Thoracic Wall and Sternum

The thoracic wall and sternum play an integral role in various normal physiologic processes that are essential in maintaining homeostasis. The physiologic roles of the thoracic wall and sternum include housing and protecting the thoracic viscera as well as providing the semi-rigid framework that supports respiratory effort and function. When the functions of the wall and sternum are altered through malformation (congenital or acquired) or trauma, homeostasis can be disrupted with results ranging from inconsequential to catastrophic. Therefore, it is incumbent on the veterinarian to understand the normal functions of the thoracic wall and sternum as well as to recognize potential consequences when these functions are disrupted. Unfortunately, clinical signs that indicate the presence of thoracic wall pathology may be either overshadowed by concurrent, more obvious, clinical signs from separate problems or be insidious in presentation and relatively difficult to detect.

Thoracic wall trauma is considered to be more common than congenital and acquired deformities,1 and traumatic injuries to the thoracic wall can be categorized as blunt or penetrating [1-4]. Blunt injuries to the thoracic wall result from vehicle accidents, adverse interactions with other animals or humans, falling from heights, and crushing injuries. The pliant nature of the thoracic wall in small animals has been suggested as a primary reason that blunt trauma may not always be manifest by visible pathology to the thoracic wall [5-10]. However, owing to the enclosure of vital thoracic organs, absence of visibly obvious pathology does not preclude the possibility of damage to these organs. Many reports have indicated that injury to pulmonary and cardiac tissues are common sequels to blunt injury despite the lack of visible damage to the thoracic wall [2,11-13]. When injuries to the thoracic wall are apparent, it should be assumed that damage to the underlying organs has also occurred, and therapy addressing this damage may take priority over other less threatening injuries. Pulmonary damage, alterations of the pleural space, disruption of tracheobronchial structures, damage to the heart and great vessels, and diaphragm rupture are common potential sequels to blunt thoracic trauma.

Penetrating injuries to the thoracic wall are not as common as blunt injury and result from high- and low-velocity projectiles, animal bites, and impalement (accidental or purpose driven). The integrity of the pleural space and underlying organs becomes a primary concern in that loss of the integrity and function can be rapidly fatal. Penetrating wounds must also be considered contaminated and the potential for infection realized [3]. The degree of trauma resulting from penetration is dependent on several factors. Among these are the type of tissue, the mass, shape, size, and velocity of the penetrating object, and the behavior of the object on penetration [14,15]. Generally speaking, the more kinetic energy transmitted to the tissues, the greater the tissue damage will be. This generalization, however, does not take into account that vital functions may be completely disrupted by even relatively little tissue damage, depending on the organ involved. Penetrating wounds to the thoracic wall alone would rarely be a cause of major concern if not for the role the thoracic wall plays in respiration and in protecting vital organs.

Deformities of the thoracic wall and sternum, as previously mentioned, are much less common than is traumatic injury [1]. The pathologic results of deformities can alter normal physiologic function of the chest wall and major organ systems housed within the thoracic cavity [1,3,6,16]. However, such disruption of function is not common and is relative to the severity of the deformity. Congenital deformities include pectus excavatum, pectus carinatum, and various rib and spinal deformities. Finding a significant congenital deformity of the thoracic wall and/or sternum is not an automatic indication for surgical or medical intervention because in many cases those affected are asymptomatic [16,17]. Acquired deformities of the thoracic wall may be a result of neoplasia or infection. Neoplastic disorders may arise from soft tissue or skeletal structures of the thorax or be a metastatic extension from a distant site [17]. Infections can result from bacterial or fungal invasion secondary to chest wall trauma or migrating foreign bodies. These infections can present as mass lesions or can disrupt the integrity of the thoracic wall, leading to pleural space and possibly pulmonary disease.

In this chapter, I focus on the basics of anatomy and physiology to provide sufficient information for the reader to recognize pathophysiology of selected disorders of the thoracic wall and sternum.

