ABSTRACT
Spontaneous pneumothorax is a common surgical disease that is a surgical emergency. It can be divided into primary (caused by microscopic blebs <1 cm in diameter) and secondary (asthmatic, catamenial, neonatal, caused by emphysematic bullae or chronic respiratory obstruction) varieties. This surgical entity has been closely associated to a variety of electrocardiographic (ECG) changes, which are pathophysiologically explained by spatial changes in the anatomical structure of the mediastinum caused by increased hemithoracic pressure. Several reports on ECG variations due to pneumothorax that masquerades as myocardial ischemia have been previously recorded. However, when the underlying disease involves two pathological entities, in this case pneumothorax and myocardial infarction, time limits can be pressing. Herein, we describe an interesting case of a patient who presented with left secondary spontaneous pneumothorax associated with acute myocardial infarction. It is an intriguing and rarely encountered case in which the patient's anamnesis can easily mislead the clinician and valuable time can be wasted.
Subject(s)
Myocardial Infarction/complications , Pneumothorax/complications , Chest Tubes , Electrocardiography , Humans , Intubation, Intratracheal/instrumentation , Male , Middle Aged , Myocardial Infarction/diagnosis , Pneumothorax/diagnosis , Pneumothorax/surgery , Thrombolytic Therapy , Treatment OutcomeABSTRACT
Physiology changes of the pleura in spontaneous pneumothorax (SP) patients are not known with its etiology remaining unclear. The aim of the study was to investigate the pleural electrophysiology profile of SP patients and to compare it with the normal pleural electrophysiology. Specimens from nine patients who underwent surgery for persistent SP were obtained after wedge resection (apical visceral) and apical pleurectomy (apical parietal) alongside with parietal specimens over the 8th-9th rib (caudal parietal). Specimens were mounted in Ussing chambers and trans-mesothelial resistance (R(TM)) was determined as a permeability indicator. Amiloride (Na(+) channel inhibitor) was used as an ion channel transportation inhibitor. R(TM) of apical visceral, apical parietal and caudal parietal pleura of SP patients was increased (P=0.042, 0.025 and 0.001, respectively) when compared to disease-free specimens obtained from lung lesion patients. Amiloride was unable to increase R(TM) in all cases. Histopathology of apical and caudal parietal specimens revealed inflammatory infiltration. In conclusion, pleural electrophysiology is altered in SP patients when compared with the electrophysiology of disease-free specimens. A similar observation was made for caudal pleura suggesting diffuse process that possibly involves inflammation as shown by the histopathology.
