Affiliations: Université Catholique de Louvain Brussels, Belgium,
University of Ottawa Ottawa Hospital Ottawa Health and Research Institute Ottawa, ON
Correspondence to: Franck Verschuren, MD, Service des Urgences, Clin Universitaires St. Luc, Avenue Hippocrate 10, Bruxelles B 1200, Belgium; e-mail: email@example.com
We read with interest the article by Dr. Rodger and coworkers in a recent issue of CHEST (July 2001)1 regarding the use of a bedside combination of plasma d-dimers and alveolar dead space measurement in excluding pulmonary embolism. The authors showed on 246 study patients that the adjunction of the capnographic measurement of the alveolar dead space to the d-dimer determination allowed the sensitivity to increase from 83 to 97.8% in ruling out pulmonary embolism without additional diagnostic testing.
The d-dimer assays used in the study (latex and whole-blood agglutination tests), even if the most extensively studied rapid d-dimer assays, may be subject to criticism for their suboptimal sensitivity (varying from 65 to 89%), especially since the emergence of new, rapid enzyme-linked immunosorbent d-dimer assays, which have been validated as screening tests for the exclusion of pulmonary embolism with a sensitivity of 99.5%.2–3 Consequently, the benefit of associating agglutination d-dimer tests and alveolar dead space fraction measurements in order to better rule out pulmonary embolism (sensitivity 97.8%) is similar to the performance of a rapid enzyme-linked immunosorbent d-dimer assay alone. Therefore, a new question arises to know if alveolar dead space determination with capnography brings some additional information in case of positive d-dimer values (> 500 ng/mL) with the rapid enzyme-linked immunosorbent assay.
As explained by Colp and Stein4in the editorial of the same issue of CHEST, we are concerned by the diagnostic performance of alveolar dead space measurement in excluding pulmonary embolism. In a recent multicenter study by Kline et al,5 the alveolar dead space fraction, determined with volumetric capnography, showed a low sensitivity (67%), probably because a proved pulmonary embolism may physiologically be associated with normal alveolar dead space due to a reflex hypocarbic bronchoconstriction or, in case of pulmonary infarction, atelectasis or small peripheral embolisms.
In conclusion, we believe that the interest of capnography as a screening test for pulmonary embolism has still to be evaluated, and that this very interesting article brings more questions than answers.
We agree that enzyme-linked immunosorbent d-dimer assays have been shown to have higher sensitivity than latex and whole-blood agglutination d-dimer assays.1 However, this higher sensitivity comes at a cost of lower specificity (excluding fewer patients without pulmonary embolism suspected of having pulmonary embolism), less rapid turnaround time, and capital expenditures to set up the enzyme-linked immunosorbent d-dimer assays that are not required for latex and whole-blood agglutination tests. Hence, in smaller hospitals, adoption of latex and whole-blood agglutination d-dimers is more realistic than enzyme-linked immunosorbent assays or rapid enzyme-linked immunosorbent d-dimer assays.
We share the concern of Dr. Verschuren and Dr. Thys that alveolar dead space measurement and these easily adoptable d-dimer assays do not have excellent sensitivity on their own. However, upon further validation, we are optimistic that the combination of low alveolar dead space fraction and negative d-dimers will be able to exclude pulmonary embolism at the bedside in the large proportion of patients with suspected pulmonary embolism.
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