Anatomy

The thoracic cage provides the dorsal, lateral, and ventral peripheral boundaries of the thoracic cavity, which contains all or part of the heart and great vessels, lungs, pleurae and pleural space, trachea, esophagus, thymus, lymph nodes, and nerves of the somatic and autonomic systems. Also protected by the thoracic cage are the diaphragm, liver, gallbladder, stomach, and all or part of the spleen, right kidney and adrenal gland, intestines, and abdominal extensions of the great vessels and autonomic nerves [18]. The morphology of the thoracic wall can generally be described as a laterally compressed cone with the base as the caudal extent and the apex cranial. The lateral compression results in a greater dimension in the dorsoventral direction [16,18]. The skeletal components include the sternum, thoracic vertebral bodies, and ribs. The sternum is composed of 8 individual bones called sternebrae, which make up the floor of the thoracic cage. The cranial- and caudal-most sternebrae are specifically designated as the manubrium and xiphoid process, respectively. Interposed between the sternebrae are cartilaginous plates, and extending caudally from the xiphoid process is the flattened xiphoid cartilage. The dorsal aspect of the thoracic cage is formed by the 13 thoracic vertebral bodies and the vertebral extremities of the ribs. Thirteen pairs of ribs constitute the lateral walls of the thoracic cage, each with osseous dorsal and cartilaginous ventral components. Each rib has synovial articulations dorsally with the vertebrae in two locations, the head with the vertebral bodies (or body) at or near the intervertebral disc and the tubercle with the transverse process. Ventrally the first 9 pairs of ribs have synovial articulations with the sternum. The first pair with the manubrium, pairs 2 to 7 with the corresponding intersternebral cartilage plates, and pairs 8 and 9 share an articulation site at the last intersternebral cartilage. Pairs 10 to 12 attach to the preceding rib through the ventral costal cartilages and form the costal arch. The 13th pair are commonly known as floating ribs because they do not articulate with the sternum and the ventral cartilaginous portions are enclosed in the surrounding abdominal muscles [6,16,18] The diverging nature of the sternum and vertebral bodies and the increasing arch of the ribs from cranial to caudal account for the aforementioned cone shape [18].

The soft tissue components of the thoracic wall include the costal parietal pleura, the endothoracic and external thoracic fasciae, and various muscles that are important structurally as well as functionally for respiration. The parietal pleura is a serous membrane that has a layer of mesothelial cells supported by a layer of delicate elastic fibers. The parietal pleura also lines the surface of the diaphragm [18,19]. The parietal pleura is supported by the endothoracic fascia which is deep to the thoracic musculature. The external thoracic fascia covers the external surfaces of the muscles and the chest wall [18].

The intercostal muscles are confined within the space between each rib. Closest to the parietal pleura are the internal intercostals. These muscles extend from the cranial borders of ribs 2 to 13 and course in a cranioventral direction to insert on the caudal border of the preceding rib.16,18 In the interosseous area of the thoracic cage, this arrangement results in the ribs being pulled in a caudal direction. Other muscles of the thoracic wall also function to pull the ribs caudally. These include the external intercostals of the caudal-most interspaces, rectus abdominus muscles on the ventral aspect, the costal portions of the external abdominal oblique muscle at the ventrolateral aspect of the chest wall, the caudal portion of the serratus dorsalis located caudodorsally, and the transverses thoracis on the internal surface of the ventral thorax [16,18,20,21]. The external intercostals, as the name implies, lie lateral or external to the internal intercostals. These muscles arise from the caudal border of ribs 1 to 12 and course caudoventrally to insert on the cranial border of the succeeding rib [16,18]. The fibers run at a right angle to the fibers of the internal intercostals and in the craniodorsal interspaces have essentially the opposite action, that of pulling the ribs cranially. The other muscles of the thoracic wall that pull ribs cranially include the interchondral portion of the internal intercostals, rectus thoracis located cranioventrally, the scalenus on the ventrolateral aspect, and the cranial portion of the serratus dorsalis on the dorsolateral aspect of the chest wall [16,18,20,21]. The other muscles that cover the thoracic wall and function in mobility of the spine and thoracic limb include the epaxial muscles over the dorsal thoracic region, the serratus ventralis on the craniolateral surface, the rhomboideus and trapezius muscles over the craniodorsal walls, the pectoral muscles on the ventral surface, and the latissimus dorsi along the lateral wall [16,18]. Finally, loose subcutaneous tissues, the cutaneous trunci muscle and the skin form the outer layers and covering of the thoracic wall.

