Assessment of Regional Lung Function Disturbances as a Contributive Factor in the Occurrence of Spontaneous Pneumothorax and Hemopneumothorax
 
D. Subotic*, D. Mandaric*, S. Pavlovic**, T. Kuljic*
 
  *Institute for Lung Diseases, University Clinical Center, Belgrade;
**Nuclear Medicine Institute, University Clinical Center, Belgrade


The correct citation of this article for reference is:

Subotic D, Mandaric D, Pavlovic S, Kujic T: Assessment of Regional Lung Function Disturbances as a Contributive Factor in the Occurrence of Spontaneous Pneumothorax and Hemopneumothorax. The Internet Journal of Thoracic and Cardiovascular Surgery 2000; Vol3N1: http://www.ispub.com/journals/IJRDM/Vol3N1/pneu.htm . Published January 14, 2000; Last Updated January 14, 2000. Please add "Date Accessed".


Quick Links
Introduction
Material and methods
Results
Discussion
Conclusion
References


Introduction (back to Quick Links)

Spontaneous pneumothorax (SP) represents 2.7-7.1% of all lung diseases 1. Spontaneous haemopneumothorax (SHP), occurring in 0.9-6.8% patients with SP, although presenting as medical urgency more frequently than SP, shares with it the identical etiology and any underlying pathology. Many clinical aspects of both SP and SHP have been well analysed resulting in broad consensus concerning etiology, diagnostics and treatment, that is conservative in more than 90% cases 2. This is particularly important in patients with SHP, since the more aggressive therapeutic approach to this condition resulted in significantly lowered mortality - from 20-25% (early fifties) to 3-5% that is now most frequently reported 3.
Unlike clinical aspects of both conditions, pathophysiology of pneumothorax is still not absolutely clear. More than 100 years ago it was demonstrated at post mortem (West 1884) that the normal, healthy pleura could not be ruptured in situ with pressures less than 200 mmHg. That clearly indicated that pleura needs to be weakened before rupture 4. Electron microscopy studies of lung specimens obtained during lung biopsies in patients with SP rendered additional data concerning the ultrastructure of blebs and bullas and the surrounding lung tissue - dominant findings were increase in interstitial mass and proliferation of epithelial cells both being usually reported as responses to pulmonary stress or insults 5. It became clear long ago that rupture of blebs occurs as the consequence of their “isolation” from the surrounding lung tissue, that, usually in combination with abrupt decrease in atmospheric pressure, makes them follow the Boyl-Mariot low - as external pressure falls, the non communicating gas within blebs will expand, thus increasing the pressure gradient across the wall of the bleb 67.  Rare publications dealing with SP in the acute phase of the disease point out the absence of gravitational gradient of lung expansion in the lung affected by SP as a consequence of  gravitational gradients of pleural surface pressure being abolished by pneumothorax 8. As lungs with pneumothorax in most studies demonstrated airway closure at low lung volumes, it is suggested that it could be the chief cause of ventilation maldistribution in SP 9. So, disagreement still exists concerning the exact mechanism of blebs “isolation” from the surrounding lung tissue.
In this study, two kinds of investigations were performed in patients with healed SP and SHP. The first kind represents routine respiratory function tests with measurement of diffusion parameters; the second kind of investigation represents scintigraphic evaluation of lungs with determination of pulmonary clearance as the indicator of lung epithelial permeability.
The aim of the first kind of investigation is to assess the eventual presence of asymptomatic lung emphysema as the underlining cause of SP and SHP; the second kind of investigation is expected to confirm or deny the existence of regional lung function disturbances and eventual damages of alveolo-capilar membrane in the lungs that had been faced with SP and SHP.
The fact that performed conservative treatment neither eliminates nor disturbs the distribution of preexisting morphological changes of the affected lung that can be responsible for the occurrence of SP and SHP, justifies this kind of investigation in a series of patients with healed SP and SHP.
 

