Discussion:
Pneumomediastinum relates to the accumulation of air in the mediastinal structures. It may result from blunt trauma leading to thoracic injury, esophageal perforation, or hollow viscus rupture. It can also occur spontaneously without any structural lung or mediastinal abnormalities in the absence of trauma, called SPM. In general, SPM can be caused by intrathoracic (involving trachea and major bronchial airways, esophagus, lung, and pleural cavity) or extra-thoracic (head, neck, or peritoneum) processes. SPM is a non-traumatic entity that occurs due to increased intrathoracic pressure leading to alveolar rupture. As the mediastinal pressure is more negative than the pulmonary parenchyma, the air enters the pulmonary interstitium. It dissects along the perivascular sheets to reach the hilum from where it spreads to the mediastinum. This phenomenon is described as the Macklin effect.(9) Occasionally, pneumopericardium can also occur with leakage of air into the pericardial space. (10) It is worth emphasizing, spontaneous alveolar rupture can occur even with no prior history of pulmonary disease or esophageal perforation and is usually precipitated by cough, emesis, physical exercise, labor, or upper airway infection.
The exact mechanism of ST-segment changes secondary to SPM remains unclear. The most common EKG findings associated with SPM are the loss of R wave in the precordial leads and diminution of QRS voltages or ST-segment elevation in inferior leads (11-15). Previously described mechanisms propose cardiac rotation, right ventricular dilatation, and insulation effect caused by air accumulation between the cardiac structures and the chest wall as the cause of such changes. Secondly, SPM may lead to myocardial stretch leading to stretching and narrowing of the coronary arteries, which may masquerade as ST-elevation myocardial infarction with a troponin leak (15). We further postulate the EKG changes associated with pneumopericardium in our cases could be related to the direct inflammatory effect from air leakage between the pericardium and the chest wall leading to a presentation similar to acute pericarditis. Such ST-T changes may give an initial diagnostic clue of the presence of pneumopericardium accompanying SPM. The concurrent pneumopericardium diagnosis may be relevant if caused by fistula formation from the adjacent intra-abdominal structures as mortality rates can be as high as 50-70% in such cases. (16, 17) Given the lack of abdominal symptoms and CT findings not suggestive of an intra-abdominal or esophageal source in Case 1, an esophagram was not performed. The esophagram in the second described case was performed as the patient presented with hyperemesis, leading to Boerhaave syndrome suspicion. These patients appear sicker on presentation with hypotension and shock due to chemical mediastinitis, and a pleural effusion often accompanies findings of SPM. (18)
Management of SPM is mainly conservative with avoidance of trigger factors, analgesia, bed rest, and oxygen therapy in the absence of complications such as hemodynamic instability, pneumothorax, suspected chemical mediastinitis, or tamponade effect by the coexisting pneumopericardium.