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Thoracic Trauma: The Do�s and Don�ts of Chest Triage

Andrea L. Looney, DVM
MSPCA/Rowley Memorial Animal Hospital
Springfield, MA

Thoracic injury is common in dogs and cats following trauma. Thoracic trauma seldom occurs as an isolated injury; patients are often in shock and may have other significant injuries. The immediate priorities of management apply equally to all cases of trauma. A global approach, aimed at assessing and supporting all vital organs is necessary to successfully manage these patients. Since trauma, specifically that to the thorax, is a leading cause of small animal death, the goal of this lecture will be to outline first some basics of general trauma management, then progress through the diagnosis and management of specific traumatic thoracic injuries.

Trauma is defined as any insult to the body. Obviously the variety of insults is tremendous. One thing we have learned via observation of emergency cases at referral and tertiary care facilities is that a systemic approach to the care of traumatized victims will indeed save lives. The "Golden period" defines the time following injury wherein effective therapy ensures a good chance of survival. Speed and quality of emergency care invariably determines morbidity and mortality. To effect a response, a primary survey involves triage of major body systems that follows the ABC�s of emergency care and gives at termination, a summary or total evaluation of the animal�s stability. Life-threatening problems are then treated immediately, according to their level of priority, utilizing a team-oriented approach (at least 2-3 people are necessary for a successful resuscitation).

In veterinary medicine, there are really three intervals in which death results from trauma, and as such, three times in which intervention may be crucial to survival. The first hour following trauma has classically been recognized in human medicine as the "survival hour." It is within this time that most deaths occur as a result of catastrophic, unsalvageable injury to the respiratory and cardiovascular system. Tragically, many patients do not survive, but historically those that do survive long enough to be transported to the hospital, often survive the traumatic ordeal itself. The next 2-4 hours are what we as clinicians recognize as the "Golden period." This is the most common presentation in the veterinary hospital. Prompt, aggressive treatment makes a difference in survival. Most treatable cardiovascular and respiratory injuries are seen in this period. The third interval occurs 3-5 days after the traumatic event. With attention to detail, recognition of hidden injuries, and appropriate monitoring, the insidious declines, organ failures and imminent sepsis in the traumatized patient can be avoided.

Initial Survey

The initial step in managing any traumatized animal is obtaining a history of the INCIDENT, vs. the patient, with specific reference to the mechanism of the injury. Encounters with automobiles, animal fights, traps, burns, weapons, and abuse are common traumatic injuries seen by veterinarians. Have the technician or assistant stay with the owner of the animal, as attention to the human counterparts is a very important aspect of handling the incident. The animal is then transferred to the emergency-ready area of the hospital where the team assesses A-airway, B-breathing, C-cardiovascular status and neurologic status of the patient, in that order. Life-threatening problems are treated immediately, stabilizing before moving on to the next system. Vital signs are collected as quickly as possible. Blood samples are taken for minimal database and include packed cell volume, total solids (protein), blood glucose, ACT, and urine specific gravity.

The body systems important in trauma triage are the following: a.) Arterial bleeding: often seen with open long bone fractures, hemothorax, or splenic and liver fractures; b.) Respiratory system: consider both oxygenation and ventilation; c.) Cardiovascular system: consider both pump and volume; d.) Neurologic system: consider both central and peripheral neurologic injury; e.) Tertiary systems (liver, kidney, spleen, bladder); and f.) Musculoskeletal systems. In order to consider any arterial bleeding and the cardiovascular system, tissue perfusion is assessed. In shock, blood is preferentially distributed to coronary and carotid arteries. We can assess coronary supply via ECG tracings, and carotid supply via neurologic (cranial nerve) status. Blood is then delivered to the liver, mesentery and finally to the skin. Evidence of urine output is suggestive of adequate renal perfusion and warming of extremities usually suggests adequate perfusion to the skin. Our goal is to assure this preferential perfusion via fluid therapy, thermoregulation, oxygenation, and proper monitoring.

Secondary Survey

Once the initial survey is completed, and the animal stabilized, a secondary survey begins. This starts with detailed evaluation of potential life-threatening injuries in the thorax, the focus of our discussion today. While the list of thoracic pathologies secondary to trauma is quite lengthy, I will attempt to focus on the more common problems encountered in clinical medicine as well as mechanisms to diagnose and effectively treat these entities. A recent study noted that clinical signs were not present in over 75% of dogs with injuries documented by radiographs, blood gases, or ECGs. In other words, the fate of many traumatized animals is determined by the ability of the clinician to recognize clinical signs once they become aware of the possibilities of problems associated with thoracic trauma. In humans, fractures of the first and second rib are the hallmark of severe thoracic trauma. Although first rib fractures are rare in dogs and cats due to anatomic differences (such as the forelimb musculature being more protective), cranial rib fractures may cause a mortality rate as high as 36% in small animals. Death is due to associated neurologic injuries, cardiac injuries (such as aortic and pulmonary artery transection), and pulmonary disease complicated by brachial plexus injury and subclavian artery injury. Pulmonary contusions are seen in 55% of all thoracic injury.

