Showing posts with label Injury. Show all posts
Showing posts with label Injury. Show all posts

Monday, February 17, 2014

Calcaneofibular Ligament Injury

Background

Ankle injuries are among the most common injuries that present to physician offices and emergency departments (EDs) because the ankle is the most frequently injured joint in the body.[1, 2, 3, 4, 5, 6, 7, 8] Ankle injuries are a major cause of time loss from work or other daily activities and constitute up to 25% of all time-loss injuries from running and jumping sports.[9, 10] Sprains account for 85% of ankle injuries and, of these sprains, 85% are caused by inversion injuries. An inversion sprain results in an injury to the lateral ligaments, one of which is the calcaneofibular ligament (CFL). Most ankle sprains can be managed with a short period of immobilization followed by rehabilitation therapy, but chronic instability is best treated surgically.[11]

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Ankle Sprain and Sprains and Strains.

NextEpidemiologyFrequencyUnited States

An estimated 1 ankle inversion injury occurs per 10,000 people per day, or 23,000 ankle inversion injuries per day. Of these ankle inversion injuries, the CFL is the second most common ligament injured after the anterior talofibular ligament (ATFL).

PreviousNextFunctional Anatomy

The CFL courses from the distal fibula to the calcaneus by extending from the distal anterior margin of the lateral malleolus to insert onto the posterior lateral tubercle of the lateral wall of the calcaneus.[8, 12, 13] The CFL lies deep to the peroneal tendons, is cylindrical in shape, and, because it crosses 2 joints, it acts as a subtalar joint stabilizer.

PreviousNextSport-Specific Biomechanics

The CFL is 20-30 mm long, 3-5 mm thick, and 4-8 mm wide, and the angle of the CFL from the fibula to the calcaneus is 10 º -45 º posterior to the axis of the fibula. Except in the extremes of inversion, the CFL is in a lax position. With an inverted ankle, strain on the CFL is highest in dorsiflexion; thus, when the ankle is dorsiflexed or in a neutral position, the CFL is the lateral ligament that is most often injured in inversion sprains. Although isolated CFL tears are uncommon, CFL tears in combination with ATFL tears are the second most common injury pattern (20% of injuries). Midsubstance rupture of the CFL remains the most common injury pattern, although a number of fibula or calcaneus avulsion-type injury patterns exist.[14]

PreviousProceed to Clinical Presentation , Calcaneofibular Ligament Injury

Sunday, February 16, 2014

Talofibular Ligament Injury

Background

Ligamentous injuries of the ankle are common among athletes.[1, 2] Inversion injuries of the ankle account for 40% of all athletic injuries. The anterior talofibular ligament (ATFL) and the calcaneofibular ligament (CFL) are sequentially the most commonly injured ligaments when a plantar-flexed foot is forcefully inverted. The posterior talofibular ligament (PTFL) is rarely injured, except in association with a complete dislocation of the talus.[3, 4, 5]

Ligamentous injuries of the ankle are classified into the following 3 categories, depending on the extent of damage to the ligaments:[6, 7, 8, 9, 10]

Grade I is an injury without macroscopic tears. No mechanical instability is noted. Pain and tenderness is minimal.Grade II is a partial tear. Moderate pain and tenderness is present. Mild to moderate joint instability may be present.Grade III is a complete tear. Severe pain and tenderness, inability to bear weight, and significant joint instability are noted.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Ankle Sprain and Sprains and Strains.

Related Medscape Reference topics:

Ankle Impingement Syndrome

Ankle Sprain

Ankle Taping and Bracing

Related Medscape resources

Resource Center Exercise and Sports Medicine

Resource Center Joint Disorders

Specialty Site Orthopaedics

NextEpidemiologyFrequencyUnited States

Approximately 3600 cases of talofibular ligament injury per 100,000 people are reported per year.

PreviousNextFunctional Anatomy

The lateral articular capsule of the ankle can be divided into anterior and posterior segments. The anterior segment attaches proximally to the anterior portion of the distal tibia superior to the articular surface and to the border of the articular surface of the medial malleolus. The posterior segment attaches distally to the talus just posterior to its superior articular facet and attaches laterally to the depression in the medial surface of the lateral malleolus.[3, 4, 5]

The ATFL is intracapsular and attaches anteriorly to the anterior border of the distal fibula and laterally to the neck of the talus. The PTFL attaches posteriorly to the digital fossa of the fibula and laterally to the lateral tubercle on the posterior portion of the talus.

PreviousNextSport-Specific Biomechanics

The talofibular ligaments along with the CFL are components of the lateral ligament complex. This complex becomes stressed when the ankle is inverted and plantar flexed.[11] Supination of the foot in neutral flexion usually results in injury of the CFL. Supination and adduction injuries tear both the ATFL and the CFL.

