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Symptom Relief After Large-Volume Thoracentesis in the Absence of Lung PerfusionLarge-Volume Thoracentesis and Dyspnea FREE TO VIEW

Mary E. Klecka, MD; Fabien Maldonado, MD, FCCP
Author and Funding Information

From the Department of Internal Medicine (Dr Klecka) and Division of Pulmonary and Critical Care Medicine (Dr Maldonado), Mayo Clinic, Mayo Foundation for Medical Education and Research, Rochester, MN.

Correspondence to: Fabien Maldonado, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Gonda 18, Mayo Clinic, 200 1st St SW, Rochester, MN 55905; e-mail: Maldonado.Fabien@mayo.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(5):1141-1143. doi:10.1378/chest.13-1523
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The physiologic basis for relief from dyspnea after therapeutic thoracentesis remains poorly understood. Here, we describe the case of a 46-year-old man with large recurrent pleural effusion with absent perfusion to the affected lung who experienced dramatic dyspnea relief after large-volume thoracentesis. This patient’s improvement in breathlessness cannot be attributed to improved gas exchange and suggests the primary physiologic basis for the relief in dyspnea is a change in respiratory system mechanics or work of breathing.

Figures in this Article

Patients with large pleural effusions often experience dramatic and immediate relief from dyspnea after therapeutic thoracentesis. Although this is a well-recognized phenomenon, the physiologic basis for such relief remains poorly understood.

One commonly proposed mechanism is that therapeutic thoracentesis allows for lung reexpansion, ventilation of previously atelectatic lung, and improved ventilation-perfusion matching, subsequently leading to dyspnea relief. This would explain why therapeutic thoracenteses do not appear helpful in patients with nonexpandable lung. This hypothesis contrasts with the concept of length-tension inappropriateness, which posits that chest wall mechanics, rather than gas exchange, best explain the perception of dyspnea relief.

A 46-year-old man was referred for dyspnea and diagnosed with fibrosing mediastinitis (FM) after developing massive hemoptysis during bronchoscopy. Despite treatment with itraconazole, his dyspnea progressed to be present at rest. A CT scan of the chest revealed a large left pleural effusion occupying one-half of the hemithorax. Prethoracentesis ultrasound revealed the presence of an inverted diaphragm (Fig 1). Thoracentesis yielded 2.5 L of a serous transudate. Pleural manometry showed an opening pressure of 4.1 cm H2O with a gradual decrease to –12.2 cm H2O after complete fluid drainage, consistent with normal pleural elastance. Echocardiogram showed no evidence for constrictive pericarditis secondary to FM that could explain the pleural effusion. CT angiogram with venous protocol revealed bilateral pulmonary vein obstruction secondary to FM, with high-grade stenosis of the right superior pulmonary vein and complete obstruction of both left-sided pulmonary veins (Fig 2): the presumed cause of his left pleural effusion. A quantitative perfusion scan after complete pleural drainage (within 2 h) demonstrated negligible (3%) perfusion to the left lung, with 97% of total perfusion directed to the right lung (Fig 3). There was also decreased perfusion of the right upper lobe due to occlusion of the right upper lobe pulmonary artery.

Figure Jump LinkFigure 1. Prethoracentesis ultrasound reveals inverted diaphragm and large pleural effusion.Grahic Jump Location
Figure Jump LinkFigure 2. CT angiography with three-dimensional reconstruction shows high-grade stenosis of the right superior pulmonary vein and occlusion of the right upper lobe pulmonary artery, as well as complete occlusion of the left pulmonary veins.Grahic Jump Location
Figure Jump LinkFigure 3. Perfusion scan demonstrating little to no perfusion of the left lung.Grahic Jump Location

Despite the absence of perfusion to the left lung, the patient reported dramatic improvement in dyspnea after thoracentesis. Subsequent therapeutic thoracenteses resulted in the same stereotypical response. After therapeutic thoracentesis, the patient could perform strenuous exercise for many hours without limitation. As the effusion would reaccumulate, his severe dyspnea would recur to be present with minimal effort. On a linear analog scale, dyspnea from 0 (no dyspnea) to 100 (maximum dyspnea), his predrainage score was 75, and postdrainage score was 0. He ultimately underwent tunneled indwelling catheter placement with complete relief of symptoms.

To our knowledge, this is the first case describing a dramatic improvement in dyspnea after thoracentesis in a patient with absent perfusion to the affected lung. This patient’s improvement in breathlessness cannot, therefore, be attributed to improved gas exchange and suggests that the primary physiologic basis for the relief in dyspnea is a change in respiratory system mechanics and/or work of breathing.

The mechanism of relief after large-volume thoracentesis was first investigated by Brown et al,1 who described significant relief after thoracentesis despite a lack of improvement in lung volumes or gas exchange in patients with large pleural effusions. The authors concluded that this relief could be due to a placebo effect. Subsequent studies supported these findings, suggesting that improvement in dyspnea is typically observed despite minimal or absent improvement in lung volumes or gas exchange.1-4 In most cases, the bulk of the effusion appeared to be mainly accommodated by an increase in chest wall dimensions.