Vascular supply to the thoracic wall is generally through the intercostal arteries and veins. The arteries originate either from the costocervical trunk or the dorsal intercostals from the thoracic aorta and course along the caudal border of the ribs to anastomose with the ventral intercostal arteries arising from the internal thoracic arteries that lie on the internal surface of the ventral thoracic wall. Branches of the ventral intercostals can be found on the cranial and caudal aspect of the ribs. The intercostal veins course with the arteries along the caudal border of the ribs and drain into the azygous vein between the vertebral bodies and thoracic aorta [18].

Innervation to the thoracic wall is primarily from branches of the thoracic spinal nerves. The intercostals nerves arise from the ventral branches and course with the arteries and veins along the caudal border of the ribs [18].

Physiology

Respiration can be divided into four major functions: pulmonary ventilation, diffusion of O2 and CO2 between alveoli and the blood, transport of O2 and CO2 within the blood to the cells of the body, and regulation of ventilation [22]. The anatomic morphology of the thoracic wall contributes primarily to pulmonary ventilation. The cone-like shape of the thoracic cage and the muscle attachments allow for expansion and contraction of the thoracic cavity. Because the diaphragm is located near the base of the "cone," as it contracts the craniocaudal dimension of the thoracic cavity is increased. The combination of rib morphology, rib articulation with the spine and sternum, and thoracic wall musculature lead to a "bucket-handle" type of motion to the ribs [6,23]. As the ribs are pulled in a cranial direction by thoracic wall muscles, the sternum moves further away from the spine and the arches of the ribs become more abaxially positioned. This results in an increase in both the dorsoventral and lateral dimensions of the thoracic cavity. Those muscles that function to pull the ribs cranially are called muscles of inspiration while those that pull the ribs caudally are muscles of expiration.

By convention it has been thought that the external and internal intercostal muscles have distinctly inspiratory and expiratory functions, respectively. This convention has changed and the individual effects of these muscles on respiration are determined more by topography and nervous input [20,21]. It is now thought that the external intercostals in the craniodorsal interspaces and the interchondral portion of the internal intercostals (a.k.a. parasternal intercostals) are inspiratory and pull the ribs in a cranial direction [20,21].

The parasternal intercostal contribution to the cranial movement of the ribs is estimated at approximately 80% []. The interosseous portion of the internal intercostals and the external intercostals of the caudal-most interspaces are expiratory and pull the ribs caudally [20,21].

The pleural space contained within the thoracic cavity is, in actuality, only a potential space. This is because the subatmospheric or negative pressure within the space keeps the pulmonary pleura held in contact with the parietal pleura of the thoracic wall. This negative pressure is created by fluid movement into and out of the pleural space [22]. Starling's forces and pleural membranes that are porous allow protein-containing interstitial fluid to transude into and out of the pleural space. The net effect of capillary hydrostatic pressures and colloid osmotic pressures between systemic capillaries and pulmonary capillaries favors flow from the systemic capillaries through the pleural space and absorption into the pulmonary capillaries. As the volume of fluid increases above that which is necessary for lubrication of the pleural surfaces, the lymphatic vessels pump excess fluid away. The pumping action of the lymphatic system helps to produce the negative intrapleural pressure. Fluid flow dynamics and the lymphatic actions produce a "liquid coupling" between the pulmonary and parietal pleural surfaces. This coupling allows complete transmission of changes in the thoracic cavity volume to the lungs [19]. So, as thoracic cavity dimensions are increased in response to respiratory muscle action, the lungs are able to expand.

The thoracic wall and lungs have an elastic nature that is independent of each other. Without fluid coupling, the thoracic wall would expand to a point where, when relaxed, a specific thoracic volume (Vo) would exist [6]. When muscles of inspiration increase the thoracic volume above Vo, the thoracic wall has a tendency to recoil inward until Vo is reached. If thoracic volume is less than Vo, the thoracic wall has a tendency to spring outward, again until Vo is reached [6]. The elastic nature of the lungs, without fluid coupling, would result in an inward collapse to a point where only a residual volume of air remained. The opposing elastic recoil of the thoracic wall and lungs, with fluid coupling, has a point where balance is achieved. That is, the inherent tendency of the lungs to collapse is prevented by the inherent tendency of the thoracic wall to spring outward and vice versa. At this point of balance, the thoracic volume is less than Vo and the volume within the lungs is the functional residual capacity (FRC) [6,23]. When the muscles of inspiration cause expansion of the thoracic volume, the lungs also expand owing to fluid coupling. This results in an increase in the negative pleural pressure, which generates negative pressure within the airways and alveoli relative to the atmosphere (transpulmonary pressure) and allows air to flow into the lungs. Because the thoracic volume is held to less than V, the inherent tendency of the thoracic wall to spring outward actually assists in the inspiratory effort until Vo is reached or exceeded. Then, when inspiratory muscle contraction ceases, the thorax passively returns to the point of balance.

