Sports medicine physiatrists are well versed in collaborative work with other health professionals, and therefore have a unique ability to function as the leader of the interdisciplinary sports medicine team. The sports medicine event physician must be prepared for any injury that may occur on the field, including neurologic, musculoskeletal, and medical emergencies. Rapid assessment of the situation is necessary so that the medical team can be activated when there is potential for life- or limb-threatening injury. A comprehensive review of every issue that can be encountered on the field is beyond the scope of this chapter, and the focus will be on common sports medicine emergencies.

Pre-Event Planning

Proper management of any sporting event emergency requires pre-event preparedness. The first step is determining if an athlete’s health puts them at increased risk of injury. For school-based sports, a pre-participation exam is generally required, and the team physician should be aware of any medical conditions that may predispose an athlete to injury or illness. Many adults, and participants in mass participation events, may not have discussed their exercise program with a physician and may have undiagnosed medical conditions that could affect their health during competition.

The medical director or event physician must develop an emergency action plan (EAP). At a minimum, the EAP should incorporate the following: establishment of a chain of command to define the responsibilities of all parties involved, clear protocols for notification of emergency personnel, and access to early defibrillation.¹ The EAP should be reviewed and rehearsed at least annually.¹ Mass participation events may require additional planning. This includes pre-event planning with emergency responders and area medical facilities, given the potentially large number of injured participants. Planning for potential hazardous conditions and monitoring of weather conditions is also the responsibility of the medical director.² Detailed responsibilities of the team physician are discussed in Chapter 25.

Initial Assessment of the Injured Athlete

Initial assessment of the down athlete must be performed in a systematic fashion and begins with CAB (circulation, airway, breathing), followed by a focused neurologic evaluation.³ While previously known as the ABCs, newer recommendations emphasize that maintenance of circulation is the primary goal of cardiopulmonary resuscitation (CPR). Any athlete with altered consciousness must also be presumed to have suffered a cervical spinal cord injury, and strict spine precautions should be put in place, particularly for the contact sport athlete or an unwitnessed fall (Table 27–1).

Circulation

In the event of a primary cardiac event, with either absent or irregular pulse, immediate CPR should begin, with maintenance of cervical spine stabilization. Early access to an automated external defibrillator (AED) is necessary. Neurogenic shock due to a cervical spinal cord injury may present with bradycardia and diminished pulses and hypotension. Hypovolemic shock, with a rapid, diminished pulse, may be associated with splenic injury or other causes of rapid internal blood loss.⁵

Airway Maintenance with Cervical Spine Protection

Athletes should be assessed not only for airway patency but also for the ability to protect the airway. Inline cervical spine stabilization should be maintained at all times. The jaw-thrust chin-lift maneuver, rather than the head tilt, is recommended, as it leads to less cervical spine movement.⁴ Mouth guards should be removed, and in the helmeted athlete, the facemask should be removed as quickly as possible (Fig. 27–1).

Breathing and Ventilation

Adequate ventilation should be verified with auscultation. If necessary, a bag-valve device and facemask are often sufficient for on-the-field ventilation. Definitive airway control (with laryngeal mask airway, endotracheal tube, or esophageal tracheal Combitube) should be done only in the presence of trained personnel, and is indicated in the following situations: apnea, severe closed head injury, high cervical spine injury (due to inhibition of phrenic nerve output), or any inability to maintain adequate ventilation.^5,6

Cervical Spine Precautions

The next step includes evaluation of mental status, neurologic deficit, and cervical spine status.³ Once the athlete is alert and oriented, assessment begins with detailed cranial nerve exam, and motor and sensory testing of the limbs.⁷ If this is all normal and there is no further concern for cervical spine injury, evaluation can proceed with cervical spine palpation, then gentle active range of motion with and without support. The athlete may then sit, then stand. Any abnormalities or neck pain at any point necessitates full cervical spine precautions.

Exposure

In athletes with equipment, the jersey and shoulder pads should be cut to allow access to the chest, if this has not already been performed. The athlete should be protected from extremes of temperature.