The PTFL is the strongest of the lateral ligaments, and extreme inversion with plantar flexion is required to place the PTFL under stress; as a result, the PTFL is less commonly injured.[11] Transient subluxation or dislocation of the talus from the tibial mortise usually results in injury of all 3 lateral ligaments. Prevention of anterior displacement of the talus is primarily a function of the ATFL. Little additional motion occurs when the CFL also is damaged. Instability to inversion is greater when both the CFL and the ATFL are injured than when either ligament is injured alone.

PreviousProceed to Clinical Presentation , Talofibular Ligament Injury

Saturday, February 15, 2014

Groin Injury

Introduction and Frequency

Groin injuries are commonly encountered by physicians and clinicians who treat athletes of all ages at all levels of competition. Groin injuries are particularly common in activities in which forceful adduction of the hip occurs; examples include skating, ice hockey, swimming, and soccer. In fact, as many as 10% of ice hockey–related injuries and 5% of soccer-related injuries are groin injuries.[1, 2] This article focuses on acute and chronic groin injuries related to sporting activities. Groin injuries resulting from major trauma (eg, multiple trauma, penetrating injuries) are not addressed, except to note that they require emergent medical evaluation.

The images shown below illustrate the relevant anatomy of the pelvis relating to groin injuries.

Pelvis, symphyseal aspect. Pelvis, symphyseal aspect. Pelvis, frontal view. Pelvis, frontal view. Pelvis, lateral aspect. Pelvis, lateral aspect.

Give special consideration to children, adolescents, and females with groin pain, because these conditions in this patient population may be erroneously attributed to minor trauma when they are, in fact, serious and require medical or surgical intervention. Evaluate any child aged 2-15 years with groin pain and an antalgic gait, especially if he or she has a fever. Avascular necrosis (AVN) of the hip, Legg-Calve-Perthes disease, septic arthritis, and slipped capital femoral epiphysis must be ruled out.[3] Consider early orthopedic consultation in any such case.

Hip pain in the adolescent athlete must take into consideration the relatively weaker growth plate of certain bony structures in the hip, and it should prompt the clinician to consider the diagnosis of apophyseal avulsion fractures. Apophysitis and apophyseal fractures are more common in skeletally immature athletes, in whom the physis is the weakest link in the muscle – tendon – bone complex.[4] Moreover, remember that children and adolescents may report knee pain that is actually referred from pathology in the hip, or vice versa. That is, complaints of both hip and lower-extremity pain in children and adolescents merit a detailed physical examination of the affected joint and surrounding structures.

The initial evaluation and conservative treatment for adult female athletes may be similar to that of male athletes. However, epidemiologic findings suggest that differences in female body mechanics may lead to subtly different injury patterns and a need for specialized rehabilitation services.[5] Although anatomic differences are obvious, several factors play important roles in determining injury patterns in female athletes. These factors include (1) differences in metabolism, circulation, and cardiorespiratory capacity; and (2) differences in body shape, size, and composition. An example of such is the higher rate of patellofemoral disorders in female athletes, possibly accounted for by an increased quadriceps angle, less developed vastus medialis, and greater degree of genu valgum.[6]

For patient education resources, see the Sports Injury Center, as well as Muscle Strain and Hernia.

Go to Female Athlete Triad, Low Energy Availability in the Female Athlete, and Osteitis Pubis for complete information on these topics.

NextFunctional Anatomy and Sport-Specific Biomechanics

See the following images, which illustrate the relevant anatomy.

Pelvis, symphyseal aspect. Pelvis, symphyseal aspect. Pelvis, frontal view. Pelvis, frontal view. Pelvis, lateral aspect. Pelvis, lateral aspect. Thoracoabdominal and proximal lower-extremity muscThoracoabdominal and proximal lower-extremity musculature.

The hip joint is formed by the femoral head and its articulation with the acetabulum. The femoral neck and its bony prominences, the greater trochanter laterally and the lesser trochanter medially, are the attachment points for the major muscle groups of the hip. The abductor muscles of the hip, the gluteus medius and minimus, and the external rotators of the hip attach to the greater trochanter; the gluteus maximus, the main extensor of the hip joint, along with the hamstrings, attaches to the femur just distal to the greater trochanter. The lesser trochanter is the site of attachment for the iliopsoas muscle, the major hip flexor.[7]

The main blood supply to the femoral head and neck is the medial femoral circumflex artery, a branch of the common femoral artery. Disruption of the blood supply, through direct trauma (fractures of the femoral neck) or through vaso-occlusive disorders (sickle cell crisis), is related to the development of avascular necrosis of the femoral head.