The change in volume of the lungs and thoracic cavity in response to changes in pressure is called compliance [6,22,23]. The compliance of the lungs and the thoracic wall together make up the total compliance of the pulmonary system. When the ability of either the thoracic wall or the lungs to change volume in response to change in pressure occurs, the total compliance will change. The effort required to generate sufficient negative transpulmonary pressure to overcome the compliance of the pulmonary system and the resistance to airflow within the airways for inspiratory flow or to overcome resistance to expiratory flow is the work of respiration. The work of respiration will be altered if compliance is altered [1,6]. If thoracic wall compliance is decreased because of trauma or disease, the work of respiration will increase.

Trauma

Blunt Trauma

Blunt trauma to the thorax induces tissue injury by transference of the kinetic energy of the impacting object to the chest wall without creating an opening between the pleural space and thoracic organs and the external environment. The greater the kinetic energy transmitted the greater potential for damage to the thorax. Additionally, the energy is also transferred to the thoracic organs with potential damage to those organs. Direct trauma produces crush and shear injury to the soft tissues and skeletal structures. Low-speed trauma produces a localized crushing injury to the tissues [1]. With this type of trauma the skin may appear relatively undamaged owing to the resilience of the cutaneous epithelium. Underlying tissues such as muscle and bone however, may exhibit a greater degree of damage. Muscle tissue is extremely sensitive to pressure [25]. This sensitivity can result in muscle damage with localized rhabdomyolysis, and myoglobin, potassium, phosphorus, and creatinine phosphokinase are released into the surrounding tissues. When more than 200 grams of muscle are injured, the serum myoglobin levels can be increased and myoglobin may be detected in the urine [26]. Despite the fact that myoglobinemia is rapidly cleared, it must be remembered that the products of myoglobin breakdown are nephrotoxic [27,28]. Skeletal muscle contains more potassium than any other body structure [29]. Extensive damage to muscle tissue with muscle necrosis can lead to hyperkalemia []. Phosphorus can leak from damaged muscle tissue and contribute to hyperphosphatemia [31]. Creatinine phosphokinase is an enzyme released from damaged muscle; an increase in levels of creatinine phosphokinase is a sensitive indicator of muscle injury from any cause, and the increase will parallel the degree of damage. Muscle that has been injured in this manner becomes edematous and swollen and loses its elasticity and ability to contract efficiently. This decreases the compliance of the thoracic wall and, therefore, increases the work of respiration. However, the resulting pain may contribute to a decreased respiratory effort, which may contribute to hypoventilation.

Higher speed trauma produces shearing injury in addition to crushing [1]. Shearing injury results when two adjacent tissues with different specific gravities are suddenly accelerated or decelerated [1,32]. Because of the specific gravity variation, the momentum of the tissues during the abrupt change is also different. This generates shear forces at the junction of the two tissues. If the shear forces exceed the inherent elasticity of the tissue junction, the result will be a separation between the tissues. Although soft tissue damage of the thoracic wall is rarely a major cause of morbidity or mortality [1], it is critical to remember that the kinetic energy of the impact is also transmitted to the thoracic organs, and crush and shear injuries may occur to these structures.

