BAROTRAUMA is a complication of mechanical ventilation that may manifest by pulmonary interstitial emphysema, pneumothorax, pneumomediastinum, and subpleural air cysts. [1] Systemic air embolism has recently been recognized to occur as a complication of mechanical ventilation, during which air has been detected in the coronary and cerebral arterial circulations. [2–4] The mechanism of systemic air embolization resulting from positive-pressure ventilation has not been elucidated. We present a patient who, during pancreatic debridement, developed a tension pneumothorax and systemic air emboli, as documented by transesophageal echocardiography (TEE).

A 58-yr-old man (weight, 64 kg) with a 3-week history of necrotizing pancreatitis treated with intravenous fluids, antibiotics, and parental hyperalimentation developed fever, worsening abdominal discomfort, and bacteremia. Multiple bacterial cultures of pancreatic fluid, abdominal fluid, and blood culture identified methicillin-resistant Staphylococcus aureus. Operative pancreatic debridement with gastrostomy and jejunostomy tube placement was planned.

With an intravenous line, right radial arterial line, and a right internal jugular triple-lumen central line in place, anesthesia was induced with etomidate and fentanyl. Succinylcholine was administered to facilitate tracheal intubation. Anesthesia was maintained with inhaled sevoflurane and intravenous fentanyl infusion, and muscle relaxation was achieved with intermittent boluses of pancuronium. Mechanical ventilation was initiated with a tidal volume of 1000 ml and a respiratory rate of 10 breaths/min. Dopamine and insulin infusions were continued throughout the surgery.

Approximately 2 h into the procedure during retroperitoneal debridement, the patient became acutely cyanotic as oxygen saturation measured by pulse oximetry decreased to 30%. Ventilation became extremely difficult because of high airway resistance (peak airway pressures increased from 36 to more than 50 cm H2O) as the end-tidal CO2decreased to 5 mmHg. The patient developed a sinus tachycardia at a rate of 160 beats/min and hypotension with a systolic blood pressure of 40 mmHg. Lung auscultation revealed distant bilateral breath sounds. The precipitating causes of electromechanical disassociation, including pulmonary embolus, hypovolemia, cardiac tamponade, acidosis, hypoxia, and tension pneumothorax, were considered. The patient's resuscitation included 100% oxygen, chest compressions, crystalloid volume resuscitation, angiocatheters placed in the second intercostal space of the anterior chest wall bilaterally followed by bilateral chest tube thoracostomies, and several boluses of epinephrine, sodium bicarbonate, and calcium chloride. While an emergent chest radiograph was ordered, an examination with the TEE, which is always readily available in our operating room, was performed to further evaluate the possibility of pulmonary embolus, cardiac failure, or tamponade.

The TEE examination revealed normal left ventricular function and normal valvular function. The right ventricle (RV) appeared moderately dilated, but with normal function and without septal changes to suggest an acute increase in RV pressure or volume. The absence of intracardiac septal defects was confirmed by the absence of abnormal color Doppler flow and by the lack of contrast material seen in the left side of the heart after intravenous injection of agitated saline solution. An interesting and unexpected finding was that a stream of air bubbles was seen in the left atrium and left ventricle (Figure 1). The source of air bubbles was presumed to be from the tracheobronchial tree; thus, we attempted to isolate each bronchus to localize the source and eliminate the systemic air emboli. The endotracheal tube (ETT) was first advanced into the right mainstem bronchus (confirmed by fiberoptic bronchoscopy) to eliminate left lung ventilation. The bubbles seen in the left side of the heart on TEE disappeared when the right lung was selectively ventilated (Figure 2). When the ETT was pulled back into the trachea, the air bubbles in the left heart reappeared. Bilateral tube thoracostomies were performed, and a "rush of air" was heard as the left-sided chest tube was placed. The patient's hemodynamic parameters improved immediately, confirming the relief of a tension pneumothorax. The streaming of air in the left side of the heart as seen on TEE disappeared after the pneumothorax was evacuated. An emergency chest radiograph revealed bilateral chest tube placement without a pneumothorax. After surgery was completed, the patient was transported to the intensive care unit intubated, mechanically ventilated, and requiring dopamine for blood pressure support.