Neurologic

Head Injury

Concussions/mild traumatic brain injuries are relatively common, particularly in contact sports. Among 20 high school sports, the overall concussion incidence has been found to be 2.5 per 10,000 athlete exposures, with the highest rates in football, boys ice hockey, and boys lacrosse.⁸ While not a true sporting emergency, recognition of when a concussion may have occurred is imperative so that the athlete can be removed from play immediately. It is important to remember that a concussion can occur from a blow to the head or a blow to the body with forces transmitted to the head. The majority of concussions do not involve loss of consciousness. The athlete with a suspected concussion should not be allowed to return to play on the same day and should follow a medically supervised, gradual return to exercise and sport only once asymptomatic.⁹ Boden et al found that of athletes who suffered a catastrophic brain injury while playing football, 39% were playing with symptoms from a previous injury, reinforcing the need for recognition and removal from play following a concussion.¹⁰

Athletes who require transport for advanced imaging following concussion include patients who exhibit any of the following: focal neurologic deficits, persistent alterations in mental status, Glasgow Coma Scale scores of 13 or less, and the possibility of a skull fracture.¹¹ The following life-threatening injuries can be encountered on the field and require recognition and transport: skull fracture, second impact syndrome, and brain hemorrhage.

Skull fractures can occur following a blow to the head and should be suspected in the presence of swelling or ecchymosis around the eyes (raccoon eyes) or behind the ear over the mastoid process (Battle’s sign), visible bony defect, or evidence of cerebrospinal fluid (CSF) leakage¹² (Fig. 27–2). The majority can be managed conservatively, but surgical intervention may be necessary if the fracture is compound or significantly depressed.¹²

Second impact syndrome (SIS) is a rare condition that can occur in adolescent athletes that suffer a second head injury while still symptomatic from an earlier head injury. The pathophysiology behind SIS is thought to be a loss of cerebral autoregulation that can lead to cerebral vascular congestion, increased intracranial pressure, and brain herniation.¹³ A thin subdural hematoma can be seen on imaging but is not generally thought to be large enough to explain the elevated intracranial pressure.¹⁴ SIS progresses rapidly, and athletes may become comatose within minutes.¹³ Even with intervention, this usually results in death or severe disability. Treatment consists of rapid intubation and transport for emergent decompression.

Intracranial hemorrhage is a leading cause of sports-related fatalities. Epidural hematomas are more common in nonhelmeted sports, while subdural hematomas are more common in football.¹²

An epidural hematoma (EDH) can be rapidly fatal if not recognized. It occurs when an athlete is struck in the head with a ball traveling at high velocity, such as in baseball and golf.¹¹ EDH is often associated with a temporal bone fracture and rupture of the middle meningeal artery. A posterior fossa EDH can be seen with occipital skull fracture. The classic description is of a brief loss of consciousness, followed by a lucid interval before progressive neurologic deterioration.¹⁵ Lateralizing signs, or the presence of Cushing’s triad (hypertension, bradycardia, and respiratory depression), are signs of uncal herniation. If present, a dilated pupil is seen ipsilateral to the side of the bleed, due to compression of the oculomotor nerve. There is often no underlying parenchymal lesion, so with prompt recognition and evacuation of the clot, excellent recovery can be expected.¹⁵

Subdural hematomas (SDHs) are the leading cause of brain injury–related deaths in American football¹³ and often result from bleeding of the cortical vessels or tearing of the bridging veins. Unlike an EDH, there often is associated parenchymal damage with SDH, which may lead to morbidity even if the SDH is treated. SDH can progress rapidly but can sometimes present days later. Symptoms include increasing headache, vomiting, blurred vision, and altered cognition.¹² If severe, the athlete may be unconscious or have lateralizing signs. Rapid decompression is indicated in cases of progressive neurologic decline. In cases without neurologic signs, an SDH can be monitored with serial imaging.

