Systemic Arterial Air Embolism in Penetrating Lung Injury Aaron S. Estrera, MD, Lawrence J. Pass, MD, and Melvin R. Platt Division of Thoracic and Cardiovascular Surgery, The University of Texas Southwestern Medical Center at Dallas, Parkland Memorial Hospital, Dallas, Texas

Systemic arterial air embolism is frequently unrecog- nized as a cause of death among patients with isolated penetrating lung injury. Between 1975 and 1983 at Park- land Memorial Hospital, the complication of systemic arterial air embolism developed in 9 patients with pen- etrating lung injury (six gunshots and three stabbings). Eight patients were either in profound shock or experi- enced cardiac arrest and all were intubated and on positive-pressure ventilation, frequently on a manual resuscitator bag before or at the time of diagnosis. The diagnosis was made by direct visualization of air in the coronary vessels in all 9 patients, and in 3 air was also aspirated from the left ventricular apex and aortic root. In addition, 5 patients had clinically significant hemopty-

ystemic arterial air embolism as a complication of S penetrating lung injury is a relatively recent observa- tion. Its acceptance as a specific clinical entity has been very slow in coming, a situation not too dissimilar from what took place at the turn of the century regarding a little-known entity called "pleural shock' syndrome. Pleural shock, as originally described by Roger in 1864 [l], was characterized by the sudden onset of hemodynamic collapse, seizures, and, at times, sudden death occurring as a complication of thoracentesis, therapeutic pneumo- thorax, and pulmonary resection [ 1-41, Initially, this phe- nomenon was attributed to cardioinhibitory or vasomotor effects and other so-called pleural reflexes, which were somehow triggered by invasive procedures involving the pleural cavity [3, 41. Subsequently, air embolism was suspected to be the underlying mechanism. The clinical report by Brandes [5] and the later animal experiments by Van Allen and co-workers [6] and Moore and Braselton [7] established the definitive relationship between systemic arterial air embolism and the phenomenon of pleural shock.

Reports of air embolism complicating penetrating lung injury have appeared in the literature only in the past two decades. To our knowledge, no case has been reported in any of the major wars of this century. In 1966, Chiu and associates [8] were first to confirm the occurrence of coronary artery air embolism in the presence of lung

Accepted for publication Mar 10, 1990

Address reprint requests to Dr Estrera, Division of Thoracic and Cardio- vascular Surgery, The University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 752354879,

sis. At operation, only an isolated injury to the lung was found in 7 of the 9 patients. Arterial air embolism is a highly lethal complication; 6 of our patients died, a mortality rate of 66%. Thus, it clearly behooves us to be more alert to the possible occurrence of this complication among all victims of penetrating chest trauma. We must accept that systemic arterial air embolism is an estab- lished complication of penetrating lung injury and must recognize that it occurs much more frequently than has been previously reported. Prompt diagnosis coupled with aggressive efforts at cardiopulmonary resuscitation is crucial for successful management of patients with air embolism.

(Ann Thorac Surg 1990;50:257-61)

injury in an animal experiment in which a dog's lungs were lacerated and ventilated with high (40 mm Hg) intrabronchial pressure. In 1973, Thomas [9] published the first clinical report of 4 patients with penetrating lung injury in whom this complication developed. This report caused skepticism and stimulated controversy in many trauma centers in this country, including our own; how- ever, subsequent laboratory investigations and clinical experiences [9, 101 confirmed the earlier observations of Chiu and Thomas. The recent autopsy study by King and associates [ 111 conclusively documented the occurrence of this complication; these investigators even suggested that systemic arterial air embolism may frequently be the cause of death among patients with isolated penetrating lung injury.

Between 1975 and 1983 at Parkland Memorial Hospital, one of us (A.S.E.) personally managed 9 patients in whom systemic arterial air embolism developed after penetrating lung injury. This report retrospectively analyzes this group of patients.

