Year : 2007 | Volume
: 24 | Issue : 3 | Page : 102--104
Pneumomediastinum with subcutaneous emphysema in a silico tuberculosis patient
Ramakant Dixit1, Lokendra Dave2,
1 Department of Tuberculosis & Chest Diseases, J. L. N. Medical College, Ajmer., India
2 Department of Medicine, Gandhi Medical College, Bhopal, (India)., India
Assistant Professor in Respiratory Medicine, 381/26, Ramganj, Ajmer-305001.
The present communication describes a case of pulmonary tuberculosis with silicosis that developed pneumomediastinum with subcutaneous emphysema following anti-tuberculosis chemotherapy. Possible mechanism of such complication and its clinical significance are also described.
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Dixit R, Dave L. Pneumomediastinum with subcutaneous emphysema in a silico tuberculosis patient.Lung India 2007;24:102-104
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Dixit R, Dave L. Pneumomediastinum with subcutaneous emphysema in a silico tuberculosis patient. Lung India [serial online] 2007 [cited 2020 Feb 23 ];24:102-104
Available from: http://www.lungindia.com/text.asp?2007/24/3/102/44227
Air in the mediastinal tissue is referred to as pnemomediastinum. It is not a common clinical condition, although it may occur in a wide variety of different disorders. Most cases of pnemomediastinum probably are the result of alveolar rupture into the bronchovascular sheath, from momentary shearing force due to sudden pressure discrepancy between them, mainly in the presence of alveolar overdistension , . It is suspected by the presence of subcutaneous emphysema, mainly in the region of neck or may be diagnosed mainly by its characteristic radiological features , .
The present communication describes a case of pneumomediastinum with subcutaneous emphysema in a silicotuberculosis patient after starting anti-tuberculosis therapy.
A 35-year-old male patient was admitted for breathlessness, cough, loss of appetite and fever. He was nonsmoker, nonalcoholic and vegetarian. For the past two and a half years he was working in a stone-drilling factory. Prior to this he was a housekeeper for 10 years.
He was asymptomatic and healthy prior to this employment. For last one year, he used to feel dry cough and breathlessness while at work but these symptoms became persistent in the last six months and gradually increasing in severity. Over the last four months, he developed fever and loss of appetite. He also gave history of four episodes of mild blood in his sputum in last 15 days.
On examination patient was febrile, dyspnoeic but without cyanosis, clubbing and lymphadenopathy. Examination of respiratory system revealed bilateral crackles in upper lung fields. Routine examination of blood and urine were normal except raised erythrocyte sedimentation rate (42 mm in the first hour). Sputum smear examination was negative for acid-fast bacilli in three samples. Pyogenic culture of sputum was sterile. Skiagram chest revealed bilateral reticulo-nodular infiltrates with areas of confluent opacities in upper and mid zones. Mantoux test was reactive (20mm induration at 72 hours) and sputum microscopy by concentration method revealed few acid-fast bacilli. His ECG and blood chemistry was within normal limits. Spirometry revealed a mild restrictive type of ventilatory defect. He was negative for HIV antibodies and Rh factor.
Based on history, clinical examination and investigation reports, a diagnosis of pulmonary tuberculosis with silicosis (silicotuberculosis) was made. Although lung biopsies and CT scan could not be performed, the diagnosis of silicosis was strongly considered based on significant clinical history (positive occupational history co relating with clinical symptoms) and suggestive radiological picture on chest radiography. He was put on antituberculosis drugs, steroids and supportive therapy. After taking third dose of directly observed treatment for tuberculosis, patient complained of increase in cough frequency followed by feeling of crepitus swelling over neck, shoulder and chest with mild chest pain. On examination subcutaneous emphysema was noted on the neck, chest and shoulder. There was no additional information on respiratory and cardiac auscultation. There was no pulsus paradoxus and Hamman's sign was absent.
A repeat chest radiography showed similar lesions along with a sharp line of lucency outlining the left cardiac border. Mediastinal and subcutaneous air was also noticed but there was no pneumothorax [Figure 1]. Patient was treated with reassurance and kept under observation for five days. The previous treatment was also continued. Complete resolution of the subcutaneous emphysema was noted at the end of two weeks. There was no recurrence of pneumomediastinum thereafter.
