Burn natural history, complications and prognosis: Difference between revisions

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<br />
 
==Overview==
[[Burn (injury)|Burn]]<nowiki/>s injuries is a common  condition that involves complications such as the [[disability]] . If left untreated,  progresses from early stage of [[Burn (injury)|burn]] to advanced skin [[Scar tissue|scar]] and [[contraction]]. Common complications of [[Burn (injury)|burn]]<nowiki/>s injuries include [[infection]], [[bedsores]], post-burn [[seizures]], [[hypertrophic]] scars and [[keloids]], [[Respiratory]] complications, systemic [[complications]]. There is a cure for [[Burn (injury)|burn]]<nowiki/>s injuries  and the treatment focuses on the stage of the [[Burn (injury)|burn]]( size and [[Depth of field|depth]]) so [[fluid resuscitation]], wound [[Excision repair|excision]], [[grafting]] and coverage, [[infection]] control and [[nutritional]] support can be part of the management of the [[Burn (injury)|burn]] injuries.<br />
==Natural History==
Patients with [[Burn (injury)|burn]] injury If left untreated<ref name="pmid10907433">{{cite journal| author=Janzekovic Z| title=The burn wound from the surgical point of view. | journal=J Trauma | year= 1975 | volume= 15 | issue= 1 | pages= 42-62 | pmid=1090743 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1090743  }}</ref>,  may progress to develop<ref name="urlFiona Wood | Australian surgeon | Britannica">{{cite web |url=https://www.britannica.com/biography/Fiona-Wood |title=Fiona Wood &#124; Australian surgeon &#124; Britannica |format= |work= |accessdate=}}</ref>:
 
<br />
 
*[[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<ref name="pmid1090743">{{cite journal |vauthors=Janzekovic Z |title=The burn wound from the surgical point of view |journal=J Trauma |volume=15 |issue=1 |pages=42–62 |date=January 1975 |pmid=1090743 |doi= |url=}}</ref><ref name="pmid12443718">{{cite journal |vauthors=Chan BP, Kochevar IE, Redmond RW |title=Enhancement of porcine skin graft adherence using a light-activated process |journal=J Surg Res |volume=108 |issue=1 |pages=77–84 |date=November 2002 |pmid=12443718 |doi=10.1006/jsre.2002.6516 |url=}}</ref>. ( "[[Hypermetabolic]] response to moderate-to-severe [[Burn (injury)|burn]] injury and management", section on 'Early excision and grafting' and "Burn wound)
 
*post-burn [[seizures]],
 
*[[Scar tissue|scar]] tissue called [[hypertrophic]] scars and [[keloids]],
 
*[[Respiratory]] complications:  include [[inhalation]] injuries<ref>A review of the complications of burns, their origin and importance for illness and death - Abstract [http://www.ncbi.nlm.nih.gov/pubmed/448773 J Trauma. 1979 May;19(5):358-69.] Accessed February 27, 2008</ref><ref name="pmid448773">{{cite journal |vauthors=Sevitt S, Schmoldt A, Benthe HF, Haberland G, Ward CW, Thompson HC, Eisenstein TK, Schmoldt A, Benthe HF, Haberland G |title=A review of the complications of burns, their origin and importance for illness and death |journal=J Trauma |volume=19 |issue=5 |pages=358–69 |date=May 1979 |pmid=448773 |pmc=420673 |doi=10.1097/00005373-197905000-00010 |url=}}</ref>[[aspiration]] of fluids by unconscious patients, [[bacterial]] [[pneumonia]], [[pulmonary edema]], [[obstruction]] of [[pulmonary]] [[arteries]], and postinjury [[Respiratory failure|respiratory]] failure.  The three basic categories of direct-[[inhalation]] injuries are [[inhalation]] of dry heat and [[soot]], [[Carbon monoxide poisoning|carbon monoxide]] poisoning, and [[smoke inhalation]].
 