The resistance of skeletal structures of the thoracic cage to injury through blunt trauma is attributed to inherent resilience [2,4,6,9]. Despite this resilience, the lack of obvious skeletal damage does not preclude the possibility of severe, even life-threatening soft tissue or thoracic organ damage because considerable force is required to induce fracture and that force is also transmitted to the thoracic organs. Blunt trauma that results in fractures of the thoracic cage most commonly is from a direct force applied to the lateral body wall resulting in rib fractures [4]. Ventral-dorsal compression of the thorax from bite wounds or falls from heights can result in sternal and rib fractures, but these are considered rare [4,33]. Research has shown that local bending and shear are some of the primary loading modes during impact trauma [34]. When the force or load applied to skeletal components exceeds the ultimate strength, the failure point is reached and a fracture is produced. Interestingly, the rate at which a force is applied to the cortical bone of ribs will affect the material characteristics of the bone. The ultimate strength of the bone is lower if the load is applied slowly. Conversely, high-speed application results in a higher ultimate strength. This property is known as viscoelasticity [35]. This property can affect the amount of kinetic energy absorbed by the bone when a force is applied. Slow application of load to failure results in less kinetic energy absorbed and the resulting fracture will likely be a simple two-piece fracture with minimal energy released and subsequently minimal damage to the surrounding tissues. High-speed load to failure will result in an increase in absorbed kinetic energy and a more complex fracture with more surrounding tissue damage [35]. The proximity of the pleural space and lungs to the thoracic cage puts them at risk when a fracture occurs; the more complex the fracture, the higher the risk to these vital structures. Rib and sternal fractures alter the function of the thoracic cage by decreasing compliance. However, in simple nondisplaced fractures and displaced fractures that will not damage the underlying pleural space and lung, therapy should be directed at the underlying pulmonary damage and pain rather than at the fractures. If the fracture fragments endanger these vital organs, then therapy is directed at stabilization of the fragments.

Flail Chest

When the trauma to the thoracic wall is severe enough to fracture adjacent ribs (at least two) in two locations, the result is flail chest. This complex fracture eliminates the costal arch support of the section of thoracic wall between the fractures. The section "flails" asynchronously with normal thoracic motion and is characterized by inward displacement during inspiration and outward displacement during expiration. The degree of paradoxical motion is determined by the pleural pressure becoming more negative during inspiration and the action of the parasternal intercostal (interchondral internal intercostal) muscles which pulls the flail segment inward [36,37]. This paradoxical motion can be a dramatic clinical finding, which may overshadow the less apparent but clinically more significant damage to the thoracic organs. It has been shown in a nontraumatic model of flail chest in the canine that arterial blood gases and the respiratory pattern did not change while the flail segment existed. This suggests that the severe effects of traumatic flail chest are a result of pulmonary damage, pleural space disruption, and the accompanying pain from the trauma rather than the paradoxic motion of the flail segment [5,38]. Disruption of the thoracic wall from fractured ribs will decrease the compliance of the thoracic cage and the work of respiration will increase; however, the accompanying pain causes a restriction in the ventilatory efforts. Understanding the pathophysiology of flail chest has refocused primary therapy from flail segment stabilization to improving respiratory function and pain control [1,5]. If the trauma or fracture fragments have resulted in pleural space disruption or if they endanger the pulmonary parenchyma, it is important that therapy also include restoration of the pleural integrity and stabilization of the fractures.

Penetrating Trauma

Penetrating injury usually results when a mechanical force is abruptly applied to a focal area and the integrity of the thoracic wall and pleural space is breached. The resulting damage is from severe stretching and crushing of tissues in the direct path of penetration. Penetration of the thoracic wall itself would not be a primary cause of concern except that the pleural space and thoracic organs may be damaged. The severity of penetration injury depends on the resulting degree of dysfunction and the degree of damage to vital organs.

Low-velocity penetration injury is essentially limited to the confined area because relatively little energy is transferred from the penetrating object to the tissues. Simple bite wounds, stabs, arrows, and some pneumatically propelled projectiles are examples of low-velocity penetration. Cutaneous and subcutaneous tissue, muscle, fascia, and possibly bone are damaged in the path of penetration. When the parietal pleural layer is penetrated and direct communication with the external atmosphere occurs, the negative pressure within the pleural space is lost and air now fills the pleural space. Fluid coupling of the thoracic wall and parietal pleura with the visceral pleura and lung is disrupted and the inherent elasticity of the lung causes an inward collapse while the thoracic wall expands. The individual compliance of the lungs and thoracic wall decreases and the work of respiration necessarily increases. Without the assistance of the thoracic wall, the lungs are unable to expand adequately and the degree of negative transpulmonary pressure needed to allow efficient airflow into the airways is not generated. The result is an expanded thoracic cage and a compensatory rapid shallow respiratory pattern [6].

