Pneumothorax and Lung Lobe Torsion: Emergency Management to Reduce Mortality
Theresa W. Fossum, DVM, PhD, DACVS
Tom and Joan Read Chair in Veterinary Surgery, Director, Clinical Programs and Biomedical Devices, Michael E. DeBakey Institute Professor of Surgery, Texas A&M University College of Veterinary Medicine
College Station, TX, USA
Traumatic pneumothorax is the most common type of pneumothorax in dogs. It most often occurs as a result of blunt trauma (i.e., vehicular accidents, being kicked) which causes parenchymal pulmonary damage to the lung and a closed pneumothorax. Pneumomediastinum may be associated with pneumothorax or tracheal, bronchial, or esophageal defects, or it may be due to subcutaneous air migration along fascial planes at the thoracic inlet.
Tracheal rupture may occur due to trauma; it is especially associated with overinflation of the endotracheal tube cuff in cats. Tracheoscopy may be the method of choice for documenting tracheal rupture. The primary signs of tracheal rupture are pneumomediastinum and subcutaneous emphysema; pneumothorax is rare. It is important to distinguish tracheal rupture without pneumothorax from that causing pneumothorax.
Spontaneous pneumothorax occurs in previously healthy animals without antecedent trauma and may be primary (without underlying pulmonary disease) or secondary (with underlying disease such as pneumonia, pulmonary abscess, neoplasia, chronic granulomatous infection, or pulmonary parasitic infection, such as with Paragonimus spp.).
Traumatic pneumothorax is most common in young dogs because they are more likely to be hit by cars or to suffer other trauma resulting in pulmonary damage. For similar reasons, males may be more commonly affected than females. Spontaneous pneumothorax usually occurs in large and deep-chested breeds; however, it may occur in small dogs. Purebred dogs, particularly Siberian Huskies, may be more commonly affected than mixed breed dogs.
Pneumothorax due to trauma usually causes acute dyspnea. Trauma is often not reported, making differentiation between traumatic and spontaneous pneumothorax difficult. Although the history of dogs with spontaneous pneumothorax varies depending on underlying etiology, most animals have acute onset of dyspnea. Occasionally a chronic cough or fever may be noted. Recurrence of dyspnea in an animal previously treated for pneumothorax suggests spontaneous rather than traumatic pneumothorax.
Physical Examination Findings
Most animals with pneumothorax have bilateral disease and are presented for treatment 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 with trauma-induced pneumothorax. Most animals with pneumothorax show a restrictive respiratory pattern (i.e., rapid, shallow respirations).
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. Radiographs should be carefully evaluated for underlying pulmonary disease (e.g., abscess, neoplasia) or associated trauma (e.g., rib fractures, pulmonary contusion). Pulmonary blebs found in some animals with spontaneous pneumothorax are seldom visible radiographically, although CT is more sensitive for finding these lesions. If imaging does not identify the lesion, surgical or thoracoscopic identification of bullae is indicated.
Medical management of pneumothorax consists of initially relieving dyspnea by thoracentesis. If the pleural air accumulates quickly or cannot be managed effectively with needle thoracentesis, a chest tube should be placed. 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 recurrent pneumothorax if surgery is not performed.
Surgical therapy of animals with traumatic pneumothorax is seldom necessary. However, nonsurgical management of spontaneous pneumothorax usually results in an unsatisfactory outcome. Thoracoscopic treatment of bullous emphysema has been reported in dogs. Mechanical pleurodesis of the lungs may reduce the recurrence of pneumothorax in animals that undergo surgery for spontaneous pneumothorax. Mechanical pleurodesis damages the pleura, causing it to thicken.
If an underlying pulmonary lesion is readily identified (i.e., pulmonary abscess or neoplasia) and can be localized to one hemithorax, an intercostal thoracotomy allows lobectomy to be performed more readily than from a median sternotomy approach. However, dogs with spontaneous pneumothorax usually have diffuse, bilateral pulmonary disease with multiple bullae. A median sternotomy allows visualization of all lung lobes and partial resection of any diseased lobes. Mechanical pleurodesis might be of benefit in dogs with spontaneous pneumothorax to reduce recurrence.
Lung Lobe Torsion
Any mechanism that increases mobility of a lung lobe seems to favor 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. This 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 may be chylothorax that caused LLT. LLT has been reported secondary to previous thoracic surgery in which lung lobes are manipulated and remain partly collapsed after thoracic closure. LLT has typically been reported most commonly in the right middle lung lobe; however, in a recent study right middle lobe torsion was predominant in large dogs while left cranial lobe torsion was more common in small dogs (D'Anjou et al, 2005). Underlying thoracic disease was found in only 5 of 15 dogs in the aforementioned study. Midlobar torsion of the right caudal lung lobe has been reported in a dog (Hofeling et al, 2004).
Deep-chested, large-breed dogs, especially Afghan hounds, are more commonly affected; however, five of 22 dogs with LLT in a recent study were toy breeds (Neath et al, 2000). Young, male pugs appear to be predisposed to LLT (Rooney et al, 2001; Murphy et al, 2005). Lung lobe torsion in Afghan hounds may be associated with chylothorax. In large breed dogs and pugs, LLT frequently occurs spontaneously without previous history of disease or trauma. LLT in other small breeds is often secondary to primary pleural effusion, thoracic surgery, or trauma. LLT is rare in cats. Middle-aged dogs are more commonly affected, but LLT may occur in animals of any age.
In a recent study of 22 dogs with LLT, dyspnea was the most common reason for examination (Neath et al, 2000). Coughing and hemoptysis can also occur and may be chronic in nature. Some animals may be anorectic and depressed. There may be a previous history of pneumothorax, pneumonia, or trauma or all three.
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 vary depending on the volume of pleural fluid, the presence or absence of preexisting disease, and the duration of the torsion. The most consistent finding is pleural effusion accompanied by an opacified lung lobe. Initially, air bronchograms are present in the torsed lobe and may be seen running in an abnormal direction. 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. Bronchoscopy typically reveals a bronchus that is occluded and appears to be "twisted". Sometimes the tissue at the site seems edematous. There may or may not be blood in the bronchi.
Spontaneous correction of a torsed lung lobe is uncommon because of 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 generally is severe enough that attempts to salvage the lobe are not warranted. Recurrence has been reported after surgical correction where lobectomy was not performed.
Before attempting to derotate the affected pedicle, clamp it with a noncrushing forceps to prevent release of toxins into the bloodstream or fluids into the dependent lobes. Untwisting the lobe before its removal may help facilitate identification of the vascular structures and bronchus for ligation; however, in many cases the lobe cannot be easily returned to its normal position because of extensive adhesions. A transfixation suture or Miller's knot can often be used in such cases to ligate the vessels and bronchus. Check the remaining lobes for position and normal expansion. Culture the pulmonary parenchyma after 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.