Thoracic trauma: keys to success (Proceedings)

Article

Traumatized small animal patients represent a population in which a standardized approach to diagnosis centered on thorough background knowledge of traumatic injuries coupled with a complete physical examination will allow for rapid therapeutic interventions and optimization of patient care.

Traumatized small animal patients represent a population in which a standardized approach to diagnosis centered on thorough background knowledge of traumatic injuries coupled with a complete physical examination will allow for rapid therapeutic interventions and optimization of patient care. The following paragraphs will detail the pathophysiology, diagnostic methods, and emergency medical treatment for injuries sustained due to both blunt and penetrating thoracic trauma from an anatomically based approach.

Thoracic injury occurs most commonly as a result of blunt trauma. Common causes include being hit-by car, falling from a height (high-rise syndrome), big-dog-little-dog interactions, and human-animal interactions. Penetrating injury (projectile induced injury, big-dog-little-dog interactions, and impalement injuries) occurs with less frequency than blunt thoracic injuries, but it must be recognized that both can result in immediately life threatening problems.

Trauma Associated Pleural Space Disease:

Pneumothorax, Hemothorax, and Diaphragmatic Hernia make up the three acute trauma associated pleural space diseases. Patients with clinically significant trauma associated pleural space diseases will likely display signs of tachypnea, dyspnea, and muffled heart and lung sounds on auscultation of the thorax.

Pneumothorax is the accumulation of air in the pleural space between the parietal and visceral pleura. Pneumothorax is classified as "open" when air enters the pleural space from an external wound, or "closed" when air enters the pleural space due to pulmonary or mediastinal injury. Tension pneumothorax occurs when air accumulates within the pleural space via a one-way-valve effect allowing air to enter, but not leave the pleural space. The resultant accumulation of air (and thus pressure) within the pleural space limits pulmonary expansion (ventilation) and venous return resulting in severe compromise to both the cardiovascular and respiratory systems. Pneumothorax is the most common of the trauma-associated pleural space diseases occurring in up to 47% of all dogs and cats with thoracic trauma. During our initial assessment of the traumatized patient, if we assume that a pneumothorax is present, we will make extra effort to both document and treat the condition.

Diagnosis of clinically significant pneumothorax is based on thorough auscultation of the chest and observation of the patient for signs of dyspnea. Positioned in sternal recumbency, patients with pneumothorax will tend to have decreased lung sounds dorsally to diffusely. Pneumothorax may be unilateral or bilateral. If pneumothorax is suspected based on auscultation and clinical signs, or if the clinician is unsure of the presence or absence of pneumothorax, thoracocentesis should be performed. Thoracocentesis is both diagnostic and therapeutic for pneumothorax. Radiographs of the thorax are not necessary for the acute diagnosis of a clinically significant pneumothorax and they may jeopardize the stability of the patient. When performed, radiographic evidence supportive of pneumothorax includes retraction of the lung from the chest wall (loss of vascular markings in this space), consolidation of lung lobes, and on lateral radiograph, the appearance of the heart "floating" on a cushion of air. The latter radiographic finding is due to the falling of the heart to the side of the atelectatic "down" lung.

Clinical evaluation of the patient's tolerance for its pneumothorax should guide treatment. Thoracocentesis may be performed with the patient in lateral or sternal recumbency. Most commonly, dyspneic patients will prefer to be sternal. Necessary equipment for thoracocentesis includes a 60cc syringe, three-way-stopcock, extension set and needle or catheter, or butterfly catheter.a-d In sternal recumbency, the needle or catheter is inserted through the skin off of the cranial edge of a rib (to avoid the neurovascular bundle) in the 8th – 11th interspaces. The needle or catheter is inserted perpendicular to the chest wall and advanced a few millimeters at a time with intermittent aspiration of the syringe until air is retrieved. If air is retrieved, the thoracic cavity should be completely evacuated until negative pressure is attained. When thoracocentesis is performed in lateral recumbency, the needle or catheter should be inserted at the highest point of the arch of the ribs. Most dyspneic animals will not tolerate being held in lateral recumbency. Numerous acceptable methods for thoracocentesis exist.