Thoracic injury is assessed via many means. Subcutaneous emphysema may occur with trauma but in itself is usually of little significance. Crepidus may be an indication of SQ emphysema or isolated rib fractures. If the blow has been severe enough to cause scapular or spinal fractures, chances are good that underlying pulmonary parenchymal or cardiac damage is present. Rib fractures can interfere with ventilation if the animal splints to reduce pain or occasionally, rib fractures may injure a major vessel; But, in and of themselves, these are rarely life threatening. Animals that have been injured cranially, especially in the cervical spinal cord or early thoracic spinal cord, may have an absence of pain (spinal shock or actual cord injury), OR rib cage, muscular, or sternal pain which is referred. The pattern of respiration can be informative. Patients with pneumothorax, effusions, and diaphragmatic hernia tend to have a rapid, shallow pattern, whereas pulmonary injury generally results in slower, more labored (abdominal) respiration. Bear in mind, however, that pain may limit chest movements and cause a shallower pattern. Slow, shallow breathing and paradoxical respiration may occur with head or cervical spinal trauma. Thoracic auscultation is performed to detect areas of dullness (hemothorax or diaphragmatic hernias), or harsh adventitious lung sounds (pulmonary contusions). Simultaneous auscultation and percussion can be used to diagnose pneumothorax; likewise, decreased lung sounds may indicate the same.

Thoracic radiographs are not indicated for initial assessment. They provide little additional information for the risks involved. It is quicker and safer to perform needle thoracocentesis to detect the presence of air or fluid than to take radiographs in a compromised patient. When initial stabilization is obtained, radiographs can be performed. It is well to remember that signs of thoracic injury may not be evident on initial assessment, especially on radiographs or even electrocardiographs; periodic reassessment is therefore mandatory to prevent respiratory or cardiovascular impairment from being overlooked. Physical exam, arterial blood gas analysis, and pulse oximetry are the tools used to evaluate thoracic injury in the emergency room.

A word or two on thoracocentesis. This technique is usually performed in the seventh or eighth intercostal space, with the patient standing, in sternal or lateral recumbency. The dorsoventral location of the puncture within the intercostal space is influenced by whether fluid or air is to be aspirated. An 18-20 gauge needle, or better yet, a short plastic catheter (either intravenous or thoracic) is used. A 3-way stopcock and a 20-60 ml syringe are attached to the needle wither directly or by a section of IV extension tubing. The neurovascular bundle is on the caudal edge of the rib. The skin is pulled cranially first, the needle inserted at a 90-degree angle to the skin surface, the skin let go, and the thoracic peritoneum is entered at a 45-degree angle with the needle pointing cranially. We use sedation of valium and oxymorphone or butorphanol IM or IV if the animal is extremely anxious or painful. Clipping and prep are done IF time allows. Local infiltration of bupivicaine or lidocaine are rarely utilized in an emergency situation but can be very helpful in reducing sensory thresholds if multiple taps are anticipated.

Arterial blood gas sampling is an easy art to master with practice. If the animal appears to have a tension pneumothorax or severe parenchymal damage, percutaneous placement of an arterial catheter may be indicated for repeat blood gas analysis. The most common site for arterial sampling is the dorsal metatarsal artery. This artery is most superficial in the proximal metatarsus, medial to the extensor tendons, between the second and third metatarsal bones. A second site is the dorsal pedal artery that courses medial to the long digital extensor tendon at the level of the proximal tarsus. Peripheral vasoconstriction and hypothermia secondary to shock yield falsely elevated pHs as well as falsely decreased PaO2 and PaCO2. In the presence of severe hypoperfusion, hypercapnia and acidemia at the tissue level are better detected in central venous blood vs. arterial blood; however, the latter better reflects respiratory status.

