|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 312-314
A letter in response to recurrent subcutaneous emphysema in a treated tuberculosis patient: Is there any association?
Department of Pulmonary Critical Care and Sleep Medicine, VMMC and Safdarjang Hospital, New Delhi, India
|Date of Web Publication||1-Jul-2014|
Department of Pulmonary Critical Care and Sleep Medicine, VMMC and Safdarjang Hospital, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Ray A. A letter in response to recurrent subcutaneous emphysema in a treated tuberculosis patient: Is there any association?. Lung India 2014;31:312-4
|How to cite this URL:|
Ray A. A letter in response to recurrent subcutaneous emphysema in a treated tuberculosis patient: Is there any association?. Lung India [serial online] 2014 [cited 2020 Jul 13];31:312-4. Available from: http://www.lungindia.com/text.asp?2014/31/3/312/135805
Apropos of the article written by Ete et al.  where a female patient with past history of tuberculosis presented with shortness of breath and swelling of face, I would like to furnish the following comments:
- The patient has been rightly labeled as spontaneous mediastinal emphysema as she developed the mediastinal emphysema during spontaneous breathing (and not on positive pressure breathing). Now subcutaneous emphysema associated with positive pressure ventilation, palpebral cutaneous tension, palpebral occlusion, airway compromise, dysphagia, dysphonia, pneumoperitoneum etc., has been defined as "severe" or "extensive subcutaneous emphysema". , As in the case described by the authors there was palpebral occlusion it can also be appropriately labeled as "severe" or "extensive" subcutaneous emphysema which also connotes the severity of the subcutaneous emphysema which the patient had.
- In the letter the authors deliberated on the possible cause for the recurrent subcutaneous emphysema in the patient. In this regard, the pathophysiology of recurrent subcutaneous emphysema can perhaps be explained by the Macklin effect.  According to this concept air passing through ruptures in alveoli tracks through bronchovascular sheaths to reach the mediastinum which has somewhat negative pressure with respect to the pressure in the pulmonary parenchyma. Once in the mediastinum the air would further move along tissue planes taking the path of least resistance into the subcutaneous tissue producing subcutaneous emphysema. Some air may rupture through delicate mediastinal fascia to produce pneumothorax. Since the least resistance is offered by the subcutaneous tissue space there is preferential accumulation of air in this space and not in other areas like the pleural space. This is exemplified in this case by the fact that there were minimal pneumothorax but severe subcutaneous emphysema. This is explained in [Figure 1].
|Figure 1: Macklin effect suggests that the air leak caused due to alveolar rupture tracks along the bronchovascular sheath to the mediastinum and then to the subcutaneous tissue along the path of least resistance. Some air may enter the pleural space after rupture of mediastinal pleura|
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- Various techniques have been reported to aid in the resolution of severe subcutaneous emphysema like incisions on the skin, fenestrated catheters, chest tubes with or without suction etc., Incidentally, we had described a novel method of using fenestrated central venous catheter to treat this condition (manuscript in press). These catheters or drainage tubes act as conduits for removal of air from the subcutaneous tissues. This is exemplified in [Figure 2] and [Figure 3]. While fenestrated catheters inserted in the subcutaneous plane act to remove air in subcutaneous tissue directly, the intercostal drainage catheters provide an alternate way for exit of air in the mediastinum (tracking along bronchovascular sheaths from the site of alveolar rupture) through the pleural space rather than into the subcutaneous tissue. But what is important to appreciate is that these methods aim to treat the cosmetic aspect (decreases the subcutaneous emphysema) but has no effect on the underlying air leak which had led to the migration of air to the mediastinum and subcutaneous tissue. If the underlying air leak does not heal (spontaneously or by help of interventions like decreasing or discontinuing positive pressure ventilation in appropriate cases) then there would be re-appearance of subcutaneous emphysema once the catheters or tubes are taken out. This was probably the reason why the authors had noted "recurrence" of subcutaneous emphysema on removing the intercostals drainage catheters. A more cautious approach in the index case might have been to clamp the intercostal drainage catheters and to look for increase in subcutaneous emphysema (followed by prompt removal of the clamps once the increase in emphysema has been appreciated) and to remove the intercostals drainage catheters once no increase in subcutaneous emphysema has been confirmed.
|Figure 2: The intercostal drainage catheter (icd) catheter creates a path of reduced resistance as a result of which the air in the mediastinum tracks along the pleural space (into the icd catheter) and not into the subcutaneous space|
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|Figure 3: A fenestrated catheter or subcutaneous incisions serve to provide an escape route for the air out of the subcutaneous space|
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- The decision to submit the patient to pleurodesis is surprising as even after splinting the two surfaces of the pleura together the air would continue to track into the subcutaneous tissue (provided the site of air leak is active). Thus, the subcutaneous emphysema would probably recur again as shown in [Figure 4].
|Figure 4: After pleurodesis the air in the mediastinum would not enter into the pleural space but will still continue to track into the subcutaneous space|
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- The old history of tuberculosis of the patient, the clinical picture of tracheal deviation and CT picture of parenchymal fibrosis hint to residual damage of lung by tuberculosis. The fact that the shortness of breath in this patient antedated the development of swelling by 2 weeks (the minimal pneumothorax on the CT scan seems unlikely to explain dyspnea in this patient) also might hint at a possible airway involvement. It would be indeed enlightening to know about past symptoms of cough with or without sputum (after resolution of tuberculosis and before the development of severe subcutaneous emphysema), old spirometry suggestive of obstructive airway disease or expiratory CT scans suggestive of air trapping in this patient. Since it is known that post tubercular obstructive airway disease (PTOAD) might occur in more than 30%  of pulmonary tuberculosis patients it behooving to consider a diagnosis of PTOAD since it fits the larger picture and might also explain the genesis of air leak in this patient.
| References|| |
|1.||Ete T, Mondal S, Sinha D, Nag A, Chakraborty A, Pal J, et al. Recurrent subcutaneous emphysema in a treated pulmonary tuberculosis patient: Is there any association? Lung India 2014;31:197-8. |
|2.||Cesario A, Margaritora S, Porziella V, Granone P. Microdrainage via open technique in severe subcutaneous emphysema. Chest 2003;123:2161-2. |
|3.||Srinivas R, Singh N, Agarwal R, Aggarwal AN. Management of extensivesubcutaneous emphysema and pneumomediastinum by micro-drainage: Time for a re-think? Singapore Med J 2007;48:e323-6. |
|4.||Macklin CC. Transport of air along sheaths of pulmonic blood vessels from alveoli to mediastinum: Clinical implications. Arch Intern Med 1939;64:913-26. |
|5.||Menezes AM, Hallal PC, Perez-Padilla R, Jardim JR, Muiño A, Lopez MV, et al. LatinAmerican Project for the Investigation of Obstructive Lung Disease (PLATINO) Team. Tuberculosis and airflow obstruction: Evidence from the PLATINO study in Latin America. Eur Respir J 2007;30:1180-5. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]