Once stabilized by restoring negative intrathoracic pressure and treating concurrent life threatening conditions, surgical exploration of the thorax is warranted in patients with open pneumothorax as damage to the internal structures, debris, and necrotic tissue are likely to be present. Closed traumatic pneumothoraces are often self-limiting with thoracocentesis or continuous pleural drainage (via thoracostomy tube) and rarely require surgical intervention.

Hemothorax is the accumulation of blood in the pleural space between the parietal and visceral pleura. Hemothorax may result from injury to the vessels of the thoracic wall, pulmonary vessels, great vessels, or the heart. The incidence of traumatic hemothorax based on radiographic evidence was found to be 8.7% in one series of dogs with fractures.5 The incidence of clinically significant hemothorax is lower and that of massive hemothorax is unknown.

Clinically significant hemothorax is suspected based on a thorough physical examination and confirmed through thoracocentesis or thoracostomy tube placement. Signs of shock (tachycardia, slow CRT, pale mucous membranes, weak pulses, cool extremities, etc,) will likely be seen early on in clinically significant hemothorax. Signs of respiratory tract compromise (tachypnea, dyspnea, dull lung sounds ventrally) may also be noted. Similar to cases of suspected pneumothorax, thoracocentesis is both diagnostic and therapeutic for hemothorax (see above). Thoracocentesis for suspected cases of hemothorax should be performed in the ventral third of the chest in the 6th – 8th interspaces with the patient positioned in sternal recumbency. Blood removed via thoracocentesis after blunt trauma may be re-administered via a blood administration set (auto-transfusion) as long as it is collected with a closed system.

Radiographs of the thorax are rarely necessary for the diagnosis of a clinically significant hemothorax and they may jeopardize the stability of the patient. Hemothorax will manifest radiographically as pleural fissure lines, retraction of the lung from the thoracic wall, and a positive silhouette with the heart and diaphragm (making identification of their specific borders difficult).

Most cases of hemothorax due to blunt trauma rarely require any management more aggressive than thoracocentesis. However, if >7mL/Kg of blood is retrieved via thoracocentesis or if there is other evidence of ongoing hemorrhage, a thoracostomy tube should be placed. If >30mL/Kg is retrieved, exploratory thoracotomy / sternotomy may be necessary. Surgical exploration of the thorax is always recommended in cases of penetrating thoracic injury.

Diaphragmatic hernia is the third of the acute trauma associated pleural space diseases. The pathophysiology surrounding diaphragmatic hernia in the dog and cat is thought to center on an acute rise in intra-abdominal pressure with the major energy dissipation directed cranially toward the diaphragm. Compared with other injuries identified in thoracic trauma patients, diaphragmatic hernia is relatively uncommon. Diaphragmatic hernia was reported in 5.8% of dogs sustaining fractures as a result of motor vehicle accidents. Diagnosis of diaphragmatic hernia is based on a thorough assessment of the respiratory system based on physical examination, and is aided by a variety of imaging techniques.

Clinical findings in dogs and cats with diaphragmatic hernia are varied and will depend on which organs are herniated, presence of concurrent injuries (in one study, 38% had concurrent thoracic injuries and 48% had no other clinical signs6), and acuteness of the injuries. Acutely, signs of cardiovascular (shock) and respiratory compromise will predominate.

Imaging techniques including survey radiography, positional radiography, positive contrast celiography, upper gastrointestinal contrast study, ultrasound, and computed tomography may aid in the diagnosis of diaphragmatic hernia.7 Radiographic findings include gross evidence of liver lobes, bowel loops, spleen or stomach within the pleural space. Abdominal radiographs may be helpful to identify organs "missing" from the abdomen. Often in cases of diaphragmatic hernia, concurrent pneumo/hemo thorax is present and pulmonary contusion may also be noted making definitive diagnosis challenging.