Brain contusion and parenchymal hemorrhages result from neuronal and vascular injury and continue to evolve over 24 to 48 hours,¹¹ therefore requiring serial monitoring. They can occur from direct trauma or deceleration/acceleration injury, with injury most often seen in the inferior frontal and temporal lobes.¹¹

Intracerebral hemorrhage can occur from congenital vascular lesions such as aneurysm or arteriovenous malformation, and therefore may be rapidly progressive. Serial imaging is generally recommended. Subarachnoid hemorrhage (SAH) can also arise from congenital vascular lesions and will present with severe headache. A large amount of subarachnoid blood can lead to vasospasm, but most SAHs are not life threatening.¹¹

Cervical Spine Injury

Spinal cord injuries are most common in American football, ice hockey, rugby, downhill skiing/snowboarding, and equestrian sports.¹⁶ Rule changes such as eliminating spear tackling in American football and checking from behind in hockey have helped to decrease the incidence of cervical spine injuries.¹⁶

Cervical spine injuries can occur from a number of mechanisms but the most common is an axial load to the head with a slightly flexed cervical spine. In this position, the cervical spine functions like a segmented column, which will buckle under load.¹⁶ Any athlete complaining of neck pain or neurologic symptoms in any limb should be evaluated for a cervical spine injury.

Transient Quadriplegia (TQ)

TQ is, by definition, a transient neurologic dysfunction and may be better termed “cervical cord neuropraxia.” Generally, the athlete has no neck pain but will complain of sensory symptoms of numbness or paresthesias, with or without weakness, in more than one limb. There are three types: plegia (complete loss of motor function), paresis (motor weakness), and paresthesia (sensory symptoms only). One common presentation is burning hands syndrome, which is a variant of central cord syndrome and presents with painful paresthesias in both hands. Symptoms of TQ generally resolve within 15 minutes but can take up to 48 hours.^16,17

Extremes of neck flexion or extension can cause momentary cord compression through a pincer mechanism.¹⁸ Acquired or congenital cervical stenosis is thought to increase the risk for development of this condition. In a study by Torg et al, over half of American football players who returned to play experienced a second occurrence.¹⁷ It is important to note that while unilateral symptoms consistent with a stinger are common, bilateral stingers are exceedingly rare. Any athlete with symptoms in more than one extremity should be presumed to have a cervical spine injury, with immediate initiation of full cervical spine precautions and transport to a hospital for full evaluation.

Cervical Spine Stabilization

Cervical spine stabilization of the athlete with a suspected cervical spine injury begins with immobilization of the head and neck. No traction should be applied, as excessive distraction may cause further injury.⁶ The player will need to be moved onto a spine board or other immobilization device.

Transfer to a spine board can occur with either a log roll or the eight-person lift.¹⁹ (The person who is stabilizing the head and neck is responsible for leading the transfer. If the athlete is supine, the eight-person lift is generally recommended.²⁰ If the athlete is prone and must be log-rolled, ideally this should occur directly onto the spine board to avoid moving the athlete twice. The log roll requires at least four to five people. While log rolling the athlete, attempts to move the cervical spine into neutral position should stop if any of the following are encountered: increased pain, neurologic symptoms, airway compromise, mechanical resistance, or the patient is apprehensive.⁴ If the athlete is not wearing a helmet, a cervical collar should be put in place prior to transfer. The body should be secured with at least three straps and then the head should be secured with the use of pads and/or straps or tape with two points of contact. The thumbs are often taped together over the chest to keep the arms in place. A vacuum mattress may also be used but still requires a long spine board underneath. However, it may be more comfortable for the patient and can be used with concomitant pelvis or femur fracture. A team physician or athletic trainer should accompany the athlete to the hospital, both for continuity of care and to help with equipment removal.

Sports-Specific Equipment Removal

In 2001, the Inter-Association Task Force for Appropriate Care of the Spine-Injured Athlete recommended leaving the helmet and shoulder pads in place for transport in football and ice hockey.⁷ With helmet and shoulder pads in place, the neck is kept in neutral alignment. Additionally, removal of the equipment is challenging and can lead to increased movement of the cervical spine. The National Athletic Trainers’ Association (NATA) recently released an executive statement, which was later amended, indicating that protective equipment may be removed prior to transport in the appropriate situation with trained professionals. There are also instances in which the helmet and shoulder pads should be removed prior to transport (Table 27–2). Helmet and shoulder pads work as a unit to keep the spine in neutral and should always be removed together in American football and ice hockey (all or none principle).

