Burn natural history, complications and prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Eman Alademi, M.D.[2]
Overview
Burns injuries is a common condition that involves complications such as the disability . If left untreated, progresses from early stage of burn to advanced skin scar and contraction. Common complications of burns injuries include infection, bedsores, post-burn seizures, hypertrophic scars and keloids, Respiratory complications, systemic complications. There is a cure for burns injuries and the treatment focuses on the stage of the burn( size and depth) so fluid resuscitation, wound excision, grafting and coverage, infection control and nutritional support can be part of the management of the burn injuries.
Natural History
Patients with burn injury If left untreated[1], may progress to develop[2]:
- infection and sepsis": 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]. ( "Hypermetabolic response to moderate-to-severe burn injury and management", section on 'Early excision and grafting' and "Burn wound)
- post-burn seizures,
- scar tissue called hypertrophic scars and keloids,
- Respiratory complications: include inhalation injuries[5][6]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[7] 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] . The risk of MODS increases with burn wounds >20 percent total body surface area (TBSA), increasing age, male gender, sepsis, hypoperfusion, and under-resuscitation[9][10]. Approximately 50 percent of patients who succumbed to the burn injury had been diagnosed with MODS[11]. 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[12][13]. 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[14].
Prevention:
Prevention of sepsis from burn wound infection is the most promising approach and illustrated by:
1. physiologically: such as the recognition of the importance of burn surface area, infection control and nutritional support and skin grafting and coverage,, [15]However, this was not reflected in improving survival and many patients still died of shock and infection
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. [17][18][19].
References
- ↑ Janzekovic Z (1975). "The burn wound from the surgical point of view". J Trauma. 15 (1): 42–62. PMID 1090743.
- ↑ "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.
- ↑ 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.
- ↑ Janzekovic Z (1975). "The burn wound from the surgical point of view". J Trauma. 15 (1): 42–62. PMID 1090743.
- ↑ 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). - ↑ 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.
- ↑ Herndon DN, Tompkins RG (2004). "Support of the metabolic response to burn injury". Lancet. 363 (9424): 1895–902. doi:10.1016/S0140-6736(04)16360-5. PMID 15183630.
- ↑ McCowen KC, Malhotra A, Bistrian BR (2001). "Stress-induced hyperglycemia". Crit Care Clin. 17 (1): 107–24. doi:10.1016/s0749-0704(05)70154-8. PMID 11219223.
- ↑ "Burn-Induced Coagulopathies: a Comprehensive Review".
- ↑ Herndon DN, Tompkins RG (June 2004). "Support of the metabolic response to burn injury". Lancet. 363 (9424): 1895–902. doi:10.1016/S0140-6736(04)16360-5. PMID 15183630.
- ↑ "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.