Thoracoabdominal Injuries

  • Hamish KerrEmail author
  • Brady Bowen
  • Deborah Light
Part of the Contemporary Pediatric and Adolescent Sports Medicine book series (PASM)


Trauma to the thorax and abdomen can occur during participation in sports. This chapter reviews some of the more common presentations of such injuries and how such injuries should be best managed. Thoracic injuries reviewed include internal injuries such as pneumothorax, pulmonary contusion, hemothorax, commotio cordis, and cardiac contusion. Chest wall injuries are also reviewed such as rib fractures, costochondritis, and slipping rib syndrome plus sternal and scapular fractures. Abdominal injuries reviewed are focused on internal organ trauma to the spleen and liver, kidney, pancreas, and bowel. There is attention to the effect of Epstein-Barr virus and infectious mononucleosis, seen very frequently in high school and collegiate athletes. Finally, groin pain and athletic pubalgia are described.

In addition to anatomy and clinical presentation, imaging modalities that characterize such trauma are reviewed for each diagnosis. Prevention of thoracoabdominal injuries and return-to-play decisions are described at the chapter conclusion.


Pneumothorax Commotio cordis Costochondritis Infectious mononucleosis Athletic pubalgia 

Intrathoracic and Intra-abdominal Injuries

A soccer player sustains trauma to his abdomen in a collision with an opponent. The player is taken out of the game, only to return within 2 min feeling little ill effect. He is noted to be coughing but is able to continue. After the game, he is complaining of left upper quadrant abdominal pain. The athletic trainer relates that the player has had a recent upper respiratory tract infection.

Did the player sustain a splenic rupture because of underlying splenomegaly, caused by infectious mononucleosis, or is this an abdominal wall hematoma or muscle strain? Alternatively, could the coughing be indicative of an intrathoracic injury, such as a pneumothorax?

This scene illustrates the difficulties involved in diagnosing injuries to the chest and abdomen. Unless there is a low threshold to pursue investigation, athletes may suffer serious consequences. Injuries to the chest and abdomen are often more subtle in presentation than other injuries, such as an acute ligament rupture. Thoracoabdominal injuries are uncommon, and catastrophic events can occur if an intra-abdominal or intrathoracic injury is unrecognized. Awareness of the organs that can be injured, and how such injuries may present, is the best defense against missing potentially life-threatening thoracic and abdominal trauma [1].


The thorax contains the heart, the great vessels, and the lungs. The lungs are surrounded by two layers of pleurae protected by the ribs and the thoracic musculature. The diaphragm divides the thoracic and peritoneal cavities with a variable position throughout respiration [2]. The expulsive motion of the diaphragm can raise the right crus to the level of the fourth anterior costal cartilage. Importantly, the abdominal contents may be raised well into the chest and exposed to chest wall trauma.

The peritoneal cavity contains solid organs, such as the liver, spleen, and pancreas, plus hollow viscous organs, including the stomach and the small and large intestines. Also in this area are the lower ribs, the abdominal wall musculature, vascular structures, the bladder, and retroperitoneal organs and spaces.

Clinical Evaluation

Thoracic Injury

Athletes with a thoracic injury may present with chest wall pain and, often, shortness of breath. Inspection for ecchymosis can also be helpful with intrathoracic injuries incurred in sport. Pulmonary auscultation is essential for assessment for lung pathology. Cardiac auscultation may be indicated for myocardial contusion or arrythmias. Further examination may include palpation for tenderness over a suspected rib fracture.

Abdominal Injury

Athletes can present with an immediate onset of pain or a more insidious onset [1]. Athletes who have a history of a high-risk mechanism, such as a rapid deceleration or high-energy impact, or who have continuous, persisting abdominal pain should be examined.

Physical exam should begin with the measurement of vital signs, which may be normal or reflect a state of shock. Inspection for ecchymosis and tenderness on abdominal palpation helps detect the potentially affected organ. Abdominal wall muscular contusion can be difficult to distinguish from intra-abdominal injury. Contusions are usually only tender over the area of sustained injury, and pain may be evident with contraction of the underlying muscle. Conversely, intra-abdominal injuries may elicit tenderness from various angles of palpation.

Among athletes with significant abdominal trauma, 50% will have a negative initial exam, so reexamination can be crucial. One estimate is that 20% of patients with an acute hemoperitoneum have an initial benign abdominal exam [3].

Liver or spleen injuries can bleed, causing intra-abdominal irritation and pain. Pain is often mild, without palpable tenderness. Injuries to hollow viscera and the pancreas cause peritonitis, often resulting in severe pain. Initially, this is localized to the site of injury. Peritoneal signs, such as referred tenderness and loss of bowel sounds, are found with progression of intra-abdominal injury. Auscultation for bowel sounds can be misleading, as the presence of bowel sounds does not exclude injury. Walking or coughing can also precipitate pain. Retroperitoneal injuries may occur without peritoneal signs when there is minor trauma. Hematuria is often the only clinical manifestation of renal trauma.

Coexisting Injuries

It has been well recognized that lower chest wall trauma places the upper abdominal organs at risk for injury. Most commonly, a blow to the lower left chest wall can result in an injury to the spleen [1]. Conversely, several case reports exist in the literature of abdominal impact resulting in an intrathoracic injury, such as a pneumothorax. One such report by Roberts [4] described an ice hockey player who was checked into the boards and sustained an impact over his left lower ribs. Initial concern for a splenic injury proved unfounded, and he was allowed to return to the game. However, he was too uncomfortable to continue, and assessment afterward revealed a 15% pneumothorax on chest x-ray. Hence, pulmonary injury from abdominal trauma can occur without disruption of the diaphragm. Diaphragm rupture is uncommon but is usually left sided (70–90%), as the liver appears to protect the right side.

Diagnostic Assessment

Laboratory investigations , including serial determination of hematocrit, diagnostic imaging, and diagnostic peritoneal lavage (DPL), can be performed in a hospital setting. DPL has become less commonly performed with the increased availability of diagnostic ultrasound and computed tomography (CT). A chest x-ray is usually indicated. An erect view is helpful to exclude air under the diaphragm, suggesting bowel perforation.

An emerging imaging modality for chest and abdominal trauma is diagnostic ultrasound, which has useful applications in the evaluation of thoracic trauma and may be a better diagnostic tool than supine x-ray for pneumothoraces and lung contusions [5, 6, 7].

Abdominal CT scan after blunt trauma has 67% sensitivity in its ability to predict the need for surgery in a pediatric population [8]. The negative predictive value was 98.7% in the same study. A combination of clinical exam and CT scan did not miss any significant injuries. Serial examination may be performed in a hospital setting. CT scan alone may miss clinically significant injuries.

CT is the best choice for imaging solid organs such as the liver and spleen [9] and remains the gold standard in evaluating blunt abdominal trauma in hemodynamically stable patients [10, 11, 12, 13] though diagnostic ultrasound has advantages. While ultrasonography is not as sensitive for intra-abdominal trauma, does not provide as much anatomic detail, does not allow for injury grading [14], and remains operator dependent, it does have a role, for instance, in the hemodynamically unstable patient [15, 16]. Hoffman et al. described a sensitivity of 85% and a specificity of 99% in detecting intra-abdominal injuries [16], while Berkoff suggests sensitivity of 60% (95% CI 49–70) [17]. Ultrasound visualizes free intraperitoneal fluid well, though it may not identify the injured organ [18]. Conditions identified on ultrasound in unstable patients will eventually require CT to identify the injury and to guide management [18]. The use of abdominal ultrasound for evaluation of unstable patients has been described by the term “focused assessment with sonography for trauma” (FAST) [19]. The FAST examination aims to recognize peritoneal fluid/blood, which typically arises from a solid organ injury. A hypotensive athlete who has suffered abdominal trauma with a positive finding on a FAST examination has a higher likelihood of operative management [17, 19, 20, 21, 22, 23, 24, 25, 26].


Field treatment for shock, before and during transfer to a trauma center, is essential when shock is detected. Intravenous access with a large-bore cannula should be established at two sites with rapid infusion of 0.9% saline, rather than dextrose-containing fluids.

Current surgical goals are for organ salvage and repair, rather than removal of injured intra-abdominal organs. Indications for removal revolve around uncontrolled bleeding, particularly when associated with coagulopathy. In such circumstances, the risks of surgery are outweighed by the benefit of achieving hemostatic control, with a low likelihood of control being achieved any other way. Once stabilized, discharge with home observation is often practical. However, caution is required regarding delayed rupture of the spleen at 7–10 days.

Thoracic Injuries

Thoracic injuries generally result from rapid deceleration or high-energy impacts, which occur most frequently in high-speed, high-energy contact sports, such as bicycling, skiing, football, hockey, and boxing [15]. Statistically, adolescents have a higher incidence of penetrating thoracic trauma relative to younger children, who have higher rates of blunt thoracic trauma [27]. Road traffic accidents and pedestrian injuries have been reported as the leading cause of thoracic injuries, with sports-related injuries occurring much less frequently [28]. However, evolution of “extreme sports” may increase the potential for high-energy impacts and may be especially dangerous in the setting of remoteness from immediate medical attention. In one study, 6.1% of injured snowboarders sustained chest trauma, whereas only 2.7% of skiers had similar injuries [29].

Lung Injuries


This is the most common intrathoracic injury after blunt thoracic trauma [30]. Among all children who sustain high-energy thoracic trauma, approximately one quarter to one third will develop a pneumothorax [31, 32]. Pneumothorax related to sporting activity or injury is relatively uncommon. Spontaneous occurrences have been reported in a number of sports such as soccer [33] and weight lifting [34]. Pneumothorax as a result of blunt trauma during sports generally involves deceleration of the athlete’s thorax against a moving or a stationary object, as has been reported in skiing and snowboarding [35], bicycling [36], football, and ice hockey [37].

Tension pneumothorax occurs in 1–2% of patients with a spontaneous pneumothorax [38]. Pneumothorax results from the loss of air from the lung into the pleural space. If no mass effect is caused by this air, the injury is referred to as a simple pneumothorax. However, if the loss of air into the pleural space continues, tension can result with concomitant shift of the mediastinum away from the side of the pneumothorax. Such a tension pneumothorax requires immediate decompression with a needle into the chest cavity and, optimally, by a tube thoracostomy. If this is not done, the continued pressure and mediastinal shift will lead to respiratory compromise by inhibition of airflow into the working lung and to cardiac compromise by a reduction in venous return to the heart.

Pneumothorax, whether simple or tension, can occur spontaneously from rupture of a bleb, from a sudden compressive force to the chest with a resulting rupture of the lung parenchyma, or from a displaced rib fracture that penetrates the lung. Both simple and tension pneumothoraces are associated with tachypnea, dyspnea, and sudden chest pain, though these findings may be quite subtle with a simple pneumothorax. Of those with spontaneous pneumothorax, up to 87% will present with chest pain and 43% with shortness of breath [39].

On examination, a simple pneumothorax may present with a small shift of the mediastinal structures to the side of the pneumothorax, whereas tension pneumothorax is associated with a shift to the opposite side. Physical examination may also demonstrate decreased breath sounds on auscultation and hyperresonance to percussion on the side of the lesion. Tension pneumothorax is also associated with tachycardia, neck vein distension, and hypotension.