Impalement injury is another type of low-velocity penetration in which a foreign object traverses and remains transfixed within the thoracic wall. This uncommon injury is generally the result of collision or impact between the body and an immovable object []. Even though this injury is classified as penetrating, it can be argued that there are characteristics of blunt trauma as well [40,41]. The distance and trajectory of the penetration dictate which (if any) thoracic organs or other body areas may also be involved. In impalement injury, the foreign object may fill the wound sufficiently such that the pleural space is effectively closed and also provide a tamponade effect to the surrounding organs or vessels [4,42,43]. It is recommended for this reason that the impaling object not be blindly removed from the body but left in place and stabilized for transport to a hospital for removal under direct visualization and controlled surgical conditions [40-43]. It may be necessary to cut and shorten the object for patient extrication and this should be done with extreme care so as not to cause further disruption or accidental dislodgement. Impaled wounds may be contaminated with unusual pathogens from the environment as well as with resident microorganisms from cutaneous tissues and potential hollow viscus disruption [43].

Bites are a relatively common source of low-velocity penetrating thoracic wounds. Bite wounds, like impalement, also have characteristics of blunt trauma but they also introduce the potential of severe tearing injury away from the point of penetration owing to the scissor action of teeth and the shaking that may accompany a bite wound. The blunt trauma aspect of bite wounds to the thoracic wall is a relatively common source of fractures [4,5,8]. Tearing of the intercostal muscles and potential fracture can severely disrupt the thoracic wall and pleural space such that pulmonary herniation may occur [6]. Occasionally, the cutaneous epithelium may remain intact despite complete disruption of muscular and skeletal structures. When this occurs, the skin may move in a paradoxic manner and mimic flail chest [6]. As with other penetrating thoracic wounds, microorganism contamination is inevitable, with the possibility of subsequent infection. The spectrum of contaminating organisms includes normal cutaneous flora and numerous intraoral microorganisms.

Penetrating injury through high-velocity projectiles most commonly results from either accident or malicious intent. As mentioned previously, the amount of kinetic energy a penetrating object transfers to the tissues dictates the amount of damage. Several formulas calculate the amount of kinetic energy. The simplest of these is: KE = 1/2 mv2

Where KE is the kinetic energy, m is the mass of the projectile and V is velocity []. As is readily seen from the equation, velocity is the most important factor when it comes to kinetic energy transfer and therefore tissue damage. The transfer of energy to the tissues produces injury in various ways. Lower velocity projectiles, such as those from air guns, damage tissues primarily through crushing and laceration. Higher velocity projectiles also have crushing and laceration components in the path of penetration, but they also produce a temporary cavity that is formed by forward acceleration of the tissues in the wake of the projectile, which causes radial stretch of the wound cavity. Cavitation can lacerate tissues, create contusions, damage vascular lining, and rupture large vessels. The greater the energy transferred to the tissue, the further from the bullet track these injuries will extend. Another method of injury is through shock waves that travel ahead of and to the sides of the projectile. At lower velocities these shock waves produce little damage, but at high velocity the pressure created can be significant [14].

Another factor includes the type of tissue penetrated. The major characteristics of body tissues that influence the degree of damage are specific gravity (density) and elasticity []. These characteristics have differing influences on the degree of tissue damage when penetrated by a high-velocity projectile. Tissues that have a high specific gravity will incur greater damage whereas tissues that are highly elastic will have less damage. Muscle has a relatively high density and some elasticity and, therefore, is severely damaged. The variable density of bone may divert the trajectory of the projectile. If the bone is fractured by the projectile, the created fragments can in turn become projectiles [45].

Structural Deformities

Pectus Excavatum

Pectus excavatum (PE) is a morphologic deformity of the thoracic wall characterized by sternal and costal cartilage abnormalities that can result in dorsoventral flattening of the thorax to concave deformation of the ventral thoracic wall [1,3,6,16]. Although the condition is generally considered congenital in small animals, the etiology is largely unknown. Various theories exist as to the cause, including defective development of cartilage and bone such that the sternum and costal cartilages are readily deformed by respiratory pressure gradients; anatomic variations in soft tissue attachments to the sternum; excessive costal cartilage growth; and abnormal intrauterine pressures [1,3,46]. Because PE is seen most commonly in brachycephalic dogs and Burmese cats and has been reported in cases of mucopolysaccharidosis, it is feasible that a genetic basis for the condition exists [1,6,46-48]. It is also possible that there is an acquired aspect of PE as can be seen in humans with upper airway obstruction [1,46,49,50]. In brachycephalic dogs the upper airway obstruction that results from brachycephalic airway syndrome may lead to an increase in the negative pleural pressure, which deforms the immature cartilage and bone of the thorax. Generally, the condition is localized in the caudal sternal area but cranial sternal deformities have also been reported [51].

