Estimation of diaphragm length in patients with severe chronic obstructive pulmonary disease

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Abstract

In patients with advanced chronic obstructive pulmonary disease (COPD) diaphragm function may be compromised because of reduced muscle fibre length. Diaphragm length (LDi) can be estimated from measurements of transverse diameter of the rib cage (DRc) and the length of the zone of apposition (LZapp) in healthy subjects, but this method has not been validated in patients with COPD. Postero-anterior chest radiographs were obtained at total lung capacity (TLC), functional residual capacity (FRC) and residual volume (RV) in nine male patients with severe COPD (mean [S.D.]; FEV1, 23 [6] %pred.; FRC, 199 [15] %pred.). Radiographs taken at TLC were used to identify the lateral costal insertions of the diaphragm (LZapp assumed to approach zero at TLC). LDi was measured directly and also estimated from measurements of LZapp and DRc using a prediction equation derived from healthy subjects. The estimation of LDi was highly accurate with an intraclass correlation coefficient of 0.93 and 95% CI of ∼±8% of the true value. LDi decreased from 426 (64) mm at RV to 305 (31) mm at TLC. As there were only small and variable changes in DRc across the lung volume range, most of the LDi changes occurred in the zone of apposition. Additional studies showed that measurements of LDi from PA and lateral radiographs performed at different lung volumes were tightly correlated. These results suggest that non-invasive measurements of LZapp in the coronal plane (e.g. using ultrasonography) and DRc (e.g. using magnetometers) can be used to provide an accurate estimate of LDi in COPD patients.

Introduction

The effectiveness of the diaphragm as an inspiratory muscle in the face of the large increase in functional residual capacity (FRC) that occurs in advanced chronic obstructive pulmonary disease (COPD) is controversial (De Troyer, 1997). While many studies of transdiaphragmatic pressure (PDi) during tidal breathing have been made in COPD (Sharp et al., 1977, Druz and Sharp, 1982, Levine et al., 1988, Martinez et al., 1990) so far it has not been possible to estimate the accompanying dynamic changes in diaphragm length (LDi). The nearest approach has been to make static measurements of LDi at different lung volumes. Most measurements have been made using plain chest radiographs (Braun et al., 1982, Loring et al., 1985, Rochester and Braun, 1985, Sharp et al., 1986, Petroll et al., 1990). Scans using either computerised tomography (CT; Whitelaw, 1987, Cassart et al., 1997, Pettiaux et al., 1997) or magnetic resonance imaging (MRI; Gauthier et al., 1994) allow three-dimensional reconstruction of the whole diaphragm; unfortunately the time resolution of both techniques is poor (<1 Hz) and studies can only be made with the subject lying. Cine-radiography has better time resolution (around six frames/sec) and has been used to a limited extent (Wade, 1954, Gandevia et al., 1992) but entails significant radiation exposure.

To measure LDi (muscle and central tendon) the lengths of the zones of apposition of the diaphragm against the chest wall on the right and left sides (LZapp,r and LZapp,l) respectively, and the cross-sectional lengths of the two domes are summed. On radiographs the costal insertions of the diaphragm in the coronal plane are assumed to attach to the rib at or just below the caudal limit of the costo-phrenic angle at total lung capacity (TLC). With CT and MRI the origin has been assumed from anatomical land marks or external markers have been applied to the skin. All three imaging techniques can be used to measure LDi at TLC and at smaller lung volumes.

Loring et al. (1985) suggested that the length of the right and left domes in the mid-axillary coronal plane could be estimated from the internal diameter of the rib cage (DRc) in that plane plus an additional length which reflected the curvature of the domes. They obtained postero-anterior radiographs in three normal subjects at three different lung volumes. The effect of dome curvature could be expressed by multiplying DRc by a constant which was essentially similar in each subject and at each lung volume. Thus they were able to estimate changes in LDi in normal subjects by measuring external diameter of the rib cage with a pair of magnetometers and using ultrasonography over the lateral rib cage to measure LZapp,r (LZapp,r equalled LZapp,l on the radiographs). Ultrasonography was also used to measure the thickness of the ribcage, which was subtracted from the diameter measured by the magnetometers to obtain DRc. The temporal resolution with ultrasonography is potentially higher (∼30 Hz) than that with other methods of imaging.

Petroll et al. (1990) extended these studies by measuring LDi from postero-anterior radiographs taken at five different lung volumes between TLC and residual volume (RV) in 16 normal subjects. They found small differences in dome curvature at different lung volumes but showed that LDi could be estimated accurately by the equation:LDi (mm)=2(0.98LZapp,r+0.46DRc+35),R2=0.94

If this equation could be applied to patients with COPD it would permit the use of surface measurements to measure dynamic LDi during tidal breathing. However, the applicability of this equation to COPD cannot be assumed; obvious differences are that in COPD changes in DRc with volume may differ from control subjects (due to alterations in rib-cage shape and mechanics) and the diaphragm domes are often flatter and may exhibit more change in curvature with lung volume. In patients with COPD there are significant distortions in chest shape over the vital capacity range (Sharp et al., 1977) so that the relative changes in LDi between the coronal and sagittal planes may be different from those in control subjects. Moreover, in contrast to the relative consistency of dome shape with volume in the coronal plane the diaphragm usually flattens completely in the sagittal plane at TLC (Gauthier et al., 1994).

In the present study we report measurements of LDi made from postero-anterior radiographs at TLC, FRC and RV in nine men with severe COPD. Similar measurements were made from lateral chest radiographs taken at the same lung volumes in three patients to correlate measurements of LDi in the coronal and sagittal planes. We had two distinct objectives: (i) to compare our measurements with the limited available literature using plain radiography or CT and (ii) to determine whether the equation of Petroll et al. (1990) derived in healthy subjects could predict static diaphragm length at different lung volumes in patients with severe COPD.

Section snippets

Patients

The main study was performed on nine male patients with severe COPD due to smoking but no significant neuromuscular or skeletal disease and no prior chest surgery. An additional study was performed on three other patients (two male, one female). All patients had a history of recurrent admissions to hospital for infective exacerbations and most had been treated for recurrent oedema due to cor pulmonale. The patients were all smokers or ex-smokers and their anthropometric and lung function data

Results

All patients had evidence of severe airflow obstruction with mean FEV1 (SD) of 0.71 (0.15) L and FVC of 2.81 (0.69) L. They were markedly hyperinflated with mean FRC of 7.2 (0.6) L, TLC 8.5 (0.7) L and RV 5.7 (0.7) L. These values are shown as percent predicted in Table 1. Five patients had an arterial PO2 breathing room air of less than 8.0 kPa. Seven patients had hypercapnia (PaCO2 >6.0 kPa).

Group data for the measures of diaphragm length in the mid-coronal plane at the three lung volumes are

Discussion

We have been able to find only three previous reports of diaphragm length measurements in patients with severe COPD. Rochester and Braun (1985) using plain chest radiographs provided measurements of LDi only at RV with a total length of 442 (68) mm (sum of 1/2 length in PA view and length in lateral view), compared with 550 (94) mm in the present study of three additional patients. Cassart et al. (1997) used spiral CT to provide measures of LDi in the coronal plane in 10 patients at FRC (454

Acknowledgements

JFT held the Australian Lung Foundation-Boehringer Ingelheim Chronic Airflow Limitation Scholarship and NP received a Wellcome-Ramaciotti Travel Grant. The research was supported by the Asthma Foundation of New South Wales and the National Health and Medical Research Council of Australia.

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