Zusammenfassung
Ein Verbrennungstrauma mit Beteiligung bereits ≥20 % der Körperoberfläche kann bis zum Multiorganversagen mit fatalen Folgen führen. Es entsteht eine systemische Reaktion u. a. mit signifikanter Flüssigkeitsverschiebung aus dem intravasalen in den interstitiellen Raum und somit eine Ödembildung. Bei der Entstehung eines Verbrennungsschocks spielt neben der Hypovolämie auch die Aktivierung der zahlreichen Mediatoren eine zentrale Rolle. Dieses Kapitel befasst sich hauptsächlich mit systemischen Reaktionen der Verbrennungskrankheit bei schwerverbrannten Patienten. Dabei werden die Mechanismen auf zellulärer Ebene und der Effekt der wichtigsten Mediatoren beschrieben sowie die Auswirkung auf einzelne Organsysteme dargestellt.
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Literatur
Arturson G (1996) The plasma kinins in thermal injury. Scand J Clin Lab Invest 107:153–161
Arturson G (1996) The pathophysiology of the burn wound and pharmacological treatment. The Rudi Hermans Lecture. In: Burns 22:255–274
Baron DM, Metnitz PGH (2009) Metabolische Veränderungen bei Brandverletzungen – Pathophysiologie und Therapie. Anästhesiol Intensivmed Notfallmed Schmerzther 44:494–499
Baxter CR, Cook WA, Shires GT (1966) Serum myocardial depressant factor of burn shock. Surg Forum 17:1–2
Buhling F, Lieder N, Kuhlmann UC, Waldburg N, Welt T (2007) Tiotropium suppresses acetylcholine-induced release of chemotactic mediators in vitro. Respir Med 101:2386-2394
Burch JM, Moore EE, Moore FA (1996) The abdominal compartment syndrome. Surg Clin North Am 76:833–842
Cartotto R, Callum J (2012) A review of the use of human albumin in burn patients. J Burn Care Res 33:702–717
Chong SJ, Wong YC, Wu J, Tan MH, Lu J, Moochhala SM (2014) Parecoxib reduces systemic inflammation and acute lung injury in burned animals with delayed fluid resuscitation. Int J Inflam. doi: 10.1155/2014/972645. Epub 2014 Jan 21
Davis CF, Moore FD Jr, Rodrick ML, Fearon DT, Mannick JA (1987) Neutrophil activation after burn injury: contributions of the classic complement pathway and of endotoxin. Surgery 102:477–484
Deitch EA (1990) Intestinal permeability is increased in burn patients shortly after injury. Surgery 107:411–416
Demling RH (2005) The burn edema process: current concepts. J Burn Care Rehabil 26:207–227
Diao L, Marshall AH, Dai X, Bogdanovic E, Abdullahi A, Amini-Nik S, Jeschke MG (2014) Burn plus lipopolysaccharide augments endoplasmic reticulum stress and NLRP3 inflammasome activation and reduces PGC-1a in liver. Shock 41:138–144
Friedl HS, Till GO, Tentz O, Ward PA (1989) Roles of histamine, complement and xanthine oxidase in thermal injury of skin. Am J Pathol 135:203–217
Gauglitz GG, Herndon DN, Kamolz LP, Jeschke MG (2009) Die Pathophysiologie von Verbrennungswunden. In: Karnolz LP, Herndon DN, Jeschke MG (Hg) Verbrennungen. Springer Berlin, Heidelberg, New York
Gauglitz GG, Williams FN, Herndon DN, Jeschke MG (2011) Burns: where are we standing with propranolol, oxandrolone, recombinant human growth hormone, and the new incretin analogs? Curr Opin Clin Nutr Metab 14:176–181
Gelfand JA, Donelan M, Burke JF (1983) Preferential activation and depletion of the alternative complement pathway by burn injury. Ann Surg 198:58–62
Goodman-Gilman A, Rall TW, Nies AS, Taylor R (1990) The pharmacological basis of therapeutics. 6th Edn, MacMillan New York
Grunwald TB, Garner WL (2008) Acute burns. Plast Reconstr Surg 121:311e–319e
Harms B, Bodai B, Demling R (1981) Prostaglandine release and altered microvascular integrity after burn injury. J Surg Res 31:27–28
Hettiaratchy S, Dziewulski P (2004) ABC of burns. Pathophysiology and types of burns. BMJ Vol 328
Ishitsuka Y, Moriuchi H, Hatamoto K, Yang C, Takase J, Golbidi S, Irikura M, Irie T (2004) Involvement of thromboxane A2 (TXA2) in the early stages of oleic acid-induced lung injury and the preventive effect of ozagrel, a TXA2 synthase inhibitor in guinea-pigs. J Pharm Pharmacol 56:513–520
Jackson DM (1953) The diagnosis of the depth of burning. Br J Surg 40:588
Jeschke MG, Finnerty CC, Emdad F, Rivero HG, Kraft R, Williams FN, Gamelli RL, Gibran NS, Klein MB, Arnoldo BD, Tompkins RG, Herndon DN (2013) Mild obesity is protective after severe burn injury. Ann Surg 258:1119–1129
