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 Table of Contents  
ORIGINAL ARTICLE
Year : 2023  |  Volume : 6  |  Issue : 1  |  Page : 2-6

Assessment of excursion and thickness of diaphragm by ultrasound during acute exacerbation of chronic obstructive pulmonary disease and correlation with severity of airway obstruction


1 Department of Respiratory Medicine, A. J. Institute of Medical Sciences and Research Centre, Mangalore, Karnataka, India
2 Department of Respiratory Medicine, Chamarajanagar Institute of Medical Sciences, Yadapura, Karnataka, India

Date of Submission17-Dec-2022
Date of Decision08-Mar-2023
Date of Acceptance14-Mar-2023
Date of Web Publication29-Apr-2023

Correspondence Address:
Dr. M Vishnu Sharma
Department of Respiratory Medicine, A. J. Institute of Medical Sciences and Research Centre, Kuntikana, Mangalore, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/japt.japt_38_22

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  Abstract 


Background: Diaphragm dysfunction in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) leads to increased morbidity and mortality. Early diagnosis of diaphragm dysfunction and aggressive management to improve the diaphragm function and may improve the outcome in AECOPD. Aims and Objectives: This study aimed to assess diaphragmatic excursion by ultrasound during AECOPD and correlation with the severity of airway obstruction. Materials and Methods: Sixty patients admitted with AECOPD were evaluated. Ultrasonography was done to assess the diaphragm excursion and thickness. Airway obstruction was classified as moderate, severe, and very severe by measuring forced expiratory volume in 1 s (FEV1). Comparison of excursion and thickness of the diaphragm in the study patients was done with normal values and analyzed using Student's t-test. Values of measured FEV1 were correlated with the normal values of excursion and thickness of the diaphragm and statistical analysis was done by ANOVA test. Results: Forty-six males and four females were included in the study. Thirty-four percent (17) had moderate COPD, 60% (30) had severe COPD, and 6% (3) had very severe COPD. The mean excursion and thickness of the diaphragm in the study patients were less when compared to the normal values. In moderate COPD, the mean excursion of the diaphragm was 29.94 mm, whereas in those with severe and very severe COPD, the mean excursions were 26.77 mm and 23.33 mm, respectively. Statistical analysis by ANOVA test was done to compare the diaphragm excursion and severity of COPD. The P = 0.039 was considered statistically significant. Patients with moderate COPD (34%) showed a mean diaphragm thickness of 2.82 mm, and those with severe (60%) and very severe (6%) COPD showed a diaphragm thickness of 2.23 mm and 2.00 mm, respectively. Statistical analysis by ANOVA test was done to compare the diaphragm thickness and severity of COPD. The P < 0.001 was considered statistically significant. Conclusions: Patients with AECOPD have reduced excursion and thickness of the diaphragm in comparison with normal subjects. Diaphragm dysfunction increases as the severity of airflow obstruction in COPD increases.

Keywords: Assessment of excursion and thickness of diaphragm, diaphragm dysfunction, severity of airway obstruction, ultrasound: acute exacerbation of chronic obstructive pulmonary disease


How to cite this article:
Sharma M V, Chandrik Babu S R. Assessment of excursion and thickness of diaphragm by ultrasound during acute exacerbation of chronic obstructive pulmonary disease and correlation with severity of airway obstruction. J Assoc Pulmonologist Tamilnadu 2023;6:2-6

How to cite this URL:
Sharma M V, Chandrik Babu S R. Assessment of excursion and thickness of diaphragm by ultrasound during acute exacerbation of chronic obstructive pulmonary disease and correlation with severity of airway obstruction. J Assoc Pulmonologist Tamilnadu [serial online] 2023 [cited 2023 May 29];6:2-6. Available from: https://www.japt.in//text.asp?2023/6/1/2/375459




  Introduction Top


Ultrasound is a simple, noninvasive, portable, and relatively less expensive investigation for the assessment of functional status of the diaphragm.[1] In patients with chronic obstructive pulmonary disease (COPD), measurement of thickness, and movements of the diaphragm are useful to detect dysfunction of the diaphragm.[2] It is measured at the zone of apposition of the diaphragm. The zone of apposition of diaphragm is the area where the upper abdominal contents meet the lower rib cage. Ultrasonography (USG) is useful to measure the degree of lung hyperinflation. The severity of lung hyperinflation correlates with the severity of COPD.[3] Severe diaphragm dysfunction as measured by USG is associated with NIV failure and increased mortality during acute exacerbation of COPD (AECOPD).[4]

