Pneumothorax

Pneumothorax is defined as the accumulation of free air or gas in the pleural space. This accumulation of air may come from three general sources but rupture of the visceral pleura with secondary leakage from the lung via a pleuropulmonary leak is the most common cause. Alternatively, atmospheric air may enter from disruptions to the esophageal, tracheal, bronchial, or chest walls. Gas may also be formed within the pleural space from infection with gas-forming organisms, although this is a rare occurrence.

Pneumothorax may be categorized into four broad categories: traumatic, iatrogenic, spontaneous, and infectious. Traumatic pneumothorax is the most common form and develops when disruption of the integrity of the lung, esophagus, or thoracic wall allows air to leak into the pleural space. Traumatic pneumothorax can be further subdivided according to whether there has been loss of integrity to the chest wall (open pneumothorax) or no discernible disruption (closed pneumothorax). Iatrogenic pneumothorax is a consequence of thoracotomy, but also can occur as a result of inadvertent trauma to the lungs during diagnostic or therapeutic procedures. Spontaneous pneumothorax is defined as a pneumothorax that occurs with no history of prior trauma and results from a pleuropulmonary leak, which is usually found at a site of pulmonary tissue damage secondary to a variety of underlying causes. Pneumothorax may also occur secondary to infection of the pleural space with a gas-producing organism.

Regardless of underlying etiology, the progression of the pneumothorax depends on the defect size, ability to seal itself, and whether it acts as a one-way valve or allows air to enter and exit the pleural space. The patient's respiratory pattern may also influence progression of the pneumothorax.

Physiology and Pathophysiology

The visceral (pulmonary) pleura is the serous membrane tightly adhered to the lungs, following all irregularities of their surfaces [1]. The parietal pleura covers the walls of the thoracic cavity and diaphragm, as well as the inner surface of the mediastinum. The pleurae of dogs and cats are approximately 20 microns thick [2]. The pleurae form two complete sacs on either side of the chest and are referred to as the pleural cavities. The right pleural cavity is larger than the left owing to the displacement of the mediastinum to the left caudal to the heart. Except for a thin film of capillary fluid moistening the flat mesothelial cells of the pleurae, the visceral pleura lies in contact with the parietal pleura. This fluid effectively couples the lungs to the thoracic wall while allowing the lungs to move within the thoracic cavity during the phases of respiration. Owing to the fluid coupling of the two pleural surfaces and negative intrathoracic pressure, changes in thoracic volume confer changes in lung volume.

Only during pathologic conditions in which fluid or air accumulate between these two layers does the pleural cavity exist as a true cavity. The opposing elastic recoil of the lung and thorax creates negative interpleural pressure relative to both atmospheric and alveolar pressure [3]. For optimal function, the pleural space must be devoid of both air and fluid. Fluid secreted into the pleural cavity normally is reabsorbed by lymphatics underlying the parietal pleura. The relative negative total gas pressure of the surrounding tissue favors absorption of gas from the pleural space.

With introduction of air into the pleural space, as occurs with pneumothorax, the pressure of gas in the space approaches or eventually reaches atmospheric pressure. By comparison, the pressure within the surrounding tissues remains subatmospheric. This pressure difference favors reabsorption of the pneumothorax, with each gas being reabsorbed independently. Pleural oxygen diffuses down its concentration gradient (from approximately 149 mm Hg to 40 mm Hg), out of the pleural cavity and into the interstitial fluid. With the loss of oxygen from the pleural space, the volume of gas decreases and the relative concentration of nitrogen increases. The residual oxygen and nitrogen within the pleural space, followed by carbon dioxide and water vapor, continue to be absorbed until all gases are evacuated from the cavity. The rate of resorption depends on several factors, including: the quality of the pleural surface (pathologic conditions leading to increased pleural thickness will decrease the resorptive rate), the total surface area of the thoracic cavity, and the initial volume of air to be resorbed. Oxygen therapy has been shown to hasten the resolution of pneumothorax by decreasing the alveolar nitrogen partial pressure and, therefore, venous nitrogen pressure [4,5]. The increased gradient between pleural and alveolar space nitrogen facilitates its diffusion from the pleural to the alveolar space, thus speeding the absorption of the pleural air.