Material and Methods (back to Quick Links)

The analysis included 21 patients with healed SP and SHP that had underwent a treatment in the acute phase in the aforementioned institute. Pneumothorax group (SP group) consisted of 11 persons with healed spontaneous pneumothorax and the haemopneumothorax group (SHP group) consisted of 10 persons with healed spontaneous haemopneumothorax. In both groups investigation was performed 4-12 months after discharge.
First part of the investigation consisted of respiratory function tests including diffusion parameters and body pletismography. The following parameters were analysed: vital capacity (VC), total capacity (TLC), residual volume (RV), functional residual capacity (FRC), FEV1, Tiffeneau-index, diffusion capacity (Dco), coefficient of diffusion (D/VA) and FEF50.
The second part of the investigation included determination of pulmonary clearance and lung scintigraphy. By measuring the rate of decrease of radioactivity of inhaled aerosol - 99m Tc DTPA, it is possible to discover impairments of the alveolo-capilar membrane integrity. Pulmonary clearance, expressing this rate, represents the indicator of pulmonary epithelial permeability. The DTPA complex was labeled by the standard procedure with 1480 mBq 99mTc in 1 ml of 0,9% NaCl. With his nose occluded, the patient inhales the aerosol during 2.5 minutes. The aerosol is produced in a nebulizer connected with oxygen, with diameter of particles 0.8 micrometers. Data acquisition was performed in 4 standard projections. After the completion of acquisition, perfusion lung scintigraphy was done using Tc-labeled albumine macroagregates (99Tc-MAA) in 4 standard projections.
Values of the pulmonary clearance were determined by the analysis of dynamic curves using the commercial programme and were expressed as T1/2 - time that is necessary for the radioactivity to decrease to the half of maximal value.
Obtained results were statistically analysed using t-test for paired samples, X2 test and Fisher’s test.
 

Results (back to Quick Links)

Structure of the analysed groups is presented on the Table 1.

Table 1. Structure of the groups

 

sex

age

height

weight

side

 

M

F

X + SD

X + SD

X + SD

L

R

SP

11

0

37.0 + 13.39

179 + 7.3

70 + 12.0

5

6

SHP

8

2

34.5 + 10.22

181 + 9.1

71 + 12.4

5

5

* SP - spontaneous pneumothorax
*SHP - spontaneous haemopneumothorax


Results of spirometry, diffusion parameters and pletismography of the patients from the SP-group are presented on the table 2.

Table 2. Values of lung function tests (SP- group)

VC

TLC

RV

FRC

FEV1

Tiffenau

Dlco

Dlco/VA

FEF50

pred.

4.95 0.55

7.02 0.50

1.87 0.35

3.36 0.22

4.11 0.54

80.90 0.85

10.52 2.14

1.88 0.30

5.31 0.72

act.

4.35 1.84

7.72 1.54

2.85 0.73

4.64 1.08

3.65 1.41

72.27 13.0

8.87 2.41

1.22 0.24

3.45 2.02

t-test

1.22

- 1.77

- 4.81

- 3.71

1.68

2.64

3.31

5.83

4.60

P

> 0.05

< 0.05

< 0.001

< 0.001

> 0.05

< 0.05

< 0.001

< 0.001

> 0.001

In this group, elevated values of FRC and RV indicate some degree of lung hyperinflation. Slight obstructive ventilatory disorders existed in 4 cases in this group and of moderate degree in only one. In this group, Tiffenau-index was significantly less than predicted values. Also, unlike the SHP- group, forced expiratory flows measured at low lung volumes, were below the predicted values. In this group, unlike the SHP- group, significant difference existed not only for diffusion coefficient, but also for diffusion capacity compared with the predicted values. The analysis of percent-values revealed that differences in diffusion coefficient were more significant than those of diffusion capacity (mean value of 66.55 + 13.41% vs. 83.88 + 12.11%). Also, in 4 patients diffusion coefficient was 60% or less, that was not the case with the diffusion capacity.

Results of the analysis of the same parameters in the SHP-group are presented on the table 3.

