In phases of dyspnoea, expiration was not prolonged. Work of breathing did not seem to be elevated; she did not perform pursed lips breathing, which questioned a typical asthma attack. In addition, at least some improvement from beta-agonists and systemic corticosteroids would have been expected in an asthma ISRIB attack. The pre-bronchodilator resistance curve in Fig. 1 showed airway obstruction exclusively during expiration. A totally normal inspiratory resistance is atypical for severe bronchial obstruction. This phenomenon was

seen in repeated lung function tests. However, for one test, in 1 out of 3 manoeuvres, the expiratory resistance was completely normal. Despite a relevant increase of intra-thoracic gas volume (ITGV), the crossing of the resistance curve with the x-axis gave no hint for trapped air as it normally occurs with the inspiratory part crossing on the left and the expiratory part crossing on the right of point zero. All the pathologic changes seen in lung function testing can be explained by the tongue

being put forward into the mouthpiece of the Fleisch pneumotach exclusively during exhalation. This manoeuvre was impossible when performing the spiroergometry. There, the spirometer is integrated in the mask and cannot be obstructed by the tongue. As expected, in the later Decitabine cell line setting, bronchial obstruction was not detectable. The combined findings, including the episodes of fever of unknown origin, reassured us with our diagnosis of a Munchhausen’s check syndrome complicating her known asthma. In asthma refractory to treatment, Munchhausen’s syndrome should be taken into consideration.2 It may mimic asthma as well as complicate a pre-existing asthma. In this

case, the fact that the young women worked in a paramedical profession and that she obviously suffered from mental anorexia could have been a hint to an increased likeliness of Munchhausen’s syndrome. There exists no conflict of interest. “
“Subcutaneous emphysema and pneumomediastinum occur frequently in critically ill patients in association with alveolar rupture, blunt or penetrating trauma, soft-tissue infections, or any condition that creates a gradient between intra-alveolar and perivascular interstitial pressures.1 We report a case where patient presented with severe shortness of breath and subcutaneous emphysema that was secondary to direct communication of cavitary tuberculosis lesion of left upper lobe into the soft tissue of chest wall. A 46-year-old male who worked in a factory presented with complaints of breathlessness, with swelling over the chest for past two days. This was sudden in onset after a bout of coughing leading to an initial swelling at the left side of the chest and then spreading to whole chest, neck, arm and face over the next few hours. There was history of low-grade fever and cough with expectoration for the past one year.