In all sports, the goal is neutral alignment of the spine. If the athlete’s equipment does not permit this, or in the helmeted athlete if the equipment does not immobilize the head adequately, then removal of equipment in a safe manner is indicated to achieve neutral alignment and adequate stabilization.⁴

When the decision is made to immobilize or transport a helmeted athlete, the facemask should be removed as quickly as possible, regardless of current respiratory status.⁷ This may be done with an electric screwdriver, but medical personnel should also be equipped with cutting tools in case the screws cannot be removed.^6,20

Helmet Removal

This requires at least three trained professionals and many more for lifting the athlete.⁷ The first trained professional maintains alignment and stabilization from the top of the head. As the equipment is loosened by the second person, the third person will take over control of the cervical spine from the front, using the athlete’s chest to help stabilize the forearms. The shoulder pads should already have been cut down the front and the straps under the arms. The first step is cutting/removal of the chin strap. Next the ear pads are removed one at a time, using a tongue depressor or similar object. The third person takes control of the head one side at a time as the ear pad is removed. The helmet is then deflated with an 18-gauge needle, if needed. The person who was controlling the head and neck from the top now works to remove the helmet and shoulder pads while the third person maintains alignment. First the athlete must be lifted a few inches off the surface. The person at the head controls the count. The helmet should be rolled forward to clear the occiput. It should not be pulled outward from the sides, as this only tightens the fit. The shoulder pads can then also be pulled off around the head before the athlete is lowered and a cervical collar is put in place (Fig. 27–3).

Musculoskeletal

Acute Compartment Syndrome

Acute compartment syndrome (ACS) is caused by increased intracompartmental pressure within a closed limb compartment that can impair local circulation and tissue perfusion.²¹ ACS is a surgical emergency and unless the pressure is quickly relieved, necrosis and permanent disability may occur.²¹ Soft tissue injuries can cause ACS, but fractures are the most common cause.^22,23 It is estimated that the annual incidence of ACS ranges from 1 to 7.3 per 100,000.^21,24 The thigh, leg, and forearm are most frequently affected (Figs. 27–4 and 27–5).

Symptoms include pain (often severe), sensation of tightness, and potentially paresthesias and weakness. Late findings include pulselessness and pallor, although these findings may not always be present. ACS is defined as intracompartmental pressures greater than 30 mm Hg for normotensive patients and greater than 20 mm Hg for hypotensive patients.²¹ Pressures greater than 30 mm Hg for over 6 hours can lead to irreversible damage.²⁵ The initial management begins with removal of any casts or dressings and closely examining the limb.²¹ The limb should be kept at the level of the heart, as elevation will reduce arterial inflow, while if the limb is dependent swelling will increase pressures further.²⁶ Radiographs may be performed to evaluate for any fracture. Intracompartmental pressures may be measured; however, if there is strong clinical concern for ACS, prompt surgical decompression via fasciotomy should be performed for definitive treatment.

Dislocation/Fracture

Knee Dislocation

Knee dislocations are an uncommon event in sports medicine; however, prompt diagnosis and treatment are imperative to prevent neurovascular compromise. Knee dislocations are often associated with significant ligamentous injury, and therefore the treating provider should always maintain a high index of suspicion following significant knee trauma. Patients can spontaneously reduce their dislocated knee; thus, the true incidence is likely underestimated and difficult to accurately confirm.^27–29 Knee dislocations are classified by the position of the tibia relative to the femur (anterior, posterior, lateral, medial, or rotatory)^27,30 (Fig. 27–6).

The most common mechanism of injury in athletics is forced hyperextension, typically resulting in an anterior (tibia anterior to femur) dislocation.²⁸ Prompt recognition is important, given the high rate of vascular injury to the popliteal artery or vein, which is a medical emergency. Fibular nerve injury, fracture, compartment syndrome, and significant ligamentous injury can also be seen.^29,30 Patients characteristically complain of severe pain and instability of the knee. There may or may not be obvious deformity (Fig. 27–7).

An immediate neurovascular assessment should be performed. Treatment of a knee dislocation includes reduction, immediate splinting of the knee in extension, and transport to the emergency department. Early angiography should be considered to evaluate for popliteal artery injury. Emergent surgical intervention should be considered if there is an open dislocation, popliteal artery injury, irreducible dislocation, or an associated compartment syndrome.