The diagnosis is confirmed by chest x-ray, but as noted previously, tension pneumothorax should not await chest x-ray for treatment. Figure 7.1 illustrates a CT of a left pneumothorax which remains the gold standard for diagnosis. Ultrasound has gained increased interest given its growing availability, feasibility, and lack of radiation exposure, of particular importance in the pediatric population. Though investigation is ongoing, studies have suggested improved sensitivity and comparable specificity of ultrasound compared to supine chest x-ray for detecting pneumothorax [40, 41]. One study demonstrated that prehospital critical care providers were able to learn the techniques, correctly diagnose, and retain the skills needed to identify sonographic signs suggestive of a pneumothorax [42], a practice that could be applied by appropriately trained sports medicine physicians [17].
Fig. 7.1

Left pneumothorax. Courtesy of David Mooney, MD, Children’s Hospital, Boston, MA

Tube thoracostomy and suction at −20 cm H2O are all that is required for the treatment of most pneumothoraces. Thoracoscopic talc pleurodesis has been shown to be an effective intervention in recurrent or persistent spontaneous pneumothoraces [43]. The athlete can resume normal activity within a few days of discharge or as other injuries allow. Occasionally, a small, simple pneumothorax of 20% or less can be treated without tube thoracostomy if the patient is asymptomatic and has no other injuries. This approach requires careful observation and repeat chest x-ray to document stability. Regardless of treatment type, recurrence rates of primary spontaneous pneumothorax are reportedly high in children, up to 54% [44]. Return to physical activity should be delayed until complete resolution of the pneumothorax [45]. Symptoms of primary spontaneous pneumothorax often resolve within 24 h, even prior to resolution of the pneumothorax [46]. Therefore, return to play should be determined on a case-by-case basis. Current guidelines recommend avoidance of air travel within 2–3 weeks following a pneumothorax, due to concern that a volume of air trapped in the pleural cavity may expand and develop into a tension pneumothorax in the lower cabin pressure of a commercial airplane in flight [47].

Pulmonary Contusion

Pulmonary contusion is a bruise of the lung associated with hemorrhage and edema into the lung parenchyma [15]. It can result from a sudden deceleration in which the lung strikes the chest wall, from a concussive blow to the chest that compresses the lung or from a displaced rib fracture [30]. Children appear prone to this injury in the absence of a rib fracture because of the compressive nature of the rib cage [31]. As a result, the force of impact is transmitted to the lungs, rather than being absorbed by the ribs, which may not fracture. It is important to identify pulmonary contusion, as some patients will go on to develop pneumonia or acute respiratory distress syndrome (ARDS).

Patients present with cough, hemoptysis, and dyspnea. Exam shows diminished breath sounds, crackles, or both. Chest x-ray findings vary from fluffy, patchy infiltrates to consolidation and are diagnostic in 85–97% of patients [48, 49]. The extent of pulmonary contusion on CT scan can help to predict the risk of developing ARDS [50]; however, the role of CT in the pediatric patient with chest trauma remains controversial [51]. Ultrasound is emerging as an alternative diagnostic tool in thoracic trauma and may be a useful alternative to CT for assessment of the extent of pulmonary contusion [7].

Fluid intake should be minimized, if possible, to reduce pulmonary edema. Supportive ventilation is necessary in severe instances. Pulmonary contusion after athletic injury is usually self-limited, without long-term sequelae. Once resolved, an athlete can resume training but should do so gradually, because exercise tolerance and pulmonary reserve will be reduced.


Hemothorax may result from injury to the lung parenchyma or any of the intrathoracic vessels that may be lacerated by a traumatic rib fracture. In the setting of trauma, a pneumothorax may accompany this hemorrhage, causing a hemopneumothorax. Clinically relevant hemothoraces occur in 14% of children sustaining blunt-force chest injury [31]. Blood in the thorax is often asymptomatic, unless the volume is large. In this instance, hemothorax can present similarly to tension pneumothorax, with decreased breath sounds and hypotension. Dullness to percussion is noted over the area of pooled blood. Treatment involves supporting ventilation and circulation with intravenous fluids and then placing a chest tube once transferred to an appropriate setting.

Cardiac Injuries

Commotio Cordis

Commotio cordis is a cause of sudden cardiac arrest resulting from blunt, nonpenetrating trauma to the precordium. It is often of apparently low energy and results in cardiac arrhythmias in the absence of any structural injury to the heart or surrounding tissues [52]. The epidemiology of commotio cordis has been studied in the United States over the last several decades with the use of a commotio cordis injury registry, first described by Maron et al. in 1995 [52, 53, 54, 55]. Most cases occur in teenage males, with a mean age of 15 years, and it has been speculated that the more compliant chest cage of younger athletes may make them more susceptible to these impacts. Over half of reported commotio cordis events occur during organized competitive sports, with the remainder occurring during practice or daily activities. The majority of blows resulting in commotio cordis are the result of a small projectile impacting the chest, such as a baseball, lacrosse ball, or hockey puck, while the rest are from bodily contact [56].

Animal models have been developed that suggest a specific and rare combination of circumstances is required to produce commotio cordis [57, 58, 59]. An impact must occur directly over the precordium, with a small enough surface area to transmit all of the energy from the collision to the heart [52, 59]. If this occurs exactly at the time of ventricular repolarization, just before the peak of the T wave, there is a 10–20 ms period of susceptibility that can result in ventricular fibrillation [54, 57, 58, 59, 60]. In animal models, when a blow occurs outside this time, other arrhythmias may result, including heart block or bundle branch blocks [57].

Commotio cordis had previously been thought to have a high fatality rate with a low likelihood of reversal, despite the lack of structural injury [52, 53]. However, with increasing awareness and availability of automated external defibrillators (AEDs) at sporting events and in the community, the percentage of patients who survive commotio cordis has increased from 10 to 15% before 2000 to greater than 50% during the period from 2006 to 2012. Predictors of survival are prompt defibrillation and occurrence in a competitive event (during which rapid response and AED availability are more likely) [56].

Protective equipment such as chest guards and softer “safety balls” have been used to try to prevent blunt cardiac trauma, but evidence that such equipment prevents commotio cordis is lacking [61]. The most recent registry report at the time of this writing indicated that almost 40% of commotio cordis victims were wearing chest protectors at the time of the event, suggesting that current equipment may not offer sufficient protection [56]. In some cases this may be due to incomplete coverage of the precordium, or migration of equipment during movement [52, 54], but commercially available chest wall protectors failed to prevent ventricular fibrillation in an animal model of commotio cordis despite complete coverage of the cardiac silhouette [62].

For survivors of commotio cordis, a comprehensive cardiac work-up is necessary to rule out structural defects, conduction abnormalities, or other cardiac diseases that could have led to arrhythmia or arrest. Return-to-play decisions depend on the presence of underlying cardiac disease and should occur in consultation with a cardiologist. Some experts suggest avoiding return to sports with risk of chest impact after a commotio cordis event, at least until an older age [55].

Cardiac Contusion and Other Blunt Cardiac Injuries

In the setting of thoracic trauma, structural injuries to the myocardium must be considered. Such injuries may range in severity from contusion to free wall or septal wall rupture, valvular injury, and coronary artery or great vessel injury [63, 64]. Cardiac contusion (also referred to as contusio cordis) may result from a direct blow to the chest or from a rapid deceleration of the heart, causing it to strike the rib-sternum complex. Most injuries occur to the right ventricle, due to its proximity to the anterior chest wall. It has been reported in contact sports [65, 66, 67] but is more common in high-speed events such as motor vehicle accidents.

If blunt cardiac trauma is suspected due to mechanism or associated injuries, patients should be referred for further diagnostic testing. The use of cardiac enzymes for diagnosis and prognosis of cardiac contusion has been a topic of debate in the literature [68, 69, 70, 71, 72, 73] and is complicated by the fact that there is no agreed-upon gold standard for comparison. Creatine kinase (CK) and creatine kinase-myocardial band (CKMB) have not shown diagnostic utility [68]; however, the combination of a normal cardiac troponin and normal electrocardiogram (EKG) is predictive of the absence of clinically significant cardiac trauma [70, 71, 72]. Most experts recommend obtaining an EKG and cardiac troponin if cardiac trauma is suspected, and further evaluation such as echocardiography should be obtained if the results are abnormal. Patients with EKG abnormalities or elevated troponin should be monitored for 24–48 h, as most dysrhythmias will occur during the first 24–48-h period after injury [64, 69, 70, 74, 75]. In the absence of EKG or troponin abnormalities, asymptomatic patients can resume normal activities as other injuries allow.

Chest Wall Injuries

Rib Fractures

Acute Rib Fractures

Rib fractures are considered the most common serious injury of the chest wall [76, 77]. Children are more vulnerable to intrathoracic injuries than adults, even in the absence of rib fracture, because of the increased elasticity and flexibility of their thoracic cage, which allows energy to be transmitted to the intrathoracic structures [78]. A fracture of the rib in a pediatric patient is more likely to be associated with other more significant injuries than in adults [79] and should increase clinical suspicion of other intrathoracic or intra-abdominal trauma.

Rib fractures can be divided into upper zone (first four ribs), midzone (ribs 5–8), and lower zone fractures (ribs 9–12) [80]. The most commonly fractured ribs from direct impact in any age group are the midzone ribs [77]. Fractures of the upper zone or lower zone ribs, multiple fractures, and flail segments are less likely to be isolated injuries than other patterns of rib fractures and may result in injury to surrounding structures [76, 80]. Acute traumatic impact fractures of the first and second rib are often associated with neck trauma and vascular injuries, as well as pneumothorax, lung laceration, and hemothorax. Direct impact fractures of the lower ribs may injure the kidneys, liver, or spleen. Splenic trauma has been reported in up to 20% of left lower rib fractures and acute liver trauma in up to 10% of right lower rib fractures [77]. Fractures of the first rib and the floating rib are generally thought to be more common in sports [76]. Isolated fractures of the first rib were initially described primarily as stress fractures or overuse injuries in athletes or physical laborers [81, 82, 83], though more are being reported in contact sports participants.

First rib fractures in sports may also occur from indirect trauma as a result of forceful opposing muscle contraction [83] and have been reported in tennis players, surfers, windsurfers, rowers, dancers, gymnasts, and basketball players [84, 85, 86, 87, 88, 89, 90]. Fractures from indirect trauma occur with hyperabduction of the arm and falling on an outstretched arm, as well as sudden muscle contraction [83, 84, 91, 92]. The intercostal muscles and serratus anterior pull inferiorly, while the scalene muscles pull superiorly. The anterior scalene muscle produces bending forces at the subclavian sulcus, which is the usual fracture site [93].

Floating lower rib fractures may also occur with indirect trauma [76]. They are caused by avulsion of the attachments of the external oblique muscles and latissimus dorsi muscles with sudden contraction [76]. These types of fractures have been reported in baseball players and batters [76, 94].

The diagnosis of acute rib fractures is often indicated by a history of a traumatic event. The pain may initially be diffuse and gradually localize over the affected rib. Direct palpation, deep inspiration, coughing, twisting, or flexion to the side may exacerbate the pain. If there is accompanying lung or pleural injury, there may be subcutaneous emphysema. While these findings should prompt evaluation for rib fracture, clinical examination alone is not sensitive for detecting many rib fractures [95]. First rib injury may be particularly challenging, as palpation of the first rib is difficult.

