The incidence of occult pneumothorax is reported to be 5% in literature(2). Tension pneumothorax in tracheal intubation of emergency is a more rare but deleterious event, especially when predisposing factors cannot be known in view of acute profound hypoxemia. Tension pneumothorax both are negatively impacted by positive ventilation and has similar hemodynamic and respiratory consequences, while at the same time, extreme air-trapping can also lead to barotrauma(3). We collect several rare cases of tension pneumothorax of different etiology. Sunil Kumar Garg(4) and Erik Nygaard Andresen(5) present iatrogenic pneumothorax. Iatrogenic pneumothorax is a complication caused by procedures such as transthoracic needle aspiration, thoracentesis, transbronchial biopsy, pleural biopsy, and positive pressure ventilation. Even, nebulization and nasogastric feeding tube can cause similar phenomenon because of misuse. Therefore, education and training should be a continuous process. And approaches to all interventions should be taught to all medical workers so that they can be in a better position to understand the consequences of any deviation from standard. Yuki Yoshimatsu(6) and Khoa Anh Nguyen(7) describe the same situation because of the patient's own special condition including neurofibromatosis -related lung disease and congenital tracheal stenosis. High-resolution chest CT of patients, of course, may show anatomical abnormality including bullae, cysts, emphysema, and ground glass opacities. And congenital abnormality like tracheal stenosis and emphysematous could exist in absence of clinical symptoms and signs. Needless to say, knowing the patient's laboratory tests and examinations in detail are very essential. Ayman(8) and Steven(9) think present history of patients is also important, which include asthma, drug addiction and so on. Asthma‑related airway inflammation and alpha-1 antitrypsin deficiency caused by tobacco use and cocaine were the major cause for emphysematous, which is inducing factor of pneumothoraxes and the rupture of bullae. The rupture of bullae during manual ventilation is more serious by the rapid cardiorespiratory deterioration after intubation and start of controlled ventilation(1). If signs of circulatory compromise are not obvious and other indirect signs like jugular vein enlargement remain unnoticed, the diagnosis could be set with great delay. And the patient mentioned above had a known history of smoking and drinking, which may be the cause of pneumothoraxes.
The inability to ventilate a patient after successful intubation is a rare but emergent situation and may be caused by obstruction of the endotracheal tube, mainstem bronchus intubation, esophageal intubation, severe bronchospasm, or bilateral tension pneumothorax(10). It is recommended that observation of small occult pneumothoraxes, without tube thoracostomy in patients not receiving mechanical ventilation, is safe(8). But, in patients undergoing mechanical ventilation, chest tube is indispensable appliance to prevent development of tension pneumothorax. As for confirmation of tracheal tube placement, observation of passing through vocal cords during laryngoscopy, auscultation, observing symmetrical chest expansion and observation capnography or end-tibal carbon dioxide can be valid(11). However, the fiberoptic scope was not advised, on account of poor quality of the image obscured by secretions and blood, especially in blunt trauma patients.
Drawing lessons from the past, firstly, the patient should be fully evaluated before intubation including laboratory tests and examinations, present history and physical examination like auscultation of breath sounds in both lungs and palpation of the abdomen. Secondly, early control of the airway to ensure oxygenation, ventilation and protection against aspiration is paramount. Capnography to measure end-tibal carbon dioxide is a very practical prop, especially when auscultation breath sound is not clear. When intubation complications occur, the cannula should not be hastily removed and the patient's symptoms should be carefully evaluated again. In the emergency intubation items, if pulmonary shunt is present from the collapsed or atelectatic lung, the low mixed venous PO2 from low cardiac output will cause arterial hypoxemia. Breath sounds must be assessed immediately after tube insertion and periodically thereafter. Thirdly, if at any time breath sounds become decreased or lost, the position of the endotracheal tube has been confirmed before assuming that the patient has suffered a hemothorax or pneumothorax. Patients exhibited both hypoxemia, hypotension and signs of low cardiac output. They probably should elevate jugular venous pressure from impeding of venous return, which would cause an elevated intracranial pressure. The resultant increased intrathoracic pressure impeded venous blood return and ultimately led to cardiovascular collapse. Therefore, the diagnosis of tension pneumothorax can be proved by the patient’s clinical signs listed as before. Tension pneumothorax was suspected and should be managed with insertion of an 18‑gauge intravenous catheter in the second intercostal space, followed by chest tube insertion.