Fat Embolism

Fat emboli can occur following fracture or severe injury to soft tissues, and are often small and widespread, as opposed to a focal blood clot.³¹ Fat emboli are thought to occur in all patients with long-bone fractures, but only a subset of patients will actually become symptomatic.^31,32 Two possible mechanisms exist: direct entry of a fat globule—for example, from the marrow of a long bone—into the bloodstream³³ or a plasma-derived fat emboli caused by agglutination of fat.³³ It is felt that the pliable nature of the fat emboli can contribute to passage through the pulmonary capillary system with subsequent embolization to the skin or brain.³⁴

The subset of patients who become symptomatic can present with pulmonary symptoms from a pulmonary fat embolism, neurologic symptoms from a cerebral fat embolism, or more widespread and systemic dysfunction from fat embolism syndrome, which can also include pyrexia, tachycardia, and a pathognomonic petechial rash.^31,32 Management of fat emboli, and even fat embolism syndrome, is largely focused on supportive measures.³¹ Early surgical fixation of long-bone fractures has been shown to reduce the risk of symptomatic fat emboli.^35,36

Other Organs

Lung

Flail Chest

Rib fractures in athletes can occur following blunt trauma to the chest wall. A flail chest can occur with fracture of three or more consecutive ribs in at least two places and is accompanied by paradoxical motion of the flail segment (flail segment collapses on inspiration and expands during expiration).³⁷ Athletes present with acute, sharp thoracic pain after a single traumatic event³⁸ (Fig 27–8).

Initial management begins with addressing the patient’s CAB. Morbidity is generally related to the underlying lung injury, such as pulmonary contusion, pneumothorax, or hemothorax,³⁹ and for this reason, the patient should be transported immediately to the hospital for further management. Definitive management of flail chest remains controversial given the lack of adequate studies comparing surgical fixation of the segment versus nonoperative treatment.³⁹ In general, rib fractures can take up to 6 to 8 weeks to heal. Athletes can often return to noncontact sport earlier in the recovery period, depending on their pain tolerance, but return to contact sports should be held off until there is clinical and radiographic evidence of healing.

Pneumothorax

A pneumothorax is defined as air that has accumulated outside of the pleural space and within the chest cavity itself.³⁸ The amount of air that accumulates can continue to progress and eventually become a life-threatening tension pneumothorax, which is a medical emergency.

A spontaneous pneumothorax occurs secondary to the rupture of subpleural blebs or bullae, and is often seen in young males who are tall and thin.^38,40 A traumatic pneumothorax can be formed by either blunt or penetrating trauma to the chest wall and can be the result of rupture of a pulmonary bleb or parenchymal laceration from a rib fracture or the penetrating instrument.³⁸ Any athlete in a contact sport is at risk to develop a traumatic pneumothorax and may be seen with concomitant trauma to the abdomen or flank.⁴¹

Athletes with a pneumothorax will present with pleuritic chest pain and shortness of breath. Those with a tension pneumothorax will be acutely ill.³⁸ With a large pneumothorax, there may be asymmetrical expansion of the chest wall, hyperresonance to percussion, and decreased breath sounds on the affected side.⁴² With a tension pneumothorax, there may also be tachycardia, hypotension, and deviation of the apical cardiac impulse and trachea contralateral to the side of the collapsed lung.⁴² These signs are not always consistent, and it can be more challenging to diagnosis a tension pneumothorax than once thought.^43,44 Worsening hypoxia, diminishing blood pressure, and hemodynamic instability are reasons to proceed with needle thoracostomy, rather than waiting for medic arrival and transportation. This is done by inserting a large-bore needle (14- to 16-gauge) in the second intercostal space in the midclavicular line. Some recent literature questions the effectiveness of this approach, with concerns that standard catheters are not long enough to penetrate through chest wall tissue^45,46 (Fig. 27–9).

