TENSION PNEUMOPERICARDIUM: A CASE HIGHLIGHTING THE IMPORTANCE OF EARLY DETECTION IN BLUNT POLYTRAUMA

Objectives: Twenty-two-year-old male motorcyclist presented as Motor Vehicle Accident, going approximately 50 miles per hour. Initial evaluation revealed GCS (Glasgow coma scale) of 8. The patient was hypotensive, tachycardic, with diminished breath sounds bilaterally. Once intubated, a right-sided chest tube was placed, with an improvement in oxygen saturation. However, the oxygen saturation dropped again, a left-sided chest tube was placed. There was limited response to blood product, and FAST exams showed no pericardial effusion or evidence of cardiac trauma. While in Computed Tomography (CT), pneumopericardium was immediately identified. The patient was taken for pericardiocentesis, pulses were lost before the start of the procedure. A resuscitative thoracotomy was performed, the pericardial sac was tense, and upon opening, a gush of air was released. Once the pneumopericardium was released, cardiac activity was noted, and blood pressure improved. The patient was taken immediately to the Operating Room for right thoracotomy, which was extended into a clamshell, and no obvious injury was identified. Due to persistent hypotension, an exploratory laparotomy and splenectomy were done due to splenic laceration. During abdominal exploration, cardiothoracic surgery completed a bronchoscopy where no tracheobronchial injuries were found. The patient had persistent hypotension, and the chest was re-evaluated for the source of bleeding. A hemostatic patch was placed in the right superior chest at the site of persistent ooze, and the chest and abdomen were packed. The patient was brought to the Intensive Care Unit for further resuscitation, where the patient later succumbed to his injuries.

Pneumopericardium is an exceptionally uncommon phenomenon in the setting of blunt polytrauma. It is imperative for trauma providers to identify tension pneumopericardium despite its rarity. Most commonly, blunt trauma results in a deceleration injury which causes a sudden surge of intrathoracic pressure causing alveolar damage. One explanation of the physiology of pneumopericardium causing tamponade is demonstrated by the Macklin Effect. The Macklin Effect is described as pulmonary parenchymal tears leading to air escaping along facial planes, which can leak into the pericardium at weak points in the sac. This patient demonstrated this, as his tamponade physiology did not improve with chest tube placement, and he became worse with mechanical ventilation in addition to no tracheobronchial injuries identified on bronchoscopy. Trauma surgeons should have tension pneumopericardium in their differential diagnosis when there is tamponade physiology without visualized pericardial effusion, especially if the condition worsens with intubation.

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