There are approximately 18 bursae located throughout the hip joint. The superficial bursa located over the greater trochanter is a common source of pain as a result of inflammation; the deep bursa, or the gluteus medius bursa, is another common source of hip pain. The deep bursa lies between the gluteus maximus tendon and the posterolateral prominence of the greater trochanter.[7]

The hip is the largest joint in the body. The range of motion of the hip joint is impressive, second only to that of the shoulder joint. This factor, combined with the fact that the hip joint bears weight and is subjected to repetitive stress, makes this joint extremely susceptible to injury. In an Australian study of 29 elite soccer players, Verrall et al suggested that the development of chronic groin injury may be preceded by hip stiffness—that a restricted range of motion of the hip may in fact be a risk factor for this condition.[8] Even minor groin injuries can be difficult to rehabilitate.

Most groin injuries are related to stress and strain on the hip joint and the surrounding bony and muscular support structures of the pelvis. The most common injuries can be divided into acute and chronic injuries. The most common acute injuries are soft-tissue contusions and hematomas that result from direct force. The most common chronic conditions are strains of the muscle–tendon unit.[9]

Acute groin injuries may result from direct trauma encountered in contact sports (eg, football, ice hockey, basketball, rugby, soccer) and noncontact sports (eg, gymnastics). Acute muscle strains are commonly encountered in activities in which forced adduction of the hip occurs (eg, soccer, football, rugby, ice hockey, swimming [particularly with the breaststroke]) or in activities in which forced abduction of the hip occurs (eg, any sporting activity in which the athlete may perform a split, either accidentally or forcefully).

The causes of acute groin injuries may be considered causes of chronic (overuse) injuries. Chronic groin injuries tend to occur in those who participate in activities that promote overuse of the groin area (eg, swimming [particularly the breaststroke], ice hockey, speed and figure skating, soccer, running).

Go to Hip Pointer, Hip Tendonitis and Bursitis and Pediatrics, Sickle Cell Disease for complete information on these topics.

PreviousNextApproach to History Taking and Physical Examination

The approach to the athlete with groin pain can challenge the clinician for a variety of reasons.[10] The description and location of the pain is often vague. The anatomy of the groin can be clinically difficult to define.

The groin consists of the area where the abdomen meets the legs and includes the structures of the perineum. The groin, therefore, includes the following: the lower rectus abdominis musculature, the inguinal region, the symphysis pubis, the upper portions of the adductor muscles of the thigh, and the genitalia, as well as the scrotum in males.

The history and physical examination should be approached systematically to avoid missing the diagnosis. The clinician should assess for the onset of pain and whether the athlete can recall the inciting event, if any. The clinician should discuss factors that aggravate and alleviate pain, especially those pertinent to the sport in which the athlete participates.

The physical assessment requires the exposure of as much of the groin and hip as permitted, and the examination must include the following: inspection for symmetry and anatomic irregularity; palpation of the affected area for deformity; assessment of the range of motion of the articular structures near the area; rotation of the hip joint; observation for discrepancy of leg length; and evaluation of the patient's gait, including the performance of sprints, jumps, and activities that exacerbate the athlete's pain.

The differential diagnosis must take into consideration a number of medical conditions that affect the groin region in all individuals, not solely athletes.[4] These include the following:

Intra-abdominal disorders – Appendicitis, inflammatory bowel diseaseGenitourinary abnormalities – Urinary tract infections; sexually transmitted diseases; gynecologic, scrotal, and testicular abnormalities; nephrolithiasisReferred lumbosacral pain from lumbar disc diseaseHip joint disorders – Osteoarthritis, Legg–Calve–Perthes disease, synovitis, slipped capital femoral epiphysis, osteochondritis desiccans

Because an estimated 27-90% of patients with groin pain have more than one coexisting injury, it is possible for clinicians to diagnose and manage one injury while a second injury goes unrecognized and untreated.[4, 11] The importance of a wide differential diagnosis is clearly evident from such a statistic.

The specific historical and physical examination findings germane to specific groin injuries will be discussed in the sections that follow. The patterns of pain described by patients, however, suggest types of pathologic processes at and around the hip joint. Pain that is aggravated by use and alleviated with rest suggests a structural problem, such as that encountered with osteoarthritis. Constant pain suggests an infectious, inflammatory, or neoplastic process.[7]

Go to Urinary Tract Infection in Females and Urinary Tract Infection in Males for complete information on these topics.

PreviousNextClinically Encountered Groin InjuriesImpact injuries

Impact injuries, such as those that occur during football, hockey, or other contact sports that produce high-speed collisions, usually result in contusions. However, such injuries may cause fractures of the pelvis (iliac wing); they may exacerbate previously asymptomatic inguinal hernias; and, in rare cases, they may produce bladder, testicular, or even urethral (straddle) injuries.

