Fatal pulmonary emboli in hospitalised patients: a necropsy review. Replies

<p>We read with interest the recent article by Alikhan et al , in which they reviewed necropsy reports to find out the number of deaths due to fatal pulmonary embolism in hospitalised patients.[1] There seem to be a number of confusions in this paper.<br>1. Acute infection was the most common medical illness found in patients who had died from pulmonary embolism, in particular respiratory infections. The authors state that the pathophysiology of venous thromboembolism in the presence of acute infection remains to be fully defined and then quote recent evidence that respiratory viruses are capable of infecting endothelial cells and causing a shift from anti- coagulant to pro-coagulant activity.[2] Such a proposed mechanism would presumably increase the likelihood of pulmonary thrombosis, not thromboembolism from deep venous thromboses.<br>2. The authors recognise that without denominator numbers for the surgical and medical patient groups, no interpretation is possible regarding the actual incidence of fatal pulmonary embolism. However, they themselves then go on to make a number of comparisons between surgical and “non-surgical” groups.<br>3. Pulmonary emboli were recorded as the cause of death when the necropsy report stated that embolism was the main or contributing cause of death. Many things get written down as contributing towards death, as any pathologist knows. The authors also state that it is difficult to distinguish between fatal, contributory, and incidental emboli when the definitions and interpretations are based on pathologists’ opinions over a long time period. One obvious way to address this difficulty would be for the authors to ask a pathologist to help them interpret the necropsy reports.</p> <p><br>References<br>1. Alikhan R, Peters F, Wilmott R, et al. Fatal pulmonary emboli in hospitalised patients: a necropsy review. J Clin Pathol 2004;57:1254-7.<br>2. Visseren FL, Bouwman JJ, Bouter KP, et al. Procoagulant activity of endothelial cells after infection with respiratory viruses. Thromb Haemost 2000;84:319-24.