Zusammenfassung
Die pathophysiologischen Abläufe nach akzidentellem Trauma zeigen einen phasischen Verlauf der immunmodulatorischen Reaktion. Ein operatives Trauma durch eine sekundäre Operation stellt hierbei eine zusätzliche Noxe dar. Je nachdem, in welcher Phase der posttraumatischen Inflammation dieser Second Hit einwirkt, können mehr oder weniger starke Störungen der Homöostase bis hin zum postoperativen Multiorganversagen auftreten. Größere sekundäre Operationen innerhalb der ersten 2–3 Tage nach dem Trauma scheinen ein deutlich größeres Operationsrisiko aufzuweisen und sollten – sofern keine dringliche Indikation besteht – auf einen späteren Zeitpunkt verschoben werden, insbesondere wenn die Lungenfunktion eingeschränkt ist (pO2/FiO2-Quotient<280 mmHg). Für die Planung von Operationen ab dem 4. Tag scheinen ein pO2/FiO2-Quotient>280 mmHg, eine stabile Kreislaufsituation, eine Thrombozytenzahl >100.000–150.000/µl und steigende globale Gerinnungstests im Referenzbereich, eine moderate Inflammation (C-reaktives Protein, Interleukin-6), eine ausgeglichene Flüssigkeitsbilanz und bei Schädel-Hirn-Trauma ein Hirndruck <15–20 mmHg oder fehlende Hirndruckzeichen im CCT ein akzeptables Operationsrisiko anzuzeigen.
Abstract
The pathophysiological consequences of accidental trauma have a phasic course as far as the immunomodulatory response is concerned. An operative trauma inflicted by a secondary surgical intervention is an additional burden. Depending on the inflammatory phase during which this secondary hit takes effect, homoeostasis may be impaired to varying degrees, even to the extent of causing multiple organ failure. Major operations within the first 2–3 days after trauma appear to involve a greater risk, particularly if they are performed while respiratory function is impaired (pO2/FiO2 ratio <280 mmHg), and should be postponed – whenever possible – until a later time. For surgical interventions after day 3 a pO2/FiO2 ratio above 280 mmHg, stable circulatory function, a platelet count above 100,000–150,000/µl, normal global coagulation tests, no more than moderate systemic inflammation as indicated by C-reactive protein or interleukin-6 levels, a normal fluid balance and, in the case of traumatic brain injury, absence of any signs of elevated intracranial pressure suggest an acceptable level of risk.
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Literatur
Bone RC (1996) Sir Isaac Newton, sepsis, SIRS, and CARS. Crit Care Med 24: 1125–1128
De Bel E, Goris R (2000) Systemic inflammation after trauma, infection, and cardiopulmonary bypass: is autodestruction a neccessary evil? In: Baue E, Faist E, Fry D (eds) Multiple organ failure – pathophysiology, prevention, and therapy. Springer, Berlin Heidelberg New York, pp 71–81
Ertel W, Keel M, Bonaccio M et al. (1995) Release of anti-inflammatory mediators after mechanical trauma correlates with severity of injury and clinical outcome. J Trauma 39: 879–885
Faist E, Baue AE, Dittmer H et al. (1983) Multiple organ failure in polytrauma patients. J Trauma 23: 775–787
Flohe S, Lendemans S, Schade F et al. (2004) Influence of surgical intervention in the immune response of severely injured patients. Intensive Care Med 30: 96–102
Galle C, De Maertelaer V, Motte S et al. (2000) Early inflammatory response after elective abdominal aortic aneurysm repair: a comparison between endovascular procedure and conventional surgery. J Vasc Surg 32: 234–246
Gebhard F, Pfetsch H, Steinbach G et al. (2000) Is interleukin 6 an early marker of injury severity following major trauma in humans? Arch Surg 135: 291–295