Any patient with lower abdominal or pelvic impact injury that causes severe groin pain, loss of function, or blood in the urine should be immediately evaluated by a physician. Findings from anteroposterior radiographs of the pelvis, hip images, and dipstick urinalysis are usually sufficient to rule out a serious acute injury. If no bony injury is discovered, conservative measures, namely, rest, application of ice for the first 24-48 hours, compression, and nonsteroidal anti-inflammatory drugs (NSAIDs), may be implemented. A urologist should also evaluate the patient for hematuria.

Hip pointer

The hip pointer encompasses both impact and strain injuries of the hip. Forced extension of the hip may result in a sprain or avulsion of the sartorius muscle at its attachment to the iliac crest. These injuries are severely painful and difficult to rehabilitate. Contusions to the anterior superior iliac crest may involve the attachment of the sartorius muscle as well as the lateral femoral cutaneous nerve, causing pain and paresthesias to radiate down the lateral aspect of the thigh. In some of these cases, especially those in which trochanteric bursitis is suspected, a local anesthetic or steroid injections may be given (at the physician's discretion) to treat severe pain.[12]

Groin pull

Acute strain injuries of the groin are epitomized by the groin pull. Multiple muscles, including the iliopsoas muscle, the adductor group, and the gracilis muscle, attach to the medial portion of the femur or pubis and help keep the legs together and flex the thigh. Falling, running, and quickly changing directions, as well as kicking or doing the splits (either intentionally or otherwise) can result in these injuries. Groin pulls can cause pain in the groin that radiates down the inside of the thigh.

The injury is usually focused at the musculotendinous junction and involves disruption of the fibers to various degrees and, occasionally, hematoma formation, which may delay healing. These weakened areas are repaired by fibroblasts, but they continue to be susceptible to repeat injury for a long time.[5] In fact, in a review of 1292 National Hockey League players, those with a previous groin injury had twice the risk of repeat injuries as that of athletes without a previous injury.[13] Furthermore, veteran hockey players had an injury rate 5 times greater than that of rookie players.[13]

In another review, the National Hockey League statistics revealed that adductor strains occurred 20 times more frequently during training camp than during the regular season, possibly related to the benefits of a strength-training program and to the fact that off-season deconditioning may contribute to these injuries.[4]

Sometimes, the relevant muscles may actually tear loose from their bony attachments, taking a piece of the bone with it. If these avulsion fractures are severely displaced, surgical repair may be required. Most groin pulls eventually respond to conservative treatment that consists of rest, the application of ice, compression, and the use of NSAIDs. These injuries may be adequately managed by the team physician or trainer.

Injuries of the muscle–tendon units

Several muscle–tendon units are commonly strained and injured in athletes. The muscle most commonly strained and injured in the abdomen and groin is the adductor longus muscle.[9] Other muscle–tendon units that must be considered include the rectus femoris, the rectus abdominis, the sartorius, the gracilis, and the iliopsoas.

The rectus abdominis strain is an injury that may cause acute or chronic groin pain. This strain results from injury to the rectus muscle of the abdominal wall, which attaches to the pubis. This injury is fairly common in skaters, hockey players, and swimmers (especially breaststrokers). Severe tears and sprains of the rectus muscle are slow to recover; they may result in significant hematoma formation; and, on rare occasions, they may require surgical repair or reinforcement.[14]

Strain of the adductor longus may be managed in a variety of ways, depending on the location of the injury. Physical examination may reveal whether the injury lies within the muscle belly or within the tenoperiosteal attachment. Injuries to the muscle belly are best managed with gentle stretching, strengthening, and liberal return to activity. Injuries to the tenoperiosteal attachment require more conservative management: rest until the patient is pain free; gentle stretching and strengthening over a period of weeks; running and sprinting; and, lastly, running and sprinting combined with rapid changes in direction.[15]

Hernias

Hernias of the abdominal wall must be considered in patients who present with abdominal or groin pain. Hernia pain can be confused with pain due to chronic conditions encountered in a variety of sporting activities. Therefore, hernias represent a pathologic process that is frequently overlooked in the athlete. In fact, only 8% of patients with abdominal or inguinal hernias had detectible hernias on physical examination.[9] Therefore, a high index of suspicion is recommended when evaluating patients with groin or abdominal pain, and a hernia must be considered in the differential diagnosis. Herniography depicts a disorder in 84% of patients, and more importantly, 50% of these patients with abdominal wall defects do not have pain.[9]