If pneumothorax is suspected, the athlete should refrain from further physical activity or any other endeavor that can increase intrathoracic pressure.⁴⁷ A chest radiograph is the initial study of choice.⁴⁸ For athletes without other injury, a pneumothorax of around 15% or less can simply be observed, and the pleural air will often be resorbed without further treatment.⁴¹ Daily chest films are recommended, and if the pneumothorax does not resolve or if it becomes larger, then tube thoracostomy is required.⁴¹ Once the pneumothorax has resolved, the athlete can return to activity. This is also true for tension pneumothorax.⁴¹ Pleurodesis can be considered in individuals with recurrence of pneumothorax.⁴²

Spleen

Splenic Rupture

The spleen is one of the most commonly injured intra-abdominal organs following blunt trauma, but can also rupture spontaneously.⁴⁹ It is important to be aware that splenic injury can result from even trivial mechanisms, such as a collision with another player, and should remain on the differential for any athlete complaining of abdominal pain and discomfort.⁵⁰ In most adults, the spleen does not extend inferiorly past the rib cage, unless it is otherwise enlarged, but in children the rib cage does not completely cover the spleen. Additionally the thoracic cage in children is more compliant and can transmit more energy, increasing the risk for injury.⁵⁰

Splenic injury can present with a wide range of sometimes vague symptoms.⁵⁰ These symptoms include abdominal pain, radiating pain to the left shoulder (Kehr’s sign), nausea, lightheadedness, sweating, abdominal guarding, and possible syncope.⁴⁹ A high index of suspicion should be maintained and combined with a careful history and physical exam, which includes questions about possible mechanism of injury, prior illness, fever, or hematologic disorders.⁵⁰ Physical exam can demonstrate abdominal tenderness, rebound tenderness, or guarding.⁵⁰ The clinician must assess for hemodynamic stability.

If there is concern for a possible splenic injury, prompt transport to a hospital for further imaging and hemodynamic monitoring is of utmost importance.⁵⁰ Field management should focus on maintaining an athlete’s CAB and supportive management until transport can occur. Surgical management may be indicated with hemodynamic instability or severe injuries, but selective nonoperative management has been a mainstay of treatment for hemodynamically stable patients.^50,51 Delayed splenic rupture can occur in up to 8% of patients, potentially caused by pseudoaneurysm, splenic abscess, secondary tearing of the parenchyma, or delayed hemorrhage.⁵⁰

Return to play following splenic injury remains controversial. Recommendations range from 3 weeks to 3 months before return to contact activities, with close monitoring of the athlete.^49,50

Splenic Rupture in Association With Infectious Mononucleosis

Infectious mononucleosis (IM) is caused by the Epstein-Barr virus and has been stated to eventually infect almost 90% of adults.⁵² Splenic enlargement is nearly universal in this disease and can occur within the first few weeks of infection; it is associated with not only increase in size but also increase in fragility of the tissues of the spleen.^52,53 While rupture is rare, it is associated with significant morbidity.⁵² The current consensus for return to play is that light noncontact activities can be initiated 3 weeks from symptom onset, and the athlete should be afebrile, asymptomatic, well hydrated, and without a palpable spleen or liver.^52,53 Return to contact activities is more controversial. The majority of splenic ruptures occur within the first 3 weeks of illness, but cases have been noted as far out as 7 weeks from the start of illness.⁵² One review notes that splenic rupture rarely occurs after 28 days, so based on these findings return to play after one month is a reasonable plan with close monitoring.⁵³

Testicle

Testicular Rupture

Testicular rupture is a very rare entity, given the anatomic location and mobility of the scrotum, but it can be seen with blunt trauma during a sporting event. The mechanism is often a direct blow that causes compression and tearing of the usually strong tunica albuginea. The athlete will complain of acute pain, with significant testicular edema, ecchymosis of the scrotum, and exquisite tenderness of the testis on exam.⁵⁴ The swelling and pain can make a physical exam challenging, and ultrasound can be used to help diagnose.⁵⁵ Early surgical repair is the mainstay of treatment and results in a far less risk of orchiectomy than delayed surgery or conservative treatment.⁵⁶

Testicular Torsion

Testicular torsion is a urological emergency that results from the twisting of the spermatic cord causing ischemia and pain in the affected testicle, and should be considered in the differential diagnosis of testicular rupture.^57,58 Torsion can be subdivided into two categories: extravaginal and intravaginal. Extravaginal torsion involves the testes, spermatic cord, and process vaginales and is seen primarily in neonates in conjunction with undescended testes.^57,58 Intravaginal torsion occurs within the tunica vaginales and is often the result of a congenital malformation of the process vaginales that allows the testis to rotate freely within the tunica vaginales, called a bell-clapper deformity.^58,59 Intravaginal torsion most commonly occurs in adolescent boys ages 12 to 18 but can occur at any age.^57,58 Venous engorgement from the torsion causes edema, hemorrhage, and subsequent arterial compromise.⁵⁹ The amount of torsion can range from 90 to 180 degrees (incomplete torsion) to 720 degrees (complete torsion causing disruption of the testicular artery).^57,59

