The main findings of this study were: (1) functionally sizeable collateral channels are frequent between lobes in emphysema: given that there are bronchoscopic attempts to exclude lobes to emulate LVRS, the likelihood is that 66% of lobar occlusions will not result in significant volume loss due to the presence of these interlobar collaterals; and (2) the degree of heterogeneity on CT and V/Q scintigraphy does, in part, predict the likelihood of collaterals—that is, those judged to have homogeneous disease are highly likely to have interlobar collaterals.
The presence of collateral ventilation was first confirmed by Van Allen and colleagues in 1930. Collateral ventilation is present in the normal lung but its importance in the distribution of ventilation is negligible because the resistance to airflow is higher in collateral channels than in the airway.
24 Observations in necroscopic emphysematous human lungs, however, showed that the resistance to collateral airflow in the lungs of patients with emphysema is low in comparison with that in normal lungs.
17 Three levels of collateral ventilation have previously been described in human lungs: 1–2 μm pores of Kohn,
25 30 μm channels described by Lambert,
26 and 80–150 μm interbronchiolar communications in humans described by Martin.
27 Morrell
et al discovered that segmental collateral ventilation occurred to a much greater extent in the emphysematous lung than in the normal lung.
28Although surprisingly not described in the more recent reviews, the older medical literature provides some support for the concept of poorly characterised interlobar communications. Hogg
et al17 first considered the possibility of collateral ventilation in patients with emphysema, demonstrating intralobar collateral ventilation between segments and interlobar collateral ventilation across the major fissure in patients with emphysema. Rosenberg and Lyons demonstrated significant interlobar collateral ventilation occurring at physiological pressures in five excised lungs with emphysema and pneumonia. Furthermore, they carried out radioactive
133xenon studies on some of the lung preparations after the collateral flow measurements were made.
29 Other investigators have recently reported that ventilation scintigraphy using
133xenon performed on days 3 and 15 after placement of BLVR prostheses showed reduced and delayed wash in of
133xenon into the ostensibly occluded upper lobes and accelerated wash out of
133xenon from the non‐occluded lower lobes.
23 The faster wash out of the lower lobes and persistent upper lobe ventilation are most likely the result of diffusion of
133xenon into the upper lobes through interlobar collaterals.
We sought to identify factors that may help to predict patients with significant interlobar collateral ventilation. Van Allen
et al found that gas diffusion occurred easily within lobes but only crossed the fissure when the lobes were overdistended.
24 Our findings show that air might flow through interlobar collateral channels betweens lobes at physiological pressures and it is notable that all patients were hyperinflated. However, there was no statistical relationship between collateral ventilation and the extent of interlobar fissure or the exact degree of hyperinflation. In fact, a comparison between the collateral group and the no collateral group showed no significant difference in any demographic characteristic on pulmonary functional variables. In particular, our results did not indicate that collateral ventilation increased with age, as has previously been reported.
30 Interestingly, we found a significant relationship between collateral ventilation and radiological scores (p
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0.04). This finding suggests that interlobar collateral ventilation occurs to a much greater extent in homogeneous emphysema than in heterogeneous emphysema.
We recognise that our study has some limitations. Firstly, we analysed patients only at the severe end of the spectrum and used one or two lungs from included patients (although no differences were noted when repeat measures were removed, the sample size is inherently small). The other major issue is the lack of a “gold standard visual scoring system” regarding emphysema heterogeneity. Nuclear V/Q scintigraphy has proved useful in demonstrating the considerable heterogeneity of the pattern of emphysema.
31 However, when applying a semiquantitative scoring system of visual assessment of perfusion scintigrams, correlation between scores of perfusion heterogeneity and functional outcome has been weak.
32 The mismatch relationship between heterogeneity scores from chest CT scans and V/Q scintigraphy has two main implications: (1) it confirms that the two techniques measure different properties of the lungs—namely, structure and function, respectively—and therefore provide complementary information; and (2) the low prevalence of a homogeneous distribution in V/Q scintigraphy shows that the technique is relatively sensitive for subtle differences in regional lung function (as reflected by perfusion) even in patients in whom visual inspection of the chest CT scan suggests an even distribution of structural alterations by emphysema among all lung areas.
Much of the controversy surrounding LVRS involves the variability of the response by patients, limitations in the magnitude of the response, costs, and concerns about the duration of improvement. Air leak remains the major morbidity following LVRS. Knowledge of the precise incidence, extent, and aetiology of interlobar collaterals may be important in predicting the likely success of LVRS and innovative alternative strategies (such as bronchoscopic valves, prostheses, or glues) for severe emphysema.
Interlobar collateral ventilation in emphysema may explain clinically observed phenomena such as persistent air leaks following lobectomy or segmentectomy, the failure of lobes to collapse when selectively intubated in intensive care or during anaesthesia, and the development of giant bullae in some patients with emphysema.
33 They may also be relevant to the spread of infectious pathogens and malignant cells between lobes. More research is needed to find other techniques which will predict those patients without interlobar collateral ventilation who might be more likely to benefit from bronchoscopic lung volume reduction techniques and to link interlobar collateral ventilation with local/nodal lung cancer metastatic spread patterns.
In conclusion, it is apparent from the present study that interlobar collateral ventilation is an underrecognised significant phenomenon (66% in the present study) in severe emphysema that may have important pathophysiological correlates for a range of clinical circumstances. Although a comparison between the collateral and no collateral groups revealed no significant differences in any demographic, pulmonary function, or histopathological variables, interlobar collateral ventilation occurred to a much greater extent in those with radiologically homogeneous emphysema than in those with heterogeneous emphysema. Heterogeneity of emphysema may therefore predict patients with a significant or reduced risk of interlobar collateral ventilation. Future studies need to address the particular relevance of interlobar collaterals in the success of LVRS techniques.