The goal of arterial blood sampling is to determine the animal�s efficiency of oxygenation and ability to ventilate. Oxygenation is determined by calculating the Alveolar-arterial oxygen gradient (A-a gradient). The formulae used for this are the following: When the animal is breathing room air (21%): "A" = (barometric pressure � 47)(0.21) � PaCO2/0.8. "a" is simply the measures PaO2. Thus the A-a gradient = A � a. The normal A-a gradient is 0-10. Questionable oxygenation A-a gradients = 11-20. Hypoxic respiratory emergencies cause A-a gradients >21, often in the range of 30-35. A-a gradients are used instead of PaO2 because both hypoventilation and impaired gas exchange can cause hypoxemia; the higher the gradient, the more significant gas exchange impairment (parenchymal damage) is evident. In general though, patients with PaO2 levels below 80 mmHg require oxygen supplementation. A PaO2 of less than 60 mmHg with an inhaled oxygen content exceeding 50% indicates a need for mechanical ventilation.

The animal�s ability to ventilate is assessed by examining the PaCO2. Hypoventilation is a decreased ability to rid the body of CO2, and indicated by increased PaCO2. Hypoventilation in an animal without significant head trauma is indicative of severe contusion. Patients with PaCO2 values exceeding 50 mmHg require mechanical ventilation. The PaCO2 and PaO2 are variables obtained using various point of care testing devices such as the iSTAT, STATpal, and NOVA or standard bench-top laboratory blood gas analyzers.

Pulse oximetry measures oxygen saturation but does not provide a measurement of acid-base or ventilatory status. This technique allows the instantaneous estimation of arterial oxyhemoglobin via transmission of light through a skin fold. Although the arterial oxyhemoglobin saturation (SaO2//SpO2) is not linearly related to the arterial O2, it provides information on oxygen delivery and is most useful when used as a continuous, real-time monitor. Instruments are relatively inexpensive, safe, easy to use, and well tolerated by patients. The PaO2 contributes only 0.003 volume percent to the total blood oxygen content. Thus, the most important measures of tissue oxygenation are hemoglobin concentration and percent saturation. In this case, the pulse oximeter is indeed a useful monitor of tissue oxygen delivery given that the animal has normal hemoglobin concentration and is not peripherally vasoconstricted (shock, pain, hypotension, drugs) to preventing proper absorption of light and pulsatile blood flow.

If oxygenation or ventilation is impaired, a number of conditions should be initially considered. Amongst these are: a.) airway obstruction; b.) pneumothorax; c.) flail chest or rib fractures; d.) hemothorax; e.) pulmonary contusions; f.) diaphragmatic hernia. The management of several of these pathologies will be the emphasis of the remainder of this handout.

Airway Obstruction

Ensuring a patent airway is the first priority in trauma management. The examiner should assess the pattern of respiration and listen carefully to breath sounds, while palpating and visually inspecting the oral cavity, larynx, and trachea. Severe or complete obstruction of the airway will result in exaggerated inspiratory efforts or apnea. Often these are secondary to severe head (palatal, mandibular, or pharyngeal injury or to regurgitation of a recently ingested meal from the middle or side of the road. Locating the obstruction is a priority, but if the head was injured, the neck was probably injured as well. Care should be taken to avoid any unnecessary movement of possible unstable spinal or spinocranial luxations. Use of head and backboards are encouraged.

The quality of breath sounds may help in determining the level of obstruction. Oropharyngeal obstructions tend to be "gurgly;" while laryngeal or upper tracheal obstructions are "raspy" or stridorous. Suctioning or sponging can be used to clear the airways. Where airway obstruction is only partial, oxygen supplementation may be sufficient to temporarily stabilize the patient. This can be applied via a face-mask, hood, or nasal/tracheal cannula. The latter method is preferred where oxygen flow rates of 100-200 ml/kg/min are recommended. When a more complete airway obstruction is present, aggressive measures such as transtracheal oxygen cannula, or tracheostomy are required. The author urges ruling out pneumothorax via needle throacocentesis prior to intubating (with cuff inflation) any animal traumatized cranial to the waist. Closed aggressive ventilation may quickly worsen any pneumothorax (especially a tension pneumothorax) and increase chances of hemothorax leaks as well as cardiovascular compromise.


Closed pneumothorax may result from perforation of the lungs, airways, or esophagus. Most begin unilaterally but progress bilaterally. A tension pneumothorax develops from a closed pneumothorax and occurs when tissue acting as a one-way valve allows air to enter the pleural space during inspiration, but not to exit during expiration. The resulting supra-atmospheric pressure severely compromises ventilation as well as venous return, leading to death within minutes. Patients with pneumothorax have rapid, shallow, respirations. With tension pneumothorax, jugular and/or femoral venous distension is occasionally observed. Lung sounds are not only decreased, but often one can simultaneously percuss and auscultate ("ping") to hear an increased resonance.