Some debate exists as to the optimal time for surgical intervention in cases of diaphragmatic hernia. One study found increased mortality in cases in which surgery was performed within 24 hours of the inciting trauma as well as after one year following trauma. However, a more recent study found excellent survival when patients were operated within 24 hours of trauma. Surgical management of patients with diaphragmatic hernia should be delayed if possible until patient stability is achieved. Indications for immediate surgery include the inability to stabilize patients medically (recognizing that surgical intervention may not improve the patients condition), those with evidence of strangulation of abdominal viscera, ongoing hemorrhage, concurrent injury for which emergency surgery is necessary, or those with a distended stomach within the thoracic cavity that cannot be decompressed via tube or trochar catheter. Mean mortality in cases of diaphragmatic hernia is approximately 10-20%.

Trauma Associated Pulmonary Disease:

Pulmonary contusion refers to a lesion of the lung that occurs after a compression-decompression injury to the chest wall that results in hemorrhage and edema leading to alveolar collapse and lung consolidation.10-11 Pulmonary contusion is the most common injury identified after blunt chest trauma in people and is very commonly recognized in animals that have undergone thoracic trauma. Pathophysiologic mechanisms for pulmonary contusion include the Spalling effect, inertial effect, and implosion effect. Various types of pulmonary contusion have been described.

All of the above forces and types of contusion culminate in the development of hypoxemia due to ventilation/perfusion mismatch, shunt, diffusion impairment, and hypoventilation.15 Diagnosis of pulmonary contusion should be based on strong suspicion in all cases of trauma supported by consistent physical examination findings, and confirmed radiographically. Pulmonary contusion should be suspected in all animals that have sustained thoracic trauma until proven otherwise. Thoracic radiography must not jeopardize the stability of the patient. Ventrodorsal radiographic views should NOT be performed on hemodynamically unstable or dyspneic patients.

Clinical signs of pulmonary contusion may be noted immediately after trauma or may not manifest for a number of hours. Clinical findings of tachypnea and dyspnea are most commonly recognized. Coughing and hemoptysis may also be noted. Auscultation of the chest in patients with pulmonary contusion may reveal a spectrum of findings ranging from mild increases in lung sounds to overt crackles. Conversely, in areas of the lung that are completely consolidated, decreased airflow may be noted. Each hemithorax may be differentially affected by pulmonary contusion. Auscultation must be interpreted in light of the likelihood that other thoracic lesions are present (pleural space diseases). If rib fractures are noted on physical examination, underlying pulmonary contusion should be expected.

Radiographic evidence of pulmonary contusion may not be present immediately after trauma, and may worsen over the first one-to-two days. Supportive radiographic evidence includes patchy interstitial or alveolar densities. Other radiographic evidence of thoracic trauma is commonly present.

Treatment of patients with evidence of pulmonary contusion is primarily supportive. Oxygen therapy should be administered to optimize oxygen saturation (minimum >94%) (as measured by a pulse oximeter) or PaO2 (>75mmHg) as measured by arterial blood gas analysis. Patients that are not able to maintain oxygen saturation with moderate respiratory effort in the face of 50-60% inspired oxygen concentration will require ventilatory support. Fluid support should be directed to maintain mean arterial pressure at least 75mmHg in the face of a relatively normal heart-rate, adequate urine output (minimum 1ml/Kg/hr), normal lactate, normal base-excess, and normal cardiac output. There is much debate as to the optimal fluid resuscitation choice in patients with pulmonary contusion, but no firm conclusions. Crystalloids, blood products, and colloids all have their place in fluid resuscitation. We should strive to avoid excessive fluid therapy (volume overload) as such situations may worsen pulmonary contusion. In the absence of hypovolemic shock, fluids should be administered sparingly to patients with pulmonary contusion.

Pharmacologic agents used in the treatment of pulmonary contusion over the years include furosemide, corticosteroids, and antibiotics. Furosemide is not indicated unless fluid overload has occurred and the patient must be monitored such that hypovolemia does not develop. The use of glucocorticoids for treatment in pulmonary contusion is very controversial. Some laboratory animal studies show some benefit, while others do not. The only clinical study in veterinary medicine to evaluate the use of corticosteroids for treatment of pulmonary contusion showed no decrease in the duration of hospitalization or oxygen therapy. At the present time, corticosteroids are not recommended for the management of pulmonary contusion. The incidence of bacterial pneumonia after pulmonary contusion in dogs is quite low (1%), however, this incidence is much higher in people. Because of the very low incidence of pneumonia, antibiotic therapy cannot be recommended. If a patient develops signs compatible with pulmonary infection, culture and sensitivity testing of transtracheal or bronchoalveolar lavage samples should be performed and antibiotic therapy begun immediately.