The cardiopulmonary effects of progressive pneumothorax have been investigated in both anesthetized and conscious dogs [6-11]. As the pleural surfaces separate, and elastic recoil is abolished, the thoracic cavity expands with simultaneous collapse of the lungs, although degree of lung collapse is disproportionately greater than that of thoracic cavity expansion [10]. In addition to a decrease in tidal volume, the collapse of the lung creates a ventilation/perfusion mismatch, leading to diminished arterial partial pressures of oxygen [10,12]. This fall in PaO2 leads to a concomitant increase in respiratory rate via a vagally mediated elimination of the abdominal expiratory muscle activity [7]. As pneumothorax progresses, hypoxemia induces resistance vessels of the lungs to undergo vasoconstriction (hypoxic vasoconstriction), in an effort to reduce ventilation-perfusion mismatch by diverting blood from hypoxic regions and to maintain PaO2. Initially, early compensatory mechanisms are capable of maintaining alveolar ventilation despite reductions in tidal volume, but as the degree of pneumothorax increases, they are overcome and additional cardiopulmonary derangements become evident [10,11]. It is also of clinical significance that many compensatory mechanisms are abolished during anesthesia, augmenting the cardiorespiratory depression in anesthetized patients with pneumothorax [13]. Respiratory rate, central venous pressure, and alveolar-to-arterial O2 tension difference increase in a linear relationship proportional to the degree of pneumothorax, while tidal volume, and arterial and mixed-venous pH and PaO2 decrease in a linear relationship and a manner inversely proportional to the degree of pneumothorax. Heart rate and mean arterial pressure are not significantly affected by mild to moderate pneumothorax [10,11]. As the pneumothorax progresses, cardiovascular effects become more evident. Increased intrathoracic pressure may impair venous return directly by compression of the great vessels and indirectly by eliminating the thoracic pump. Additionally, pulmonary artery pressure elevation and myocardial ischemia may diminish cardiac output.

Tension pneumothorax occurs when the torn edge of lung or thoracic wall forms a flap and acts as a one-way valve allowing air to enter but not to exit the pleural space. Air accumulation may be rapid and initial pathophysiologic changes described above can rapidly progress to cardiopulmonary collapse if not promptly detected and treated. As supra-atmospheric pressure develops in the pleural space, severe compression atelectasis of the lung, flattening of the diaphragm, and compression of the major vessels occur. These events lead to ventilatory impairment, profound hypoxemia, and dramatically reduced venous return, which are ultimately fatal if not aggressively treated.

Although it is clear that increasing volume of air within the pleural space correlates with the degree of cardiorespiratory dysfunction, underlying lung pathology has a substantial impact on clinical presentation. In normal experimental subjects, pneumothorax equivalent to 150% of the calculated lung volume were well tolerated [11]; however, patients with concurrent pulmonary disease and ventilatory compromise may exhibit pathophysiologic derangements with much smaller volumes of pneumothorax. Furthermore, concurrent head trauma, fractures, large airway disruptions, diaphragmatic hernias, myocardial contusions, and intra-abdominal disease seen in trauma patients with pneumothorax may further compromise these patients.

Syndromes and Pathogenesis

The categorical designation of a patient with regard to underlying etiology is an important step in logical diagnostic and therapeutic decision-making.