Patients with PE may show an increased work of respiration, and this suggests a decrease in the compliance of the pulmonary system. Abnormal anatomy of the sternum and costal cartilage will decrease compliance of the thoracic wall, and pulmonary compression will decrease pulmonary compliance. Clinically, this can be seen as varying degrees of tachypnea, exercise intolerance, dyspnea, and cyanosis. Other signs may include recurrent respiratory infection, cardiac murmurs, vomiting, weight loss, and decreased growth [1,46]. Deviation of the heart owing to PE can lead to heart murmurs, conduction abnormalities, and apparent enlargement [1,6,16,46,52]. It is important to differentiate potential congenital cardiac defects from the secondary effects of cardiac compression and malposition. Many of the clinical abnormalities associated with PE can be alleviated or eliminated by repair of the defect.

Diagnosis of PE is usually made by thoracic palpation. However, in some, the flattening of the chest is not as apparent as evidenced by diagnosis later in life when clinical signs indicate a potential cardiovascular or respiratory problem. Radiographs of the thorax can provide a means of objective measurement of the relative degree of PE. The frontosagital index is a ratio between the width of the chest at the 10th vertebral body and the dorsoventral measurement from the ventral surface of the 10th vertebra to the sternum. The range of normal ratios for non brachycephalic dogs is 0.8 to 1.4, for brachycephalic dogs is 1.0 to 1.5, and for cats is 0.7 to 1.3. The vertebral index has also been used and is calculated as the dorsoventral measurement from the dorsal surface of the vertebral body selected to the sternum and the dorsoventral measurement of the vertebral body itself. Non brachycephalic dogs have a vertebral index range of 11.8 to 19.6, brachycephalic dogs from 12.5 to 16.5, and cats from 12.6 to 18.8.52 Although these measurements and ratios can help classify the degree of PE and help to determine anatomic improvement after repair procedures, they do not necessarily correlate to the severity of clinical presentation or physiologic abnormalities [1].

Other Congenital Deformities

Pectus carinatum is essentially the reverse of pectus excavatum and is described as a protrusion deformity of the sternum [16,53]. Because the thoracic cage of small animals is laterally compressed, this condition would be inherently difficult to detect. In fact, to the author's knowledge, no cases have been reported in small animals. Other chest-wall deformities include missing ribs, extra ribs, and rib malformations. Toxin exposure in utero may lead to these types of abnormal skeletal formations []. Although there are scattered reports of such anomalies in the veterinary literature, they are often incidental findings. Severe spinal malformations such as scoliosis and kyphosis may lead to thoracic cage malformation and decreased compliance [46]. The abnormality may also lead to pulmonary restriction with decreased compliance and abnormal respiratory function []. These abnormalities are also rare, and reports in the veterinary literature are uncommon.

Acquired Deformities

Acquired deformities of the thoracic wall that lead to dysfunction are uncommon. Such deformities can present as mass lesions readily visible externally or as a mild chest-wall thickening with significant intrathoracic extension that leads to respiratory or cardiovascular dysfunction [3,6,17]. These deformities include primary chest-wall tumors, metastatic tumors, and pyogranulomatous or purulent infection.

Infection

The contaminating nature of penetrating wounds raises the potential of clinical infection at or near the site of the wound. The infectious process may produce cellulitis, abscesses, or granulomas. Various aerobic and anaerobic bacteria and fungal organisms have been isolated from thoracic-wall lesions. Migrating foreign bodies such as grass awns ("fox tails") may be the source of the infection, and the degree of tissue involvement can be extensive. Lesions from infectious microorganisms can adversely affect the function of localized areas of the thoracic wall through alteration of muscle action and destruction of musculoskeletal tissues. However, extension of the infection into the pleural space and organs of the thoracic cavity can produce more serious conditions such as pyothorax, lymphadenopathy, and pulmonary infiltration [17]. Therapy for infectious conditions may be simple drainage and appropriate antimicrobial medications, but it may require extensive debridement or excision of diseased tissue to facilitate resolution. In this case, therapy may also contribute to altered thoracic function.