An athlete with an acute testicular torsion would present with sudden onset of pain in the scrotum often followed by nausea, vomiting, and a low-grade fever. Examination would be consistent with a swollen, inflamed, tender hemiscrotum; absent cremasteric reflex; and no relief of pain with elevation of the scrotum.⁵⁹ This clinical picture can be confused with epididymitis, which is not a surgical emergency. Differentiating clinical signs include a present cremasteric reflex and pain relief with scrotal elevation in epididymitis.^58,59 Epididymitis is also associated with a more gradual onset of symptoms and is seen more frequently in an older population.⁵⁸ There is a nearly 100% salvage rate if treatment occurs within 6 hours of onset; this rate drops to 50% to 70% salvage up to 12 hours and 10% to 20% within 24 hours.^58,59

Quick diagnosis and surgical treatment are the goals of care of an individual with testicular torsion.^57–59 If prompt surgical care cannot be accomplished, then an attempt at manual derotation can be made. It is recommended to cool the testis and perform a local block with an anesthetic agent if available.^57,58 About 66% of the time the testis rotates medially, so the examiner should first attempt to rotate the testis laterally toward the thigh. If this does not relieve symptoms, then next the examiner should try to rotate the testis medially away from the thigh.^57,58 The success rates for manual derotation vary widely.⁵⁸

Sporting injuries are one of the most common causes of testicular injury, and all male athletes should be encouraged to wear adequate and appropriate protective equipment.⁵⁴

Sudden Cardiac Arrest

Sudden cardiac death (SCD) is the leading cause of mortality in young athletes during exercise.^60–62 Physical activity may trigger an acute cardiovascular event or sudden cardiac arrest in young individuals with silent hereditary or congenital heart disease. Cardiac conditions are generally grouped into the following categories: vascular, anatomic, dysrhythmias, metabolic, ion channelopathies, infectious, traumatic, and idiopathic⁶³ (Table 27–3). The survival rate after sudden cardiac arrest (SCA) remains poor and has been reported as low as 11%.⁶⁴ Early defibrillation is the strongest determinant of survival following cardiac arrest; thus, close access to an AED is imperative.^65,66

The incidence of SCA is well debated. The incidence in high school–aged athletes has previously been reported as 1:100,000 to 1:300,000.^61,62 A more recent study showed that the estimated rate of SCD in collegiate sports is approximately 1 per 50,000.⁶¹ Coronary artery disease is the most common cause of SCA in athletes aged 35 or older. Hypertrophic cardiomyopathy (HCM) was historically found to be the most common cause of SCD in young American athletes. In a recent study, there were fewer cases of definitive hypertrophic cardiomyopathy than previously described, and the most common finding at autopsy was instead autopsy-negative sudden unexplained death, without any structural abnormality found.⁶⁷ High-risk groups include males, black athletes, and basketball athletes.⁶⁷

Several dysrhythmias can be associated with sudden collapse, including long Q-T syndrome, second- and third-degree heart block, and aberrant atrioventricular pathways.^63,68 Dysrhythmias can also be caused by metabolic imbalances, such as those associated with altered levels of serum sodium, potassium, and calcium.⁶³ Commotio cordis is the second most common cause of sudden cardiac death in young athletes and is most common in boys less than 18 years old, and is seen in the absence of morphologic injury or preexisting disease.⁶² If a high-velocity impact to the chest wall occurs during ventricular repolarization, it can induce an R-on-T phenomenon that causes ventricular fibrillation.⁶⁹ Sports that can be associated with commotio cordis include baseball, ice hockey, and karate. Survival after commotio cordis has been reported to be only 15%.⁷⁰ The use of softer balls or pucks and the use of chest barriers can help prevent commotio cordis. Rapid recognition of the dysrhythmia and early cardiopulmonary resuscitation with the appropriate use of AEDs have resulted in improved outcomes for patients with arrhythmias resulting from blunt cardiac injury and can be potentially lifesaving.⁷¹