A chest x-ray is often sufficient to establish the diagnosis and exclude other diagnoses, such as a pneumothorax or hemothorax. Dedicated rib series are more sensitive than conventional chest x-ray for detection of rib fracture, though their utility in minor chest trauma is debated [96, 97]. Patients with significant chest trauma should be referred to the emergency department for evaluation with a CT scan, which can also assess for associated intrathoracic and intra-abdominal injuries. An emerging diagnostic modality in the assessment of acute rib fracture is thoracic ultrasound. Some early studies suggest that ultrasound is effective and may be more accurate than x-ray in detecting rib fractures in the acute setting [95, 98, 99, 100]. Ultrasound is also useful and potentially more accurate than x-ray in the assessment of other injuries associated with rib fractures, including pneumothorax and pulmonary contusion [5, 6, 7].

The majority of rib fractures heal with rest. The goal of therapy for uncomplicated rib fractures is pain relief, improvement of ventilation, prevention of worsening injury, and a safe return to sport. Pain is usually controlled with oral analgesics. Ice may also be used. Deep breathing should be encouraged to prevent atelectasis. Taping is controversial and may lead to increased splinting, pulmonary complications, and atelectasis. Activities should be modified until symptoms resolve, and training should be resumed gradually. Return to play should only be considered in patients whose symptoms resolve and who have minimal pain with palpation.

Rib Stress Fractures

Stress fractures are relatively uncommon in the ribs as compared to the lower extremities, but they have been described in youth and adult athletes [101, 102, 103]. Most published information on rib stress fractures is in the form of case reports, with such reports indicating that these injuries occur predominantly in the first rib or in the middle ribs [102, 104].

First rib stress fractures have been reported mostly in overhead sports such as baseball, basketball, tennis, and weight lifting [81, 82, 83, 89, 104, 105, 106], as well as in surfers, swimmers, and dancers [84, 85, 107]. Unlike with acute traumatic first rib fractures, isolated first rib stress fractures are infrequently associated with other significant injuries of the vasculature or the lung (Fig. 7.2) [93].
Fig. 7.2

First rib stress fracture

Stress fractures of the middle to lower ribs are reported mostly in patients who engage in swinging or pulling activities such as golf and rowing [104, 108, 109, 110, 111]. Etiological factors associated with these sorts of fractures include improper technique, equipment problems, and lack of flexibility and strength [108, 111, 112]. Onset of symptoms is often preceded by an increase or change in physical activity or training [113]. Stress fractures of the ribs in rowers are postulated to be caused by excessive action of the serratus anterior muscle [114].

An athlete with a rib stress fracture typically presents with insidious onset of pain, either in the scapular region in the setting of a first rib fracture or with lateral, posterior, or anterior chest pain in the case of middle rib injury [93, 111]. Diagnosis is often delayed due to the nonspecific symptoms, which may be misdiagnosed initially as a muscle strain [102, 109].

In a study by Lord et al., plain radiographs revealed stress fractures in 16 cases of 19 rib fractures performed 2 weeks after the injury [109]. However, plain radiographs may initially be negative with stress fractures prior to callus formation, and diagnosis typically requires a triple-phase bone scan [101, 102, 103]. CT scans and magnetic resonance imaging (MRI) may also be useful for definitive diagnosis [115]. Rest from sport is suggested for a period of 4–6 weeks, though there is little evidence regarding the best approach to return to sport [116, 117]. Delayed union and nonunion are the most common complications of first rib stress fractures in throwing athletes. In patients with recalcitrant pain, referral to an orthopedic surgeon may be necessary [90].

Slipping Rib Syndrome

Slipping rib syndrome (also referred to variably in the literature as rib-tip syndrome, clicking rib syndrome, or rib pain syndrome) was first described in the early twentieth century and is characterized by an abnormal movement of the lower ribs resulting in intercostal nerve impingement and pain. This diagnosis has remained somewhat elusive, in part due to variation in definitions within the literature. Scott and Scott described the more inclusive “painful rib syndrome” as the clinical presentation of pain in the lower chest or abdomen, a tender spot on the lower costal margin, and reproduction of pain by pressing that spot [118]. Slipping rib syndrome may also mimic abdominal pathology, due to its common presentation with upper abdominal pain [119]. The condition typically involves the eighth, ninth, and tenth ribs. These ribs are attached to each other by fibrous tissue in adults and by cartilaginous tissue in children. It is believed that when these connections are weakened or ruptured by trauma, the ribs can slip and impinge on the intercostal nerve, producing pain [120]. Rib-tip syndrome is usually unilateral; however, it may be bilateral [118, 121]. This condition particularly affects running, vigorous arm exercise, arm abduction, and swimming [101]. It has been reported more frequently in adults but nevertheless is a cause of rib and upper abdominal pain in adolescent and collegiate athletes [122, 123, 124].

Pain is often localized to the upper abdomen, epigastrium, or inferior costal regions. Some patients report a slipping movement of the ribs or a popping sensation. Pain may vary from mild to severe and often is reproduced by movement [118]. Symptoms can often be reproduced upon clinical examination by hooking the fingers under the inferior rib and pulling anteriorly, referred to as the “hooking maneuver” [125]. A positive test reproduces the patient’s pain and results in a click. Direct tenderness over the cartilage is another frequent finding. The diagnosis is clinical, and diagnostic imaging is generally not helpful, although it may exclude other conditions. Intercostal nerve blocks may be useful in establishing the diagnosis. Ultrasound has been described in adult patients as a means to observe cartilage subluxation during movement [126].

No definitive consensus exists as to the best management for slipping rib syndrome [127]. Conservative management for mild cases includes reassurance and avoidance of aggravating motions. Some patients have reported favorable outcomes with single or multiple local anesthetic nerve blocks [119, 128], and corticosteroids added to an injection may be beneficial. Surgical excision of costal cartilage for recalcitrant cases has demonstrated efficacy in both adults and children [120, 122, 129, 130].

Costosternal Syndromes (Costochondritis)

A variety of diagnostic terms have been used in this group of syndromes, including costochondritis, costosternal syndrome, and anterior chest wall syndrome. Costochondritis is a common cause of atraumatic chest pain in children and adolescents and is characterized by pain and tenderness of the costochondral junction without swelling [131]. This condition may account for 9–22% of cases of pediatric chest pain [132, 133]. The sites most typically involved are the second through fifth ribs [131]. Costochondritis may be preceded by an upper respiratory infection or by exercise that stresses the upper body, and symptoms may persist for several months [134].

Diagnosis of costochondritis is clinical, based on a history of chest pain and by exclusion of other etiologies [134]. Anterior chest wall tenderness may be localized to one or more costochondral junctions, and movement of the arm on the ipsilateral side may also reproduce the pain [131, 134].

The course is usually self-limited, and most patients recover spontaneously from the condition. Anti-inflammatory agents, ice, muscle relaxants, and injection of lidocaine (with or without corticosteroid) have been used in selected cases [134, 135]. Stretching exercises may also be of benefit [136]. Patients should be reassured of the benign course of this condition and can continue to participate in sports as tolerated.

Sternal Fractures

Sternal stress fractures have been reported in golfers, weight lifters, and wrestlers [101, 137, 138]. Acute traumatic sternal fractures are frequently seen in association with deceleration injuries and/or direct blows to the chest in adults, though a case series in children suggested that more minor blunt trauma may be a common mechanism in this age group [139]. Isolated sternal fractures from direct impact do not pose significant risk to the athlete. Injuries to the sternum have traditionally led to a search for associated cardiac, great vessel, and pulmonary injuries caused by the anatomic proximity of these structures, but associated morbidity with these injuries is low. Studies in both Europe and the United States have shown the mortality associated with isolated sternal fractures to be less than 1%, and the incidence of associated blunt cardiac injury to be low [140, 141, 142]. Nevertheless, it is important that one carefully assess the pediatric patient who presents with a sternal fracture for symptoms of other potentially associated injuries. These include pneumothorax, pulmonary contusion, and cardiac contusion.

Sternal fractures are often better seen on lateral sternal x-rays than on standard anterior-posterior (AP) chest films, because most of these fractures are oriented transversely. Standard radiographs can also be challenging to interpret in pediatric patients, due to the variable pattern of ossification centers in the sternum [139, 143]. In cases in which a fracture is questionable, CT scans are more sensitive but may not improve detection of clinically significant sternal fractures [144]. Ultrasound is a promising diagnostic tool for sternal fracture, with recent reports suggesting better accuracy than traditional radiographs [145, 146].

If intrathoracic trauma is suspected in the setting of a sternal fracture, further imaging and assessment are warranted. Otherwise asymptomatic pediatric patients with isolated sternal fracture can be safely discharged home [139].

Scapular Fractures

Scapular fractures represent less than 1% of all skeletal injuries and 5% of shoulder fractures [147, 148]. It is uncommon for scapula fractures to occur in isolation [149], and presence of a scapula fracture should prompt consideration of other thoracic injuries [150]. Fractures of the scapula are rare in athletes, with the majority of reported cases occurring in football players [147, 148, 151]. Injuries occur during tackling, when the shoulder is in abduction and the scapula is pulled away from the chest wall where it is unable to dissipate direct force.

There are eight types of scapular fractures. They are classified by anatomic location: body, glenoid rim, glenoid fossa, anatomic and surgical neck, acromion, spine, and coracoid process. The majority of scapular fractures are body fractures [151]. Approximately 10% of fractures occur in the acromion, coracoid, and spine [115].

A scapular fracture may present with symptoms that are similar to a rotator cuff injury [151]. Cain and Hamilton reported that rotator cuff injuries were initially suspected in half of football players who were diagnosed with scapular fractures [147]. Clinical examination reveals weakness with abduction and external rotation of the shoulder. Pain and weakness in the shoulder region are exacerbated with movement. Localized tenderness, swelling, and hematoma formation over the fracture site may also be present.

Scapula fractures are often not seen on standard scapula x-rays (AP, lateral, and axillary views). In one study, 43 out of 100 scapular fractures were missed on initial radiographs [149]. Therefore, specialized views such as the scapula Y, CT, or MRI may be necessary.

Treatment of nondisplaced scapular fractures is usually conservative and involves rest from sports and physical therapy. The application of ice is recommended for the first 48 h. A sling may also be used for immobilization, along with early range of motion exercises for 2–4 weeks. Rehabilitation should then focus on strengthening, and full return to sport may take several months [151]. In severe cases, surgical fixation should be considered.

Abdominal Injuries

Ten percent of all abdominal injuries have been reported to result from sports-related trauma [152]. Football [153, 154], rugby [155], soccer [156, 157, 158], and wrestling [159] are the most common contact sports for abdominal trauma. Noncontact sports, such as downhill skiing [160, 161, 162, 163], water skiing [164], and horseback riding [153, 165], result in high-speed deceleration mechanisms and may result in very serious injuries.