Thoracic radiographs are not indicated for initial assessment. It is quicker and safer to perform needle thoracocentesis to rule out pneumothorax. If repeated thoracocentesis is required, a chest tube should be placed and continuous suction drainage used. Usually, these systems are used only with dogs because of the amounts of air being drained, apparatus size, and amount of required tubing. Such factors make use in cats cumbersome.

Open Chest Wounds

These may be associated with extensive diffuse contamination of the chest cavity and pneumothorax. Wounds should be occluded immediately with Vaseline-impregnated gauze and a chest wrap. Often, these animals survive to hospital admission because their open wounds are recumbent side down or covered with an owner�s blanket. Unfortunately, these wounds are not only a source of air entering the chest, but vicious nosocomial infections. Antibiotics utilized to treat open chest wounds include enrofloxacin and metronidazole (known for their excellent tissue-penetrating abilities), the penicillins (great for anaerobes and gram positive organisms, bactericidal), and the cephalosporins (especially useful if hollow viscus or cranial abdominal trauma is suspected). These wounds may be explored, debrided, and closed under general anesthesia when the animal is cardio-respiratory stable in 2-5 days.


Pleural effusion, especially hemorrhagic, should be ruled out in any patient with unresponsive shock. Signs of blood loss and hypovolemic shock generally precede respiratory distress. The internal thoracic vessels, intercostal vessels, or internal mammary vessels are often the source of hemothorax. Thoracic auscultation reveals dullness ventrally. Hemothorax should not be excluded based off of a negative thoracocentesis. The chances of a positive tap are increased by the use of a multi-fenestrated catheter and multiple taps. Autotransfusion can be considered in a massive hemothorax until an alternative source of blood is available.

Exactly how much blood to remove from a hemothorax is a very controversial issue. The accumulation of blood may increase intrapleural pressure enough to provide tamponade for cessation of bleeding, but a substantial hemorrhagic effusion may cause a significant decline in pulmonary function. It is generally recommended that blood be removed if it is causing a significant decrease in pulmonary function. The quantity removed should be only the amount needed to relieve respiratory distress.

Pulmonary Contusions

Pulmonary contusions constitute the most common injuries following thoracic trauma. Damage to the lung causes hemorrhage and edema into the interstitium, alveoli, and small airways. Hypoxemia occurs and pain induced hypoventilation is contributory. Decreased cardiac output commonly occurs and is significant because it occurs when tissue demands for oxygen are greatest. Hemoptysis, or the presence of blood or bloody fluid in the oropharynx and trachea indicates severe chest contusions. Thoracic auscultation may reveal moist rales, and/or bronchial sounds. Contusions MAY be confirmed on thoracic radiographs appearing as alveolar or interstitial infiltrates. Contusions may not appear or be evident for up to 6-12 hours post trauma. Arterial blood gas monitoring and clinical signs are the most sensitive means of detecting respiratory compromise.

Treatment of pulmonary contusions centers around supportive care and maintaining adequate tissue oxygenation. Fluid therapy restores adequate cardiac output. Careful monitoring is used to avoid overload (CVP monitoring). Hypertonic saline solutions or dextrans are a useful adjunctive therapy directed at rapidly restoring circulatory function without causing deleterious pulmonary effects. Animals with dyspnea and hypoxmia require oxygen therapy. Nasal oxygen is most useful. Pain associated with thoracic trauma inhibits ventilation so analgesia via opioids (systemic, oral, patch), sedatives, or even epidural or spinal blocks is warranted. Pain also reduces cough, promotes atelectasis, and predisposes to pulmonary infection. Diuretics are not recommended unless fluid overload or pulmonary edema occurs. Cage rest assists recovery of mild cases, but severe cases benefit from positional changes and physical therapy.

Flail Chest and Rib Fractures

Flail chest is the result of two or more rib fractures of two or more adjacent ribs. Rib fractures compromise respiration secondary to pain and often are the tip of the iceberg indicative of much underlying lung pathology. Immediate stabilization is generally not required. Fractures of cranial ribs are often indicative of severe cardiovascular trauma, while fractures of the caudal ribs should arouse suspicion of possible cranial abdominal trauma. Placing the animal in sternal recumbency with flail side covered and down may limit pain and further injury, but wrapping the chest often decreases compliance instead of stabilizing fractures.


Embolisms occurring secondary to trauma may be of three types: air, fat, or thromboembolic. Fat embolisms occur very commonly in people with thoracic trauma one hour to three days following initial injury. It is theorized that lung injury is produced when lipases hydrolyze neutral triglycerides to liberate unsaturated fats toxic to the pulmonary parenchyma. This fat may precipitate diffuse coagulopathies or ARDS (adult respiratory distress syndrome).

