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.