Pneumomediastinum or mediastinal emphysema may develop under three circumstances-(i) mediastinal sepsis from gas forming organism introduced from soft tissues nearby, commonly the head and neck, (ii) traumatic disruption of large gas containing structures i.e. esophagus and trachea, frequently in association with positive pressure ventilation, or from the retro-peritoneal space, (iii) damage to alveoli and to bronchioles, allowing gas to leak along the bronchovascular bundle towards the mediastinum  . The last mechanism is the most common mechanism where alveolar rupture may occur as a result of marked increase in intra-alveolar pressure secondary to conditions like violent cough especially with glottis closed, asthmatic paroxysms, strenuous vomiting etc  . It has also been reported in pulmonary tuberculosis, pneumonia, bronchogenic carcinoma and sometime in the absence of any demonstrable predisposing disease and absence of any trauma, when it is called primary pneumomediastinum ,, . The pressure gradient between the intra-alveolar air pocket and the contiguous blood vessels lining the alveoli favors their rupture. The air so escaped enters the perivascular sheath, courses its way either towards the visceral pleura or towards the lung hilum and mediastinum. If the former is ruptured a condition of homolateral pneumothorax occurs while a sequel of the dissection to the lung hilum results in mediastinal emphysema  .
Pneumomediastinum in tuberculosis is uncommon , , however, in interstitial lung diseases, it is very rare  . Severe coughing in tuberculosis has been proposed to precipitate the rupture of the alveoli  . Adhesions between visceral and parietal pleura are too common over the areas of tuberculous lung. A tear of such pleural symphysis into the subcutaneous tissues may also produce emphysema, giving rise to typical crepetus  . Interstitial lung disease produces areas of uneven lung expansion with hyperinflation and areas of atelectasis. It is also assumed that there is an increase risk of rupture in the hyper inflated areas of lung, leading to interstitial emphysema  . Further, it is also said that in both tuberculosis and silicosis, local airway obstruction with distal air trapping can cause alveolar rupture and subsequent pneumomediastinum  . Any one or more of the above mechanism might be possible for the development of pneumomediastinum with subcutaneous emphysema due to both pulmonary tuberculosis and silicosis in our case and the process might have been fueled by the lysis of tuberculous foci by anti tuberculosis drugs.
Central chest pain is the commonest symptom of pneumomediastinum and mimic myocardial infarction or pericarditis with exacerbation by movements and breathing and relief by leaning forward in sitting position. Dyspnoea, dysphasia and dysphonia may be present. On examination, widespread surgical emphysema is usually present. A characteristic, though not specific sign, noted in about 50% cases is the Hamman's sign, a crackling sound or crunching sound heard at the sternal edge with patient sitting forward or in the left lateral decubitus position with the heart sounds  . Chest radiography reveals the free mediasinal air as sharp lines of increased lucency enhancing the mediastinal viscera, outlining the cardiac borders and widening the superior mediastinum. Other radiological signs include 'continuous diaphragm' sign, 'ring around the artery' sign (air around the right pulmonary artery in frontal view), 'V' sign (the confluence of innominate veins outlined in frontal view), pneumopericardium and presence of retrosternal air on lateral skiagram  .
Conservative treatment is indicated in majority of pneumomediastinum as spontaneous absorption of air occurs within a week. It has also been shown to improve by breathing high concentration oxygen replacing nitrogen by rapid absorption of oxygen, especially in non-surgical pneumomediastinum. Reassurance, observation and analgesia apart from removal of precipitating cause is all, that is needed in most of these cases. Special attention is required when pneumomediastinum complicates into pneumothorax, cardiac temponade, air block (because of splinting action of peribronchial air causing further occlusion of airways), pulmonary arterial hypertension and stridor  , which can occur in some cases.
In conclusion, the present report describes a self limiting case of pneumomediastinum in a patient of silicotuberculosis with an emphasis to make clinicians aware of this uncommon complication and its significance, that may arise in their day today pratice.
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