Treatment for hernias is conservative and includes rest; the application of ice; gentle range-of-motion exercises; and, ultimately, surgical repair with mesh reinforcement of the abdominal wall (in more serious conditions). In comparing the recovery times for patients after hernia repair, Stoker and colleagues cited differences when open surgical repair was compared with laparoscopic repair. The authors suggested that full recovery may require as long as 2-3 weeks in patients with open surgical repair, whereas patients who undergo laparoscopic repair are more likely to resume participation in 1 week.[16]

Sportsman's hernia

The sportsman's hernia, or Gilmore groin, was first described by O.J. Gilmore in 1980.[17] It is a syndrome characterized by chronic groin pain that is associated with a dilated superficial inguinal ring, although the exact cause of this injury is largely speculative and likely multifactorial.[4] The true incidence of sportsman's hernia remains controversial; some authors believe it is only a rare cause of groin pain in athletes, but others believe it is the most common cause of chronic groin pain.[4]

The term "sportsman's hernia" is a misnomer, however, as there is typically no demonstrable hernia or defect in the groin or the abdominal wall. The definition of the sportsman's hernia, therefore, is any condition that causes persistent unilateral pain in the groin without a demonstrable hernia.[18]

The classic operative findings include laddering of the external oblique in conjunction with separation of the conjoint tendon from the ligament and laxity of the transversalis fascia.[19] Other studies have suggested abnormalities with the rectus abdominis insertion, avulsions of the internal oblique muscle fibers at the pubic tubercle, or entrapment of the ilioinguinal or genitofemoral nerves.[20]

Historically, the pain is described as chronic, located near the pubic tubercle, maximal on the evening of vigorous exercise or on the morning afterward, and exacerbated by activities that increase the intra-abdominal pressure. It is believed that sportsman's hernias are the result of chronic, repetitive trauma or stress to the musculotendinous portions of the groin, the pain of which develops insidiously, rather than acutely or dramatically. The sportsman's hernia is more commonly encountered in male than female athletes, and predictors of the development of groin injuries observed in professional hockey players included previous injury, nonaggressive conditioning in the off-season, and veteran, or older, players.[18]

On digital examination, the superficial inguinal ring is dilated. Evidence of herniation may or may not be palpable. The point of most tenderness is often the ipsilateral pubic tubercle. Pain can be elicited with a Valsalva maneuver or a resisted sit-up. Examination of the hip joint and evaluation of the athlete's gait typically reveal weakness with adduction.

Conservative therapies may temporarily alleviate the patient's pain, but definitive surgical management is recommended. Over 9 years, Gilmore repaired 360 injuries with a technique that used 6-layered reinforcement of the weakened transversalis fascia. Approximately 97% of his patients returned to competitive sports by the 10th week after postoperative care.[19] When conservative therapy does not result in alleviation of symptoms, surgical exploration is indicated, and placement of prosthetic meshes or patches, with or without neurectomy or ablation of the ilioinguinal nerve, has demonstrated success.[18]

Hip fracture or dislocation

The most severe and potentially debilitating groin injury is the hip fracture or dislocation. This injury normally results from a violent or high-speed collision or fall, for example, in skiing or playing hockey. The pain is usually severe and associated with an inability to bear weight and with a shortening and rotation of one leg inward or outward. Other severe injuries may be associated with the amount of force required to fracture or dislocate a hip. Immobilization and immediate medical attention and reduction (within the first few hours) are required to maximize the potential for recovery.

Stress fractures

Stress fractures of the femoral neck and the pubic ramus are the 2 most common stress fractures of the groin region.[21] Stress fractures are caused by repetitive minor trauma to the bones or muscular attachments. Therefore, these injuries are categorized somewhere between acute injuries and chronic injuries. Most stress fractures occur secondary to running (eg, in joggers or military recruits), although additional risk factors include relative osteoporosis in young female athletes secondary to nutritional or hormonal imbalances, muscle fatigue, changes in foot gear and training, or changes in intensity and/or duration of training.[21]

Stress fractures in the groin or hip can be difficult to diagnose and treat; these injuries most commonly occur at the femoral neck and inferior pubic ramus.

Femoral neck stress fractures are especially troublesome because they may lead to AVN of the femoral head and long-term disability. These may appear as a cortical irregularity or haziness on plain radiographs, but a magnetic resonance image (MRI) or a bone scan is usually required for the definitive diagnosis. The treatment is conservative, and recovery, although usually complete, may take months, especially if the athlete's activity is not significantly curtailed.

Avulsion fractures

Avulsion fractures of the hip must be considered in young athletes who give a history of severe, sudden-onset, and well-localized pain over a bony prominence. The relative weakness of the apophysis of the adolescent skeleton predisposes the young athlete to a variety of avulsion fractures. Examples include the following: avulsion of the anterior inferior iliac spine due to forceful flexion of the hip by the rectus femoris, avulsion of the ischial tuberosity by the hamstrings, and avulsion of the anterior superior iliac spine caused by the sartorius muscle.