Neoplasia

Tumors of the thoracic wall can originate from skeletal structures or soft tissues; the type of tumor will determine the biologic behavior. Although tumors of the thoracic wall are considered uncommon, it is important to differentiate between benign and malignant tumors in order to plan the appropriate therapy. Benign tumors can often be removed without wide or radical types of excision, and a cure can be expected. Malignant tumors should be removed with a variable margin of normal tissue, depending on the tumor type and the tissues involved. Those that have a high probability of recurrence should have large borders of normal tissue removed three dimensionally around the tumor [56]. The extent of the surgical excision may not only affect the function of the thoracic wall but will dictate the type of closure or thoracic wall reconstruction required.

Primary tumors affecting the supporting skeletal structures of the thoracic wall are malignant more often than they are benign [1,3,6,16,46,57]. Most authors report that osteosarcoma is the most common type of malignant rib tumor, with chondrosarcoma being second [1,3,6,16,46,57]; however, some authors have this order reversed [17]. The common site of occurrence in dogs for both types of tumor is the costochondral junction; rarely the sternum is the site [1,3,16,57]. These tumors are often firmly attached to other tissues of the thorax, making them relatively immobile. This characteristic may be an indication of malignancy [46]. Younger to middle-aged dogs seem to be affected more often with these tumors [1,16,57,58]. The occurrence of these tumors in this location in the cat is rare [57].

The most common bone tumor in dogs is osteosarcoma; approximately 25% occur in the axial skeleton, with 10% of those occurring in the ribs [59]. Clinically, dogs with osteosarcoma of the thorax present with a palpable mass of the ribs or sternum that may be painful [59], although many authors describe them as nonpainful [16,17,57]. Dyspnea has been reported as a clinical sign by various authors with suggestions that pulmonary impingement owing to intrathoracic extension, pleural effusion, and pulmonary metastasis may be the cause [1,16,57,58]. Others state that respiratory signs owing to these conditions are not commonly seen [59]. One characteristic that is generally agreed on is that the biologic behavior of osteosarcoma in the rib is similar to that in other locations. Locally, osteosarcoma is aggressive, with lysis and production of bone and replacement with neoplastic tissue [59]. Early metastasis is a hallmark of osteosarcoma with the lungs as the primary location for tumor spread [6,57,58]. This predilection for metastasis is responsible for the poor prognosis for osteosarcoma. The median survival times for patients treated by en bloc excision and excision plus adjunctive chemotherapy are 3 and 8 months, respectively [59-61]. The poor prognosis emphasizes the need for accurate diagnosis.

Chondrosarcoma seems to have a predilection for flat bones; it occurs in these 61% of the time [59]. In dogs, the range of occurrence on the ribs is from 6% to as high as 33%, according to various sources [17,57]. In cats, common locations near the thorax are the scapula and vertebrae; rarely, if ever, the ribs or sternum. Ostensibly not as aggressive as osteosarcoma, this tumor may attain large dimensions before diagnosis. It is locally invasive, invades the pleural space, and may cause pleural effusion [17]. Metastasis is reported to be slower than with osteosarcoma and the prognosis is somewhat better [17,59]. A wide variation exists in reported median survival times for dogs with chondrosarcoma of the ribs, but they are considerably longer than with osteosarcoma, with sources reporting survival up to 1080 days [59,61]. As with osteosarcoma, therapy for chondrosarcoma is en bloc resection of the tumor with reconstruction of the thoracic wall if needed.

Metastatic neoplasms of the thoracic wall have been described and the ribs are considered a common site, whereas the sternum is rarely reported [1,59]. When metastasis to the ribs (and other bones) occurs, it seems to be localized near the diaphyseal area near the nutrient foramen rather than the costochondral junction [17,59]. The incidence of metastasis of osteosarcoma to other bones such as the ribs may be increased following chemotherapy regimens [59].

Primary tumors of thoracic soft tissues include various sarcomas (e.g., fibrosarcoma, hemangiosarcoma, hemangiopericytoma, and malignant fibrous histiocytoma) and occasional discrete cell tumors (i.e., mast cell tumor) [3,46,62]. Wide three-dimensional surgical excision is recommended for these tumors. If removal requires en bloc excision of the thoracic wall, reconstruction may be required.