Figure 1. The transesophageal four-chamber view reveals numerous air bubbles in the left atrium (LA) and left ventricle (LV). No air bubbles are seen in the right atrium (RA) and right ventricle (RV). 

Figure 1. The transesophageal four-chamber view reveals numerous air bubbles in the left atrium (LA) and left ventricle (LV). No air bubbles are seen in the right atrium (RA) and right ventricle (RV). 

Figure 2. Shown is the same four-chamber view as  Figure 1 as the ETT is advanced into the right mainstem bronchus (occluding the left mainstem bronchus). Note the air bubbles in the left atrium (LA) and left ventricle (LV) have disappeared. 

Figure 2. Shown is the same four-chamber view as  Figure 1 as the ETT is advanced into the right mainstem bronchus (occluding the left mainstem bronchus). Note the air bubbles in the left atrium (LA) and left ventricle (LV) have disappeared. 

His postoperative course was notable for prolonged mechanical ventilatory support for respiratory failure and persistence of necrotizing pancreatitis with severe infectious complications. His renal function deteriorated, and he became dependent on hemodialysis. He suffered from frequent tonic-clonic seizures controlled with barbiturate infusions. His mental status gradually improved during the following 4 months, and he became alert and fully oriented, able to follow commands, and move all four extremities. He eventually weaned from mechanical ventilation and was transferred to a rehabilitation facility.

Barotrauma has been estimated to occur in 0.5–38% of critically ill patients. [5] Ventilator-induced barotrauma develops after an overdistended alveolus ruptures and air is introduced into the perivascular adventitia. Air dissects along perivascular sheaths to the mediastinum, causing pneumomediastinum. Air may then vent into the pleural space, causing pneumothorax, or decompress into the tissues of the neck, causing subcutaneous emphysema, or into the peritoneum, causing pneumoperitoneum. Rupture of a subpleural air cyst may also cause a pneumothorax. Risk factors thought to predispose to barotrauma include alveolar distention resulting from high tidal volumes, high inflation and inspiratory airway pressures caused by low lung or chest wall compliance, and positive end-expiratory pressures. [5,6]

Pneumothorax occurring during general anesthesia is a rare event; nevertheless, pneumothorax accounted for 3% of anesthetic complications identified by the American Society of Anesthesiologist's Closed Claims Project. [7] Pneumothorax was related to the performance of regional blocks in 40% of reported cases, by airway instrumentation in 19%, barotrauma in 16%, and central line placement in 7%. Barotrauma remains the most likely cause of pneumothorax in this case. It is unlikely that a pneumothorax developed from airway instrumentation because the intubation was uneventful and atraumatic. A pneumothorax resulting from central line placement was not contributory because the pneumothorax developed on the contralateral side from the right internal jugular central line placement. Obstructed expiratory flow resulting from mechanical malfunction of the breathing circuit has been associated with the development of pneumothorax; however, the circuit had been functioning normally. A pneumothorax caused by the surgical dissection cannot be ruled out.

A systemic air embolus may occur from the presence of a venous air embolism and an intracardiac or intrapulmonary shunt (paradoxical embolism). An intracardiac shunt is unlikely because the TEE revealed no evidence of an atrial or ventricular septal defect. Air in the venous circulation can overcome the "filtering mechanism" of the pulmonary circulation and become a systemic air embolus, [8,9] but no evidence of air in the right atrium or ventricle was found on TEE examination. The most likely explanation is that the air embolism occurred from the existence of a bronchovenous connection from the left bronchial tree to the pulmonary veins. This possibility could include rupture of an overdistended alveolus or subpleural cyst, causing a pneumothorax with coincidental laceration of a pulmonary vein creating a bronchopulmonary venous fistula. The increased intrathoracic pressure and tension pneumothorax may have provided a pressure gradient for air to enter the pulmonary veins. Because the stream of air bubbles in the heart disappeared when the ETT was advanced into the right mainstem bronchus (occluding the left mainstem bronchus) and when the left-sided pneumothorax was relieved with a chest tube, the bronchovenous connection presumably originated from the left bronchial tree.