Clinical Experience

Before 1975, we were skeptical, as were many other investigators, that systemic air embolism could complicate pulmonary injury. In 1975, however, our skepticism ended when a young man was admitted to the emergency department with a gunshot wound to the left chest. Resuscitation, including emergency department thoracot- omy, was unsuccessful. During resuscitation, however, localized crepitation was palpable deep in both groins. Although this was initially believed to be subcutaneous emphysema, needle aspiration revealed air in the femoral

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258 ESTRERA ET AL AIR EMBOLISM IN LUNG INJURY

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punctured site.

arteries. Systemic arterial air embolism was confirmed by visualization of air in the coronary vessels and by aspira- tion of a large volume of air from the left ventricular apex and aortic root (Fig 1). Vigorous air leak with foamy air-blood admixture exuding from both the entry and exit wound of the left upper lobe of the lung was also noted; this was the only clinically significant injury found. It was evident that the patient died of massive systemic arterial air embolism. After this incident, concerted efforts were made to diagnose this complication among victims of penetrating chest injury. During the ensuing 8-year pe- riod, 8 additional patients were examined by one of us (A.S.E.). The clinical summaries of these cases are pre- sented in Table 1.

The patients ranged in age from 15 to 42 years; 6 sustained gunshot wounds and 3 sustained knife wounds. Three patients who arrived in the emergency department without vital signs and with cardiopulmonary resuscitation in progress had thoracotomy performed there. Five patients were in profound shock and were rushed to the operating room; only 1 patient was in stable condition on arrival, and he required an urgent thoracot- omy for massive hemothorax.

All patients were intubated and on positive-pressure ventilation, frequently with a manual resuscitator bag, at

the time the diagnosis of systemic air embolism was made. At operation, every patient had either a deep puncture wound or a through-and-through wound of the lung in close proximity to the hilum. In 7 of the 9 patients, the lung injury was the only clinically significant finding. Of the other 2, 1 patient had a superficial avulsive-type laceration of the lateral wall of the left ventricle and the other had a thoracic spinal cord injury (T-4 level). Five patients had massive amounts of blood suctioned from the endotracheal tube, severely compromising mechanical ventilation. In every patient, the diagnosis of air embo- lism was made by direct visualization of air in the coro- nary vessels; in 3 patients, a large volume of air was also aspirated from the left ventricular apex and aortic root. In 4 patients, vigorous air leaks with blood exuding from the wound or wounds of the lung were noted. Four patients survived the operation; 3 were discharged with complete recovery, and 1 died a week later with severe neurological deficit.

Comment The incidence of systemic air embolism complicating penetrating lung injury remains obscure for several rea- sons. First, the clinical manifestations of systemic air

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ESTRERA ET AL 259 AIR EMBOLISM IN LUNG INJURY

Table 1. Air Embolism Complicating Penetrating Lung l n j u y (Parkland Memorial Hospital, 1975-1983)

Patient Age Operative Procedure No. (yr) Sex Type of injury Clinical Presentation and Findings Diagnosis Outcome

1 34 M

M

F

M

M

F

M

F

M

GSW (L) chest Agonal, shock, massive hemothorax

EDT (anterior); through-and- through wound of LUL with vigorous air leak

Air in coronary vessels; air aspirated from femoral arteries, LV apex, and aortic root

Air in the coronary vessels; air aspirated from LV apex and aortic root

v e s s e 1 s Air in coronary

Died

Left posterolateral thoracotomy; deep wound of LUL; blood in endotracheal tube

Died 2 22

14

24

GSW (L) chest Hypotensive, massive hemothorax; sudden cardiac arrest

GSW (L) chest

GSW (R) chest

Agonal, shock, massive hemothorax

EDT (anterior); through-and- through wound LLL; blood in the endotracheal tube

thoracotomy; through-and- through wound RUL with large air leak and bleeding from the wounds; RUL lobectomy

thoracotomy; substantial amount of blood in endotracheal tube with difficulty of ventilation; deep puncture wound LLL; LLL lobectomy

Left anterior thoracotomy; avulsive wound in the lateral LV; through-and- through wound LUL with vigorous air leak; LUL lobectomy

Right posterolateral

Left posterolateral

Died

Air in coronary vessels

Survived; discharged

Hypotensive, massive hemothorax; stabilized with volume replacement; sudden cardiac arrest

