Theresa W. Fossum, DVM, MS, PhD, DACVS
Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX, USA
Traumatic pneumothorax is the most frequent type of pneumothorax in dogs. It most often occurs due to blunt trauma (i.e., vehicular accidents, being kicked by a horse), which causes parenchymal pulmonary damage to the lung and a closed pneumothorax. When the thorax is forcefully compressed against a closed glottis, rupture of the lung or bronchial tree may occur. Alternately, pulmonary parenchyma may be torn due to shearing forces on the lung. Pulmonary trauma occasionally results in subpleural bleb formation, similar to those seen with spontaneous pneumothorax. Open pneumothorax occurs less commonly, but is also frequently due to trauma (i.e., gun shot, bite or stab wounds, lacerations secondary to rib fractures). Some penetrating injuries are called "sucking chest wounds," because large defects in the chest wall allow an influx of air into the pleural space when the animal inspires. These large, open chest wounds may allow enough air to enter the pleural space that lung collapse and marked reduction in ventilation occur. There is a rapid equilibration of atmospheric and intrapleural pressure through the defect, interfering with normal mechanical function of the thoracic bellows, which normally provides the necessary pressure gradient for air exchange. Pneumomediastinum may be associated with pneumothorax, tracheal, bronchial, or esophageal defects, or may be due to subcutaneous air migration along fascial planes at the thoracic inlet.
Spontaneous pneumothorax occurs in previously healthy animals without antecedent trauma and may be primary (i.e., an absence of underlying pulmonary disease) or secondary (underlying disease such as pulmonary abscesses, neoplasia, chronic granulomatous infections, pulmonary parasites such as Paragonimus, or pneumonia are present). Based on the histologic appearance of the pulmonary lesion, both cysts and bullae have been reported in dogs. Primary spontaneous pneumothorax in dogs may be due to rupture of subpleural blebs; the remaining lung tissue may appear normal. These blebs are most commonly located in the apices of the lungs. Secondary spontaneous pneumothorax is more common in dogs than the primary form. In these animals, the subpleural blebs are associated with diffuse emphysema or other pulmonary lesions. It has been shown that volume strain from expansive pressure within the lung increases disproportionately at the apex as height increases. A majority of affected people are cigarette smokers, suggesting that the underlying pulmonary disease could be a result of interference of the normal function of alpha-1-antitrypsin in inhibiting elastase. It is believed that alpha-1-antitrypsin is inactivated in people who smoke, allowing increased elastase-induced destruction of pulmonary parenchyma.
Physical Examination Findings
Most animals with pneumothorax have bilateral disease and present with an acute onset of severe dyspnea. Other evidence of trauma (i.e., rib fractures, limb fractures, traumatic myocarditis, pulmonary contusions) may be evident in animals sustaining trauma. Most animals with pneumothorax exhibit a restrictive respiratory pattern (i.e., rapid, shallow respirations). If hypoventilation causes hypoxemia, they may appear cyanotic, and the heart and lung sounds are often muffled dorsally. Dogs are able to tolerate massive pneumothorax by increasing their chest expansion. Respiration becomes ineffectual in animals with tension pneumothorax as the chest becomes barrel-shaped and fixed in maximal extension. This condition is life threatening. Occasionally, subcutaneous emphysema will be noted in animals with pneumomediastinum and pneumothorax. The air may migrate from the mediastinal space to the thoracic inlet and be noticeable under the skin over the neck and trunk.
Thoracic radiographs should be delayed until after thoracentesis in dyspneic animals. Pneumothorax usually occurs bilaterally in animals because air easily diffuses across the thin mediastinum. Pneumothorax results in an increased width of air-filled space in the pleural cavity. The most sensitive view is a horizontal-beam, laterally recumbent thoracic radiograph. On a recumbent lateral thoracic radiograph, the lungs collapse and retract from the chest wall and the heart usually appears to be elevated from the sternum. This apparent elevation of the heart is not noticeable on a standing lateral radiograph. Partially collapsed or atelectic lung lobes appear radiopaque when compared to the air-filled pleural space. As the lungs collapse, the vascular pattern will not extend to the chest wall; this may be particularly noticeable in the caudal thorax on a ventrodorsal view. Radiographs should be carefully evaluated for underlying pulmonary disease (i.e., abscess, neoplasia) or associated trauma (i.e., rib fractures, pulmonary contusion). Pulmonary blebs found in some animals with spontaneous pneumothorax are seldom visible radiographically. This is probably because the large blebs have ruptured causing the pneumothorax. In such cases, surgical identification of bulla is necessary. Air-filled bullae may be incidental findings on thoracic radiographs of some animals. Pneumomediastinum is characterized by the ability to visualize thoracic structures (i.e., aorta, thoracic trachea, vena cava, esophagus) that are not usually apparent on thoracic radiographs.