The pediatric literature documents the occurrence of systemic air embolization as a complication of mechanical ventilation. Collections of air have been found in the aorta, carotid, and subclavian arteries on radiographs in neonates suffering from barotrauma. [10,11] Recently intravascular gas has been documented in the coronary and cerebral circulations by computed tomography scan and post-mortem autopsy in an adult, presumably resulting from mechanical ventilation. [2]

Lack of recognition may explain the apparent rarity of systemic air embolization because signs and symptoms are easily attributable to other causes, and air itself is difficult to detect. Central nervous system complications of air emboli caused by obstruction to flow, subsequent platelet activation, and release of vasoactive substances [6,12] may range from nonspecific findings such as a change in mental status to more serious sequelae, including seizure activity or cerebral infarction. Dramatic recovery has been described after gas is cleared and capillary flow returns. [4] Our patient exhibited several signs of central nervous system injury, including confusion, unresponsiveness, and seizure activity. Myocardial ischemia or infarction may also occur as a result of systemic air embolization although no suggestive electrocardiographic changes were observed in our patient. Air is difficult to detect because of the necessity of only small quantities of air to produce life-threatening symptoms, the transient nature of the event, and rapid clearance of intravascular gas, especially if it is oxygen-rich. [4] Ultrasound, however, is remarkably sensitive to the presence of intravascular air.

In summary, we have described an unusual case of pulmonary barotrauma resulting in tension pneumothorax and systemic air embolization. Systemic air embolism associated with mechanical ventilation may be far more common than recognized may be an explanation for the occurrence of dramatic clinical features, including mental status changes, seizures of unknown etiology, or myocardial injury in critically ill patients. This case represents an in vivo documentation of systemic air embolization by transesophageal echocardiography as a complication of mechanical ventilation in a patient who survived.

Haake R, Schlichtig R, Ulstad DR, Henschen RR: Barotrauma: Pathophysiology, risk factors, and prevention. Chest 1987; 91:608-13
Weaver LK, Morris A: Venous and arterial gas embolism associated with positive pressure ventilation. Chest 1998; 113:1132-4
Kane G, Hewins B, Grannis FW: Massive air embolism in an adult following positive pressure ventilation. Chest 1988; 93:874-6
Marini JJ, Culver BH: Systemic gas embolism complicating mechanical ventilation in the adult respiratory distress syndrome. Ann Intern Med 1989; 110:699-703
Petersen GW, Baier H: Incidence of pulmonary barotrauma in a medical ICU. Crit Care Med 1983; 11:67-9
Hall JB, Schmidt GA, Wood LDH: Principles of Critical Care. New York, McGraw-Hill, 1992, pp 590-2
Cheney FW, Posner KL, Caplan RA: Adverse respiratory events infrequently leading to malpractice suits. Anesthesiology 1991; 75:932-9
Butler BD, Hills BA: Transpulmonary passage of venous air emboli. J Appl Physiol 1985; 59:543-7
Katz J, Leiman BC, Butler BD: Effects of inhalation anaesthetics on filtration of venous gas emboli by the pulmonary vasculature. Br J Anaesth 1988; 61:200-5
Blanco CE, Rietveld LAC, Ruys JH: Systemic air embolism: A possible complication of artificial ventilation. Acta Paediatr Scand 1979; 68:925-7
Brown ZA, Clark M, Jung AL: Systemic gas embolus. Am J Dis Child 1977; 131:984-5
Marcus RH, Weinert L, Neumann A, Borow KM, Lang RM: Venous air embolism: Diagnosis by spontaneous right-sided contrast echocardiography. Chest 1991; 99:784-5