Study objectives: To review the etiology and
pathophysiology of pneumomediastinum in severe blunt trauma, with a
special interest in one of its possible origins, the Macklin effect.
The Macklin effect relates to a three-step pathophysiologic process:
blunt traumatic alveolar ruptures, air dissection along bronchovascular
sheaths, and spreading of this blunt pulmonary interstitial emphysema
into the mediastinum. The clinical relevance of the Macklin effect was
Setting: A university hospital serving
as a reference trauma center.
Patients: A selection of
51 patients with severe blunt trauma between 1995 and 2000.
Inclusion criteria: Severe trauma or high-speed
deceleration justifying chest CT; if chest CT demonstrated a
pneumomediastinum, bronchoscopy and esophagoscopy were performed to
rule out tracheobronchial or esophageal injury.
Design: Retrospective analysis of patients’ clinical
files, chest CT, and bronchoscopy and esophagoscopy reports. The
Macklin effect was diagnosed when an air collection adjacent to a
bronchus and a pulmonary vessel could be clearly identified on the
chest CT. Clinical relevance of the Macklin effect was statistically
evaluated regarding its repercussions on the pulmonary gas exchange
function, the respective durations of intensive care and total hospital
stay, and the associated injuries.
(39%) Macklin effects and 5 tracheobronchial injuries (10%) were
identified. One tracheobronchial injury occurred simultaneously with
the Macklin effect. The presence of the Macklin effect affected neither
the clinical profile nor the result of pulmonary gas analysis on
hospital admission, but was associated with a significant
(p < 0.001) lengthening of the intensive care stay.
Conclusions: The Macklin effect is present in 39% of
severe blunt traumatic pneumomediastinum detected by CT. Its
identification does not rule out a tracheobronchial injury. The Macklin
effect reflects severe trauma, since it is associated with
significantly prolonged intensive care stay.