Lendemans S, Kreuzfelder E, Waydhas C et al. (2004) [Clinical course and prognostic significance of immunological and functional parameters after severe trauma]. Unfallchirurg 107: 203–210
Moore FA, Sauaia A, Moore EE et al. (1996) Postinjury multiple organ failure: a bimodal phenomenon. J Trauma 40: 501–510
Mutlu LK, Woiciechowsky C, Bechmann I (2004) Inflammatory response after neurosurgery. Best Pract Res Clin Anaesthesiol 18: 407–424
Napolitano LM, Ferrer T, McCarter RJ et al. (2000) Systemic inflammatory response syndrome score at admission independently predicts mortality and length of stay in trauma patients. J Trauma 49: 647–652
Nast-Kolb D, Waydhas C, Schweiberer L (1996) Marknagelung beim Polytrauma. Orthopade 25: 266–273
Nast-Kolb D, Waydhas C, Gippner-Steppert C et al. (1997) Indicators of the posttraumatic inflammatory response correlate with organ failure in patients with multiple injuries. J Trauma 42: 446–454
Offner P, Moore E (2000) Risk factors for MOF and pattern of organ failure following severe trauma. In: Baue E, Faist E, Fry D (eds) Multiple organ failure – pathophysiology, prevention, and therapy. Springer, Berlin Heidelberg New York, pp 30–43
Pape HC, Schmidt RE, Rice J et al. (2000) Biochemical changes after trauma and skeletal surgery of the lower extremity: quantification of the operative burden. Crit Care Med 28: 3441–3448
Pape HC, Van Griensven M, Rice J et al. (2001) Major secondary surgery in blunt trauma patients and perioperative cytokine liberation: determination of the clinical relevance of biochemical markers. J Trauma 50: 989–1000
Regel G, Pohlemann T, Krettek C et al. (1997) Frakturversorgung beim Polytrauma. Zeitpunkt und Taktik. Unfallchirurg 100: 234–248
Sauaia A, Moore FA, Moore EE et al. (1993) Pneumonia: cause or symptom of postinjury multiple organ failure? Am J Surg 166: 606–610
Scalea TM, Boswell SA, Scott JD et al. (2000) External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopedics. J Trauma 48: 613–621
Shoemaker WC, Appel PL, Bland R et al. (1982) Clinical trial of an algorithm for outcome prediction in acute circulatory failure. Crit Care Med 10: 390–397
Sido B, Teklote JR, Hartel M et al. (2004) Inflammatory response after abdominal surgery. Best Pract Res Clin Anaesthesiol 18: 439–454
Taeger G, Ruchholtz S, Waydhas C et al. (2005) Damage control orthopedics in multiple injured patients is effective, time saving and safe. J Trauma 59: 409–417
Talmor M, Hydo L, Barie PS (1999) Relationship of systemic inflammatory response syndrome to organ dysfunction, length of stay, and mortality in critical surgical illness: effect of intensive care unit resuscitation. Arch Surg 134: 81–87
Waydhas C, Nast-Kolb D, Jochum M et al. (1992) Inflammatory mediators, infection, sepsis, and multiple organ failure after severe trauma. Arch Surg 127: 460–467
Waydhas C, Nast-Kolb D, Kick M et al. (1994) Operationsplanung von sekundären Eingriffen nach Polytrauma. Unfallchirurg 97: 244–249
Waydhas C, Nast-Kolb D, Kick M et al. (1995) Postoperative Homöostasestörung nach unterschiedlich großen unfallchirurgischen Eingriffen beim Polytrauma. Unfallchirurg 98: 455–463
Waydhas C, Nast-Kolb D, Trupka A et al. (1996) Posttraumatic inflammatory response, secondary operations, and late multiple organ failure. J Trauma 40: 624–631
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Waydhas, C., Flohe, S. Kriterien der Operabilität. Trauma Berufskrankh 9, 177–181 (2007). https://doi.org/10.1007/s10039-007-1246-z
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DOI: https://doi.org/10.1007/s10039-007-1246-z