John F. Peroni
Thoracic and Airway Trauma
John F. Peroni
Traumatic injury of the equine airway and thorax are challenging events. Although some of these injuries can be managed in the field, referral to a tertiary care facility is often necessary because of the extensive medical and surgical management required. The chances of a successful outcome can be optimized by assuring that the referring veterinarian, the attending clinician, and the client/owner are aware of the details of the clinical case and know what to expect when the horse is received at the referral center. This is especially true in cases of airway injury because of the extent of follow-up treatment required to ensure a successful outcome. The ideal situation for the horse and the client is that the sequence of medical events starts and ends with the referring veterinarian, while the referral center provides the intermediate clinical management. Important aspects of respiratory tract trauma care that play a role in the successful management of the injured horse include location of the injury, the resulting hemodynamic status of the horse, the presence or absence of pneumothorax, and implementation of an effective treatment plan.
Sinus injuries often result from impact with stationary objects, falls, or kicks (see Chapter 50). They often produce depression fractures of the frontal, maxillary, and nasal bone plates, which result in epistaxis and a variable degree of respiratory impairment, depending on the extensiveness of the injury. The goal of treatment is to restore anatomic integrity to achieve a functional and esthetic outcome. Sinus fractures with mild bony depression are usually left to heal spontaneously; however, more serious crushing injuries that could heal leaving concave irregularities should instead be reduced by surgical intervention aimed at raising the depressed bone plates and restoring the anatomic contour. Most sinus injuries carry a good prognosis for return to function even when segments of bone have been lost. As long as a skin flap and possibly the underlying periosteum can be closed over the site of injury, healing is typically excellent. It is possible, however, for sinus penetration to lead to persistent secondary sinusitis, abscess formation, and chronic nasal discharge. This can be avoided with early intervention consisting of broad-spectrum antimicrobials, appropriate wound care, and sinus lavage. If sinusitis persists in the wake of a traumatic event, sequestration of bony fragments produced during the accident should be suspected. In these cases, it is important to perform careful radiographic studies to identify separated fragments of bone, which should be debrided and surgically removed. Injury to the roots of the maxillary molars is surprisingly rare but should be considered as a possible source of chronic infection if sinusitis persists after traumatic injury in this area.
Equine laryngeal trauma is not common. External laryngeal trauma may occur as a result of accidents to the throatlatch region. As a result, inflammation may lead to laryngeal edema, which may be severe enough to cause upper airway obstruction. If this occurs, an immediate temporary tracheotomy should be performed in the proximal third of the trachea to restore appropriate breathing. Even in cases of moderate laryngeal injury, the diversion of airflow through a temporary tracheostomy will provide relief of laryngeal edema. Additionally, the judicious use of nonsteroidal antiinflammatory drugs will often bring about resolution of laryngeal swelling.
The larynx may be traumatized by feed material injuring the laryngeal mucosa during the act of swallowing. Such internal injuries are more common than external trauma to the larynx, and may result in damage to the mucosa covering the laryngeal cartilages. In these situations, the clinician should be aware of the possibility of extensive granulation tissue formation at the site of mucosal injury. Granulation tissue may persist and lead to classic signs of upper airway obstruction such as stridor, exercise intolerance, and chronic coughing. Persistent granulation tissue formation can be problematic and may necessitate debridement through endoscopy and medical management consisting of antimicrobials and antiinflammatory medications administered both topically and systemically.
Internal tracheal injury is usually the result of intubation during general anesthesia. Prolonged use of high-pressure, low-volume cuffed endotracheal tubes can exert pressure on the tracheal wall and lead to ischemic necrosis of the mucosa or even the entire thickness of the wall. In horses under general anesthesia, overinflation of the cuff, traumatic intubation, and removal of the tube without deflating the cuff may result in injury to the mucosa. The diagnosis of tracheal mucosal injury is not easy and is usually made endoscopically after the horse develops chronic coughing and intermittent nasal discharge following general anesthesia.
After a few days from the injury, the tracheal mucosa may slough, and granulation tissue will form across the site. The application of topical antimicrobials may aid in the development of a bed of granulation tissue. Mucosal injury typically heals without complication, but formation of scar tissue webs across the tracheal lumen is possible and may necessitate debridement once the healing process is complete.
External tracheal injury is more common and is caused by blunt or penetrating trauma to the cervical or thoracic regions. This may result in tracheal lacerations, or tracheal avulsions and ruptures. Blunt trauma rarely causes tracheal injury because the trachea is not crushed against the spine as occurs in humans.
