Zusammenfassung
Ziel: Bei der Therapie einer Hypoxämie beim schweren akuten Lungenversagen (ARDS) mit inhalativem Stickstoffmonoxid (iNO) reagiert aus bisher ungeklärten Gründen ein Teil der ARDS-Patienten nicht mit einer klinisch relevanten Verbesserung der Oxygenierung (Nonresponder). Wir untersuchten, ob die Effekte von iNO mit radiologischen Kriterien des Lungenschadens korrelieren. Material und Methoden: Bei n = 25 ARDS-Patienten, die innerhalb von 72 Stunden vor Beginn einer iNO-Therapie ein Thorax-CT erhalten hatten, wurden retrospektiv der prozentuale Anteil des geschädigten Lungengewebes und die Grenze zwischen geschädigtem und nicht betroffenem Lungengewebe ausgemessen und letztere wiederum in Relation zum Umfang der Pleura viszeralis gesetzt. Die resultierende relative Grenzlinienlänge wurde mit der durch iNO induzierten Verbesserung der arteriellen Oxygenierung (ΔPaO2 ) in Beziehung gesetzt. Ergebnisse: Bei n = 6 Nonrespondern auf iNO (ΔPaO2 < 10 %) fanden wir eine signifikant verringerte Grenzlinie zwischen nicht betroffenem und geschädigtem Lungengewebe als Maß für das Vorliegen größerer kohärent pathologisch veränderter Lungenareale im Vergleich zu n = 19 Respondern auf iNO (ΔPaO2 > 10 %) (0,09 ± 0,02 vs. 0,21 ± 0,01; p < 0,05). Es fand sich eine moderate und signifikante Korrelation zwischen dem durch iNO induzierten ΔPaO2 und der relativen Grenzlinienlänge bei allen untersuchten ARDS-Patienten (R = 0,59; p < 0,01). Schlussfolgerung: Unsere Ergebnisse zeigen, dass bei Patienten mit ARDS die im CT darstellbare Verteilung von geschädigtem Lungenparenchym signifikant mit der Response auf iNO korreliert.
Abstract
Purpose: Inhaled nitric oxide (iNO) is an effective therapy for severe hypoxemia in most patients with acute respiratory distress syndrome (ARDS). For unknown reason, a subset of ARDS patients does not respond favorably to iNO therapy. We hypothesized that radiological manifestation of lung injury may be related to iNO response. Materials and Methods: We retrospectively analyzed data from n = 25 ARDS patients who received iNO, and underwent chest CT within 72 h prior to inhaled treatment. The morphology of coherently pathologic lung tissue was characterized by the length of the borderline between consolidated, infiltrated and atelectatic lung tissue and radiologically normal lung tissue. This quantity was expressed as relative fraction of the visceral pleural circumference and averaged over all CT slices. Furthermore we semiquantitatively determined the total volume of consolidated lung tissue as part of the whole lung. Results: In n = 6 non-responders to iNO (ΔPaO2 < 10 %), we determined a short relative borderline between normal and consolidated lung tissue due to the presence of large and coherently consolidated lung regions. In n = 19 iNO responders (ΔPaO2 > 10 %), we found significantly less coherently consolidated lung tissue evidenced by an increased relative borderline when compared to iNO non-responders (0.09 ± 0.02 vs. 0.1 ± 0.01; P < 0.05). Moreover, there was a moderate and significant correlation between ΔPaO2 induced by iNO and the relative borderline in all patients studied (R = 0.59; P < 0.05). Total fraction of consolidated lung tissue volume was not different between iNO non-responders and responders (60 ± 3 % vs. 54 ± 2 % n. s.). Conclusion: Our data demonstrate that the gross morphological distribution of pathological lung tissue influences iNO response in ARDS. Inhaled NO was most beneficial in injured lungs characterized by many small consolidated areas surrounded by normal lung tissue. The increased borderline between pathologic and normal lung tissue offers additional possibility for iNO to divert blood flow from shunt areas to ventilated lung regions, which consequently improves arterial oxygenation.
Key words
Acute respiratory distress syndrome - inhaled nitric oxide - responders - computed tomography - consolidated lung tissue
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1 R. R. und T. B. trugen in gleichem Umfang zu dieser Studie bei.
Dr. Rainer Roettgen
Klinik für Strahlenheilkunde, Charité, Campus Virchow-Klinikum, Universitätsmedizin Berlin
Augustenburger Platz 1
D-13353 Berlin
Phone: ++ 49/30/4 50-55 70 02
Fax: ++ 49/30/4 50-55 79 00
Email: r.roettgen@t-online.de