1 London, Canada 2 Leicester, UK
EditorI read the case report by Schupp and colleagues1 with interest and would like to commend them for their heroic effort. However, I want to make a comment. The authors have entitled their report Postoperative ECMO for severe intraoperative SIRS 10 hrs after multiple trauma. Having made such claims a few times in the text as well, they seem to misunderstand the concept of systemic inflammatory response syndrome (SIRS).
When the term SIRS was coined in 1992 by a consensus committee, it was clearly stated that physiological changes manifesting SIRS should represent an acute alteration from baseline in the absence of other known causes for such abnormalities.2 Dr Schupps patient could have had tachypnoea due to lung contusion and rib fractures, hypothermia due to massive blood transfusion and prolonged surgery, and tachycardia due to hypovolaemia, hypoxaemia and vasoactive drugs. What no one knows was whether this critically ill patient did mount an exaggerated inflammatory response or a minimal one. The authors were successful in achieving physiological homeostasis at the bedside. However, we simply do not know if this patient had a severe SIRS, and whether the extracorporeal membrane oxygenation (ECMO) really resolved a refractory immune response, and if so how and to what extent.
The concept of SIRS has achieved notoriety because of difficulty in its interpretation, and terms such as severe SIRS should be discouraged. Both immune paralysis3 and activation (exaggerated response) have been advocated as the pathogenesis of multiple organ dysfunction resulting from infection/inflammation. We still have little information on the inflammatory responses in critical illness and in particular when and why inflammation becomes detrimental. Terminology in sepsis has been a complex issue,4 and it is important that we try to understand it better.
R. Taneja
London, Canada
EditorThank you for the opportunity to reply to Dr Tanejas letter regarding our case report.1 This paper was meant to be a case report on the use of ECMO in a patient with severe multi-organ failure due to multitrauma. We therefore will not attempt to solve the complex nuances of inflammation terminology with this reply letter.
We agree that terms such as systemic inflammatory response syndrome (SIRS) have not been very helpful and have further complicated a field already burdened with excess terminology.5 As Drs Marshall and Taneja mentioned in their chapter on sepsis terminology, SIRS was defined as the clinical manifestations of systemic inflammation, independent of their cause.4 Although the consensus conference on definitions for sepsis and organ failure proposed SIRS as a concept, the final report included an operational definition of SIRS.2 The majority of critically ill patients will fit into the clinical SIRS criteria. This is the drawback of a broad definition and does not mean we do not understand the terminology. Initially, this patients tachypnoea was due to lung contusion and rib fractures, hypothermia due to massive transfusion and prolonged surgery, and tachycardia due to hypovolaemia, hypoxaemia and vasoactive drugs as Dr Taneja correctly points out. However, the intraoperative resuscitation process was ongoing for the 6 h duration of the procedure and continued after that in the intensive care unit. We were unable to establish metabolic and haemodynamic homeostasis with conventional resuscitation methods.
SIRS is a clinical diagnosis and does not need confirmation by laboratory tests, except for the white blood cell count in certain conditions. A raised level of cytokines and other inflammatory markers during severe trauma is a well-described phenomenon.6 Unfortunately, we did not have time during the resuscitation process to measure any inflammatory markers to confirm our clinical diagnosis. Any physician experienced in the resuscitation of a multitrauma patient will know that prolonged circulatory shock and resuscitation efforts lead to a primary multiple organ dysfunction syndrome (MODS), including such well-defined clinical conditions as acute lung injury, acute renal failure, disseminated intravascular coagulopathy, etc.2 The terminology dysfunction identifies this process as a condition in which organ function is not capable of maintaining homeostasis. In primary MODS, the participation of an abnormal and excessive host inflammatory response in both the onset and progression of the syndrome is not as evident as it is in secondary MODS. Secondary MODS develops, not in direct response to the insult itself, but as a consequence of a host response.
In our patient, most systems were in chaos for almost 12 h. With ECMO we managed to correct the hypothermia and metabolic acidosis without delay, and support the cardiorespiratory systems in a controlled way.
Understanding of the human inflammatory response is still incomplete. The unresolved debate on terminology reflects this evolutionary process.4
J. L. C. Swanevelder
M. Schupp
Leicester, UK
References
1 Schupp M, Swanevelder JLC, Peek GJ, Sosnowski AW, Spyt TJ. Postoperative extracorporeal membrane oxygenation for severe SIRS 10 h after multiple trauma. Br J Anaesth 2003; 90: 914
2 Bone RC, Balk RA, Cerra FB et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 1992; 101: 164455[Abstract]
3 Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med 2003; 348: 13850
4 Marshall JC, Taneja R. Terminology and conceptual challenges. In: Deitch EA, Vincent JL, Windsor A, eds. Sepsis and Multiple Organ Dysfunction. A Multidisciplinary Approach. London: Elsevier Science Ltd., 2002; 128
5 Vincent JL. Revised terminology on sepsis. In: Baue A, Berlot G, Gullo A, Vincent JL, eds. Sepsis and Organ Dysfunction. The Challenge Continues. Milano: Springer-Verlag Italia, 2000; 11521
6 Ertel W, Keel M, Bonaccio M, et al. Release of anti-inflammatory mediators after mechanical trauma correlates with severity of injury and clinical outcome. J Trauma 1995; 39: 87985[ISI][Medline]