Medical management of an animal with pneumothorax consists of initially relieving dyspnea by thoracentesis. If the pleural air accumulates quickly or cannot be effectively managed with needle thoracentesis, a chest tube should be placed. Tube thoracostomy is typically required in animals with spontaneous pneumothorax. Intermittent or continuous pleural drainage may be used, depending on the speed with which air accumulates. Continuous drainage may cause quicker resolution of pneumothorax in animals with large, traumatic defects. Providing an enriched oxygen environment may be beneficial, particularly in animals with concurrent pulmonary trauma (e.g., pulmonary contusion/hemorrhage). Providing analgesics to animals with fractured ribs or severe soft tissue damage may improve ventilation. Surgical intervention is seldom required in animals with traumatic pneumothorax. Thoracentesis should be performed as necessary to prevent dyspnea while the pulmonary lesion heals, usually within 3 to 5 days. Recurrence is uncommon. Conversely, animals with spontaneous pneumothorax commonly have recurrence of the pneumothorax if they are not operated.
An open chest wound should be covered immediately with any readily available material. Once admitted to the hospital, a sterile occlusive dressing should be applied as rapidly as possible and intrapleural air evacuated by thoracocentesis or tube thoracostomy.
Surgical therapy of animals with traumatic pneumothorax is seldom necessary. However, non-surgical management of spontaneous pneumothorax usually results in a less than satisfactory outcome. Mechanical pleurodesis of the lungs may decrease the recurrence of pneumothorax in animals operated for spontaneous pneumothorax.
Lung Lobe Torsion (LLT)
Any mechanism that increases mobility of a lung lobe seems to favor development of a torsion. Partial collapse of the lung (i.e., with pulmonary disease or trauma) frees it from its normal spatial relationships with the thoracic wall, mediastinum, and adjacent lung lobes. They may enhance mobility. Pleural effusion or pneumothorax, along with subsequent atelectasis of lung lobes, can allow increased movement of a lobe, predisposing to torsion. Although LLT has been reported to cause chylothorax in dogs, it is more likely that the chylothorax caused the LLT. LLT has been reported secondary to previous thoracic surgery, where lung lobes are manipulated and may remain partially collapsed after thoracic closure.
Torsion of a lung lobe results in venous congestion of the affected lobe; however, the arteries remain at least partially patent, allowing blood to enter. As fluid and blood enter the alveoli, lung consolidation occurs and the lobe becomes dark colored and firm, similar in shade to the liver. The shape of the affected lobe is often altered and it may appear displaced from its normal location within the thorax radiographically. Pleural fluid usually accumulates due to continued venous congestion.
Physical Examination Findings
Pleural effusion is consistently present in animals with LLT; therefore, findings often include muffled heart and lung sounds. Other findings may include depression, anorexia, coughing, fever, dyspnea, hemoptysis, hematemesis, and/or vomiting.
Thoracic radiographic changes are variable depending on the volume of pleural fluid, presence or absence of preexisting disease, and duration of the torsion. The most consistent finding is the presence of pleural effusion accompanied by an opacified lung lobe. Initially, air bronchograms will be present in the torsed lobe and can be seen extending toward the abdomen. Air bronchograms eventually disappear as fluid and blood fill the bronchial lumen. The presence of a noninflated, radiopaque lung lobe that persists after removal of pleural fluid should increase suspicion for LLT. Positional radiographs using horizontal beam X-rays (lateral decubitus or upright VD) are often helpful. Pleural fluid secondary to LLT may persist around the affected lobe rather than fall to the dependent side. Failure of the lobe to reinflate in the "up" or nondependent hemithorax is another indication of LLT.
Initial therapy is aimed at stabilizing the animal and alleviating respiratory distress before surgery. Thoracentesis should be performed to remove pleural fluid. Persistent or massive pleural effusion may require placement of a chest tube. Oxygen therapy given by oxygen cage or nasal insufflation is beneficial to some animals. Underlying diseases such as pneumonia should be identified and treated with appropriate antibiotic therapy. Intravenous fluid therapy is beneficial before and during surgery to maintain hydration.
Spontaneous correction of a torsed lung lobe is uncommon due to swelling of the lobe and rapid formation of adhesions. The treatment of choice for LLT is lobectomy of the affected lobe. Unless LLT is diagnosed very quickly (i.e., immediately after a surgical procedure), damage to the pulmonary parenchyma is generally severe enough that attempts to salvage the lobe are not warranted. Recurrence has been reported following surgical correction where lobectomy was not performed.
Clamp the affected pedicle with a noncrushing forceps to prevent release of toxins into the bloodstream, prior to attempting to derotate it. Untwisting the lobe before its removal may help facilitate identification of the vascular structures and bronchus for ligation; however, in some cases, the lobe cannot be easily returned to its normal position due to extensive adhesions. Check the remaining lobes for position and normal expansion. Culture pulmonary parenchyma following removal of the lobe. Submit excised tissue for histologic examination to help determine underlying causes (i.e., pneumonia, neoplasia). Place a chest tube before closing the thoracic cavity.