Estenne et al4 reported in 1983 a shift in the pressure-volume curve after large-volume drainage such that the pressures generated by the inspiratory muscles were substantially more negative at any given lung volume. This shift was shown to be secondary to a decrease in thoracic cage volume. It was, therefore, hypothesized that thoracentesis allowed previously stretched inspiratory muscles to operate on a more favorable portion of their length-tension curve. This may largely apply to the diaphragmatic muscle, which has been shown to be occasionally inverted in large effusions, sometimes resulting in paradoxical motion, a finding associated with better symptomatic outcomes after thoracentesis.5,6

The concept of length-tension inappropriateness was proposed in 1961 by Campbell et al7 as an explanation for the sensation of dyspnea.8 He postulated that breathlessness would occur when an external load resulted in a change in muscle length inappropriate to the change in tension. The pressure-volume relationship of the lungs alone was shown to be preserved, suggesting that detection of these loads likely arose from receptors in the chest wall. The beneficial effects of therapeutic thoracenteses on the sensation of dyspnea have been well described.9,10

Our case establishes that relief of dyspnea after large-volume thoracentesis likely results from changes in chest wall mechanics and/or work of breathing. This observation has direct clinical implications and could inform future studies addressing management of patients with large pleural effusions.

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

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

FM

fibrosing mediastinitis

Brown NE, Zamel N, Aberman A. Changes in pulmonary mechanics and gas exchange following thoracocentesis. Chest. 1978;74(5):540-542. [CrossRef] [PubMed]
 
Perpiñá M, Benlloch E, Marco V, Abad F, Nauffal D. Effect of thoracentesis on pulmonary gas exchange. Thorax. 1983;38(10):747-750. [CrossRef] [PubMed]
 
Karetzky MS, Kothari GA, Fourre JA, Khan AU. Effect of thoracentesis on arterial oxygen tension. Respiration. 1978;36(2):96-103. [CrossRef] [PubMed]
 
Estenne M, Yernault JC, De Troyer A. Mechanism of relief of dyspnea after thoracocentesis in patients with large pleural effusions. Am J Med. 1983;74(5):813-819. [CrossRef] [PubMed]
 
Wang JS, Tseng CH. Changes in pulmonary mechanics and gas exchange after thoracentesis on patients with inversion of a hemidiaphragm secondary to large pleural effusion. Chest. 1995;107(6):1610-1614. [CrossRef] [PubMed]
 
Wang LM, Cherng JM, Wang JS. Improved lung function after thoracocentesis in patients with paradoxical movement of a hemidiaphragm secondary to a large pleural effusion. Respirology. 2007;12(5):719-723. [CrossRef] [PubMed]
 
Campbell EJ, Freedman S, Smith PS, Taylor ME. The ability of man to detect added elastic loads to breathing. Clin Sci. 1961;20:223-231. [PubMed]
 
Bennett D, Jayson M, Rubenstein D. The perception of dyspnea. Dis Chest. 1963;43:411-417. [CrossRef] [PubMed]
 
Davies HE, Mishra EK, Kahan BC, et al. Effect of an indwelling pleural catheter vs chest tube and talc pleurodesis for relieving dyspnea in patients with malignant pleural effusion: the TIME2 randomized controlled trial. JAMA. 2012;307(22):2383-2389. [CrossRef] [PubMed]
 
Tremblay A, Michaud G. Single-center experience with 250 tunnelled pleural catheter insertions for malignant pleural effusion. Chest. 2006;129(2):362-368. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. Prethoracentesis ultrasound reveals inverted diaphragm and large pleural effusion.Grahic Jump Location
Figure Jump LinkFigure 2. CT angiography with three-dimensional reconstruction shows high-grade stenosis of the right superior pulmonary vein and occlusion of the right upper lobe pulmonary artery, as well as complete occlusion of the left pulmonary veins.Grahic Jump Location
Figure Jump LinkFigure 3. Perfusion scan demonstrating little to no perfusion of the left lung.Grahic Jump Location

Tables

References

Brown NE, Zamel N, Aberman A. Changes in pulmonary mechanics and gas exchange following thoracocentesis. Chest. 1978;74(5):540-542. [CrossRef] [PubMed]
 
Perpiñá M, Benlloch E, Marco V, Abad F, Nauffal D. Effect of thoracentesis on pulmonary gas exchange. Thorax. 1983;38(10):747-750. [CrossRef] [PubMed]
 
Karetzky MS, Kothari GA, Fourre JA, Khan AU. Effect of thoracentesis on arterial oxygen tension. Respiration. 1978;36(2):96-103. [CrossRef] [PubMed]
 
Estenne M, Yernault JC, De Troyer A. Mechanism of relief of dyspnea after thoracocentesis in patients with large pleural effusions. Am J Med. 1983;74(5):813-819. [CrossRef] [PubMed]
 
Wang JS, Tseng CH. Changes in pulmonary mechanics and gas exchange after thoracentesis on patients with inversion of a hemidiaphragm secondary to large pleural effusion. Chest. 1995;107(6):1610-1614. [CrossRef] [PubMed]
 
Wang LM, Cherng JM, Wang JS. Improved lung function after thoracocentesis in patients with paradoxical movement of a hemidiaphragm secondary to a large pleural effusion. Respirology. 2007;12(5):719-723. [CrossRef] [PubMed]
 
Campbell EJ, Freedman S, Smith PS, Taylor ME. The ability of man to detect added elastic loads to breathing. Clin Sci. 1961;20:223-231. [PubMed]
 
Bennett D, Jayson M, Rubenstein D. The perception of dyspnea. Dis Chest. 1963;43:411-417. [CrossRef] [PubMed]
 
Davies HE, Mishra EK, Kahan BC, et al. Effect of an indwelling pleural catheter vs chest tube and talc pleurodesis for relieving dyspnea in patients with malignant pleural effusion: the TIME2 randomized controlled trial. JAMA. 2012;307(22):2383-2389. [CrossRef] [PubMed]
 
Tremblay A, Michaud G. Single-center experience with 250 tunnelled pleural catheter insertions for malignant pleural effusion. Chest. 2006;129(2):362-368. [CrossRef] [PubMed]
 
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