Survival after pulmonary contusion is excellent (82% in one study of dogs managed at a University Hospital). Survival drops to approximately 30%-80% when ventilatory support is necessary.,e

Trauma Associated Thoracic Wall Injuries:

Penetrating thoracic injury whether due to gunshot, impalement, knife wound, big-dog-little-dog interaction or other cause is a surgical emergency. Intubation and positive pressure ventilatory support will allow for optimal pulmonary gas exchange and a FiO2=1.0 (100% inspired oxygen). This therapy is administered in concert with standard tools for resuscitation (fluids, analgesics, etc.). Alternatively, while the patient is being stabilized with oxygen therapy, fluid therapy, pain control, etc., the wound may be covered with a sterile dressing and wrapped such that an airtight seal can be achieved and such that the chest can be evacuated of air (relieving the open pneumothorax) via thoracocentesis or thoracostomy tube. Broad-spectrum antibiotic therapy should be initiated immediately. Injury severe enough to penetrate the thoracic wall will often result in serious compromise to the underlying pulmonary and cardiac structures. Every effort should be made to identify concurrent injuries. Pulmonary contusion should be expected. As soon as the patient is stable, surgical exploration of the wound with debridement, lavage, and surgical reconstruction is recommended.

Rib fractures are relatively common after blunt thoracic trauma. The canine thoracic wall is a relatively resilient structure. As a result, it takes relatively major trauma to result in rib fractures. Fractures of the rib invariably result in significant pain (that in the worst case scenario can cause ventilatory disturbances) and if displaced internally, may result in puncture of the lung and subsequent pneumothorax. Rib fractures noted on physical or radiographic examination should serve as a "flag" for underlying pulmonary contusion.

Flail chest is described as a "paradoxic movement of a floating thoracic segment" or "the fracture of two or more consecutive ribs in two places (ventral and dorsal)." Paradoxical movement results from the changes in intrapleural pressures. Upon inspiration, intrapleural pressure decreases and the lungs expand (move outward). Because of the instability of the flail segment, it will not move outward with the rest of the thoracic wall, instead, the flail segment will move inward (towards the more negative pressure). The reverse is true on expiration. The combination of pendulous airflow, underlying pulmonary trauma, concurrent pleural space injuries, and pain can predispose to hypoxemia and hypoventilation.

Diagnosis of a flail segment of the thoracic wall is based on physical examination through the observation of paradoxical movement of the flail segment. Radiographic evaluation may confirm the flail segment and identify concurrent injuries, but is not necessary for diagnosis.

Therapy for flail chest has changed significantly over the years and still remains under debate. Three main categories of management methods exist. Conservative management centers on the treatment of the concurrent thoracic injuries (pulmonary contusion, pleural space disease) and the provision of pain control in the form of intercostal nerve blocks and epidural opiates. Bupivicainef (0.75% solution diluted to 0.25%) can be infiltrated as a small bleb locally dorsal and ventral to rib fractures. The bleb should be placed caudal to the rib due to the anatomic location of the neurovascular bundle. It may be helpful to also block single nerves cranial and caudal to the injured rib or segment. Total dose should not exceed 1.5mg/Kg and extreme caution should be exercised so as not to compromise ventilation by blocking too many intercostals nerves. Parenterally administered opiates can result in significant compromise to ventilatory function in patients with impending respiratory failure (as indicated by a PaCO2 of >50mmHg and significant respiratory effort). Surgical management can be performed if necessary once medical stabilization is achieved, but is rarely necessary on an emergency basis. Internal and external fixation methods are described.19 Management of flail chest patients with Positive Pressure Ventilation (PPV) techniques results in the generation of a "functional splint" by forcing the flail segment to move in concert with the thoracic wall. PPV also allows for the management of the underlying pulmonary trauma. Unfortunately, PPV is plagued with complications such as pneumonia and barotrauma and is difficult to perform in a non-referral institution. Prognosis for animals with a flail segment is often dictated by the severity of the underlying intrathoracic trauma.