Hyperinflation in COPD causes diaphragm dysfunction due to the shortening of diaphragm to a suboptimal length.[5] Diaphragm has to work against a mechanical disadvantage. Hyperinflation causes air trapping which further deteriorates the diaphragmatic functions leading to poor ventilation, carbon dioxide retention, and respiratory failure leading to increased morbidity and mortality in these patients.[6] Early diagnosis of diaphragm dysfunction and management of the same may improve the outcome in AECOPD. Diaphragm dysfunction in AECOPD may indicate more severe disease and poorer outcome.

Appropriate bronchodilator therapy, controlled oxygen therapy, noninvasive ventilatory support, appropriate antibiotics, and clearance of secretions may reduce hyperinflation leading to improvement in diaphragm function during AECOPD. This in turn may help to reduce the morbidity and mortality during AECOPD.

Aims and objectives

This study was undertaken to assess diaphragmatic movement by ultrasound during AECOPD and correlation with the severity of airway obstruction.


  Materials and Methods Top


This was a cross-sectional study of 50 patients who were previously diagnosed with COPD as per GOLD guidelines and admitted with acute exacerbation. Patients with chest wall abnormality, pleural disease, other chronic respiratory diseases, coexisting cardiac disease, and neuromuscular disorders were excluded from the study. Database was collected from COPD patients who were admitted for 2 years in a tertiary care teaching hospital. Ethical clearance was obtained from the institutional ethics committee and consent from each patient was obtained before the study.

Demographic profiles, history, physical findings, relevant blood investigations, chest X-ray, ECG, and echocardiogram were done in all patients. Diaphragm movement and thickness were measured in the zone of apposition by ultrasound using M-mode 3–5 MHz and 7–10 MHz, respectively, on admission. Forced expiratory volume in 1 s (FEV1) was measured by spirometry at the time of discharge when these patients were stable.

Comparison of movement and thickness of the diaphragm in the study patients was done with normal values and analyzed using Student's t-test. The normal thickness of diaphragm in the zone of apposition was taken as 0.33 cm.[5] The values of measured FEV1 in spirometry were correlated with the normal values of movement and thickness of the diaphragm and statistical analysis was done by ANOVA test.


  Results Top


Among the 50 study patients, 92% (46) were males and 8% (4) were females. Thirty-two percent (16) belonged to the age group of 46–55 years, 50% (25) belonged to 56–65 years and 18% (9) belonged to the 66–75 years' age group [Table 1]. Among the 50 patients, 34% (17) had moderate COPD, 60% (30) had severe COPD, and 6% (3) had very severe COPD when correlated with FEV1 values [Table 2].
Table 1: Age group

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Table 2: Severity of chronic obstructive pulmonary disease

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Mean age in years, movement and thickness of the diaphragm and the mean FEV1 of the study patients was compared with the normal values [Table 3].
Table 3: Mean values of age, diaphragm thickness, excursion, and forced expiratory volume in 1 s values among study subjects (n=50)

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A comparison of the movement and thickness of the diaphragm and FEV1 of the study patients with the values of normal patients was done [Table 4]. The mean excursion (movement) and the thickness of the study patients were less when compared to the normal values. Statistical analysis was done by Student's t-test and the P value was statistically significant (P < 0.001).
Table 4: Comparison of the excursion, thickness of the diaphragm, and forced expiratory volume in 1 s of study subjects with the values of normal subjects

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Excursion of the diaphragm was compared with the severity of airway obstruction by FEV1 [Table 5]. In moderate COPD the mean excursion of diaphragm was 29.94 mm, whereas in those with severe and very severe COPD the mean excursions were 26.77 and 23.33 mm, respectively. Statistical analysis by ANOVA test was done to compare the diaphragm excursion and severity of COPD. The P = 0.039 was considered statistically significant.
Table 5: Comparison of diaphragm excursion with severity of chronic obstructive pulmonary disease among study subjects