Traumatic Pneumothorax

Pneumothorax attributable to a traumatic event has been estimated to occur in up to 87% (92/105) of pneumothorax cases and is most often the result of an automobile accident [14]. Less commonly, a bite or stab wound, gunshot or shearing injury may cause a penetrating injury and disruption of the integrity of the thoracic wall (open pneumothorax). In the absence of a pleurocutaneous defect (closed pneumothorax), air may gain access to the pleural space through a pleuropulmonary leak or disruption of the conducting airways or esophagus. This may occur from barotrauma secondary to massive, sudden increase in intrathoracic pressure, which occurs with blunt-force chest compression against a closed glottis or from shearing or tensile forces generated from impact.

Rib fractures and penetrating foreign bodies may also directly lacerate pulmonary parenchyma. Concurrent pneumothorax has been shown to occur in 56% of cats with traumatic rib fractures and 58% of dogs and cats with flail segments [15,16]. In a study that included 92 cases of traumatic pneumothorax, the most common nonrespiratory-associated injury was to the musculoskeletal system, with an incidence of approximately 50% of these cases [14]. Similarly, over one half (6/11) of dogs and cats treated for thoracic bite wounds in one study were diagnosed with pneumothorax [17]. Pneumothorax associated with high-rise syndrome has been reported to occur in 32% of dogs and in 63% of cats [18,19]. Owing to the chance of concurrent injuries, animals may be less likely to tolerate smaller volumes of pneumothorax. In addition, more aggressive treatment for the pneumothorax may be necessary in the event that the concurrent disease necessitates emergency surgical management, because anesthesia may abolish compensatory cardiorespiratory mechanisms. Interestingly, in one study, survival rate was not significantly affected by the presence of concurrent injury in treated animals [14].

Open pneumothorax results when the thoracic wall is disrupted and air is able to enter the pleural space via the wound: penetrating foreign bodies (i.e., gunshots, sticks, etc.), and combined blunt/sharp trauma secondary to bite wounds or vehicular trauma. An open chest wound results in significant compromise of pulmonary function because it allows rapid equilibration of intrathoracic pressure with atmospheric pressure with an inability to expand the lung.

Iatrogenic Pneumothorax

Iatrogenic traumas associated with diagnostic and therapeutic veterinary procedures are reported causes of pneumothorax in the dog and the cat. Pneumothorax is an accepted risk of thoracocentesis, thoracostomy tube placement, fine-needle lung aspiration biopsy, or biopsy of other intrathoracic structures [20,21]. Pneumothorax was reported to occur in 31% of dogs undergoing transthoracic needle biopsy [21]. Animals undergoing general anesthetic procedures are at risk for barotrauma to conducting airways and alveoli [22,23]. Of dogs and cats undergoing prolonged periods of therapeutic mechanically-assisted ventilation, the incidence of pneumothorax was 29% and 28%, respectively [24,25]. The combination of pulmonary pathology and positive end-expiratory pressures makes these patients particularly susceptible to the development of pneumothorax. Furthermore, the use of positive pressure ventilation may convert a simple pneumothorax into a tension pneumothorax. Pneumothorax is a reported complication of thoracolumbar disk fenestration [26]. Physical restraint during venipuncture was theorized to be the cause of pneumothorax in a kitten [27]. Other procedures in which pneumothorax has been induced include closed-chest cardiopulmonary resuscitation, central venous cannula placement, pacemaker implantation, and inadvertent diaphragmatic incision during celiotomy.

Spontaneous Pneumothorax

In the absence of a preceding traumatic event, a pneumothorax is categorized as spontaneous (with the rare exception of those caused by gas-forming bacteria). In comparison with cases of trauma-induced pneumothorax, spontaneous pneumothorax occurs much less frequently and has an estimated prevalence of 0.11%. Underlying pulmonary parenchymal pathology may be the site of the leak. Alternatively, rupture of the air-containing space within or immediately beneath the visceral pleura may lead to the pleuropulmonary communication and are referred to as blebs or bullae, depending on location.