Management for the majority of avulsion fractures is conservative and typically includes rest and gradual return to activity, aided by the use of analgesics.[22] Controversy exists regarding the management of avulsion fractures of the ischial tuberosity. Some authors advocate nonsurgical management. However, others have reported deficits in strength; function; and, in some cases, the formation of a painful callus, which prompts their advocacy of early surgical repair.[5] Depending on the size and amount of displacement of the fracture fragment, the injury may warrant surgical repair; this decision must be left to the judgment of the clinician.

AVN of the femoral head

AVN of the femoral head is a progressively debilitating condition that most often affects individuals in their third or fourth decade of life. An estimated 10,000-20,000 cases occur annually, at a mean age of 34 years. Although the pathogenesis is largely unclear, disruption of the circulatory supply to the femoral head either acutely or chronically results in cell destruction and necrosis, leading to collapse of the bony framework of the joint and resulting in arthritis.[21]

Risk factors for the development of AVN include high loads, sudden or irregular impact, and preexisting abnormalities such as dysplasia of the hip.[23] Tears of the labrum have been associated with developmental dysplasia[21] and early osteoarthritis and AVN.[23]

Ninety percent of cases of nontraumatic AVN are associated with systemic corticosteroid use for the management of asthma, chronic obstructive pulmonary disease, or autoimmune disorders. Heavy alcohol consumption has also been associated with the development of AVN.[21]

The diagnosis of AVN first begins with a high index of suspicion and radiographic confirmation of the lesion. Plain radiography may not demonstrate AVN until 3 months after the initial insult; therefore, MRI is the imaging modality of choice for identifying early AVN. MRI is both sensitive and specific (88-100%).[21]

Management includes rest, restricted weight bearing, and symptom control, although studies have demonstrated discrepancies between conservative management and early surgical core decompression.[21]

Osteitis pubis

Osteitis pubis (gracilis syndrome) is a chronic injury that causes resorption of the bone or cartilage of the pubic symphysis due to repetitive stress from kicking, lifting, running, or jumping. Osteitis pubis manifests as pain and tenderness in the region of the pubic symphysis. This injury is believed to be secondary to shearing and/or rotational movement of the pubic symphysis, and it is usually more severe when it occurs in postpartum women, in whom the injury results from the normal laxity of the pelvic ligaments during pregnancy that may persist for some time after delivery.

The patient's history reveals pain, most commonly during or after kicking. Physical examination reveals tenderness over the symphysis pubis. The pain in osteitis pubis results from limited rotation of the hip that transfers stress by shearing or by distraction across the symphysis and disrupts the joint.

Most cases of osteitis pubis are self-limited, and whether the cessation of activity or continued activity delays recovery is unclear. Most authors recommend continued flexibility training and muscle-strengthening exercises during the recovery phase of the injury. Groin support with neoprene shorts may provide some comfort.

Therapy with analgesics may be recommended. The use of corticosteroids is controversial; because corticosteroids are catabolic, some believe that their use may loosen the symphysis and result in a lack of integrity of the structure.[15] One case series, however, demonstrated a benefit when corticosteroids were used in athletes whose symptoms were 2 weeks or less in duration, whereas athletes whose symptoms lasted greater than 16 weeks required an additional 11-16 weeks for symptomatic improvement.[21]

Recovery usually occurs over 2-3 months because of the relatively poor circulation to the region. Some authors note that the average healing time for osteitis pubis is 9-10 months, although most cases are self-limited.[21]

Bursitis

The last chronic or repetitive stress injury is bursitis. The body has special fluid-filled sacs called bursae, which provide lubrication in needed areas, such as the points where muscles move over bony projections. Bursae can become inflamed and irritated, resulting in pain when the overlying muscle is used. Subtle alterations in gait or gait impairment can increase the friction transmitted to the bursal sac. The result of increased friction is thickening of the normally thin bursa wall, leading to fibrosis and a gradual inability to lubricate the outer hip. Lateral hip pain that is aggravated by direct pressure is the classic pattern associated with trochanteric bursitis.[7]

The treatment is conservative, with most cases responding to NSAIDs and rest or to corticosteroid injections, used at the discretion of a physician. Persistent and recurrent bursitis may be due to rheumatic or arthritic disease or gout, which requires special medical treatment.

