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Ultrasound lung comets: the shape of lung water

2012; Elsevier BV; Volume: 14; Issue: 11 Linguagem: Inglês

10.1093/eurjhf/hfs157

1879-0844

Eugenio Picaño, Luna Gargani,

Hemodynamic Monitoring and Therapy

This editorial refers to ‘Utility of lung ultrasound in predicting pulmonary and cardiac pressures’, by E. Platz et al., published in this issue on pages 1276–1284. ‘What shape is water?’ ‘Water doesn't have any shape!’ I said, laughing. ‘It takes the shape you give it’(Andrea Camilleri, The Shape of Water. Sellerio Editore, Palermo, 1994) For a long time, cardiologists thought that the lung was off-limits for ultrasound, and this is still standard textbook knowledge. In Harrison's classical textbook ‘Principles of Internal Medicine’, it is clearly stated that ‘because ultrasound energy is rapidly dissipated in air, ultrasound imaging is not useful for evaluation of the pulmonary parenchyma’.1 However, this is not entirely true, and lung ultrasound can offer surprising clinical dividends in several challenging conditions, from pulmonary oedema to interstitial lung fibrosis, from acute respiratory distress syndrome (ARDS) to pleural effusion and pulmonary embolism.2 In pulmonary oedema, the presence of water in the lung opens up the previously locked pulmonary acoustic window and allows cardiologists to gain spectacular insight into pulmonary congestion, which can be directly imaged and semi-quantified.3–5 The study by Platz et al.6 confirms that B-lines (also called ultrasound lung comets) are a simple, low-cost, low-technology, practical sign of extravascular lung water (EVLW). The authors show that correlation with pulmonary pressure is present—but not strong. This is not surprising, is broadly consistent with previous studies, and can be better understood if we consider the heterogeneous nature of B-lines, which can occur in three different conditions: heart failure, ARDS, and lung interstitial fibrosis. In patients with heart failure, a marked increase in pulmonary pressure and pulmonary capillary wedge pressure can cause ultrastructural changes in the walls of pulmonary capillaries, resulting in interstitial and alveolar oedema.7 In this model, the presence of B-lines is a marker of pulmonary congestion (presence of EVLW), which is somewhat related to increased pulmonary capillary wedge pressure (‘haemodynamic congestion’) and to signs and symptoms of congestion (‘clinical congestion’). However, this relationship is not strict, since the three types of congestion measure different aspects.8 In patients with impending acute heart failure, there is a long incubation period of days or weeks characterized by lung water accumulation, and in the congestion cascade, pulmonary oedema can be detected well before the appearance of clinical signs of congestion. Detection and treatment of pulmonary congestion before it is clinically evident may prevent hospitalization and progression of heart failure. The correlation between B-lines and invasively assessed pulmonary capillary wedge pressure was moderate (r = 0.48, P < 0.001) in 20 patients studied by Agricola et al. before and after cardiac surgery, in a particularly favourable setting, with each patient acting as his/her own control.9 In a larger, unselected population of 340 inpatients admitted to an adult cardiology department, Frassi et al. observed a significant but weak correlation between B-lines and pulmonary artery systolic pressure derived from echocardiography (r = 0.26, P < 0.0001).10 In 75 haemodialysis patients, Mallamaci et al. reported a mild association with pulmonary pressure (r = 0.32, P = 0.006).11 The two parameters of pulmonary (B-lines) and haemodynamic (pulmonary artery systolic or wedge pressure) congestion are therefore associated, but their correlation is very limited, as also reported by Platz et al.,6 with an r-value of 0.48. In everyday practice, a patient can show very variable degrees of B-lines (from absent to severe) for any given level of pulmonary artery pressure, depending on the duration of history of heart failure, speed of changes in pulmonary pressure, concomitant mitral insufficiency, characteristics of the alveolar–capillary membrane, oncotic pressure, lymphatic drainage capacity, and so on. On the other hand, a patient can have B-lines without haemodynamic congestion, such as in ARDS and in lung interstitial fibrosis. In the previously described heart failure model, B-lines are usually accompanied by a rise in E/e′, which is a marker of raised left ventricular filling pressures.10 Another interesting and pathophysiologically different model is acute lung injury–acute respiratory distress syndrome (ALI-ARDS), which is characterized by normal left ventricular filling pressures and normal left ventricular ejection fraction (Table 1). Recently, lung ultrasound has been applied to a pig model of oleic acid-induced lung injury, which mimics human ARDS.12 B-lines unmasked accumulation of histologically verified EVLW very early in the course of lung injury in pigs, even at a stage when no changes in haemogasanalytical parameters could be observed. In humans, B-lines can identify clinically silent pulmonary oedema in elite apnoea divers, triathlon athletes after a race, and in recreational climbers,13 suggesting again that clinical symptoms are only the tip of the iceberg of pulmonary oedema, even outside the acute heart failure syndrome. B-lines may arise not only from water-thickened but also from fibrosis-thickened subpleural septa, which are an important sign of the pulmonary interstitial syndrome, for instance in interstitial lung disease of systemic sclerosis.14 Fibrotic B-lines are diuresis resistant, whereas watery B-lines of pulmonary oedema are reduced by diuretics and/or dialysis within minutes or hours.4,11 They may be detected in patients with very early systemic sclerosis, and correlate very nicely with interstitial lung disease observed with high-resolution computed tomography (CT) scan of the chest. It is an attractive biomarker for the frequent evaluation of pulmonary involvement in patients at high risk of developing pulmonary fibrosis, since it is radiation free and inexpensive, compared with CT.15 B-lines are the shape of lung water—but they can also be the shape of interstitial fibrosis. They are not mere meteors in the ultrasound diagnostic sky, but are here to stay as part of the standard armamentarium of cardiologists as well as intensivists, nephrologists, rheumatologists, and sports physicians. They are associated with pulmonary hypertension in heart failure, but identify a different variable from haemodynamic congestion: it is water, not pressure. It is also an appealingly simple sign to learn and to teach. From a technical viewpoint, in the echocardiographic cursus studiorum where 2D echo represents elementary school, Doppler-echo secondary school, and stress echo university, B-lines correspond to kindergarten. Still, much remains to be done for a full translation of this sign from echo lab to bedside. At present, we need a better understanding of the underlying physics, more standardized methodology and analysis, clear definition of the prognostic impact in different subsets, and outcome studies with B-line-driven therapy compared with a standard approach. At least one large-scale, prospective, randomized trial is already in progress in high-risk chronic kidney disease patients with heart failure and renal insufficiency and on dialysis—the LUST Trial (Lung water by UltraSound guided Treatment to prevent death and cardiovascular complications in high-risk end-stage renal disease patients with cardiomyopathy), coordinated by eminent nephrologist Carmine Zoccali from Reggio Calabria, Italy, funded by the European Renal Association-European Dialysis and Transplant Association for ∼1 million Euros and involving >30 nephrology–cardiology centres across Europe. The results of this study will be crucial eventually to incorporate B-lines into our clinically oriented diagnostic algorithms. Conflict of interest: none declared.