much less commonly1. Burns in children <5 years of age tend to be scald injuries, with increasing flame-related burns as age increases28. Around the world, burns in the elderly population are increasing, and are predominantly flame-related. However, scald injuries are increasing substantially as well29. Finally, depending on the environment, burn injuries are more frequent in some vulnerable populations, such as those with epilepsy30.