Blebs are contained entirely within the pleura between the two layers of the lamina elastica (interna and externa), but they communicate directly with adjacent alveolar spaces [28,29]. They are most frequently found at the apices and appear as small "bubbles" or "blisters" on the surface of the lung. Bullae are lined by a combination of thickened pulmonary tissue and by emphysematous lung (Fig. 55-1). In the largest study of canine spontaneous pneumothorax cases to date, 68% of cases in which a definitive diagnosis was reached were attributable to bullous emphysema [30], supporting reports from smaller studies that blebs and bullae were the most frequent cause of spontaneous pneumothorax in the dog [31-34]. Interestingly, Siberian huskies were overrepresented in the case population studied at the University of Pennsylvania [30]. In a study of 12 dogs with spontaneous pneumothorax attributable to bullae or blebs, all 12 had lesions in one or both cranial lung lobes, with 10 of the dogs having multiple lesions. Bilateral lesions were seen in 36 to 58% of dogs and multiple lung lobes were affected by bullae in 37% of dogs [3,30]. By comparison, this condition appears to be much less prevalent in cats, with only seven cats reported in the literature [35,36].

Figure 55.1. Intraoperative view of a pulmonary bleb/bulla in a dog with spontaneous pneumothorax (Courtesy of David Holt, University of Pennsylvania).

The pathogenesis of pulmonary blebs and bullae in dogs and humans is poorly defined. Exposure to cigarette smoke has been shown to be a significant risk factor for the development of these lesions in humans [37]. In addition, increased distensile forces associated with conformation, changes in atmospheric pressure, and certain inflammatory conditions have all been theorized to predispose to their development [38-42]. Although no studies have specifically examined pathogenesis of blebs and bullae in dogs, histologic similarities between these human and canine lesions suggest that similar mechanisms in their development may exist.

Less commonly, spontaneous pneumothorax develops secondary to a specific pulmonary pathology, which has caused weakening of the alveolar walls and visceral pleura with subsequent formation of a pleuropulmonary leak. Bullae may be grossly visible in the pathologic tissue. In dogs, spontaneous pneumothorax has been associated with a variety of infectious and inflammatory conditions, including pulmonary abscesses, pneumonia, parasitic granulomas and associated pulmonary arterial thromboembolism, and heartworm disease, as well as pleuritis [30,43-47]. Neoplasia, primary or metastatic, has also been implicated in the development of pneumothorax [30,48,49].

Infectious Pneumothorax

Pneumothorax that occurs secondary to an infection with gas-producing organisms is a rare condition in dogs and cats.

Pneumomediastinum with Pneumothorax

Pneumomediastinum is defined as the presence of free air within the tissues of the mediastinum. Pneumomediastinum can be seen radiographically in some animals with pneumothorax. Additionally, air may be seen dissecting in fascial planes of the neck, the pericardium, and the retroperitoneal space. This can occur with disruption of the lower airways, esophagus, and marginal alveoli of the lung [22,50-56]. Mediastinal pleura may commonly rupture with over-distention and lead to pneumothorax, but pneumothorax cannot cause a pneumomediastinum [55,56]. When pneumomediastinum occurs, it is rarely of clinical significance, but clinicians should be aware that it may lead to pneumothorax.

Treatment for patients with minimal respiratory compromise is conservative. Placing the patient in lateral recumbency with the affected side down may be of benefit, even in patients that are mechanically ventilated. Thoracocentesis or placement of thoracostomy tubes with intermittent or continuous suction may be needed. If the leakage is secondary to positive pressure ventilation, positive end-expiratory pressure (PEEP) should be discontinued if possible. Surgery is rarely necessary and is reserved for patients that do not respond to conservative treatment. The recommended treatment of spontaneous pneumothorax involves stabilization of the patient by thoracocentesis or tube thoracostomy followed by early surgical exploration with median sternotomy for patients that do not have identifiable non-surgical disease or diffuse pulmonary disease. Cases of spontaneous pneumothorax treated surgically had a lower recurrence, 3%, and mortality, 12%, versus 50% recurrence and 53% mortality for non-surgically managed cases [30].