Meralgia paresthetica

Lateral hip pain accompanied by paresthesias or hyperesthesia is the presentation of lateral femoral cutaneous syndrome, or meralgia paresthetica. Pain that accompanies this disorder is described as a burning or an uncomfortable, heightened sensation.[7] The localized area of pain or hyperesthesia is not affected by direct pressure, movement of the hip joint, or movement of the lower back.

The lateral femoral cutaneous nerve is a pure sensory nerve whose path from the lumbosacral nerve plexus through the abdominal cavity and into the subcutaneous tissue of the thigh renders it susceptible to compression. The result of this compression is a localized area of hyperesthesia or paresthesia, in contrast to sciatica, a condition in which pain extends over a much wider area and extends down the leg and into the foot.[7]

Femoroacetabular impingement

Femoroacetabular impingement (FAI), or hip impingement, has become an increasingly recognized cause of hip pain in adolescents, adults, and athletes. It is believed to result from abnormal contact stress and joint damage around the hip, most notably from prolonged sitting, leaning forward, getting in and out of a vehicle, or performing a pivoting motion in sports. Clinically, pain may be described as either insidious or acute in onset. The clinical evaluation tool most sensitive for FAI is the flexion, adduction, and internal rotation (FADIR) test and reproduces the patient's pain along the anterolateral hip.[24]

Physiologically, it is believed to result from a bony deformity or spatial malorientation of the femoral head or the head/neck junction, acetabulum, or both.[25]

Evidence demonstrates that FAI may initiate osteoarthritis of the hip. Plain radiographic evaluation of the hip (anteroposterior pelvis and frog-leg lateral radiographs) may demonstrate pincer-type FAI, cam lesions, and osteophytes on the anterior femoral neck.[24] Arthroscopic evaluation demonstrates labral tears and acetabular cartilage lesions. It is believed that clinical and radiographic characteristics--namely, male sex, older age, Tonnis osteoarthritis grade, and elevated alpha angle--are associated with more severe intra-articular hip disease observed on arthroscopic evaluation, suggesting these characteristics may serve a predictive function in the evaluation of FAI.[26] Patients with more severe osteoarthritic changes demonstrated radiographically and patients with more severe cartilage damage observed intraoperatively are believed to have worse outcomes with treatment for FAI.[27]

Currently the mainstays of nonoperative treatment for FAI include occupational and physical therapy, restriction of activities that cause pain, core strengthening, and nonsteroidal anti-inflammatory drugs. Surgical treatment, including surgical dislocation of the hip, arthroscopy, periacetabular and rotational osteotomies, and combined hip arthroscopy with limited open exposure, may be necessary to allow full return to activity. There is, however, no long-term prospective data to determine which therapeutic modality offers the most definitive result.[28]

Other injuries

Injuries to the groin that do not involve the bones or musculature are usually the result of a direct impact. All of the soft-tissue structures of the groin are susceptible to these types of injury. Injury to the genitalia (eg, penis, testis, urethra) or bladder, or traumatic inguinal or femoral herniation may occur. Reasons to suspect these injuries include blood in the urine; severe abdominal pain and tenderness (in the event of a bladder injury); persistent nausea, vomiting, or abdominal distention; and swelling in the femoral triangle or inguinal area (in the event of a hernia). All of these symptoms merit immediate medical evaluation in a hospital setting.

PreviousNextDiagnostic Tests

Plain radiography, technetium-99 (99 Tc) methylene diphosphonate (MDP) bone scanning, ultrasonography, nerve conduction studies, peritoneal radiography, computed tomography (CT) scanning, and MRI may be useful in the diagnosis of groin injuries.

Plain radiographs may show established osteitis pubis, a stress fracture (later stages), osteomyelitis (later stages), a slipped femoral epiphysis (epiphysiolysis), or osteoarthritis. Plain radiographs are useful in demonstrating the presence of hip abnormalities; one study found that 72% of male and 50% of female athletes evaluated with plain radiography demonstrated some evidence of radiographic hip abnormality, such as cam and pincer lesions associated with femoroacetabular impingement.[31]

A99m Tc-MDP bone scan may show osteitis pubis, a stress fracture, osteomyelitis, synovitis (occasionally bursitis), sacroiliitis, a tenoperiosteal lesion, or a muscle tear.

Ultrasonograms may show a muscle tear, hematoma, inguinal hernia, or bursitis (occasionally). Dynamic evaluation of the anatomic structures in the groin area through ultrasonography adds a significant amount of information to the imaging diagnosis, most notably in the evaluation of groin hernias.[32]

Nerve conduction studies may show ilioinguinal neuropathy or obturator neuropathy.

Peritoneal radiographs may show any inguinal hernia.