5 Air in coronary vessels

Survived; discharged

18 SW (L) chest Hypotensive, massive hemothorax; stabilized with volume replacement; sudden cardiac arrest

6 GSW (L) chest Stable; massive hemothorax; proximity to the heart; sudden cardiac arrest

Air in coronary v e s s e 1 s

Survived opera tion, but died with severe neurological deficit

Died

28

SW (L) chest

SW (L) chest

Hypotensive; tension hemopneumothorax; sudden cardiac arrest

Hypotensive; massive hemothorax; T-4 level paraplegia; sudden cardiac arrest

EDT (anterior); deep laceration LUL with vigorous air leak

Median sternotomy; deep puncture wound LUL; blood in endotracheal tube

Air in coronary vessels

24

28

42

Air in coronary vessels; air aspirated from LV apex and aortic root

vessels Air in coronary

Died

GSW (R) chest Hypotensive; massive hemothorax; proximity to the heart

Median sternotomy; through- and-through wounds of middle lobe with vigorous air leak and bleeding; blood in endotracheal tube; RML lobectomy

9 Survived; discharged

EDT = emergency department thoracotomy; lobe; RUL = right upper lobe; SW = stab wound.

GSW = gunshot wound; LUL = left lower lobe; LV = left ventricular; RML = right middle

embolism are so insidious and nonspecific that the diag- nosis is rarely suspected in a seriously injured patient. Second, the diagnosis is usually made only on direct visualization of air in the coronary vessels or by aspiration of air from the left ventricle or great vessels; therefore, it is usually made only at the time of thoracotomy. Third, there is still no standard postmortem method for defini-

tive diagnosis of this entity. It is to be hoped that the technique used by King and associates [ll] will be adopted by other forensic pathologists and will improve our overall diagnostic capability.

After a penetrating chest injury, air has the potential to gain access to either the systemic venous or arterial circulation. Systemic venous air embolism was reported

260 ESTRERA ET AL AIR EMBOLISM IN LUNG INJURY

Ann Thorac Surg 1990;50:25741

as the possible cause of death in a patient who sustained a gunshot wound to the chest. In this patient, the sur- geons theorized that a massive amount of air from an associated pneumothorax entered the venous circulation through a severed subclavian vein [12]. Apart from this single patient, there have been no other similar reports. Thus, in penetrating lung injury, the major concern regarding air embolism must be focused on interruption of the systemic arterial circulation, most specifically the coronary circulation.

The traumatic creation of a serious bronchopulmonary venous fistula is the primary underlying mechanism in the development of this complication. The deep puncture stab wounds and through-and-through bullet wounds in close proximity to the hilum seen in our patients are the types of injury that create and maintain a sizable fistulous communication between the proximal bronchus and a pulmonary vein. Unlike the pulmonary artery, which is in close proximity to its accompanying bronchus along its entire course, the pulmonary vein is in close proximity to its bronchus only in the hilar region. Detailed anatomical dissections of the lung specimen were performed in 6 of our cases, and in 3 a fistulous communication was clearly demonstrated. In 3 others, the missile tract could be demonstrated to have served as the conduit between the openings in the bronchus and pulmonary vein. The presence of a fistula coupled with high positive-pressure ventilation favors movement of air from the bronchus into the pulmonary vein and then into the left atrium and the systemic arterial circulation. In addition to this anatomical feature, however, other factors, such as hemodynamic status and pressure gradient between the bronchus and pulmonary vein, are very important. In these seriously injured trauma victims, hypotension, hypovolemia, and positive-pressure ventilation create a favorable environ- ment for development of this complication.

