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Letter to the Editor—Commentary on: Ro A, Chiba S, Sagi M, Kageyama N, Hayashida M, Ikawa T, et al. Abdominal stab wounds with tension pneumopericardium confirmed by autopsy and postmortem computed tomography. J Forensic Sci https://doi.org/10.1111/1556-4029.14028. Epub 2019 Feb 20

Sir, We have read with great interest the paper by Ro et al., describing the case of a woman who died of self-inflicted stab wounds to the abdomen, with the occurrence of pneumopericardium observed both at gross autopsy examination and postmortem computed tomography (1). The amount of air, calculated to be 133 mL, entered the pericardial sac from the abdomen, through the stab wounds that had cut the apical pericardium and adjacent diaphragm and liver. The authors concluded that the death resulted from the combination of hemorrhagic shock induced by the aortic cut and obstructive shock caused by the tension pneumopericardium (TPPC) and that the volume of PPC suggested that TPPC could induce lethal cardiac tamponade through lowpressure cardiac tamponade which occurs when hemorrhagic shock and obstructive shock develop concurrently. Several years ago, we published a similar case of pneumopericardium in a 34-year-old man who committed suicide by jumping from the height of 30 m (2). It was concluded that the cause of death was hemorrhagic shock, while pneumopericardium was considered a reflection of air embolism caused by the open skull fracture with laceration of the right transverse sinus of the dura. Due to the rupture at the junction of the superior vena cava and right atrium, instead of going into the right ventricle and further causing pulmonary air embolism, the air leaked out into the pericardial sac, filling it and causing pneumopericardium, clearly visible by the naked eye during autopsy. However, we do not agree with the conclusion made by Ro et al. that the air in the pericardial sac caused the cardiac tamponade (i.e., “tension pneumopericardium”) in the case they presented. As confirmed by the autopsy, the air entered the pericardial sac through the diaphragm. Normally, the effective pericardial pressure is slightly lower than the atmospheric pressure (up to 4–5 mm Hg lower) (3). After the injury, the pressure inside the pericardial sac could only become equal to the atmospheric, that is, it could not have been higher than one atmosphere (~100 kPa). That (atmospheric) pressure is not sufficient to cause “tension pneumopericardium,” regardless of the fact that the amount of air was 133 mL, because air is compressible (unlike blood)—therefore, that amount was not significant and cannot be compared to the amount of blood sufficient to cause tamponade. Additionally, the development of hemorrhagic shock through the injury of aorta requires some time and blood pumping. During that time, the air does not make sufficient pressure on both venae cavae and the heart to stop the filling of the heart; thus, it cannot cause the tamponade. The autopsy findings in the case by Ro et al. also support that there were only signs of exsanguination and no signs of cardiac tamponade, as authors stated themselves. Therefore, in the case presented by Ro et al., as well as in our case, due to the absence of signs of cardiac tamponade, pneumopericardium should not be considered the cause of death, but a vital reaction, and the sole cause of death was the hemorrhagic shock. In the case presented by Ro et al., as in our own, the air entered the pericardial sac from the outside (i.e., with the maximum pressure level corresponding to the atmospheric). In some cases, however, there is a possibility of pneumopericardium causing cardiac tamponade, but through a different injury mechanism, coming from the “inside,” by the so-called Macklin effect (4). In some cases of traumatic airway and lung injuries, for example, in asphyxias with obstruction of the upper airways, an increase in intraalveolar pressure occurs due to forced breathing attempts. This high intraalveolar pressure may cause the rupture of the marginal alveolar bases, dissecting the peribronchial and perivascular sheaths with the resulting escape of air peripherally along the vessels, sometimes resulting in pneumopericardium. In other cases, the pericardial space may also be connected directly to pleural or tracheobronchial gases as the consequence of a pericardial tear (4,5). In such cases, pericardial pressure may rise to the amounts significantly higher than the atmospheric pressure, thus causing cardiac tamponade.