A retrospective cohort study of Swedish children by Bergqvist et al. [153, 166], involving 348 injuries over 30 years, revealed 7.1% of abdominal trauma was sports related (Table 7.1). Sports involved were ice hockey (eight cases), skiing (six cases), soccer (five cases), pole vaulting (one case), and gymnastics (one case).
Table 7.1

Sports-related abdominal trauma

Intra-abdominal pathology

Abdominal wall contusions

Splenic ruptures

Ruptured jejunum

Pancreatic injury

Renal injuries

No. of patients






Source: Ref. [152]. Reprinted with permission from Elsevier

The same study contrasted recreational cycling with organized sport and found 12% of abdominal trauma in children was related to this pastime. In addition to the pathologies detailed in Table 7.1, there were liver injuries, a mesenteric rupture, muscle lacerations, a stomach rupture, and colon injuries with cycling. Ballham [167] showed that bicycle injuries had a higher injury severity index than other sports. Pediatric bicycle injury data from Puranik [168] of 211 children under 15 years old revealed 9% had internal organ injuries. The handlebar imprint can sometimes be seen along the upper edge of the abdomen (Fig. 7.3) [169]. Bicycles [170, 171, 172] and other types of sports-related vehicular use may result in the same patterns of abdominal injury that are seen in automobile accidents.
Fig. 7.3

Duodenal injury from a bicycle fall. Courtesy of David Mooney, MD, Children’s Hospital, Boston, MA

Splenic Injury

Injuries to the spleen can result from a direct force to the abdomen, especially the left upper quadrant, and from a sudden deceleration when the hilum is torn or by displacement of lower left rib fractures. Any of these mechanisms are possible in high-speed or contact sports.

The mechanism of splenic injury was explored in a study of downhill skiers [173]. In high-velocity or high-impact collisions, e.g., with a tree, a chairlift pole, or a snow fence, multiple trauma was always present (fractures or damage to multiple organs). Skiers were unable to move at the scene, and splenectomy resulted in five out of six cases (83%). With low-velocity or low-impact collisions, often just a single organ was involved. Such injuries resulted from falls on ski trails, on moguls, or on tree stumps or rocks. Presentation in these cases was often delayed for hours, while the individual continued skiing. Splenectomy was necessary in 5 of 12 cases (42%).

Machida et al. [29] found a significantly higher abdominal injury rate in snowboarders compared to skiers. Injuries to the kidney, liver, and spleen were seen in both. In snowboarders, riding mistakes after jumping and subsequent falls were responsible for 31.6% of the abdominal traumas. Skiers were more likely to have a collision as the mechanism for their abdominal injury.

Physical exam is neither sensitive nor specific for splenic injury. Therefore, patients with a concerning mechanism or pain should undergo diagnostic imaging. The most important determinant of nonoperative management of splenic rupture is hemodynamic stability, including hematocrit. Nonoperative management of splenic injuries consists of careful hemodynamic monitoring, frequent physical and laboratory examination, and, most importantly, strict bed rest. Given a stable course, a CT scan should be repeated after 5–7 days and should show stabilization or improvement of the injury. Rest and avoidance of contact sports are recommended for up to 4 months after injury. This is determined largely by the severity of the injury seen on CT and its resolution. Nonoperative splenic management seems to be more successful in children (90%) than in adults (70%) [174].

Epstein-Barr Virus, Infectious Mononucleosis, and Splenomegaly

By age 30, 90% of the population has been exposed to the Epstein-Barr virus, which causes infectious mononucleosis [175]. This may frequently be unrecognized, particularly in children. From 1 to 3% of college students are affected each year [176]. The peak incidence is in 15–24-year-olds.

A study using physical exam alone reported splenomegaly in 8% of patients with infectious mononucleosis [177]. In comparison, a study utilizing ultrasonography demonstrated that 100% of patients with infectious mononucleosis had an enlarged spleen; physical examination detected the abnormality in less than 20% of the same cases [178]. These studies indicate that physical exam alone is an insensitive tool to diagnose splenomegaly in the setting of infectious mononucleosis.

During bouts of mononucleosis, spleen length increases by 33% and peaks between 2 and 4 weeks from onset of symptoms [178]. Comparison with normative anthropomorphic measurements with ultrasound should be used to guide recommendations for return to sport after infectious mononucleosis [179, 180, 181].

Infectious mononucleosis causes the splenic architecture to become distorted, making the spleen susceptible to rupture from any increased abdominal pressure, even from sneezing or coughing. Splenic rupture in infectious mononucleosis occurs in 0.1–0.2% of cases, with the highest estimate being 0.5% [182]. The timing of this complication is predictable, being noted in the first 3 weeks of the illness. Splenic rupture is unusual beyond 3 weeks from the onset of symptoms (headache, sore throat, and fever). The prodromal period is not considered when determining the onset of the illness.

Splenic rupture is associated with abdominal pain, left shoulder pain (Kehr’s sign), or periscapular pain. Left upper quadrant abdominal tenderness may or may not be accompanied by peritoneal signs, such as generalized tenderness, guarding, and rebound tenderness. Indicators of hypovolemia, such as tachycardia and hypotension, are worrisome signs. This complication fortunately is often not fatal. Splenectomy is necessary in some instances, although nonoperative management is often successful [183]. Treatment should be individualized. There is no evidence to suggest corticosteroids reduce spleen size or shorten the duration of the illness [184].

The appropriate time to allow an athlete with infectious mononucleosis to resume his or her activity is determined by the duration of symptoms, as well as the presence of splenomegaly and risk of splenic rupture. There is concern that contact trauma may precipitate splenic rupture. In a 1976 survey of college team physicians, the respondents identified 22 cases of splenic rupture. At the time of the trauma, 41% of these were diagnosed with infectious mononucleosis. Seventeen of the student athletes were participating in football [185]. Most splenic ruptures in the setting of infectious mononucleosis, however, are spontaneous, not the result of contact.

Return-to-play recommendations in the literature have been varied [186]. To protect the enlarged spleen, which should probably be assumed to be present in all cases [184], all strenuous activity should be avoided for the first 21 days. At this point the athlete may start a graded aerobic program, avoiding contact, if the athlete is asymptomatic, afebrile, and does not have a palpable spleen. At 4 weeks, if the signs are equivocal or the athlete is at high risk for collision, an imaging study such as ultrasound should be considered [187]. It should also be noted that normal spleen size has been directly correlated with athlete size; hence, a large athlete with an appropriately sized spleen may be mistakenly diagnosed with splenomegaly if the splenic volume/body mass is not considered [180, 188].

Hepatic Injury

With the evolution of CT scanning, recognition of minor liver injuries has been enhanced. Although the spleen was previously asserted to be the most commonly injured intra-abdominal organ, the incidence of liver injuries may be similar [189]. This is not surprising considering the large size, soft substance, and unprotected position of the liver. Injury can result from a direct blow, especially to the right upper quadrant, a sudden deceleration, or by displacement of right lower rib fractures. Hepatomegaly results in an increased risk of injury, not only because of the increased size but also because an enlarged liver is softer than normal. Therefore, hepatomegaly is a contraindication to high-speed or contact sports.

The mechanism of injury, especially for lower rib fractures, is much more important than the physical exam to suggest a possible liver injury. Right upper quadrant abdominal tenderness, an abrasion/contusion over the right upper abdomen, right shoulder pain, or hemodynamic instability may be present. A CT scan is warranted with any appropriate mechanism. The typical appearance of a liver laceration is illustrated in Fig. 7.4. Unstable patients should have an immediate laparotomy. However, even high-grade injuries can be managed nonoperatively despite an imposing CT appearance, if the patient is hemodynamically stable.
Fig. 7.4

Hepatic injury . Courtesy of David Mooney, MD, Children’s Hospital, Boston, MA

Renal Injury

The kidney is the most commonly injured intra-abdominal organ in some sports, such as rugby. Renal injuries may be relatively asymptomatic, even with repeated blows, such as in boxers, or they may result in renal contusions causing microscopic or gross hematuria. Occult hematuria without radiographic evidence of injury is extremely common in several sports. It is present in 25% of boxers [164], college football players [190], and distance runners [191]. Kidney trauma from a direct blow is particularly common in football and rugby. Twenty-five percent of renal injuries and 40% of renal pedicle injuries do not demonstrate hematuria [192]. An injury to the kidney is shown by CT in Fig. 7.5.
Fig. 7.5

Left kidney injury. Courtesy of David Mooney, MD, Children’s Hospital, Boston, MA

Gross hematuria should be evaluated in the hospital. Nonoperative management is appropriate as long as the athlete is not in shock, there is no expanding hematoma, and no free extravasation of urine seen on intravenous contrast CT. Complete healing is essential before return to sports. Most renal injuries heal within 6–8 weeks. Microscopic hematuria may persist for 3–4 weeks after injury.

Younger patients require special attention, as renal injury is more common than splenic or hepatic injury. Up to 30% of renal trauma in children is related to sport. This may be caused by a proportionally larger kidney size or a lack of musculoskeletal protection [8].


The pancreas is injured in 1–2% of abdominal trauma. A forceful blow to the upper abdomen is the most common mechanism of injury [155, 158]. For instance, a bicycle fall where the handlebar twists and “spears” the child may be the presenting history [1, 169]. As with other internal organs, there are often minimal obvious physical signs of damage. Patients can develop nausea, vomiting, and abdominal pain up to 48 h later. Typically, the pain radiates to the back. CT is the most useful imaging modality.

Bowel Injury

Bowel injury is infrequent and most commonly occurs as a result of a forceful blow to a small area over the small intestine. Physical findings may be limited. An erect chest x-ray may reveal air beneath the diaphragm, although CT is the most sensitive diagnostic imaging modality.

Groin Pain and Injuries

This is one of the more difficult problems to diagnose in athletes, especially if chronic. Soccer, hockey, hurdling, and skiing are sports where groin injuries are especially common [193]. The etiology is most commonly soft tissue injury, contusion or hematoma, and muscle-tendon strain. However, consideration of inguinal hernia, bursitis, and nerve entrapment is warranted.

Additionally, there is evidence evolving in the literature regarding the sportsman’s hernia [194]. This is a tear in the transversalis fascia in the posterior inguinal floor that Hackney [195] describes as an “incipient direct inguinal hernia.” The mechanism of injury is aggressive abduction in specific athletic situations, such as cutting maneuvers. Sportsman’s hernias are particularly common in sports such as soccer and hockey, where athletes frequently change direction at high speed [195, 196, 197]. The sportsman’s hernia is resistant to conservative therapy, and symptoms will recur after a period of rest. The key physical exam finding is tenderness at the pubic tubercle. This injury does not typically show up on routine imaging. Surgical repair of the inguinal floor will return approximately 90% of patients to full activity without pain [194].


Thoracoabdominal trauma is uncommon in pediatric athletes. Certain injuries may be preventable. Sport-specific safety equipment should be worn to minimize the risk of injury. For instance, chest barriers and safety balls in baseball may have decreased (though not eradicated) the risk of commotio cordis [52]. An AED should be present at venues.

Conditioning is also important. Appropriate core strength, including the entire trunk, will maximize protection in contact sports and minimize overuse stress in noncontact sports. Attention to proper sports technique can also minimize the possibility of overuse.

Return-to-Play Guidelines

Onsite return-to-play decisions should be based on pain resolution, unless a minor abdominal wall injury is considered likely. Vital signs should be normal and peritoneal signs absent. Further, players should be able to exercise without an increase in symptoms.