Table 3. Values of lung function tests (SHP-group)

 

VC

TLC

RV

FRC

FEV1

Tiffenau

Dlco

Dlco/VA

FEF 50

pred.

4.97

0.87

7.02

1.00

1.83

0.26

3.37

0.30

4.17

0.71

81.47

2.05

10.56

2.49

1.89

0.24

5.39

0.76

act.

5.10

1.08

7.55

1.37

2.57

0.58

5.01

1.43

4.29

0.97

85.3

10.39

10.45

2.12

1.46

0.23

5.07

1.59

t-tes

- 0.57

- 2.28

- 3.58

- 4.03

- 0.84

- 1.34

0.33

5.1

0.99

P

> 0.05

< 0.05

< 0.001

< 0.001

> 0.05

> 0.05

> 0.05

< 0.001

> 0.05

In this group, no obstructive ventilatory disorders were found. Vital capacity and forced expirium parameters were normal either with low or high lung volumes. Values of RV and FRC were significantly higher compared with predicted values that indicates the existence of some degree of lung hyperinflation. Tiffeneau-index in no patients in this group was less than 72% without significant difference in relation to predicted values. Although absolute values of diffusion coefficient were significantly lower than predicted values, analysis of percent values revealed this parameter lower than 75% only in two patients (in one patient 61%, in the another 63%). Neither absolute values, nor percent-values of diffusion capacity were significantly different from predicted values.

Comparison of the two groups concerning all parameters (expressed in percent values) is presented on the table 4. Statistically significant difference exists only for diffusion capacity, not for other analysed parameters.

Table 4. Comparison between groups (percent values)

 

VC

TLC

RV

FRC

FEV1

100FEV1/VC

Dco

D/VA

FEF/50

SP group

96.80 20.39

107 21.43

147 49.01

135.18 38.19

86.36 22.56

89.18 13.33

83.89 12.16

66.55 13.41

64.72 27.55

SHP group

103.10 13.07

107.40 9.37

143.70 38.77

148.10 34.83

102.50 10.47

104.80 10.47

99.00 11.66

76.90 12.61

92.50 18.25

t-test

0.82

0.05

-0.17

0.56

2.10

2.96

27.60

173

2.68

p>0.05

p>0.05

p>0.05

p>0.05

p>0.05

p>0.05

p<0.05

p>0.05

p>0.05


The second part of this study is perfusion and ventilatory lung scintigraphy with determination of pulmonary clearance.
Results of this investigation in the SP-group are shown on the table 5.

Table 5. Perfusion and ventilatory lung scan in the SP-group

PERFUSION

VENTILATION

affected lung

affected lung

 

normal

defects

 

normal

defects

apical

4

7

apical

4

3

basal

9

2

basal

7

-

healthy lung

healthy lung

 

normal

diminished

 

normal

diminished

apical

8

3

apical

3

4

basal

11

-

basal

7

-

Perfusion disturbances existed mainly in the apical lung parts, both at the affected and healthy side. The frequency of disturbed perfusion in the affected lung compared with the non-affected lung is greater in this group than in the SHP-group. Basal perfusion defects existed only in two cases, only in the affected lung. Beside apical and basal lung parts, diminished perfusion in this group existed in central lung zones affecting diseased side in one and the healthy side in two patients. Ventilatory disturbances also affected apical lung parts. Comparing the affected and non-affected lung, perfusion disturbances were more frequent at the diseased side, whilst ventilatory disturbances did not follow that pattern.

Results of the same investigation in the SHP-group are shown on the table 6.

Table 6. Perfusion and ventilatory lung scan in the SP-group

PERFUSION

VENTILATION

affected lung

affected lung

 

normal

defects

 

normal

defects

apical

5

5

apical

2

8

basal

9

1

basal

7

3

healthy lung

healthy lung

 

normal

diminished

 

normal

diminished

apical

6

4

apical

3

7

basal

10

-

basal

10

-

In this group, perfusion of the apical lung regions is decreased both in the healthy and in the affected lung. Only in one case decreased perfusion of the basal parts of the lung at the affected side was found, without the same finding at the healthy side in any patients. Ventilatory disturbances more frequently existed in the apical parts of the lungs on both sides with basal hypoventilation in the affected lung in 3 patients. Neither perfusion, nor ventilatory differences between the affected and non-affected lung were statistically significant in this group.
Using the Fisher’s test, no significant differences were found between the SP-group and the SHP-group concerning the aforementioned analysed parameters.