Air embolism is a relatively unrecognized cause of death in veterinary patients, and is divided into two categories, depending on whether there is involvement of the left or right side of the circulation. Venous air embolism is usually not clinically significant because relatively large amounts of air are tolerated by this route. However, arterial air embolism is rapidly lethal. Reportedly, as little as 0.5 ml of air injected into the arterial system has led to ventricular fibrillation, loss of consciousness, seizures, bradyarrhythmias, and cardiac arrest. Patients with lung lacerations receiving positive pressure ventilation may be at increased risk of developing fatal bronchoarterial fistula and should be carefully monitored for evidence of air embolism. Pulmonary thromboembolism (PTE) may occur secondary to trauma but is more commonly associated with chronic disease states such as AIHA, Cushings, protein losing glomerulonephropathy, or pancreatitis. The triad of hypoxia, hypocapnia, and dyspnea in the face of relatively normal radiographs and a traumatized lung field should make one think of PTE.

Traumatic Myocarditis

The pathogenesis of post-shock arrhythmias (traumatic myocarditis) is probably multifactorial. This appears to be much more common in dogs than in cats. Potential causes of this syndrome include blunt trauma of the heart, myocardial ischemia, and autonomic imbalance as a consequence of CNS injury. Metabolic disturbances are common following severe injury or other causes of shock syndrome; these may worsen the arrhythmias commonly seen (VPCs, idioventricular rhythm, and ventricular tachycardia). These metabolic disturbances are hypoxemia, anemia, hypokalemia, hypomagnesemia, acidemia, abnormal body temperature, pain, and pulmonary injury with hypotension.

The first step in therapy of these arrhythmias should be identification and treatment of any metabolic disturbances predisposing to arrhythmias. Nine times out of ten, simply providing oxygen therapy assists in a more rapid resolve. If the arrhythmia increases heart rate to the point that cardiac performance is inhibited or the chance of fibrillation and flutter increases, the arrhythmia may be treated with lidocaine (2-5 mg/kg/hour), magnesium sulfate (30 mg/kg over 10-15 minutes), or Procainamide (1-2 mg/kg/hour).

Diaphragmatic Hernia

Hernias secondary to trauma may present with varying degrees of respiratory compromise. Auscultation may detect diminished heart and lung sounds on the affected sides. Borborygmus may be heard on thoracic auscultation if the intestines or stomach are herniated. These findings may not be evident for days to weeks following injury. Radiograph diagnosis may be achieved if there is displacement of viscera into the thorax. Ultrasound or barium contrast studies may be necessary to discern herniation. Immediate surgical correction is contraindicated unless a rapidly expanding, gas filled viscus is present in the thorax. Only after hemodynamic stabilization is assured, is surgical correction warranted.

Lung Lobe Torsion

Lung lobe torsion is an uncommon result of severe chest trauma that forces the lung to rotate on its hilar axis. A radiographic clue is reversal of the normal pattern of bronchovesicular markings or a "ground glass" opacification of the affected hemothorax due to vascular congestion, edema and atelectasis in the affected lobe. Most cases of torsion involve the right middle lobe, and most cases occur in large breed, deep-chested dogs. Pneumothorax and pleural effusions increase the freedom of partially collapsed or injured lung lobes. Lung lobe torsion must be differentiated from edema, atelectasis, hemorrhage, neoplasia, or pneumonia. The most consistent thoracic signs are pleural effusion and opacification of the affected lobe. Pneumomediastinum may be present if the bronchus of the twisted lobe ruptures. Surgical removal is corrective even if on the thoracotomy the lobe appears normal or if it partially reinflates.

Esophageal Rupture

This should be suspected in patients with a history of major chest trauma and a pleural effusion, especially if it is left-sided or accompanied by pneumothorax. Although interscapular or substernal pain is common (along with fever and hypotension), an insidiously accumulating pneumothorax or a pleural effusion may be the only manifestation. Thoracocentesis is highly suggestive if it reveals an acidic exudative fluid, marked high amylase, or presence of rods. This is a highly lethal condition in humans with mortality approaching 2% per hour due to constricting mediastinitis. Extravasation of swallowed contrast material into the mediastinum or pleural space confirms the diagnosis. Surprisingly, endoscopy is frequently unremarkable and CT scans provide poor resolution of this area until mediastinitis is severe. Immediate surgical repair and drainage are indicated.

References available upon request from author

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