Athletes who have sustained a solid organ contusion require a normal CT scan 2–3 weeks before being allowed to return to practice. Lacerations and subcapsular hematomas require longer periods of recovery because of the greater architectural damage sustained; hence, a prolonged period of healing is necessary. If an organ has to be removed, full tissue postoperative healing takes 6–24 weeks. Strenuous activity should therefore be postponed for 6–8 weeks and contact sports for 12–24 weeks, although advice varies by surgeon.

Rib injuries should be considered on a case-by-case basis, but return to sport is usually possible in 4–8 weeks. Tullos and Erwin described a baseball pitcher who was asymptomatic with a first rib injury at 3 weeks and was able to return to pitching with a pain-free nonunion [94]. The athlete with a sternal fracture can return to play when he/she can compete in a pain-free manner. If the patient engages in contact sports, a flank jacket or other similar device can be used to protect the injury.

Clinical Pearls

  • It is essential, when assessing an athlete who has sustained trauma to the thorax or abdomen, to maintain a high level of suspicion for internal injury.

  • There may be no external sign initially, and serial physical examinations are crucial.

  • If a significant injury is suspected, the athlete should be transferred to a setting where CT imaging and advanced medical care are available.

  • Rib fractures may be traumatic from direct impact or secondary to acute muscle contraction. They may also occur as a stress injury.

  • Fractures of the first four ribs or the last two ribs, multiple fractures, and flail segments may result in injury to surrounding structures.

  • Scapular fractures are unusual in sports and are often missed initially.