In both groups pulmonary clearance was determined and expressed as T/2 i.e. the time that is necessary for the radioactivity to decrease to the half of the maximal value. This parameter reflects the lung epithelial permeability. Values of the pulmonary clearance in both groups are shown on the table 7.

Table 7. Lung clearance

 

SPONTANEOUS

PNEUMOTHORAX

SPONTANEOUS

HAEMOPNEUMOTHORAX

 

healthy lung

affected lung

healthy lung

affected lung

Smokers

31.6814.43

31.1010.28

50.9415.79

58.4222.69

Non smokers

86.8849.41

88.7550.61

   

The analysis of this parameter in both groups showed that there were no differences between the affected and non-affected lung among non-smokers. In the smokers group, the obtained values were lower comparing with non-smoker, that is not surprising.
 

Discussion (back to Quick Links)

What is the aim of assessing regional lung function changes in patients with healed SP and SHP and what is the reason for treating these two condition as separate groups?

First, it is not still established whether there is one single factor contributing to blebs isolation or if it is the consequence of the combination of many factors; is it the consequence of simple obstruction of small airways by mucous plugs or may be of its combination with regional lung function disturbances.

Second, in most scintigraphic studies in the acute phase of SP regional lung volumes are usually expressed as fractions of regional TLC. In lungs with SP, TLC is decreased so that at TLC level, units in the lung with SP are less expanded than those on the contralateral side. This fact also supports the usefulness of data obtained after full lung reexpansion has been achieved.
Third, emphysematous valve vesicles develop through local emphysematous changes representing frequent residual of many pathologic conditions in the lungs and may occur as solitary vesicles on the lung borders 10. Localised emphysema, found in all age groups and usually asymptomatic, is caracterised by this type of vesicles representing an important cause of SP 11.
Finally, having in mind that the source of intrapleural bleeding in SHP are torn adhesions between the chest wall and the collapsed lung, the aim of treating of SHP as a separate group is to reveal eventual differences in regional lung function distribution between SP and SHP that could be the cause of different effects of the elastic lung recoil - in most cases lung collapse without tearing adhesions, and only in few cases tearing of adhesions supplied by the systemic circulation.
Unlike  SP, where different imaging procedures together with the analysis of the operative specimens renders insight in the etiologic factors ( 762 pts in a 5-years period - table 8), SHP represents potential  life-threating condition, usually requiring urgent treatment. That’s why regional lung function assessment in the stable phase is practically the only possible method contributing to the better comprehension of pathophysiology base of this condition.

Table 8. Etiologic factors

 

N

%

Bleb

555

74.39

Big bulla

COPD

TB (activ)

TB (sequel.)

Bleb

COPD

Other

28

94

42

 

(16)

(21)

(2)

3.75

12.60

5.63

Tumours

Primary

Metastatic

 

8

7

 

1.07

0.98

Pneumonia

3

0.40

Silico - TB

1

0.13

Bronchiestasis

2

0.26

Lug fibrosis

3

0.40

SLE

1

0.13

M. Chiller - Chr

1

0.13

Hydatid. Cyst.