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The thickness of the diaphragm was compared with the severity of airway obstruction by FEV1 [Table 6]. Those with moderate COPD (34%) showed a mean thickness of 2.82 mm, and those with severe (60%) and very severe (6%) COPD showed a thickness of 2.23 and 2.00 mm, respectively. Statistical analysis by ANOVA test was done to compare the diaphragm thickness and severity of COPD. The P < 0.001 was statistically significant.
Table 6: Comparison of the thickness of the diaphragm and severity of chronic obstructive pulmonary disease among study subjects with normal subjects

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  Discussion Top


In our study, the majority (50%) of patients belonged to the age group of 56–65 years. In our study, COPD was more common in males. Among 50 study patients, 92% were male and 8% were female. A study by Jindal et al. showed COPD was more common among males with advancing age, low-socioeconomic status, and tobacco smoking in India.[7] This gender difference may be due to smoking habit being more prevalent in males, more exposure to pollutants, and allergens in the workplace among males.

Our study showed that diaphragmatic excursion and thickness were reduced in COPD patients during acute exacerbation as compared to normal individuals. The severity of diaphragm dysfunction was proportional to the severity of airway obstruction in COPD. In our study, diaphragm mobility and thickness reduced as the severity of COPD increased. These findings in our study correlated with previous studies.[4],[6],[8]

The mean excursion of the study subjects was 27.64 mm which was less when compared to the values of normal individuals in previous studies.[9],[10] In a study by Testa et al., the resting and forced diaphragmatic excursions were found to be 18.4 ± 7.6 and 78.8 ± 13.3 mm, respectively.[9] In another study conducted by Gerscovich et al., the mean excursion of the diaphragm was 5.69 cm.[10]

In a study done by Paulin et al., COPD patients had lower diaphragmatic mobility than the controls (36.27 ± 10.96 mm vs. 46.33 ± 9.46 mm).[11] This study also showed that reduced diaphragmatic mobility leads to increased dyspnea and poor exercise tolerance in patients with COPD. A study done by Kang, et al. in 2009–2010, on 37 COPD patients, showed a reduced diaphragm mobility was associated with carbon dioxide retention.[12]

Our study showed that the thickness of the diaphragm was reduced in COPD patients when compared to normal subjects, and also the thickness of the diaphragm decreased as the severity of COPD increased. The mean thickness of the diaphragm in our study subjects was 2.45 mm which is less in comparison to normal individuals.[9],[10] Hyperinflation and repeated exacerbations displace the diaphragm into a flattened position causing a shortening of its length with a loss of zone of opposition.

Diaphragm thickness is about 35 mm in normal patients.[13] In patients with COPD due to hyperinflation, diaphragmatic functions are impaired due to the shortening and disruption of sarcomeres. In a study done by Ueki, et al., the mean (standard deviation) thickness was found to be 4.5 (0.9) mm at total lung capacity (TLC), 1–7 (0.2) mm at functional residual lung capacity (FRC), and 1–6 (0.2) mm at residual volume (RV).[14] In a pilot study by Smargiassi, et al., showed assessment of the diaphragm function by USG could be a useful tool for studying the progression of disease in COPD patients.[3] In this study, it was found that a progressive reduction of thicknesses of the diaphragm and hyperinflation of the lung was associated with increasing the severity of COPD.

Diaphragm dysfunction and reduced thickness lead to increased work of breathing in COPD patients, especially during acute exacerbation. This results in hypoventilation and inability to withstand the increased workload leading to air trapping, hyperinflation, and CO2 retention. Hyperinflation is defined as increased FRC, increased RV/TLC, and increased TLC. In a case–control study done on 60 patients by Harsha et al., patients with severe and very severe COPD showed a risk of developing carbon dioxide retention 116 times more than that of patients with mild and moderate COPD.[15] In patients with COPD, diaphragmatic functions are impaired due to the shortening of diaphragm to a suboptimal length. Hence, diaphragm has to work against a mechanical disadvantage. In AECOPD patients, there will be air trapping which further deteriorates the ventilatory functions of the diaphragm. As a consequence of poor ventilation, there will be carbon dioxide retention and respiratory failure which is a major cause of morbidity and mortality in these patients.