  1. 1.
    Diamond DL. Sports-related abdominal trauma. Clin Sports Med. 1989;8(1):91–9.PubMedGoogle Scholar
  2. 2.
    Gray H. Anatomy of the human body. Philadelphia: Lea & Febiger; 1918.Google Scholar
  3. 3.
    Roberts WO, editor. GI trauma in sports. Indianapolis: American College Sports Medicine Team Physician Course; 2002.Google Scholar
  4. 4.
    Roberts JA. Viral illnesses and sports performance. Sports Med. 1986;3(4):298–303.PubMedGoogle Scholar
  5. 5.
    Hyacinthe AC, Broux C, Francony G, Genty C, Bouzat P, Jacquot C, et al. Diagnostic accuracy of ultrasonography in the acute assessment of common thoracic lesions after trauma. Chest. 2012;141(5):1177–83.PubMedGoogle Scholar
  6. 6.
    Irwin Z, Cook JO. Advances in point-of-care thoracic ultrasound. Emerg Med Clin North Am. 2016;34(1):151–7.PubMedGoogle Scholar
  7. 7.
    Leblanc D, Bouvet C, Degiovanni F, Nedelcu C, Bouhours G, Rineau E, et al. Early lung ultrasonography predicts the occurrence of acute respiratory distress syndrome in blunt trauma patients. Intensive Care Med. 2014;40(10):1468–74.PubMedGoogle Scholar
  8. 8.
    Sievers EM, Murray JA, Chen D, Velmahos GC, Demetriades D, Berne TV. Abdominal computed tomography scan in pediatric blunt abdominal trauma. Am Surg. 1999;65(10):968–71.PubMedGoogle Scholar
  9. 9.
    Rifat SF, Gilvydis RP. Blunt abdominal trauma in sports. Curr Sports Med Rep. 2003;2(2):93–7.PubMedGoogle Scholar
  10. 10.
    Amoroso TA. Evaluation of the patient with blunt abdominal trauma: an evidence based approach. Emerg Med Clin North Am. 1999;17(1):63–75, viii.PubMedGoogle Scholar
  11. 11.
    Gannon EH, Howard T. Splenic injuries in athletes: a review. Curr Sports Med Rep. 2010;9(2):111–4.PubMedGoogle Scholar
  12. 12.
    Richardson MC, Hollman AS, Davis CF. Comparison of computed tomography and ultrasonographic imaging in the assessment of blunt abdominal trauma in children. Br J Surg. 1997;84(8):1144–6.PubMedGoogle Scholar
  13. 13.
    Shuman WP. CT of blunt abdominal trauma in adults. Radiology. 1997;205(2):297–306.PubMedGoogle Scholar
  14. 14.
    Juyia RF, Kerr HA. Return to play after liver and spleen trauma. Sports Health. 2014;6(3):239–45.PubMedPubMedCentralGoogle Scholar
  15. 15.
    Amaral JF. Thoracoabdominal injuries in the athlete. Clin Sports Med. 1997;16(4):739–53.PubMedGoogle Scholar
  16. 16.
    Hoffmann R, Nerlich M, Muggia-Sullam M, Pohlemann T, Wippermann B, Regel G, et al. Blunt abdominal trauma in cases of multiple trauma evaluated by ultrasonography: a prospective analysis of 291 patients. J Trauma. 1992;32(4):452–8.PubMedGoogle Scholar
  17. 17.
    Berkoff DJ, English J, Theodoro D. Sports medicine ultrasound (US) beyond the musculoskeletal system: use in the abdomen, solid organs, lung, heart and eye. Br J Sports Med. 2015;49(3):161–5.PubMedGoogle Scholar
  18. 18.
    Walter KD. Radiographic evaluation of the patient with sport-related abdominal trauma. Curr Sports Med Rep. 2007;6(2):115–9.PubMedGoogle Scholar
  19. 19.
    Rozycki GS, Knudson MM, Shackford SR, Dicker R. Surgeon-performed bedside organ assessment with sonography after trauma (BOAST): a pilot study from the WTA Multicenter Group. J Trauma. 2005;59(6):1356–64.PubMedGoogle Scholar
  20. 20.
    Craig S, Egerton-Warburton D, Mellett T. Ultrasound use in Australasian emergency departments: a survey of Australasian College for Emergency Medicine Fellows and Trainees. Emerg Med Australas. 2014;26(3):268–73.PubMedGoogle Scholar
  21. 21.
    Soyuncu S, Cete Y, Bozan H, Kartal M, Akyol AJ. Accuracy of physical and ultrasonographic examinations by emergency physicians for the early diagnosis of intraabdominal haemorrhage in blunt abdominal trauma. Injury. 2007;38(5):564–9.PubMedGoogle Scholar
  22. 22.
    Melniker LA, Leibner E, McKenney MG, Lopez P, Briggs WM, Mancuso CA. Randomized controlled clinical trial of point-of-care, limited ultrasonography for trauma in the emergency department: the first sonography outcomes assessment program trial. Ann Emerg Med. 2006;48(3):227–35.PubMedGoogle Scholar
  23. 23.
    Blackbourne LH, Soffer D, McKenney M, Amortegui J, Schulman CI, Crookes B, et al. Secondary ultrasound examination increases the sensitivity of the FAST exam in blunt trauma. J Trauma. 2004;57(5):934–8.PubMedGoogle Scholar
  24. 24.
    Lentz KA, McKenney MG, Nunez DB Jr, Martin L. Evaluating blunt abdominal trauma: role for ultrasonography. J Ultrasound Med. 1996;15(6):447–51.PubMedGoogle Scholar
  25. 25.
    Ma OJ, Mateer JR, Ogata M, Kefer MP, Wittmann D, Aprahamian C. Prospective analysis of a rapid trauma ultrasound examination performed by emergency physicians. J Trauma. 1995;38(6):879–85.PubMedGoogle Scholar
  26. 26.
    Bode PJ, Edwards MJ, Kruit MC, van Vugt AB. Sonography in a clinical algorithm for early evaluation of 1671 patients with blunt abdominal trauma. AJR Am J Roentgenol. 1999;172(4):905–11.PubMedGoogle Scholar
  27. 27.
    Moore HB, Moore EE, Bensard DD. Pediatric emergency department thoracotomy: a 40-year review. J Pediatr Surg. 2016;51(2):315–8.PubMedGoogle Scholar
  28. 28.
    van As AB, Manganyi R, Brooks A. Treatment of thoracic trauma in children: literature review, Red Cross War Memorial Children’s Hospital data analysis, and guidelines for management. Eur J Pediatr Surg. 2013;23(6):434–43.PubMedGoogle Scholar
  29. 29.
    Machida T, Hanazaki K, Ishizaka K, Nakamura M, Kobayashi O, Shibata H, et al. Snowboarding injuries of the abdomen: comparison with skiing injuries. Injury. 1999;30(1):47–9.PubMedGoogle Scholar
  30. 30.
    Richardson JD, Miller FB. Injury to the lung and pleura. In: Feliciano DV, Moore EE, Mattox KL, editors. Trauma. 3rd ed. Stamford: Appleton & Lange; 1996. p. 387–407.Google Scholar
  31. 31.
    Nakayama DK, Ramenofsky ML, Rowe MI. Chest injuries in childhood. Ann Surg. 1989;210(6):770–5.PubMedPubMedCentralGoogle Scholar
  32. 32.
    Ismail MF, al-Refaie RI. Chest trauma in children, single center experience. Arch Bronconeumol. 2012;48(10):362–6.PubMedGoogle Scholar
  33. 33.
    Sadat-Ali M, Al-Arfaj AL, Mohanna M. Pneumothorax due to soccer injury. Br J Sports Med. 1986;20(2):91.PubMedPubMedCentralGoogle Scholar
  34. 34.
    Simoneaux SF, Murphy BJ, Tehranzadeh J. Spontaneous pneumothorax in a weight lifter. A case report. Am J Sports Med. 1990;18(6):647–8.PubMedGoogle Scholar
  35. 35.
    Wasden CC, McIntosh SE, Keith DS, McCowan C. An analysis of skiing and snowboarding injuries on Utah slopes. J Trauma. 2009;67(5):1022–6.PubMedGoogle Scholar
  36. 36.
    Hani R, Ennaciri B, Jeddi I, El Bardouni A, Mahfoud M, Berrada MS. Pneumothorax complicating isolated clavicle fracture. Pan Afr Med J. 2015;21:202.PubMedPubMedCentralGoogle Scholar
  37. 37.
    Partridge RA, Coley A, Bowie R, Woolard RH. Sports-related pneumothorax. Ann Emerg Med. 1997;30(4):539–41.PubMedGoogle Scholar
  38. 38.
    Erickson S, Rich B. Pulmonary and chest wall emergencies. Phys Sportsmed. 1995;23:95–104.PubMedGoogle Scholar
  39. 39.
    Robinson PD, Blackburn C, Babl FE, Gamage L, Schutz J, Nogajski R, et al. Management of paediatric spontaneous pneumothorax: a multicentre retrospective case series. Arch Dis Child. 2015;100(10):918–23.PubMedGoogle Scholar
  40. 40.
    Azad A, Juma SA, Bhatti JA, Dankoff J. Validity of ultrasonography to diagnosing pneumothorax: a critical appraisal of two meta-analyses. CJEM. 2015;17(2):199–201.PubMedGoogle Scholar
  41. 41.
    Alrajhi K, Woo MY, Vaillancourt C. Test characteristics of ultrasonography for the detection of pneumothorax: a systematic review and meta-analysis. Chest. 2012;141(3):703–8.PubMedGoogle Scholar
  42. 42.
    Lyon M, Walton P, Bhalla V, Shiver SA. Ultrasound detection of the sliding lung sign by prehospital critical care providers. Am J Emerg Med. 2012;30(3):485–8.PubMedGoogle Scholar
  43. 43.
    Adewole OO, De Keukeleire T, Phillips AS, Erhabor G, Noppen M. Effectiveness of thoracoscopic talc pleurodesis in the management of complicated spontaneous pneumothorax. J Bronchology Interv Pulmonol. 2015;22(1):48–51.PubMedGoogle Scholar
  44. 44.
    Olesen WH, Lindahl-Jacobsen R, Katballe N, Sindby JE, Titlestad IL, Andersen PE, et al. Recurrent primary spontaneous pneumothorax is common following chest tube and conservative treatment. World J Surg. 2016;40(9):2163–70.PubMedGoogle Scholar
  45. 45.
    Lorenc TM, Kernan MT. Lower respiratory infections and potential complications in athletes. Curr Sports Med Rep. 2006;5(2):80–6.PubMedGoogle Scholar
  46. 46.
    Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med. 2000;342(12):868–74.PubMedGoogle Scholar
  47. 47.
    Aerospace Medical Association Medical Guidelines Task Force. Medical guidelines for airline travel, 2nd ed. Aviat Space Environ Med. 2003;74(5 Suppl):A1–19.Google Scholar
  48. 48.
    Wagner RB, Crawford WO Jr, Schimpf PP, Jamieson PM, Rao KC. Quantitation and pattern of parenchymal lung injury in blunt chest trauma diagnostic and therapeutic implications. J Comput Tomogr. 1988;12(4):270–81.PubMedGoogle Scholar
  49. 49.
    Bonadio WA, Hellmich T. Post-traumatic pulmonary contusion in children. Ann Emerg Med. 1989;18(10):1050–2.PubMedGoogle Scholar
  50. 50.
    Daurat A, Millet I, Roustan JP, Maury C, Taourel P, Jaber S, et al. Thoracic Trauma Severity score on admission allows to determine the risk of delayed ARDS in trauma patients with pulmonary contusion. Injury. 2016;47(1):147–53.PubMedGoogle Scholar
  51. 51.
    Hershkovitz Y, Zoarets I, Stepansky A, Kozer E, Shapira Z, Klin B, et al. Computed tomography is not justified in every pediatric blunt trauma patient with a suspicious mechanism of injury. Am J Emerg Med. 2014;32(7):697–9.PubMedGoogle Scholar
  52. 52.
    Maron BJ, Poliac LC, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med. 1995;333(6):337–42.PubMedGoogle Scholar
  53. 53.
    Maron BJ, Gohman TE, Kyle SB, Estes NA, Link MS. Clinical profile and spectrum of commotio cordis. JAMA. 2002;287(9):1142–6.PubMedGoogle Scholar
  54. 54.
    Maron BJ, Estes NA. Commotio cordis. N Engl J Med. 2010;362(10):917–27.PubMedGoogle Scholar
  55. 55.
    Link MS, Estes NA, Maron BJ, American Heart Association E, Arrhythmias Committee of Council on Clinical Cardiology CoCDiYCoC, Stroke Nursing CoFG, et al. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: task force 13: commotio cordis: a scientific statement from the American Heart Association and American College of Cardiology. Circulation. 2015;132(22):e339–42.PubMedGoogle Scholar
  56. 56.
    Maron BJ, Haas TS, Ahluwalia A, Garberich RF, Estes NA, Link MS. Increasing survival rate from commotio cordis. Heart Rhythm. 2013;10(2):219–23.PubMedGoogle Scholar
  57. 57.
    Link MS, Wang PJ, Pandian NG, Bharati S, Udelson JE, Lee MY, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med. 1998;338(25):1805–11.PubMedGoogle Scholar
  58. 58.
    Link MS, Wang PJ, VanderBrink BA, Avelar E, Pandian NG, Maron BJ, et al. Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio cordis). Circulation. 1999;100(4):413–8.PubMedGoogle Scholar
  59. 59.
    Link MS, Maron BJ, VanderBrink BA, Takeuchi M, Pandian NG, Wang PJ, et al. Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. J Am Coll Cardiol. 2001;37(2):649–54.PubMedGoogle Scholar
  60. 60.
    Link MS, Maron BJ, Wang PJ, VanderBrink BA, Zhu W, Estes NA. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). J Am Coll Cardiol. 2003;41(1):99–104.PubMedGoogle Scholar
  61. 61.
    Kaplan JA, Karofsky PS, Volturo GA. Commotio cordis in two amateur ice hockey players despite the use of commercial chest protectors: case reports. J Trauma. 1993;34(1):151–3.PubMedGoogle Scholar