More commonly, kicks or impact with foreign objects will cause tracheal perforations in horses. Dyspnea is the major presenting sign of tracheal trauma, with rapid formation of subcutaneous emphysema. This is more readily seen when an incident to the cervical region disrupts the trachea. If the thoracic trachea is traumatized, it will typically collapse and be associated with a pneumomediastinum and a pneumothorax, in which case the signs of dyspnea may be severe enough to be life threatening.
A torn trachea should be suspected whenever there is subcutaneous emphysema along the neck and head. The diagnosis is confirmed by observing loss of tracheal continuity and narrowing on cervical radiographs. Occasionally, tracheal punctures may not be readily identified and may necessitate further evaluation using endoscopy. Tracheoscopy may be used to visualize the defect, but this procedure may induce further respiratory impairment and should therefore be selected only in horses that are hemodynamically stable.
Tracheal lacerations occasionally require emergency intervention. Depending on the location of the injury, it may be necessary to perform a temporary tracheostomy distal to the site of injury. If the cervical trachea is damaged, the area can be debrided with the horse standing and allowed to heal by second intention. Resection and anastomosis of a segment of the trachea has been described but is difficult to perform in horses because of the potential for reinjury during recovery from general anesthesia. Fortunately, most tracheal lacerations carry a favorable prognosis because they occur in the cervical region and are successfully treated by implementing standard wound care measures. A temporary tracheostomy will facilitate management of the wound by diverting airflow, which will further expedite healing of the injured trachea.
Thoracic trauma can be a diagnostic and therapeutic challenge, and clinicians should be prepared to institute emergency medical treatment particularly when injuries create an open thorax or in cases of severe blunt trauma. In the latter case, the signs can be deceiving because contusions, collapse, or laceration of the lung can all occur without apparent external lesions. Furthermore, the presence of cardiorespiratory signs with thoracic trauma warrants critical care management and usually necessitates referral to a hospital.
When evaluating horses with chest injuries, veterinarians may be challenged with the diagnosis and management of pneumothorax. Additionally, open chest injuries present challenges relating to pleural contamination and infection, presence of foreign material, and rib fractures. Traumatic pneumothorax, in particular, usually arises secondary to a penetrating chest injury; however, nonpenetrating blunt trauma may also cause pneumothorax by compressing and rupturing clusters of alveoli within a lung lobule, causing air to leak from the lower respiratory tract into the pleural space. Horses with acute chest trauma are often those most susceptible to severe complications and should therefore be carefully observed and managed because they may require emergency surgery.
Pneumothorax indicates the presence of free air in the pleural space. In most instances, air will be confined to the pleural space; however, the air may be contained within the adventitial tissue planes of the lung (interstitial pulmonary emphysema) or in the mediastinum (pneumomediastinum). During spontaneous normal breathing, pleural pressure is negative relative to alveolar and atmospheric pressure. Normal end-expiratory pleural pressure is subatmospheric (approximately −5 cm H2O) and becomes more negative (−7.5 cm H2O) during inspiration when the chest wall is expanded through contraction of the inspiratory muscles (mainly the diaphragm and external intercostal muscles). A negative pleural pressure is maintained throughout the respiratory cycle because of the tendency of the lung to collapse and of the chest wall to expand. When pneumothorax exists, the relationship between chest wall and lung is interrupted, and the chest wall, controlled only by recoil forces, tends to expand while the lung, under the influence of its own elastic properties, collapses. When pleural and atmospheric pressures are in equilibrium, the lung reaches its minimal volume, and further increases in pleural pressure (as air becomes trapped in the pleural cavity) lead to ipsilateral chest wall expansion and mediastinal displacement toward the contralateral hemithorax. In foals, this mediastinal shift toward the contralateral hemithorax can be detected radiographically. A tension pneumothorax occurs when a one-way valve develops either in the chest wall or the lacerated lung parenchyma. During inspiration, air enters the pleural space and accumulates because the one-way valve does not allow the inspired air to be released during expiration. In this situation, pleural pressure increases above atmospheric pressure.
Lung collapse affects pulmonary function. Total lung capacity (amount of air contained in the lung at the end of maximal inspiration) decreases, which also decreases vital capacity (the size of a maximal breath). In addition, a decrease in arterial oxygen tension occurs as a result of the low ventilation-to-perfusion ratios in poorly ventilated lung regions. This poor ventilation is a consequence of the peripheral airway closure that occurs in collapsed lung in patients with pneumothorax.
Pneumothorax also reduces cardiac function as a consequence of pressure changes within the chest cavity. When the chest is opened to the atmosphere by injury, the pressure around the heart increases to 0 mm Hg from its normal value of −5 mm Hg. This results in a decrease in venous return and reduction of cardiac output.