Trauma Associated Mediastinal Injuries:

Pneumomediastinum is the accumulation of air within the mediastinal space. Pneumomediastinum can result from a variety of injuries in both the blunt and penetrating classifications of thoracic trauma. Possible causes of pneumomediastinum include large airway rupture, alveolar rupture (with subsequent tracking through the interstitium and back into the mediastinum), esophageal rupture, or cervical wounds (air can track along the airway and vascular structures of the neck back into the mediastinum).

Pneumomediastinum is most commonly a sign of other injuries rather than a problem itself. Diagnosis of pneumomediastinum is based on thoracic radiography. Presence of pneumomediastinum should prompt examination for the underlying cause through exploration for cervical wounds, endoscopy for evaluation of the esophagus, iodinated contrast studies of the esophagus, and tracheoscopy / bronchoscopy.

Tracheal avulsion is a rather uncommon result of thoracic trauma. Tracheal avulsion is more commonly reported in the cat than in the dog and is thought to occur due to rapid and extreme hyperextension of the head and neck. The trachea is most commonly avulsed within the thorax. Animals with tracheal avulsion may show evidence of pneumomediastinum on initial radiographic evaluation and may show signs of mild to severe dyspnea. A number of animals appear to recover over the first few weeks after trauma during which time the airway is maintained by a thin reflection of mediastinal tissue. However, affected animals then develop dyspnea secondary to fixed airway obstruction as the ends of the avulsed trachea begin to stenose. Subsequent radiographic evaluation often shows lack of continuity of the tracheal silhouette. Bronchoscopic evaluation leads to definitive diagnosis. Treatment is surgical correction of the stenosis and anastamosis of the tracheal ends.

Trauma Associated Cardiac Diseases:

The cause of the arrhythmias commonly detected 12-36 hours after trauma are likely multifactorial in nature. Direct contusion to the myocardium, decreased oxygen delivery to the myocardium secondary to shock, and ischemia reperfusion injury are all likely contributors to the problem. Common arrhythmias observed based on ECG monitoring include isolated premature ventricular contractions, accelerated idioventricular rhythms, and ventricular tachycardia. Treatment should subsequently be considered if the arrhythmia is compromising perfusion or if there are signs that it could degenerate to ventricular fibrillation. Prior to pharmacologic intervention, electrolytes, volume status, blood gas, and oxygenation should be assessed such that conditions that might predispose to ventricular arrhythmias can be corrected. Lidocainei is the most commonly utilized drug for treatment of such ventricular arrhythmias and can be administered at 2-4mg/Kg IV while an infusion is running at 50-80g/Kg/min. Additional doses can safely be administered one to two more times. Tremors, seizures, and depressed mentation as well as gastrointestinal effects evidence lidocaine intoxication. Lidocaine therapy should be discontinued if signs of toxicity develop. Seizures secondary to lidocaine intoxication may respond to diazepam.j Some arrhythmias refractory to lidocaine may respond to procainamidek (6-8mg/kg IV) followed by an infusion of 10-40g/Kg/min.

*Significant portions of these proceedings were previously published for CVC.

Footnotes:

      a. Monoject 60cc Syringe, Tyco Healthcare Group, Mansfield, MA

      b. Three Way Stopcock, Medex, Hilliard, OH

      c. Extension Set 30 inch, Abbott Laboratories, North Chicago, IL

      d. B-D Precision Glide Needles, BD and Co, Franklin Lakes, NJ

      e. Beal MW, Jutkowitz LA et al. Unpublished data.

      f. Bupivicaine .75%, Abbott Laboratories, North Chicago, IL

      g. Vacutainer Brand Tube for Activated Coagulation Time of Whole Blood, Becton Dickinson, Franklin Lakes, NJ

      h. Vacutainer Brand Tube for Determinations Requiring Serum, Franklin Lakes, NJ

      i. Lidocaine 2%, The Butler Co., Columbus, OH

      j. Diazepam 5mg/ml, Abbott laboratories, North Chicago, IL

      k. Procainamide 100mg/ml, Abbott Laboratories, North Chicago, IL

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