  62. 62.
    Weinstock J, Maron BJ, Song C, Mane PP, Estes NA, Link MS. Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics. 2006;117(4):e656–62.PubMedGoogle Scholar
  63. 63.
    Bock JS, Benitez RM. Blunt cardiac injury. Cardiol Clin. 2012;30(4):545–55.PubMedGoogle Scholar
  64. 64.
    Marcolini EG, Keegan J. Blunt cardiac injury. Emerg Med Clin North Am. 2015;33(3):519–27.PubMedGoogle Scholar
  65. 65.
    Vago H, Toth A, Apor A, Maurovich-Horvat P, Toth M, Merkely B. Images in cardiovascular medicine. Cardiac contusion in a professional soccer player: visualization of acute and late pathological changes in the myocardium with magnetic resonance imaging. Circulation. 2010;121(22):2456–61.PubMedGoogle Scholar
  66. 66.
    Moye DM, Dyer AK, Thankavel PP. Myocardial contusion in an 8-year-old boy: a kick to the heart. Circ Cardiovasc Imaging. 2015;8(3):e002857.PubMedGoogle Scholar
  67. 67.
    Baccouche H, Beck T, Maunz M, Fogarassy P, Beyer M. Cardiovascular magnetic resonance of myocardial infarction after blunt chest trauma: a heartbreaking soccer-shot. J Cardiovasc Magn Reson. 2009;11:39.PubMedPubMedCentralGoogle Scholar
  68. 68.
    Bertinchant JP, Robert E, Polge A, Marty-Double C, Fabbro-Peray P, Poirey S, et al. Comparison of the diagnostic value of cardiac troponin I and T determinations for detecting early myocardial damage and the relationship with histological findings after isoprenaline-induced cardiac injury in rats. Clin Chim Acta. 2000;298(1-2):13–28.PubMedGoogle Scholar
  69. 69.
    Collins JN, Cole FJ, Weireter LJ, Riblet JL, Britt LD. The usefulness of serum troponin levels in evaluating cardiac injury. Am Surg. 2001;67(9):821–5. discussion 5–6.PubMedGoogle Scholar
  70. 70.
    Salim A, Velmahos GC, Jindal A, Chan L, Vassiliu P, Belzberg H, et al. Clinically significant blunt cardiac trauma: role of serum troponin levels combined with electrocardiographic findings. J Trauma. 2001;50(2):237–43.PubMedGoogle Scholar
  71. 71.
    Velmahos GC, Karaiskakis M, Salim A, Toutouzas KG, Murray J, Asensio J, et al. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma. 2003;54(1):45–50. discussion -1.PubMedGoogle Scholar
  72. 72.
    Rajan GP, Zellweger R. Cardiac troponin I as a predictor of arrhythmia and ventricular dysfunction in trauma patients with myocardial contusion. J Trauma. 2004;57(4):801–8. discussion 8.PubMedGoogle Scholar
  73. 73.
    Emet M, Akoz A, Aslan S, Saritas A, Cakir Z, Acemoglu H. Assessment of cardiac injury in patients with blunt chest trauma. Eur J Trauma Emerg Surg. 2010;36(5):441–7.PubMedGoogle Scholar
  74. 74.
    Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003;89(5):485–9.PubMedPubMedCentralGoogle Scholar
  75. 75.
    Bansal D, Gaddam V, Aude YW, Bissett J, Fahdi I, Garza L, et al. Trends in the care of patients with acute myocardial infarction at a university-affiliated Veterans Affairs Medical Center. J Cardiovasc Pharmacol Ther. 2005;10(1):39–44.PubMedGoogle Scholar
  76. 76.
    Miles JW, Barrett GR. Rib fractures in athletes. Sports Med. 1991;12(1):66–9.PubMedGoogle Scholar
  77. 77.
    Chang CJ, Graves DW. Athletic injuries of the thorax and abdomen. In: Mellion MB, Walsh MW, Madden C, editors. Team physicians handbook. 3rd ed. Philadelphia: Hanley & Belfus; 2001. p. 441–58.Google Scholar
  78. 78.
    Sartorelli KH, Vane DW. The diagnosis and management of children with blunt injury of the chest. Semin Pediatr Surg. 2004;13(2):98–105.PubMedGoogle Scholar
  79. 79.
    Kessel B, Dagan J, Swaid F, Ashkenazi I, Olsha O, Peleg K, et al. Rib fractures: comparison of associated injuries between pediatric and adult population. Am J Surg. 2014;208(5):831–4.PubMedGoogle Scholar
  80. 80.
    Al-Hassani A, Abdulrahman H, Afifi I, Almadani A, Al-Den A, Al-Kuwari A, et al. Rib fracture patterns predict thoracic chest wall and abdominal solid organ injury. Am Surg. 2010;76(8):888–91.PubMedGoogle Scholar
  81. 81.
    Jenkins SA. Spontaneous fractures of both first ribs. J Bone Joint Surg Br. 1952;34-B(1):9–13.PubMedGoogle Scholar
  82. 82.
    Colosimo AJ, Byrne E, Heidt RS Jr, Carlonas RL, Wyatt H. Acute traumatic first-rib fracture in the contact athlete: a case report. Am J Sports Med. 2004;32(5):1310–2.PubMedGoogle Scholar
  83. 83.
    Lorentzen JE, Movin M. Fracture of the first rib. Acta Orthop Scand. 1976;47(6):632–4.PubMedGoogle Scholar
  84. 84.
    Bailey P. Surfer’s rib: isolated first rib fracture secondary to indirect trauma. Ann Emerg Med. 1985;14(4):346–9.PubMedGoogle Scholar
  85. 85.
    Brooke R. Jive fracture of the first rib. J Bone Joint Surg Br. 1959;41-B(2):370–1.PubMedGoogle Scholar
  86. 86.
    Gurtler R, Pavlov H, Torg JS. Stress fracture of the ipsilateral first rib in a pitcher. Am J Sports Med. 1985;13(4):277–9.PubMedGoogle Scholar
  87. 87.
    Lankenner PA Jr, Micheli LJ. Stress fracture of the first rib. A case report. J Bone Joint Surg Am. 1985;67(1):159–60.PubMedGoogle Scholar
  88. 88.
    Pereira J. Stress fracture of a rib. Br J Sports Med. 1985;19(1):26.PubMedPubMedCentralGoogle Scholar
  89. 89.
    Sacchetti AD, Beswick DR, Morse SD. Rebound rib: stress-induced first rib fracture. Ann Emerg Med. 1983;12(3):177–9.PubMedGoogle Scholar
  90. 90.
    Proffer DS, Patton JJ, Jackson DW. Nonunion of a first rib fracture in a gymnast. Am J Sports Med. 1991;19(2):198–201.PubMedGoogle Scholar
  91. 91.
    Albers JE, Rath RK, Glaser RS, Poddar PK. Severity of intrathoracic injuries associated with first rib fractures. Ann Thorac Surg. 1982;33(6):614–8.PubMedGoogle Scholar
  92. 92.
    Blichert-Toft M. Fatigue fracture of the first rib. Acta Chir Scand. 1969;135(8):675–8.PubMedGoogle Scholar
  93. 93.
    Sakellaridis T, Stamatelopoulos A, Andrianopoulos E, Kormas P. Isolated first rib fracture in athletes. Br J Sports Med. 2004;38(3):e5.PubMedPubMedCentralGoogle Scholar
  94. 94.
    Tullos HS, Erwin WD, Woods GW, Wukasch DC, Cooley DA, King JW. Unusual lesions of the pitching arm. Clin Orthop Relat Res. 1972;88:169–82.PubMedGoogle Scholar
  95. 95.
    Rainer TH, Griffith JF, Lam E, Lam PK, Metreweli C. Comparison of thoracic ultrasound, clinical acumen, and radiography in patients with minor chest injury. J Trauma. 2004;56(6):1211–3.PubMedGoogle Scholar
  96. 96.
    Hoffstetter P, Dornia C, Schafer S, Wagner M, Dendl LM, Stroszczynski C, et al. Diagnostic significance of rib series in minor thorax trauma compared to plain chest film and computed tomography. J Trauma Manag Outcomes. 2014;8:10.PubMedPubMedCentralGoogle Scholar
  97. 97.
    Shuaib W, Vijayasarathi A, Tiwana MH, Johnson JO, Maddu KK, Khosa F. The diagnostic utility of rib series in assessing rib fractures. Emerg Radiol. 2014;21(2):159–64.PubMedGoogle Scholar
  98. 98.
    Chan SS. Emergency bedside ultrasound for the diagnosis of rib fractures. Am J Emerg Med. 2009;27(5):617–20.PubMedGoogle Scholar
  99. 99.
    Reissig A, Copetti R, Kroegel C. Current role of emergency ultrasound of the chest. Crit Care Med. 2011;39(4):839–45.PubMedGoogle Scholar
  100. 100.
    Kara M, Dikmen E, Erdal HH, Simsir I, Kara SA. Disclosure of unnoticed rib fractures with the use of ultrasonography in minor blunt chest trauma. Eur J Cardiothorac Surg. 2003;24(4):608–13.PubMedGoogle Scholar
  101. 101.
    Gregory PL, Biswas AC, Batt ME. Musculoskeletal problems of the chest wall in athletes. Sports Med. 2002;32(4):235–50.PubMedGoogle Scholar
  102. 102.
    Connolly LP, Connolly SA. Rib stress fractures. Clin Nucl Med. 2004;29(10):614–6.PubMedGoogle Scholar
  103. 103.
    Miller TL, Harris JD, Kaeding CC. Stress fractures of the ribs and upper extremities: causation, evaluation, and management. Sports Med. 2013;43(8):665–74.PubMedGoogle Scholar
  104. 104.
    Sinha AK, Kaeding CC, Wadley GM. Upper extremity stress fractures in athletes: clinical features of 44 cases. Clin J Sport Med. 1999;9(4):199–202.PubMedGoogle Scholar
  105. 105.
    Eng J, Westcott J, Better N. Stress fracture of the first rib in a weightlifter. Clin Nucl Med. 2008;33(5):371–3.PubMedGoogle Scholar
  106. 106.
    Leung HY, Stirling AJ. Stress fracture of the first rib without associated injuries. Injury. 1991;22(6):483–4.PubMedGoogle Scholar
  107. 107.
    Low S, Kern M, Atanda A. First-rib stress fracture in two adolescent swimmers: a case report. J Sports Sci. 2016;34(13):1266–70.PubMedGoogle Scholar
  108. 108.
    Holden DL, Jackson DW. Stress fracture of the ribs in female rowers. Am J Sports Med. 1985;13(5):342–8.PubMedGoogle Scholar
  109. 109.
    Lord MJ, Ha KI, Song KS. Stress fractures of the ribs in golfers. Am J Sports Med. 1996;24(1):118–22.PubMedGoogle Scholar
  110. 110.
    Karlson KA. Rib stress fractures in elite rowers. A case series and proposed mechanism. Am J Sports Med. 1998;26(4):516–9.PubMedGoogle Scholar
  111. 111.
    Lin HC, Chou CS, Hsu TC. Stress fractures of the ribs in amateur golf players. Zhonghua Yi Xue Za Zhi (Taipei). 1994;54(1):33–7.Google Scholar
  112. 112.
    Warden SJ, Gutschlag FR, Wajswelner H, Crossley KM. Aetiology of rib stress fractures in rowers. Sports Med. 2002;32(13):819–36.PubMedGoogle Scholar
  113. 113.
    Christensen E, IL K. Increased risk of stress fractures in the ribs of elite rowers. Scand J Med Sci Sports. 1997;7(1):49–52.Google Scholar
  114. 114.
    Gaffney KM. Avulsion injury of the serratus anterior: a case history. Clin J Sport Med. 1997;7(2):134–6.PubMedGoogle Scholar
  115. 115.
    Heincelman C, Brown S, England E, Mehta K, Wissman RD. Stress injury of the rib in a swimmer. Skelet Radiol. 2014;43(9):1297–9.Google Scholar
  116. 116.
    D’Ailly PN, Sluiter JK, Kuijer PP. Rib stress fractures among rowers: a systematic review on return to sports, risk factors and prevention. J Sports Med Phys Fitness. 2016;56(6):744–53.PubMedGoogle Scholar
  117. 117.
    Vinther A, Thornton JS. Management of rib pain in rowers: emerging issues. Br J Sports Med. 2016;50(3):141–2.PubMedGoogle Scholar
  118. 118.
    Scott EM, Scott BB. Painful rib syndrome--a review of 76 cases. Gut. 1993;34(7):1006–8.PubMedPubMedCentralGoogle Scholar
  119. 119.
    Arroyo JF, Vine R, Reynaud C, Michel JP. Slipping rib syndrome: don’t be fooled. Geriatrics. 1995;50(3):46–9.PubMedGoogle Scholar
  120. 120.
    Bass J Jr, Pan HC, Fegelman RH. Slipping rib syndrome. J Natl Med Assoc. 1979;71(9):863–5.PubMedPubMedCentralGoogle Scholar
  121. 121.
    Parry W, Breckenridge I, Khalil YF. Bilateral clicking ribs. Thorax. 1989;44(1):72–3.PubMedPubMedCentralGoogle Scholar
  122. 122.
    Porter GE. Slipping rib syndrome: an infrequently recognized entity in children: a report of three cases and review of the literature. Pediatrics. 1985;76(5):810–3.PubMedGoogle Scholar
  123. 123.
    Udermann BE, Cavanaugh DG, Gibson MH, Doberstein ST, Mayer JM, Murray SR. Slipping rib syndrome in a collegiate swimmer: a case report. J Athl Train. 2005;40(2):120–2.PubMedPubMedCentralGoogle Scholar
  124. 124.
    Turcios NL. Slipping rib syndrome in an adolescent: an elusive diagnosis. Clin Pediatr (Phila). 2013;52(9):879–81.Google Scholar
  125. 125.
    Heinz GJ, Zavala DC. Slipping rib syndrome. JAMA. 1977;237(8):794–5.PubMedGoogle Scholar
  126. 126.
    Meuwly JY, Wicky S, Schnyder P, Lepori D. Slipping rib syndrome: a place for sonography in the diagnosis of a frequently overlooked cause of abdominal or low thoracic pain. J Ultrasound Med. 2002;21(3):339–43.PubMedGoogle Scholar
  127. 127.
    Turcios NL. Slipping rib syndrome: an elusive diagnosis. Paediatr Respir Rev. 2017;22:44–6.PubMedGoogle Scholar
  128. 128.
    Spence EK, Rosato EF. The slipping rib syndrome. Arch Surg. 1983;118(11):1330–2.PubMedGoogle Scholar