The role of positive-pressure ventilation in the develop- ment of traumatic systemic air embolism is well estab- lished [8, 13, 141. Animal experiments demonstrate that during normal ventilation (inspiratory pressure of 10 to 20 mm Hg), pulmonary venous pressure is higher than intrabronchial pressure. During mechanical ventilation with inspiratory pressure up to 40 mm Hg, pulmonary venous pressure increases even more as a consequence of intrathoracic pressure transmission [8 ] . In the presence of a bronchus to pulmonary venous communication, this pressure differential tends to favor movement of blood from the pulmonary vein into the bronchial tree and thus explains the onset of intrabronchial bleeding or hemopty- sis that frequently occurs in these patients. When the ventilating pressure exceeds 40 mm Hg, however, the intrabronchial pressure increases above pulmonary venous pressure, reversing the existing pressure gradient between these two structures. This time, the pressure change allows movement of air into the pulmonary vein and into the left side of the heart. This high inspiratory pressure is easily achieved, especially during resuscita- tion. Direct measurements of inspiratory pressure among trauma victims during resuscitation have recorded pres- sures as high as 100 mm Hg [13]. This exceedingly high

ventilating pressure may also explain why body position does not appear to influence the occurrence of this com- plication. In our series, we observed this complication during a standard posterolateral thoracotomy (straight lateral position), a median sternotomy (supine position), and an anterior thoracotomy (45-degree lateral position).

Unlike massive air embolism complicating cardiopul- monary bypass procedures, in which the immediate con- cern is in the interruption of cerebral blood flow and resultant brain damage, the primary concern with sys- temic arterial air embolism complicating a penetrating lung injury is in the interruption of the coronary blood flow and resultant myocardial injury. The effects of even small amounts of air in the coronary circulation are well known (151. For patients to survive this catastrophic event, it is imperative that the diagnosis be made promptly and the source of air emboli be interrupted immediately .

Several clinical features should alert the surgeon to this complication: (1) a sudden hemodynamic collapse, usu- ally with ventricular fibrillation, in a previously stable patient; (2) hemoptysis or recovery of blood with endo- tracheal tube suctioning; (3) the presence of a vigorous air leak with foamy air-blood admixture exuding from the wound or wounds of the lung; and (4) the sudden onset of seizures.

Once the diagnosis is suspected, the hilum or pedicle of the involved lung or lobe must be clamped immediately. This maneuver, interrupting the source of air emboli, is the single most important therapeutic maneuver. Diagno- sis is confirmed by exposure of the heart and careful inspection of the coronary vessels for the presence of air bubbles while vigorous cardiac massage is initiated. This is the one rare event in trauma care for which evaluation and resuscitation must be performed simultaneously. Subsequently, a series of critical maneuvers designed to facilitate rapid removal of air from the coronary circulation is started. Ventilatory pressure is decreased, ventilation is maintained with 100% oxygen, and the patient is placed in a steep head-down position. Vigorous cardiac massage is continued while proximal aortic hypertension is in- duced by manual occlusion of the ascending or descend- ing aorta as recommended by Geohegan and Lam [16]. The left ventricular apex and aortic root are then aspi- rated; sometimes, even direct needle puncture of the coronary arteries is used to facilitate removal of air.

After these measures have been taken, cardiac rhythm is restored by defibrillation, and adequate blood pressure is maintained by infusion of vasopressors as needed. Definitive lung resection, frequently lobectomy, is then performed while the hilum remains clamped.

In the recovery period, as with any other form of systemic arterial air embolism, the main concern is the status of the patient’s cerebral function. Although none of our 3 long-term survivors had any serious neurological deficit, Yee and associates [17] reported that a few of their patients indeed had some neurological sequelae that resolved with time. It is our impression that when cere- bral circulation is seriously interfered with by air emboli complicating penetrating lung injury, the embolism is SO

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ESTRERA ET AL 261 AIR EMBOLISM IN LUNG INJURY

massive that it is probably incompatible with life. Indeed, 1 of our patients who survived the immediate postopera- tive period died a week later, having failed to recover from a severe neurological deficit.

As described by other investigators and confirmed in this report, the highly lethal complication of thoracic trauma, air embolism, often occurs among patients with isolated, easily repairable lung injuries. It behooves us to be even more cognizant of the occurrence of this compli- cation. At present there should be no more doubts as to the existence of the clinical entity of systemic arterial air embolism complicating a penetrating injury to the lung. In fact, we can assume that this complication occurs much more frequently than was previously reported, and that only conscious efforts on the part of physicians involved in the management of chest trauma are necessary for prompt diagnosis and salvage of these patients.

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