*systemic [[complications]]<ref name="pmid10907432">{{cite journal| author=Janzekovic Z| title=The burn wound from the surgical point of view. | journal=J Trauma | year= 1975 | volume= 15 | issue= 1 | pages= 42-62 | pmid=1090743 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1090743  }}</ref> 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 (injury)|burn]], with or without an [[infection]]<ref name="pmidPMID: 17925660 DOI: 10.1097/BCR.0b013e3181599bc9 A">{{cite journal| author=Greenhalgh DG, Saffle JR, Holmes JH, Gamelli RL, Palmieri TL, Horton JW | display-authors=etal| title=American Burn Association consensus conference to define sepsis and infection in burns. | journal=J Burn Care Res | year= 2007 | volume= 28 | issue= 6 | pages= 776-90 | pmid=PMID: 17925660 DOI: 10.1097/BCR.0b013e3181599bc9 A | doi=10.1097/BCR.0b013e3181599bc9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17925660  }}</ref> . The risk of [[MODS]] increases with [[Burn (injury)|burn]] wounds >20 percent [[total body surface area]] (TBSA), increasing [[age]], male gender, [[sepsis]], [[hypoperfusion]], and under-[[resuscitation]]<ref name="pmid11265031">{{cite journal| author=Cumming J, Purdue GF, Hunt JL, O'Keefe GE| title=Objective estimates of the incidence and consequences of multiple organ dysfunction and sepsis after burn trauma. | journal=J Trauma | year= 2001 | volume= 50 | issue= 3 | pages= 510-5 | pmid=11265031 | doi=10.1097/00005373-200103000-00016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11265031  }}</ref><ref name="pmidPMID: 2254977 DOI: 10.1097/00005373-199012001-0003">{{cite journal| author=Meakins JL| title=Etiology of multiple organ failure. | journal=J Trauma | year= 1990 | volume= 30 | issue= 12 Suppl | pages= S165-8 | pmid=PMID: 2254977 DOI: 10.1097/00005373-199012001-0003 | doi=10.1097/00005373-199012001-00033 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2254977  }}</ref>. Approximately 50 percent of patients who succumbed to the [[Burn (injury)|burn]] injury had been diagnosed with [[MODS]]<ref name="pmid19919684">{{cite journal| author=Williams FN, Herndon DN, Hawkins HK, Lee JO, Cox RA, Kulp GA | display-authors=etal| title=The leading causes of death after burn injury in a single pediatric burn center. | journal=Crit Care | year= 2009 | volume= 13 | issue= 6 | pages= R183 | pmid=19919684 | doi=10.1186/cc8170 | pmc=2811947 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19919684 }}</ref>. 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 (injury)|burn]] wound or [[lungs]] are the most likely sites for an [[infection]] in the severely burned patient that subsequently develops [[MODS]]<ref name="pmid151836302">{{cite journal| author=Herndon DN, Tompkins RG| title=Support of the metabolic response to burn injury. | journal=Lancet | year= 2004 | volume= 363 | issue= 9424 | pages= 1895-902 | pmid=15183630 | doi=10.1016/S0140-6736(04)16360-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15183630  }}</ref><ref name="pmid11219223">{{cite journal| author=McCowen KC, Malhotra A, Bistrian BR| title=Stress-induced hyperglycemia. | journal=Crit Care Clin | year= 2001 | volume= 17 | issue= 1 | pages= 107-24 | pmid=11219223 | doi=10.1016/s0749-0704(05)70154-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11219223 }}</ref>. 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|organ]] failure. Targeting the different cascade systems involved in the pathogenesis of burn-induced [[MODS]] is often not a feasible option<ref name="urlBurn-Induced Coagulopathies: a Comprehensive Review">{{cite web |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439938/ |title=Burn-Induced Coagulopathies: a Comprehensive Review |format= |work= |accessdate=}}</ref>.  
 
==Prevention:==
Prevention of sepsis from [[Burn (injury)|burn]] wound [[infection]] is the most promising approach and illustrated by:  
 
1. [[Physiologically-based pharmacokinetic modelling|physiologically]]: such as the recognition of the importance of burn surface area,  [[infection]] control and [[nutritional]] support and skin [[grafting]] and coverage,, <ref name="pmid15183630">{{cite journal |vauthors=Herndon DN, Tompkins RG |title=Support of the metabolic response to burn injury |journal=Lancet |volume=363 |issue=9424 |pages=1895–902 |date=June 2004 |pmid=15183630 |doi=10.1016/S0140-6736(04)16360-5 |url=}}</ref>However, this was not reflected in improving survival and many patients still died of [[shock]] and [[infection]]
 
2.[[psychologically]].<ref name="urlHistory of burns: The past, present and the future | Burns & Trauma | Full Text">{{cite web |url=https://burnstrauma.biomedcentral.com/articles/10.4103/2321-3868.143620 |title=History of burns: The past, present and the future &#124; Burns & Trauma &#124; Full Text |format= |work= |accessdate=}}</ref>
 
 
<br />
 
==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. <ref name="pmid30837206">{{cite journal |vauthors=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 |title=The epidemiology and prognosis of patients with massive burns: A multicenter study of 2483 cases |journal=Burns |volume=45 |issue=3 |pages=705–716 |date=May 2019 |pmid=30837206 |doi=10.1016/j.burns.2018.08.008 |url=}}</ref><ref name="pmid8987427">{{cite journal |vauthors=Mann R, Heimbach D, Claeyssens M, Henrissat B |title=Prognosis and treatment of burns |journal=West. J. Med. |volume=165 |issue=4 |pages=215–20 |date=October 1996 |pmid=8987427 |pmc=1303748 |doi=10.1002/pro.5560011008 |url=}}</ref><ref name="pmid20523229">{{cite journal |vauthors=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 |title=Predicting prognosis in thermal burns with associated inhalational injury: a systematic review of prognostic factors in adult burn victims |journal=J Burn Care Res |volume=31 |issue=4 |pages=529–39 |date=September 1975 |pmid=20523229 |doi=10.1097/BCR.0b013e3181e4d680 |url=}}</ref>.
 


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Latest revision as of 09:01, 12 February 2021


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)

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

2.psychologically.[16]



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

  1. ↑ Janzekovic Z (1975). "The burn wound from the surgical point of view". J Trauma. 15 (1): 42–62. PMID 1090743.
  2. ↑ "Fiona Wood | Australian surgeon | Britannica".
  3. ↑ Janzekovic Z (January 1975). "The burn wound from the surgical point of view". J Trauma. 15 (1): 42–62. PMID 1090743.
  4. ↑ 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.
  5. ↑ 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
  6. ↑ 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.
  7. ↑ Janzekovic Z (1975). "The burn wound from the surgical point of view". J Trauma. 15 (1): 42–62. PMID 1090743.
  8. ↑ 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).
  9. ↑ 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.
  10. ↑ 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).
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ "Burn-Induced Coagulopathies: a Comprehensive Review".
  15. ↑ 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.
  16. ↑ "History of burns: The past, present and the future | Burns & Trauma | Full Text".
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.

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