  129. 129.
    Fu R, Iqbal CW, Jaroszewski DE, St Peter SD. Costal cartilage excision for the treatment of pediatric slipping rib syndrome. J Pediatr Surg. 2012;47(10):1825–7.PubMedGoogle Scholar
  130. 130.
    Gould JL, Rentea RM, Poola AS, Aguayo P, St Peter SD. The effectiveness of costal cartilage excision in children for slipping rib syndrome. J Pediatr Surg. 2016;51(12):2030–2.PubMedGoogle Scholar
  131. 131.
    Fam AG, Smythe HA. Musculoskeletal chest wall pain. CMAJ. 1985;133(5):379–89.PubMedGoogle Scholar
  132. 132.
    Selbst SM. Chest pain in children. Am Fam Physician. 1990;41(1):179–86.PubMedGoogle Scholar
  133. 133.
    Pantell RH, Goodman BW Jr. Adolescent chest pain: a prospective study. Pediatrics. 1983;71(6):881–7.PubMedGoogle Scholar
  134. 134.
    Proulx AM, Zryd TW. Costochondritis: diagnosis and treatment. Am Fam Physician. 2009;80(6):617–20.PubMedGoogle Scholar
  135. 135.
    Kamel M, Kotob H. Ultrasonographic assessment of local steroid injection in Tietze’s syndrome. Br J Rheumatol. 1997;36(5):547–50.PubMedGoogle Scholar
  136. 136.
    Rovetta G, Sessarego P, Monteforte P. Stretching exercises for costochondritis pain. G Ital Med Lav Ergon. 2009;31(2):169–71.PubMedGoogle Scholar
  137. 137.
    Robertsen K, Kristensen O, Vejen L. Manubrium sterni stress fracture: an unusual complication of non-contact sport. Br J Sports Med. 1996;30(2):176–7.PubMedPubMedCentralGoogle Scholar
  138. 138.
    Baker JC, Demertzis JL. Manubrial stress fractures diagnosed on MRI: report of two cases and review of the literature. Skelet Radiol. 2016;45(6):833–7.Google Scholar
  139. 139.
    Ferguson LP, Wilkinson AG, Beattie TF. Fracture of the sternum in children. Emerg Med J. 2003;20(6):518–20.PubMedPubMedCentralGoogle Scholar
  140. 140.
    Potaris K, Gakidis J, Mihos P, Voutsinas V, Deligeorgis A, Petsinis V. Management of sternal fractures: 239 cases. Asian Cardiovasc Thorac Ann. 2002;10(2):145–9.PubMedGoogle Scholar
  141. 141.
    Athanassiadi K, Gerazounis M, Moustardas M, Metaxas E. Sternal fractures: retrospective analysis of 100 cases. World J Surg. 2002;26(10):1243–6.PubMedGoogle Scholar
  142. 142.
    Sadaba JR, Oswal D, Munsch CM. Management of isolated sternal fractures: determining the risk of blunt cardiac injury. Ann R Coll Surg Engl. 2000;82(3):162–6.PubMedPubMedCentralGoogle Scholar
  143. 143.
    Larson CM, Fischer DA. Injury to the developing sternum in an adolescent football player: a case report and literature review. Am J Orthop (Belle Mead NJ). 2003;32(11):559–61.Google Scholar
  144. 144.
    Perez MR, Rodriguez RM, Baumann BM, Langdorf MI, Anglin D, Bradley RN, et al. Sternal fracture in the age of pan-scan. Injury. 2015;46(7):1324–7.PubMedGoogle Scholar
  145. 145.
    Racine S, Drake D. BET 3: bedside ultrasound for the diagnosis of sternal fracture. Emerg Med J. 2015;32(12):971–2.PubMedGoogle Scholar
  146. 146.
    Lahham S, Patane J, Lane N. Ultrasound of sternal fracture. West J Emerg Med. 2015;16(7):1057–8.PubMedPubMedCentralGoogle Scholar
  147. 147.
    Cain TE, Hamilton WP. Scapular fractures in professional football players. Am J Sports Med. 1992;20(3):363–5.PubMedGoogle Scholar
  148. 148.
    McBryde JP. Scapular fracture in a high school football player. Phys Sportsmed. 1997;25(10):64–8.PubMedGoogle Scholar
  149. 149.
    Harris RD, Harris JH Jr. The prevalence and significance of missed scapular fractures in blunt chest trauma. AJR Am J Roentgenol. 1988;151(4):747–50.PubMedGoogle Scholar
  150. 150.
    Gottschalk HP, Browne RH, Starr AJ. Shoulder girdle: patterns of trauma and associated injuries. J Orthop Trauma. 2011;25(5):266–71.PubMedGoogle Scholar
  151. 151.
    Brown MA, Sikka RS, Guanche CA, Fischer DA. Bilateral fractures of the scapula in a professional football player: a case report. Am J Sports Med. 2004;32(1):237–42.PubMedGoogle Scholar
  152. 152.
    Bergqvist D, Hedelin H, Karlsson G, Lindblad B, Matzsch T. Abdominal trauma during thirty years: analysis of a large case series. Injury. 1981;13(2):93–9.PubMedGoogle Scholar
  153. 153.
    Bergqvist D, Hedelin H, Karlsson G, Lindblad B, Matzsch T. Abdominal injury from sporting activities. Br J Sports Med. 1982;16(2):76–9.PubMedPubMedCentralGoogle Scholar
  154. 154.
    Murphy CP, Drez D Jr. Jejunal rupture in a football player. Am J Sports Med. 1987;15(2):184–5.PubMedGoogle Scholar
  155. 155.
    Harrison JD, Branicki FJ, Makin GS. Pancreatic injury in association football. Injury. 1985;16(4):232.PubMedGoogle Scholar
  156. 156.
    Johnson WR, Harris P. Isolated gallbladder injury secondary to blunt abdominal trauma: case report. Aust N Z J Surg. 1982;52(5):495–6.PubMedGoogle Scholar
  157. 157.
    Maehlum S, Daljord OA. Football injuries in Oslo: a one-year study. Br J Sports Med. 1984;18(3):186–90.PubMedPubMedCentralGoogle Scholar
  158. 158.
    Speakman M, Reece-Smith H. Gastric and pancreatic rupture due to a sports injury. Br J Surg. 1983;70(3):190.PubMedGoogle Scholar
  159. 159.
    Wilton P, Fulco J, O’Leary J, Lee JT. Body slam is no sham. N Engl J Med. 1985;313(3):188–9.PubMedGoogle Scholar
  160. 160.
    Blankstein A, Salai M, Israeli A, Ganel A, Horoszowski H, Farine I. Ski injuries in 1976-1982: Ybrig region, Switzerland. Int J Sports Med. 1985;6(5):298–300.PubMedGoogle Scholar
  161. 161.
    Hildreth TA, Cass AS, Khan AU. Skiing injuries to the urinary tract. Minn Med. 1979;62(3):155–6.PubMedGoogle Scholar
  162. 162.
    Jurkovich GJ, Pearce WH, Cleveland HC. Thoracic and abdominal injuries in skiers: the role of air evacuation. J Trauma. 1983;23(9):844–8.PubMedGoogle Scholar
  163. 163.
    Scharplatz D, Thurleman K, Enderlin F. Thoracoabdominal trauma in ski accidents. Injury. 1978;10(2):86–91.PubMedGoogle Scholar
  164. 164.
    Kleiman AH. Renal trauma in sports. West J Surg Obstet Gynecol. 1961;69:331–40.PubMedGoogle Scholar
  165. 165.
    Pounder DJ. “The grave yawns for the horseman.” Equestrian deaths in South Australia 1973-1983. Med J Aust. 1984;141(10):632–5.PubMedGoogle Scholar
  166. 166.
    Bergqvist D, Hedelin H, Lindblad B, Matzsch T. Abdominal injuries in children: an analysis of 348 cases. Injury. 1985;16(4):217–20.PubMedGoogle Scholar
  167. 167.
    Ballham A, Absoud EM, Kotecha MB, Bodiwala GG. A study of bicycle accidents. Injury. 1985;16(6):405–8.PubMedGoogle Scholar
  168. 168.
    Puranik S, Long J, Coffman S. Profile of pediatric bicycle injuries. South Med J. 1998;91(11):1033–7.PubMedGoogle Scholar
  169. 169.
    Erez I, Lazar L, Gutermacher M, Katz S. Abdominal injuries caused by bicycle handlebars. Eur J Surg. 2001;167(5):331–3.PubMedGoogle Scholar
  170. 170.
    Friede AM, Azzara CV, Gallagher SS, Guyer B. The epidemiology of injuries to bicycle riders. Pediatr Clin N Am. 1985;32(1):141–51.Google Scholar
  171. 171.
    Kiburz D, Jacobs R, Reckling F, Mason J. Bicycle accidents and injuries among adult cyclists. Am J Sports Med. 1986;14(5):416–9.PubMedGoogle Scholar
  172. 172.
    Sparnon AL, Ford WD. Bicycle handlebar injuries in children. J Pediatr Surg. 1986;21(2):118–9.PubMedGoogle Scholar
  173. 173.
    Sartorelli KH, Pilcher DB, Rogers FB. Patterns of splenic injuries seen in skiers. Injury. 1995;26(1):43–6.PubMedGoogle Scholar
  174. 174.
    Esposito JT, Skolasky RL, McFarlane G. Injury to the spleen. In: Feliciano DV, Moore EE, Mattox KL, editors. Trauma. 3rd ed. Stamford: Appleton & Lange; 1996. p. 5225–550.Google Scholar
  175. 175.
    Kaye KM, Persson EK. Epstein-Barr virus infection and infectious mononucleosis. In: Gorbach SL, Bartlett JG, Blacklow NR, editors. Infectious diseases. Philadelphia: W.B.Saunders; 1992. p. 1646–54.Google Scholar
  176. 176.
    Brodsky AL, Heath CW Jr. Infectious mononucleosis: epidemiologic patterns at United States colleges and universities. Am J Epidemiol. 1972;96(2):87–93.PubMedGoogle Scholar
  177. 177.
    Rea TD, Russo JE, Katon W, Ashley RL, Buchwald DS. Prospective study of the natural history of infectious mononucleosis caused by Epstein-Barr virus. J Am Board Fam Pract. 2001;14(4):234–42.PubMedGoogle Scholar
  178. 178.
    Dommerby H, Stangerup SE, Stangerup M, Hancke S. Hepatosplenomegaly in infectious mononucleosis, assessed by ultrasonic scanning. J Laryngol Otol. 1986;100(5):573–9.PubMedGoogle Scholar
  179. 179.
    Hosey RG, Kriss V, Uhl TL, DiFiori J, Hecht S, Wen DY. Ultrasonographic evaluation of splenic enlargement in athletes with acute infectious mononucleosis. Br J Sports Med. 2008;42(12):974–7.PubMedGoogle Scholar
  180. 180.
    Putukian M, O’Connor FG, Stricker P, McGrew C, Hosey RG, Gordon SM, et al. Mononucleosis and athletic participation: an evidence-based subject review. Clin J Sport Med. 2008;18(4):309–15.PubMedGoogle Scholar
  181. 181.
    Hosey RG, Mattacola CG, Kriss V, Armsey T, Quarles JD, Jagger J. Ultrasound assessment of spleen size in collegiate athletes. Br J Sports Med. 2006;40(3):251–4. discussion -4.PubMedPubMedCentralGoogle Scholar
  182. 182.
    Maki DG, Reich RM. Infectious mononucleosis in the athlete. Diagnosis, complications, and management. Am J Sports Med. 1982;10(3):162–73.PubMedGoogle Scholar
  183. 183.
    Asgari MM, Begos DG. Spontaneous splenic rupture in infectious mononucleosis: a review. Yale J Biol Med. 1997;70(2):175–82.PubMedPubMedCentralGoogle Scholar
  184. 184.
    Kinderknecht JJ. Infectious mononucleosis and the spleen. Curr Sports Med Rep. 2002;1(2):116–20.PubMedGoogle Scholar
  185. 185.
    Frelinger DP. The ruptured spleen in college athletes: a preliminary report. J Am Coll Health Assoc. 1978;26(4):217.PubMedGoogle Scholar
  186. 186.
    Burroughs KE. Athletes resuming activity after infectious mononucleosis. Arch Fam Med. 2000;9(10):1122–3.PubMedGoogle Scholar
  187. 187.
    Waninger KN, Harcke HT. Determination of safe return to play for athletes recovering from infectious mononucleosis: a review of the literature. Clin J Sport Med. 2005;15(6):410–6.PubMedGoogle Scholar
  188. 188.
    Spielmann AL, DeLong DM, Kliewer MA. Sonographic evaluation of spleen size in tall healthy athletes. AJR Am J Roentgenol. 2005;184(1):45–9.PubMedGoogle Scholar
  189. 189.
    Pachter HL, Liang HG, Hofstetter SR. Liver and biliary tract trauma. In: Feliciano DV, Moore EE, Mattox KL, editors. Trauma. 3rd ed. Stamford: Appleton & Lange; 1996. p. 487–523.Google Scholar
  190. 190.
    Boone AW, Haltiwanger E, Chambers RL. Football hematuria. J Am Med Assoc. 1955;158(17):1516–7.PubMedGoogle Scholar
  191. 191.
    Alyea EP, Parish HH Jr. Renal response to exercise: urinary findings. J Am Med Assoc. 1958;167(7):807–13.PubMedGoogle Scholar
  192. 192.
    Peterson NE. Genitourinary trauma. In: Feliciano DV, Moore EE, Mattox KL, editors. Trauma. Stamford: Appleton & Lange; 1996. p. 661–93.Google Scholar
  193. 193.
    Renstrom PA. Tendon and muscle injuries in the groin area. Clin Sports Med. 1992;11(4):815–31.PubMedGoogle Scholar
  194. 194.
    Joesting DR. Diagnosis and treatment of sportsman’s hernia. Curr Sports Med Rep. 2002;1(2):121–4.PubMedGoogle Scholar
  195. 195.
    Hackney RG. The sports hernia: a cause of chronic groin pain. Br J Sports Med. 1993;27(1):58–62.PubMedPubMedCentralGoogle Scholar
  196. 196.
    Gilmore OJ. Gilmore’s groin. Sportsmed soft tissue. Trauma. 1992;3:12–4.Google Scholar
  197. 197.
    Fricker PA. Management of groin pain in athletes. Br J Sports Med. 1997;31(2):97–101.PubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of MedicineAlbany Medical CenterLathamUSA
  2. 2.Department of Internal Medicine and PediatricsAlbany Medical CenterLathamUSA

Personalised recommendations