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Trauma and Coagulopathy—Invited Critique

Trauma and Coagulopathy—Invited Critique When I first started reading “Trauma and Coagulopathy: A New Paradigm to Consider” by MacLeod, I was skeptical. I liked the “old” paradigm. Most trauma surgeons accept the theory that trauma-associated coagulopathy is a secondary phenomenon. Bleeding leads to coagulopathy, hypothermia, and acidosis, which make up the “lethal triad.” As each of these 3 components worsens after major trauma, they exacerbate one another and patients begin a downward spiral known as the “bloody vicious cycle.” The concept of abbreviated “damage-control” surgery to stop this sequence before irreversible physiologic exhaustion is the current tactic in cases of exsanguinating trauma. This approach makes intuitive sense and has been a way of life for my entire surgical career. It is a framework to educate fellows, residents, students, and staff in the clinical treatment of severely injured patients at trauma centers across around the world. However, on further consideration, I decided to seriously consider the new paradigm that coagulopathy is a primary event rather than a secondary phenomenon. The MacLeod article begins with a well-written literature review and summary of this current paradigm of coagulopathy and trauma. MacLeod then suggests the “new” paradigm based on some evidence showing coagulopathy is present immediately after trauma. The facts that patients have widely varying degrees of coagulopathy and that the coagulopathic response is unpredictable may also strengthen the argument. The new approach holds promise and leads to numerous thought-provoking questions. Are some patients more prone to bleed after major trauma? Why should genetic predisposition be relegated only to patients developing cancer or heart disease? Should our initial trauma bay laboratories include gene microarrays looking for clotting predisposition? Does a certain genetic profile predict which patients will respond to factor VIIa? Should certain patients be prescreened and wear “I’m a bleeder after trauma” medical alert bracelets? I suspect we will adopt MacLeod's new paradigm at some point in the future. However, this article does not provide a strong enough argument for making this radical shift right now. This article raises more questions than answers. Future generations of trauma surgeons may recognize this article as a classic reference from a forward-thinking trauma surgeon. They may scoff at our naiveté of the genetic predisposition for coagulopathy and our rudimentary treatments for nonsurgical bleeding. The new model is promising, but much supporting work remains to be done: basic science, translational studies, and prospective clinical trials. Until then, we should continue to teach about the “old” paradigm of secondary coagulopathy, the lethal triad, and the bloody vicious cycle. Correspondence: Dr Haut, Division of Acute Care Surgery: Trauma, Critical Care, Emergency, and General Surgery, Department of Surgery, The Johns Hopkins Hospital, 625 Osler, 600 N Wolfe St, Baltimore, MD 21287 (ehaut1@jhmi.edu). Financial Disclosure: None reported. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Surgery American Medical Association

Trauma and Coagulopathy—Invited Critique

Archives of Surgery , Volume 143 (8) – Aug 18, 2008

Trauma and Coagulopathy—Invited Critique

Abstract

When I first started reading “Trauma and Coagulopathy: A New Paradigm to Consider” by MacLeod, I was skeptical. I liked the “old” paradigm. Most trauma surgeons accept the theory that trauma-associated coagulopathy is a secondary phenomenon. Bleeding leads to coagulopathy, hypothermia, and acidosis, which make up the “lethal triad.” As each of these 3 components worsens after major trauma, they exacerbate one another and patients begin a downward spiral...
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Publisher
American Medical Association
Copyright
Copyright © 2008 American Medical Association. All Rights Reserved.
ISSN
0004-0010
eISSN
1538-3644
DOI
10.1001/archsurg.143.8.802
Publisher site
See Article on Publisher Site

Abstract

When I first started reading “Trauma and Coagulopathy: A New Paradigm to Consider” by MacLeod, I was skeptical. I liked the “old” paradigm. Most trauma surgeons accept the theory that trauma-associated coagulopathy is a secondary phenomenon. Bleeding leads to coagulopathy, hypothermia, and acidosis, which make up the “lethal triad.” As each of these 3 components worsens after major trauma, they exacerbate one another and patients begin a downward spiral known as the “bloody vicious cycle.” The concept of abbreviated “damage-control” surgery to stop this sequence before irreversible physiologic exhaustion is the current tactic in cases of exsanguinating trauma. This approach makes intuitive sense and has been a way of life for my entire surgical career. It is a framework to educate fellows, residents, students, and staff in the clinical treatment of severely injured patients at trauma centers across around the world. However, on further consideration, I decided to seriously consider the new paradigm that coagulopathy is a primary event rather than a secondary phenomenon. The MacLeod article begins with a well-written literature review and summary of this current paradigm of coagulopathy and trauma. MacLeod then suggests the “new” paradigm based on some evidence showing coagulopathy is present immediately after trauma. The facts that patients have widely varying degrees of coagulopathy and that the coagulopathic response is unpredictable may also strengthen the argument. The new approach holds promise and leads to numerous thought-provoking questions. Are some patients more prone to bleed after major trauma? Why should genetic predisposition be relegated only to patients developing cancer or heart disease? Should our initial trauma bay laboratories include gene microarrays looking for clotting predisposition? Does a certain genetic profile predict which patients will respond to factor VIIa? Should certain patients be prescreened and wear “I’m a bleeder after trauma” medical alert bracelets? I suspect we will adopt MacLeod's new paradigm at some point in the future. However, this article does not provide a strong enough argument for making this radical shift right now. This article raises more questions than answers. Future generations of trauma surgeons may recognize this article as a classic reference from a forward-thinking trauma surgeon. They may scoff at our naiveté of the genetic predisposition for coagulopathy and our rudimentary treatments for nonsurgical bleeding. The new model is promising, but much supporting work remains to be done: basic science, translational studies, and prospective clinical trials. Until then, we should continue to teach about the “old” paradigm of secondary coagulopathy, the lethal triad, and the bloody vicious cycle. Correspondence: Dr Haut, Division of Acute Care Surgery: Trauma, Critical Care, Emergency, and General Surgery, Department of Surgery, The Johns Hopkins Hospital, 625 Osler, 600 N Wolfe St, Baltimore, MD 21287 (ehaut1@jhmi.edu). Financial Disclosure: None reported.

Journal

Archives of SurgeryAmerican Medical Association

Published: Aug 18, 2008

Keywords: blood coagulation disorders,wounds and injuries

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