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Re: Fatal Thrombosis during Cardiac Surgery for Endocarditis: possible role of subclinical DIC
- Dr. Eva Kottenberg-Assenmacher, Prof. Dr. Jürgen Peters, Professor of Anesthesiology and Intensive Care Therapy, Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen (24 January 2007)
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Fatal Thrombosis during Cardiac Surgery for Endocarditis: possible role of subclinical DIC
- John Augoustides MD, FASE (4 January 2007)
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Dr. Eva Kottenberg-Assenmacher, Staff Anesthesiologist Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Prof. Dr. Jürgen Peters, Professor of Anesthesiology and Intensive Care Therapy, Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen
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To the editor: We appreciate the interest of Dr. Augoustides in our work and completely agree with his main conclusion that it is desirable to report such cases when they happen and retain blood samples for later analysis (1). However, a few comments appear appropriate. Dr. Augoustides suggests that both hypothermia and/or administration of aprotinin could have served as trigger for disseminated intravascular coagulation (DIC) followed by platelet activation. Furthermore, he submits that this is probably not the whole explanation and the answer may lie in genetic predispositions. In response, we like to point out that 1) the complication in our patient did not occur during hypothermia and that hypothermia itself was very mild (blood temperature during cardiopulmonary bypass: 32 °C) (2). Furthermore, the patient had received aprotinin already at the beginning of the case making it unlikely as a trigger. Finally, we have clearly documented in our paper that disseminated thrombosis was mediated by antibody related platelet activation. Certainly, this rules out hypothermia as a major mechanism. Thus, while all the circumstances associated with major thrombosis as mentioned by Dr. Augoustides may play a role somewhere, somehow, and in somebody, one should not jump to the conclusion that the sum of multiple predisposing circumstances makes up for a real mechanism. In fact, this would blur our vision for elucidating genuine, potentially rare molecular mechanisms for evoking catastrophic thrombosis, as described in our report. Accordingly, we wholeheartedly agree with Dr. Augoustides`s conclusion, i.e., “report these cases when they happen, and retain blood samples for analysis” (1,2). 1. Augoustides J: Fatal thrombosis during cardiac surgery for endocarditis: possible role of subclinical DIC. E-Letter 2. Kottenberg-Assenmacher E, Volbracht L, Jakob H, Greinacher A, Peters J: Disseminated intravascular clotting associated with Fc-receptor IIa-mediated platelet activation in a patient with endocarditis after aortic valve replacement. Br J Anaesth 2006; 97: 630-633 Conflict of Interest:None declared |
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John Augoustides MD, FASE, Anesthesiologist Hospital of the University of Pennsylvania, Philadelphia, PA, USA
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I read with great interest the recent report by Kottenberg- Assenmacher et al., detailing a case of fatal intravascular clotting after aortic valve replacement for endocarditis.(1) In this case, the authors have demonstrated that the mechanism was massive platelet activation that occurred shortly after administration of protamine, aprotinin, and fresh frozen plasma. The likely platelet trigger, according to the authors, was subclinical activation of coagulation by bacterial proteins. This catastrophic complication has been decribed not only in deep hypothermic circulatory arrest but also in endocarditis with clinical disseminated intravascular coagulation (DIC).(2;3) In both cases, aprotinin was utilized, and the massive intravscular coagulation occurred shortly affter protamine administration, just as in the abovementioned report. An unifying hypothesis for all three cases is DIC as the trigger for platelet activation. Deep hypothermic circulatory arrest can trigger DIC, while endocardits would have been the DIC trigger in the remaining two cases.(4) However, this is not probably not the whole explanation, given that most cardiac surgical patients with these profiles do not develop this complication. Perhaps the answer lies in genetic predispostion, an etiology that will no doubt be eluciadted in the future as the genetics of coagulation are worked out, and genetic polymorphisms are correlated with thrombotic risk. Clinicians should continue to report these cases when they happen, and retain blood samples for analysis as outlined by Kottenberg- Assenmacher et al. Perhaps as well, consultation with a hematologist would effectively focus sample analysis in the individual case, and thus help to elucidate the aetiology of this devastating complication. References 1. Kottenberg-Assenmacher E, Volbracht L, Jakob H, et al.: Disseminated intravscular clotting associted with Fc-receptor IIa-mediated platelt activation in a patient with endocarditis after aortic valve replacement. Br J Anaesth 2006; 97: 630-3 2. Augoustides JGT, Lin J, Gambone AJ, et al.: Fatal thrombosis in an adult after thoracoabdominalaneurysm repair with aprotinin and deep hypothermic circulatory arrest. Anestesiology 2005; 103: 215-16 3. Augoustides JG, Kilbaugh T, Harris H, et al.: Fatal thrombosis after mitral valve replacement for endocarditis: aprotinin and disseminated intravascualr coagulation. Anesthesiology 2006; 104: 213 4. Wilde JT: Hematological consequences of profound hypothermic circulatory arrest and aortic dissection. J Card Surg 1997; 12: 210-6 Conflict of Interest:None declared |
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