Burn natural history, complications and prognosis
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Editor-In-Chief: Eman Alademi, M.D.[1]
Natural History
If left untreated[1], patients with burn injury may progress to develop[2]:
burn infection, Wound-associated inflammation is limited by immediate debridement of devitalized tissue and tangential excision of burn tissue and wound closure, primarily by skin grafts, within 48 hours of a full-thickness burn[3][4][5]. (See "Hypermetabolic response to moderate-to-severe burn injury and management", section on 'Early excision and grafting' and "Burn wound
- infection and sepsis".
- post-burn seizures,
- scar tissue called hypertrophic scars and keloids,
- Respiratory complications: include inhalation injuries[6][7]aspiration of fluids by unconscious patients, bacterial pneumonia, pulmonary edema, obstruction of pulmonary arteries, and postinjury respiratory failure. The three basic categories of direct-inhalation injuries are inhalation of dry heat and soot, carbon monoxide poisoning, and smoke inhalation.
- SYSTEMIC COMPLICATIONS[1] like Multisystem organ dysfunction — Multiple organ dysfunction syndrome (MODS) is a progressive disorder that commonly occurs in acutely ill patients, regardless of etiology of the injury or illness. MODS exists in a continuum with the systemic inflammatory response syndrome (SIRS) which affects most patients with a severe burn, with or without an infection[8][9] . The risk of MODS increases with burn wounds >20 percent total body surface area (TBSA), increasing age, male gender, sepsis, hypoperfusion, and under-resuscitation[10][11]. Approximately 50 percent of patients who succumbed to the burn injury had been diagnosed with MODS[12]. Most patients with MODS have an inability to attenuate the inflammatory response to injury. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Multiple organ dysfunction syndrome' and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Definitions'.)
In general, the burn wound or lungs are the most likely sites for an infection in the severely burned patient that subsequently develops MODS[4]. The release of endotoxins and/or exotoxins from an infective process initiates a cascade of inflammatory mediators that leads to organ damage and ultimately organ failure. Targeting the different cascade systems involved in the pathogenesis of burn-induced MODS is often not a feasible option[13]. Prevention of sepsis from burn wound infection is the most promising approach, as illustrated by the following examples:
Burn injuries are amongst one of the most devastating of all injuries, having a great impact on the patients physically, physiologically and psychologically. Burns are still one of the top causes of death and disability in the world.[1] Physicians have searched for and formulated a myriad of treatments for burns over the centuries but these treatments mostly were of little benefit to the victims mainly because the fundamental understanding of the patho-physiological impact of burns was not known yet. There was an exponential increase in biomedical research and knowledge from the 18th to early 20thcentury in burn care, such as the recognition of the importance of burn surface area and skin grafting by Reverdin.[2] However, this was not reflected in improving survival and many patients still died of shock and infection. It was not until the past 50 years that the mortality of burns has been dramatically improved, thanks to the better understanding of the patho-physiology of burn injury. The treatment of burns is a major undertaking and involves many components from the initial first aid, assessment of the burn size and depth, fluid resuscitation, wound excision, grafting and coverage, infection control and nutritional support. Progress in each of these areas has contributed significantly to the overall enhanced survival of burn victims and this article aims to explore the history of burns to identify milestones and step-changes in each of these areas in the patient’s care. As in the case of the advancement in the treatment of trauma, these step-changes were mainly related to wars. Napoleon’s surgeon’s contributions to wound management that are still applicable today is an example. In burns, fire disasters as the Rialto fire in 1921 and Coconut Grove nightclubs fire in 1942 led to research that provided the first glimpse of the modern understanding of the patho-physiology of burns.[14]
Prognosis
Prognosis is generally depend on the etiological characteristics of the different age groups that should be considered for prevention. BI can be a reliable index of prognosis in severely burned patients. The results of the study showed that a large BI, elderly age, delayed admission after injury and combined inhalation injury are the main risk factors for extensively burned patients. [15][16][17].
References
- ↑ 1.0 1.1 "UpToDate".
- ↑ "Fiona Wood | Australian surgeon | Britannica".
