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Daniel A. Lichtenstein, MD, FCCP; Gilbert A. Mezière, MD
Author and Funding Information

Affiliations: Dr. Lichtenstein is affiliated with the Medical ICU at Hospital Ambroise-Paré. Dr. Mezière is affiliated with the Medicosurgical ICU, Centre Hospitalier de Meulan-les Mureaux.

Correspondence to: Daniel A. Lichtenstein, MD, FCCP, Service de Réanimation Médicale, Hôpital Ambroise-Paré, F-92100 Boulogne (Paris-Ouest), France; e-mail: dlicht@free.fr


Financial/nonfinancial disclosures: The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;136(6):1706-1707. doi:10.1378/chest.09-2550
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To the Editor:

We thank Drs. Reissig and Kroegel for their interest in our recently published article in CHEST (July 2008)1 on the BLUE-protocol. From their comments, we assume that they think we omitted the consideration of parenchymal anomalies, especially in cases of embolism, yielding conclusions that are erroneous.

We would remind Drs. Reissig and Kroegel that the initial step in our methodology was a purely descriptive analysis of the whole lung surface (see Table 2 in our article1). In the second step, based on the elaboration of profiles, specific territories could be, in appropriate cases, deliberately deleted. Therefore, in 53% of cases, analysis of the anterior wall alone was sufficient for establishing diagnoses (ie, pulmonary edema, embolism, pneumothorax, and pneumonia). Consequently, the criticism by Drs. Reissig and Kroegel that we may have omitted ultrasound abnormalities is unfounded.

Confusion about this issue arose because our notion of the profile was not considered. Therefore, when Drs. Reissing and Kroegel refer to the “predominant A-lines” in our study, or to “sharply demarked lesions” in multicenter studies, the territories are not specified. In the BLUE-protocol, the A-profile considered the anterior wall alone, regardless of possible posterior anomalies, and was actually the profile seen in 95% of cases of massive embolism.

Regarding now the comments of Drs. Reissig and Kroegel on the normal lung surface, apart from patients without lung disease, this pattern can be seen in: (1) patients with asthma/COPD; (2) a “few cases of strictly central localized pneumonia” (this situation, which is theoretically possible, is unlikely to occur in critically ill patients, in whom 98.5% of consolidations are pleural-based2); and (3) a “few cases of strictly central localized PE [pulmonary embolism].” If “PE” means “infarction,” these cases are likely rare and not severe (as in the case of pneumonia mentioned above); therefore, they were not included in the BLUE-protocol. If “PE” means “embolism,” we do not agree with Drs. Reissig and Kroegel: the term “central” or “proximal,” precisely defines massive embolism. This second confusion comes from the fact that both types of patients (ie, patients with nonsevere vs severe PE) generate a normal anterior lung surface (ie, the A-profile), placing patients with severe PE in our decision tree for embolism.

Third, we did not disregard the excellent articles by Reissig and Mathis (actually cited in references 37 and 40, respectively, in our article1); all the more, because we read with care studies dealing with lung ultrasound. Multicenter studies3 have demonstrated a 74% sensitivity for pleural-based lesions. We actually analyzed the posterior wall in patients with massive embolism; postero-lateral alveolar-pleural syndrome (PLAPS) was found in 52% of cases (see Table 2 in our article1). What is the meaning of these cases of PLAPS? Infarction is known to be rare in patients who have experienced massive embolism, with proximal obstruction seen early in the course of disease.4 An embolism creates a surfactant alteration and local bronchospasm, which generate small atelectases early in the course of the embolism.4 Since we are unable to distinguish small atelectases from genuine infarctions using ultrasound, we suppose that the cases of PLAPS seen in our patients were due mainly to atelectases, and not to infarctions. The posterior location of the atelectases was possibly a function of the ventilation/perfusion ratio. Even in patients with nonsevere disease, multicenter studies3 have underlined the rarity of anterior lesions in patients with embolism.

So, why did we not integrate PLAPS into the diagnosis of embolism? In the BLUE-protocol, we demonstrated that PLAPS was common in patients with pulmonary edema (all cases), pneumonia (most cases), and embolism (one-half of cases), and were therefore completely devoid of specificity for embolism. Considering that the occurrence of PLAPS indicates the presence of embolism, as Drs. Reissig and Kroegel suggest, would have definitely yielded irrelevant results.

We must point out that the results of multicenter studies3 cannot be extrapolated to our study, and vice versa. In the study by Mathis et al,3 pleural-based lesions yield a specificity of 95%, but this was explained by the analysis of control subjects (subjects with suspected embolism). Although the final diagnosis of these control subjects was not specified, we infer that they rarely included cases of pulmonary edema or pneumonia, since their rate of ultrasound lesions was only 5%; in the BLUE-protocol, 57% of patients had pulmonary edema or pneumonia. Moreover, the cases of embolism in the study by Mathis et al3 were not severe; it is known that the frequency of infarctions is an inverse function of the severity of embolism. In addition, the patients in the study by Mathis et al3 benefited from preselection, an efficient tool that improves accuracy; whereas, patients in the BLUE-protocol were not selected for one particular cause of dyspnea.

Last, surprisingly, Drs. Reissig and Kroegel write that our conclusions “may be drawn from clinical findings alone,” as if the diagnoses of the critically ill patients were clinically obvious. This is not our experience as intensivists. Even if it was true (making ultrasound useless), their criticism regarding our “questionable specificity/sensitivity” is unfounded, since our results were extracted neutrally, independent of any clinical data. Remember that the BLUE-protocol has the advantage of immediate diagnosis, with high accuracy, which is its primary purpose.

We hope these comments will clear up our differences with Drs. Reissig and Kroegel. We are glad to see that they are developing, as are we, a new tool in a field that is currently little known.

Lichtenstein D, Mezière G. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134:117-125. [PubMed] [CrossRef]
 
Lichtenstein D, Lascols N, Mezière G, et al. Ultrasound diagnosis of alveolar consolidation in the critically ill. Intensive Care Med. 2004;30:276-281. [PubMed]
 
Mathis G, Blank W, Reissig A, et al. Thoracic ultrasound for diagnosing pulmonary embolism. Chest. 2005;128:1531-1538. [PubMed]
 
Moser KH. Thrombo-embolic diseases. Harrison's principles of internal medicine. 1998;11th ed New York, NY McGraw-Hill:1105-1111
 

Figures

Tables

References

Lichtenstein D, Mezière G. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134:117-125. [PubMed] [CrossRef]
 
Lichtenstein D, Lascols N, Mezière G, et al. Ultrasound diagnosis of alveolar consolidation in the critically ill. Intensive Care Med. 2004;30:276-281. [PubMed]
 
Mathis G, Blank W, Reissig A, et al. Thoracic ultrasound for diagnosing pulmonary embolism. Chest. 2005;128:1531-1538. [PubMed]
 
Moser KH. Thrombo-embolic diseases. Harrison's principles of internal medicine. 1998;11th ed New York, NY McGraw-Hill:1105-1111
 
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