1

0.13



Obtained results of the respiratory function tests in both groups indicate the existence of some degree of lung hyperinflation that confirms similar results of other authors (Lesur, Delorme, De Troyer, Jernault). Some authors even state that a certain degree of lung hyperinflation exists up to 3/4 patients with spontaneous pneumothorax 12.
Concerning the type of the ventilatory disorder, difference between the two analysed groups is the lack of obstructive ventilatory disorder in SHP group. The cause of this difference is not clear if taking account about the similar age of patients in both groups.
Existence of obstructive ventilatory disorders in the SP-group does not differ from similar investigations in which Tiffenau-index is rarely under 60-70%. Of course, such a finding is characteristic for the primary SP, while in selective analyses depending on the existence or absence of COPD, Tiffenau-index can be significantly lower.
Among all analysed parameters, statistically significant difference between groups existed only for diffusion capacity. Diffusion disorders, registered in many published series, are by most authors attributed to the existence of multiple bullae or blebs, but not to the diffuse lung emphysema. Galy 13 states that even localized bullous lesions can induce the decrease of diffusion capacity without coexisting diffuse emphysema.
Results of scintigraphic evaluation in both groups support the literature data with more frequent difference between the affected and non-affected lung in the SP-group in terms of perfusion defects. Finding of ventilatory disorders that are most prominent in apical lung zones, and without significant differences between sides, are in some disagreement with the literature data, the latter comprising decreased ventilation at the affected side.
 

Conclusion (back to Quick Links)

Obtained results, although indicating the existence of some degree of lung hyperinflation, and supporting generally expected distribution of ventilatory and perfusion disturbances, do not render enough data for regional lung function disturbances to be considered a contributive factor in the occurrence of SP and SHP. Besides, the analysis of the pulmonary clearance did not confirm the existence of impaired integrity of the alveolo-capilary membrane.
 

References (back to Quick Links)
 

1. Ross C.A.: Spontaneous haemopneumothorax  J Thorac Surg 1952; 23 (6): 582-92. (back to text)

2. Millard F.J.C., Pepper J.R.: Pneumothorax  Respiratory Medicine, 1990, Bailliere Tindall; Vol II : 1423-26. (back to text)

3. Abyholm F.E., Storen G. Spontaneous hemopneumothorax  Thorax 1973; 28: 376-7. (back to text)

4. West S. Case of complete recovery from pneumothorax without effusion of fluid  Tr Clin Soc, London 1984; 17: 56. (back to text)

5. Tueller E.E., Crise N.R., Belton J.C., McLaughlin R.F. Idiopathic spontaneous pneumothorax  (back to text)

6. Dermksian G., Lawrence E.L. Spontaneous pneumothorax in apparently healthy flying personnel  Ann Intern Med 1959; 51: 39-51. (back to text)

7. Scott G.C., Berger R., Mcean H.E.  The role of atmospheric pressure variation in the development of spontaneous pneumothoraces
Am Rev Respir Dis 1989; 139: 659-662. (back to text)

8. Miserocchi G., D'Angelo E., Agostoni E. Topography of pleural surface pressure after pneumo or hydrothorax   J Appl Physiol 1972; 32: 296 (back to text)

9. Anthonisen N.R.  Regional lung function in spontaneous pneumothorax  Am Rev Resp Dis 1977; 115: 873-6. (back to text)

10. Ohata M., Suzuki H. Pathogenesis of spontaneous pneumothorax (with special reference to the ultrastructure of emphysematous bullae)
Chest 1980; 77: 6. (back to text)

11. Perry M.A.  On spontaneous pneumothorax  Quart J Med 1939; 8: 1. (back to text)

12. Lesur O., Delorme N., Fromaget M.J., Bernadec P., Poly M.J.  Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax
Chest 1990; 98: 341-47. (back to text)

13. Galy P., Brune J., Dorsit G., Wiesendanger T., Brune A.  Interpretation de l'abaissement de DLco/Va dans les emphysemes radiologiquement bulleux
Bull Physiopathol Resp 1968; 4: 749-62. (back to text)


Corresponding author:

Dr Dragan Subotic, MD. Ph.D.
Center for Thoracic Surgery
Institute of Lung Diseases,
University Clinical Center
Visegradska 26, 110000 Belgrade
Yugoslavia
Tel. 00 381 11 47 11 96
Fax. 00 381 11 64 69 88
E-Mail: grudhir@yubc.net 


Internet Scientific Publications, L.L.C., 1996 to 2000.

First Published: October 1996

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