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System Director, Medical Service, North Florida/South Georgia Veterans Health System, and Professor and Vice-Chairman, Department of Medicine, University of Florida.
Correspondence to: Craig S. Kitchens, MD, Veterans Affairs Medical Center, 1601 SW Archer Road, Gainesville, FL 32608-1197
As reported by Brickey and Lawlor in this issue of CHEST (see page 1667), a porcine experimental model was established to observe iatrogenic hemorrhage following transbronchial forceps biopsy (TBBx) in animals having a prolonged international normalized ratio (INR) as a result of receiving warfarin. Their porcine model has proved to be physiologically similar to the human cardiopulmonary vascular anatomy and physiology, as well as to the hemostatic system. In their first phase, these Air Force intensivists set out to determine at which INR level the animals bled following TBBx. In the second phase, they planned to determine what therapeutic maneuvers would be efficacious in the treatment and/or reversal of hemorrhage when that threshold INR level was reached and TBBx carried out. This was done in a manner in which the bronchoscopist was blinded to all therapeutic and laboratory data. Of interest to this hematologist, a preconceived notion had infiltrated its way into the design: Brickey and Lawlor were intuitively sure that there would be an answer to phase 1 which would permit them to move on soon to the more important phase 2.
Most hematologists have wrestled with the problem of patients with extraordinarily strong indications for warfarin (eg, patients with prosthetic heart valves, those with extreme hypercoagulability, or those with ongoing thrombotic episodes1 who have their anticoagulation stopped by some practitioner before an invasive procedure, whether it is cardiac catheterization, esophagogastroduodenoscopy, colon-oscopy, liver biopsy, bronchoscopy, or dental extraction.2 Such practitioners are absolutely convinced that patients who are on modern therapeutic anticoagulation will experience massive uncontrolled hemorrhage following an invasive procedure, even though there are no reports to substantiate that prejudice. While it is true that there is a baseline underlying hemorrhage rate with any of these procedures, there are no data to attribute that rate to therapeutic anticoagulation. Most bleeding that occurs is either technical or, especially, related to biopsy of a tumor, which is known to be the primary culprit when one analyzes patients who hemorrhage following biopsy.3 On the other hand, there are several reports of serious thrombosis following cessation of anticoagulant therapy in patients who are anticoagulated for good reason.1 ,4 When interventionists are asked for justification to either attenuate or stop anticoagulation, the only argument given is, "this is the way we have always done it." This approach is no longer tolerable in the era of evidence-based medicine.
The report by Brickey and Lawlor involves experimental animals, yet it complements an earlier article in CHEST5 in which humans undergoing TBBx did not experience hemorrhage, despite their abnormal prothrombin and partial thromboplastin times.
In the Brickey and Lawlor study, the animals did not experience bleeding from the biopsies despite the supratherapeutic INRs. Two animals did exsanguinate (one with an INR of 11.2, the other with an INR of 13.6) but spontaneously from bleeding ovarian cysts. Therefore, these INRs were of hemorrhagic concern but not because of the TBBx. This is most likely due to an intense amount of local tissue factor that is generated from traumatized tissue near the biopsy, which results in generation of thrombin sufficient to cause effective hemostasis despite decreased levels of vitamin K-dependent factors.
It is a leap to go from studies using animals that are otherwise well—and are not aged, atherosclerotic, or riddled with metastases—to the clinical bedside, yet articles such as this by Brickey and Lawlor and the one by Kozak and Brath5 certainly go a long way towards denting the heretofore immutable stance of most bronchoscopists that the INR must be normal. This hematologist is certain that far more morbidity and mortality have occurred by stopping anticoagulant therapy than by the biopsy of patients who are using anticoagulants and have INRs within the therapeutic range or particularly the lower end of the therapeutic range. It is already clear that major orthopaedic surgery6 can be done when the patient has an INR of 1.5 to 2.0. Therefore, it is appropriate not to cancel TBBx simply because the patient is receiving therapeutic anticoagulants. Indeed, as stated by Brickey and Lawlor, patients will continue to bleed with TBBx at a rate somewhere between 1 and 10%, but that baseline hemorrhagic rate is a technical, not hemostatic, fact.
The final point is that Brickey and Lawlor were unable to go to phase 2 of their experiment because they were unable to find any INR within a reasonable range that correlated with enough hemorrhage to determine what therapeutic maneuvers would decrease bleeding if it occurred.
References
This article has been cited by other articles:
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  K. Chinsky Bleeding Risk and Bronchoscopy: In Search of the Evidence in Evidence-Based Medicine Chest, June 1, 2005; 127(6): 1875 - 1877. [Full Text] [PDF]
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F. J.F. Herth, H.D. Becker, and A. Ernst Aspirin Does Not Increase Bleeding Complications After Transbronchial Biopsy Chest, October 1, 2002; 122(4): 1461 - 1464. [Abstract] [Full Text] [PDF]
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