Expiratory flow limitation is one of the hallmarks of COPD. Emphysema and airway dysfunction in COPD lead to dynamic hyperinflation during exercise and AECOPD.[15] Hyperinflation leads to mechanical disadvantage and limits the diaphragm movement. According to an article “No room to breathe: the importance of lung hyperinflation in COPD” published by Thomas, et al.,[16] patients with COPD reduce their physical activity due to dyspnea. Airway obstruction and skeletal muscle dysfunction in COPD result in air trapping and hyperinflation of the lung. Dyspnea in COPD leads to a vicious cycle of avoidance of physical activity, physical deconditioning, and reduced quality of life.[12] Physical inactivity in COPD predisposes to the development of comorbidities such as cardiovascular disease and metabolic syndromes.[17] Aggressive treatment of COPD with bronchodilators leads to reduced airflow limitation and improved lung emptying. Pulmonary rehabilitation in COPD leads to reduction in respiratory rate, improved skeletal muscle function, and reduction in ventilatory demand. Optimal bronchodilator therapy can reduce dyspnea and increase patient's ability to exercise, and improve the chance of a successful outcome of a pulmonary rehabilitation program. Hence, early diagnosis of diaphragm dysfunction and optimal management with reduce diaphragm dysfunction in COPD.

In addition to mechanical dysfunction in diaphragm, many pathological changes occur directly as a result of COPD and this diaphragm dysfunction correlates with the degree of severity of FEV1. In our study, among 50 patients, 60% of the patients had severe COPD, 34% had moderate COPD, and 6% had severe COPD. The number of very severe COPD patients was less in comparison to other groups. Patients who have very severe COPD will develop other comorbidities such as systolic and diastolic dysfunction of heart, cardiac arrhythmias, and cor pulmonale. Patients with comorbidities were excluded from the study; hence, the number of very severe COPD was less compared to other studies.

In our study, the mean excursion and thickness of the diaphragm decreased as the severity of COPD increased. A study done by Kang et al. hypercapnia in patients with COPD showed reduced diaphragm mobility with airflow limitation and carbon dioxide retention with increasing severity of COPD.[12] Diaphragm dysfunction leads to increased morbidity and mortality in COPD patients, especially during acute exacerbation due to hypoventilation and inability to withstand the increased workload. A study by Yamaguti, et al.[17] showed COPD patients with diaphragmatic dysfunction have a higher risk of death than those without such dysfunction. Hence, recognizing diaphragmatic dysfunction early in the course and proper control of COPD is essential to limit pathological changes and reduce morbidity and mortality in COPD. In patients with COPD loss of myosin content in diaphragmatic fibers are seen.[7] Oxidative stress and sarcomeric injury also contribute to diaphragm dysfunction in COPD.

Diaphragm and other inspiratory muscle strengthening exercise is an important modality of treatment in COPD. The main modality of the treatment of an exacerbation of COPD is by treating the infection by effective antibiotics, adequate bronchodilators, treating comorbidities, health education to the patient regarding the disease, its control by different drugs, avoiding the exacerbating factors, and pulmonary rehabilitation.[15] Pulmonary rehabilitation plays a very important role in COPD patients by increasing the strength of the diaphragm muscle. Pulmonary rehabilitation increases the quality of life, and reduces the frequency of exacerbations by increasing the strength of respiratory muscles and diaphragm. Pulmonary rehabilitation also increases the oxygen utilization by the body and reduces the psychological stress of the patient. A study done by Eaton et al.[18] showed early pulmonary rehabilitation for COPD patients admitted with an exacerbation was feasible and safe. Cachexia and malnutrition may contribute to diaphragm dysfunction in COPD.[19] Proper nutritional therapy will improve the outcome in AECOPD patients with malnutrition.[20]


  Conclusions Top


Our study showed that patients with AECOPD have reduced movement and thickness of the diaphragm in comparison with normal subjects. Diaphragm dysfunction increases as the severity of airflow obstruction in COPD increases.