Jeschke, MG (2013) Clinical review: Glucose control in severely burned patients – current best practice. Critical Care 17:232
Kao CC, Garner WL (2000) Acute Burns. Plast Reconstr Surg 101:2482–2493
Keck M, Herndon DH, Kamolz LP, Frey M, Jeschke MG (2009) Pathophysiology of Burns. Wien Med Wochenschr 159:327–226
Kobayashi L, Costantini TW, Coimbra R (2012) Hypovolemic shock resuscitation. Surg Clin North Am 92:1403–1423
Lund T, Wiig H, Reed RK, Aukland K (1987) A ‘new’ mechanism for oedema generation: strongly negative interstitial fluid pressure causes rapid fluid flow into thermally injured skin. Acta Physiol Scand 129:433–435
Lund T, Onarheim H, Reed RK (1992) Pathogenesis of edema formation in burn injuries. World J Surg 16:2–9
Mace JE et al (2012) Differential expression of the immunoinflammatory response in trauma patients: Burn vs. non-burn. Burns 38:599–606
Mandell SP, Gibran NS (2014) Early Nutrition for Burn Injury. Adv Wound Care (New Rochelle) 3:64–70
Myburgh JA, Finfer S, Bellomo R, Billot L, Cass A, Gattas D, Glass P, Lipman J, Liu B, McArthur C, McGuinness S, Rajbhandari D, Taylor CB, Webb SA (2012) CHEST Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med 367:1901–1911
Ono I, Gunji H, Hasegawa T, Harada H, Kaneko F, Matsuzaki M (1993) Effects of a platelet activating factor antagonist on oedema formation following burns. Burns 19:202–207
Ottomann C, Hartmann B (2004) Die Pathophysiologie des Verbrennungstraumas. Intensivmed 41:380–387
Perner A, Haase N, Guttormsen AB, Tenhunen J, Klemenzson G, Åneman A, Madsen KR, Møller MH, Elkjær JM, Poulsen LM, Bendtsen A, Winding R, Steensen M, Berezowicz P, Søe-Jensen P, Bestle M, Strand K, Wiis J, White JO, Thornberg KJ, Quist L, Nielsen J, Andersen LH, Holst LB, Thormar K, Kjældgaard AL, Fabritius ML, Mondrup F, Pott FC, Møller TP, Winkel P, Wetterslev J (2012) 6S Trial Group; Scandinavian Critical Care Trials Group. Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. N Engl J Med 367:124–134
Rawlingson A, Greenacre SA, Brain SD (2000) Generation of peroxynitrite in localised, moderate temperature burns. Burns 26:223–227
Samuelsson A, Farnebo S, Magnusson B, Anderson C, Tesselaar E, Zettersten E, Sjöberg F (2012) Implications for burn shock resuscitation of a new in vivo human vascular microdosing technique (microdialysis) for dermal administration of noradrenaline. Burns 38:975–983
Schwacha MG (2003) Macrophages and post-burn immune dysfunction. Burns 29:1–14
Shirani KZ, Pruitt BA Jr, Mason AD (1987) The influence of inhalation injury and pneumonia on burn mortality. Ann Surg 205:82–87
Song J1, Finnerty CC, Herndon DN, Boehning D, Jeschke MG (2009) Severe burn-induced endoplasmic reticulum stress and hepatic damage in mice. Mol Med 15:316–320
Teot L, Otmann S, Brancati A, Mittermayr R. Burn wound healing: Pathophysiology. In: Kamolz LP et al. (ed). Handbook of Burns. Springer, Wien
Ungureanu-Longrois D, Balligand JL, Kelly RA, Smith TW (1995) Myocardial contractile dysfunction in the systemic inflammatory response syndrome – role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. J Mol Cell Cardio 27:155–167
Williams FN, Branski LK, Jeschke MG, Herndon, DN (2011) What, how, and how much should patients with burns be fed?, Surgical Clinics of North America 91:609–629
Wiig H, Rubin K, Reed RK (2003) New and active role of the interstitium in control of interstitial fluid pressure: potential therapeutic consequences. Acta Anaesthesiol Scand 47:111–121
Wolfe RR, Durkot MJ, Allsop JR et al (1979) Glucose metabolism in severely burned patients.Metabolism 28:1031–1039
Yamamoto Y1, Sousse LE, Enkhbaatar P, Kraft ER, Deyo DJ, Wright CL, Taylor A, Traber MG, Cox RA, Hawkins HK, Rehberg SW, Traber LD, Herndon DN, Traber DL (2012) γ-tocopherol nebulization decreases oxidative stress, arginase activity, and collagen deposition after burn and smoke inhalation in the ovine model. Shock 38:671–676
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Fakin, R.M., Guggenheim, M., Wallner, C., Lehnhardt, M., Giovanoli, P. (2016). Pathophysiologie der Verbrennungskrankheit. In: Lehnhardt, M., Hartmann, B., Reichert, B. (eds) Verbrennungschirurgie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-54444-6_6
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