- ↑ Janzekovic Z (January 1975). "The burn wound from the surgical point of view". J Trauma. 15 (1): 42–62. PMID 1090743.
- ↑ 4.0 4.1 "UpToDate 2018".
- ↑ Chan BP, Kochevar IE, Redmond RW (November 2002). "Enhancement of porcine skin graft adherence using a light-activated process". J Surg Res. 108 (1): 77–84. doi:10.1006/jsre.2002.6516. PMID 12443718.
- ↑ A review of the complications of burns, their origin and importance for illness and death - Abstract J Trauma. 1979 May;19(5):358-69. Accessed February 27, 2008
- ↑ Sevitt S, Schmoldt A, Benthe HF, Haberland G, Ward CW, Thompson HC, Eisenstein TK, Schmoldt A, Benthe HF, Haberland G (May 1979). "A review of the complications of burns, their origin and importance for illness and death". J Trauma. 19 (5): 358–69. doi:10.1097/00005373-197905000-00010. PMC 420673. PMID 448773.
- ↑ Greenhalgh DG, Saffle JR, Holmes JH, Gamelli RL, Palmieri TL, Horton JW; et al. (2007). "American Burn Association consensus conference to define sepsis and infection in burns". J Burn Care Res. 28 (6): 776–90. doi:10.1097/BCR.0b013e3181599bc9. PMID 17925660 DOI: 10.1097/BCR.0b013e3181599bc9 A PMID: 17925660 DOI: 10.1097/BCR.0b013e3181599bc9 A Check
|pmid=value (help). - ↑ "UpToDate 2018".
- ↑ Cumming J, Purdue GF, Hunt JL, O'Keefe GE (2001). "Objective estimates of the incidence and consequences of multiple organ dysfunction and sepsis after burn trauma". J Trauma. 50 (3): 510–5. doi:10.1097/00005373-200103000-00016. PMID 11265031.
- ↑ Meakins JL (1990). "Etiology of multiple organ failure". J Trauma. 30 (12 Suppl): S165–8. doi:10.1097/00005373-199012001-00033. PMID 2254977 DOI: 10.1097/00005373-199012001-0003 PMID: 2254977 DOI: 10.1097/00005373-199012001-0003 Check
|pmid=value (help). - ↑ Williams FN, Herndon DN, Hawkins HK, Lee JO, Cox RA, Kulp GA; et al. (2009). "The leading causes of death after burn injury in a single pediatric burn center". Crit Care. 13 (6): R183. doi:10.1186/cc8170. PMC 2811947. PMID 19919684.
- ↑ "Burn-Induced Coagulopathies: a Comprehensive Review".
- ↑ "History of burns: The past, present and the future | Burns & Trauma | Full Text".
- ↑ Cheng W, Shen C, Zhao D, Zhang H, Tu J, Yuan Z, Song G, Liu M, Li D, Shang Y, Qin B, Schmoldt A, Benthe HF, Haberland G, Tarentino AL, Maley F, Kidder GW, Montgomery CW, Moroi K, Sato T, Moroi K, Sato T (May 2019). "The epidemiology and prognosis of patients with massive burns: A multicenter study of 2483 cases". Burns. 45 (3): 705–716. doi:10.1016/j.burns.2018.08.008. PMID 30837206.
- ↑ Mann R, Heimbach D, Claeyssens M, Henrissat B (October 1996). "Prognosis and treatment of burns". West. J. Med. 165 (4): 215–20. doi:10.1002/pro.5560011008. PMC 1303748. PMID 8987427.
- ↑ Colohan SM, Schmoldt A, Benthe HF, Haberland G, Ward CW, Järvisalo J, Saris NE, Palmer GC, Manian AA, Wiesmann UN, DiDonato S, Herschkowitz NN, Bauer C (September 1975). "Predicting prognosis in thermal burns with associated inhalational injury: a systematic review of prognostic factors in adult burn victims". J Burn Care Res. 31 (4): 529–39. doi:10.1097/BCR.0b013e3181e4d680. PMID 20523229.