Limitations

Small sample size and lesser number of female patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Sharma VM, Anupama N. Assessment of diaphragm functions. Pulmon 2011;13:102-7.  Back to cited text no. 1
    
2.
Sharma BB, Singh V. Diaphragmatic dysfunction in chronic obstructive pulmonary disease. Lung India 2019;36:285-7.  Back to cited text no. 2
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3.
Smargiassi A, Inchingolo R, Tagliaboschi L, Di Marco Berardino A, Valente S, Corbo GM. Ultrasonographic assessment of the diaphragm in chronic obstructive pulmonary disease patients: Relationships with pulmonary function and the influence of body composition – A pilot study. Respiration 2014;87:364-71.  Back to cited text no. 3
    
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Antenora F, Fantini R, Iattoni A, Castaniere I, Sdanganelli A, Livrieri F, et al. Prevalence and outcomes of diaphragmatic dysfunction assessed by ultrasound technology during acute exacerbation of COPD: A pilot study. Respirology 2017;22:338-44.  Back to cited text no. 4
    
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Feletti F, Malta B, Aliverti A, editors. Assessment of diaphragm function by ultrasounds. In: Thoracic Ultrasound and Integrated Imaging. Cham: Springer; 2020.  Back to cited text no. 5
    
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Baria MR, Shahgholi L, Sorenson EJ, Harper CJ, Lim KG, Strommen JA, et al. B-mode ultrasound assessment of diaphragm structure and function in patients with COPD. Chest 2014;146:680-5.  Back to cited text no. 6
    
7.
Jindal SK, Aggarwal AN, Chaudhry K, Chhabra SK, D'Souza GA, Gupta D, et al. A multicentric study on epidemiology of chronic obstructive pulmonary disease and its relationship with tobacco smoking and environmental tobacco smoke exposure. Indian J Chest Dis Allied Sci 2006;48:23-9.  Back to cited text no. 7
    
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Ottenheijm CA, Heunks LM, Sieck GC, Zhan WZ, Jansen SM, Degens H, et al. Diaphragm dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2005;172:200-5.  Back to cited text no. 8
    
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Testa A, Soldati G, Giannuzzi R, Berardi S, Portale G, Gentiloni Silveri N. Ultrasound M-mode assessment of diaphragmatic kinetics by anterior transverse scanning in healthy subjects. Ultrasound Med Biol 2011;37:44-52.  Back to cited text no. 9
    
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Paulin E, Yamaguti WP, Chammas MC, Shibao S, Stelmach R, Cukier A, et al. Influence of diaphragmatic mobility on exercise tolerance and dyspnea in patients with COPD. Respir Med 2007;101:2113-8.  Back to cited text no. 11
    
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Kang HW, Kim TO, Lee BR, Yu JY, Chi SY, Ban HJ, et al. Influence of diaphragmatic mobility on hypercapnia in patients with chronic obstructive pulmonary disease. J Korean Med Sci 2011;26:1209-13.  Back to cited text no. 12
    
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Scarlata S, Mancini D, Laudisio A, Raffaele AI. Reproducibility of diaphragmatic thickness measured by M-mode ultrasonography in healthy volunteers. Respir Physiol Neurobiol 2019;260:58-62.  Back to cited text no. 13
    
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Ueki J, De Bruin PF, Pride NB. In vivo assessment of diaphragm contraction by ultrasound in normal subjects. Thorax 1995;50:1157-61.  Back to cited text no. 14
    
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Harsha DS, Vishnu Sharma M, Nanjesh Kumar S, Bhat AC, Chandrik Babu SR, Jose B, et al. Pre morbid severity of chronic obstructive pulmonary disease and risk factor for carbon dioxide retention during acute exacerbation of chronic obstructive pulmonary disease. Res J Pharm Biol Chem Sci 2014;05:201-6.  Back to cited text no. 15
    
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Eaton T, Young P, Fergusson W, Moodie L, Zeng I, O'Kane F, et al. Does early pulmonary rehabilitation reduce acute health-care utilization in COPD patients admitted with an exacerbation? A randomized controlled study. Respirology 2009;14:230-8.  Back to cited text no. 18
    
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Vishnu Sharma M, Anupama N, Harsha DS, V.Viswambhar, Bhat AC, Basavaraj S, et al. Low body mass index and low serum albumin level as risk factors for carbon dioxide retention during acute exacerbation of chronic obstructive pulmonary disease. Int J Innov Res Sci Eng Technol 2013;2:3508-11.  Back to cited text no. 19
    
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