CT scans and MRIs may show AVN of the femoral head, disc pathology, radicular lesions, osteitis pubis, and other bone and soft-tissue injuries, as mentioned above. MRI with gadolinium has proven to be extremely valuable in the diagnosis of radiographically occult osseous abnormalities as well as soft tissue injuries like pubalgia, musculotendinous abnormalities, and bursitis.[33] MRI has been found to be 98% sensitive and 89-100% specific for injuries that involve the rectus abdominis, adductor tendon origins, and articular disease of the pubic symphysis.[33] Magnetic resonance arthrography (MRA) in the evaluation of intra-articular hip pain has been shown to be the best imaging modality for assessment of labral pathology (acetabular labral tears).[33]

Previous, Groin Injury

Tuesday, February 11, 2014

Hamstring Injury

Background

This article focuses on injuries to the hamstring muscles. The word "hamstrings" was derived from the fact that it is these muscles by which a butcher would hang a slaughtered pig.

The hamstrings are a group of muscles (ie, semimembranosus, semitendinosus, biceps femoris) located on the back of the upper leg.[1, 2] The hamstrings are a common source of injury and chronic pain in athletes. Injuries to the hamstring muscles primarily occur proximally and laterally, and they usually involve the biceps femoris. The severity of injury to the hamstring muscles is classified according to the following grades:

Grade 1 is a mild strain, with few muscle fibers being torn.Grade 2 is a moderate strain, with a definite loss in strength.Grade 3 is a complete tear of the hamstrings.

Hamstring injuries almost always occur at the proximal myotendinous junction. In the biceps femoris, this junction extends over most of its entire length. Injury usually does not occur within the tendon itself unless there is preexisting pathology.

Bony avulsion at the ischial origin may occur as well, but this is usually associated with sudden, large-force, hip-flexion injuries.[3] Avulsions are commonly seen in individuals who have been involved in waterskiing accidents in which the knee is extended and the hip is suddenly flexed as the skier falls forward.[4]

One study involving 47 football players with hamstring injuries reported an average of 14 days of convalescence before return to play.

For patient education resources, see the Sports Injury Center, Sprains and Strains Center, and Foot, Ankle, Knee, and Hip Center, as well as Muscle Strain and Ruptured Tendon.

Related Medscape topics:

Resource Center Adolescent Medicine

Resource Center Exercise and Sports Medicine

Resource Center Joint Disorders

Resource Center Trauma

Specialty Site Orthopaedics

NextEpidemiologyFrequencyUnited States

As a percentage of lower-extremity injuries, hamstring injuries peak at 33% in persons aged 16-25 years, and they most often occur in sports in which the hamstrings can be stretched eccentrically at high speed.[5, 6, 7, 8, 9, 10] Prime examples of such sporting activities include sprinting, track and field, and other running contact sports, such as football and soccer. Recreational sports such as waterskiing, in which the knee is fully extended during injury, are also common causes of hamstring injuries.[4] One study analyzed data from the National Football League’s Injury Surveillance System and found that a high percentage of hamstring injuries occur in the preseason. Over the 10-year study period, 1716 hamstring strains were noted, with slightly more than 50% occurring during the preseason. Players on the special teams units as well as wide receivers and defensive secondary were found to have an elevated risk for injury.[11]

International

An Australian study involving 1614 individuals with hamstring injuries revealed that such injuries compose 54% of the injuries in rugby, 10% of the injuries in soccer, 14% of the injuries in track, and less than 2% of the injuries in tennis, squash, ballet, and gymnastics.

PreviousNextFunctional Anatomy

The hamstrings are composed of 3 muscles, as follows:

Biceps femoris muscle (long head and short head)Semimembranosus muscleSemitendinosus muscleOrigins and insertions

All of the muscles of the hamstrings originate on the ischial tuberosity. The second head of the biceps femoris (ie, short head) originates medial to the linea aspera on the distal posterior femur.

The short head of the biceps femoris crosses only one joint to insert with the long head of the biceps femoris onto the fibular head and lateral tibial condyle.

The other hamstring muscles cross 2 joints to reach their insertions. The semitendinosus muscle forms the pes anserinus with the sartorius and gracilis tendons to insert on the medial tibial metaphysis. The semimembranosus muscle interweaves with the fibers of the semitendinosus to eventually insert onto the posteromedial tibial condyle.

Innervations

The short head of the biceps femoris muscle is also unique in that it is innervated by the peroneal portion of the sciatic nerve, whereas the long head of the biceps femoris, semimembranosus, and semitendinosus are innervated by the tibial portion of the sciatic nerve.

PreviousNextSport-Specific Biomechanics

In track and field events in which the hamstring is eccentrically contracted, the risk of a hamstring injury can be high. Contact sports such as football can result in contusions of the hamstring muscle.[12, 13] The contusion is superficial when the muscle is contracted on impact, and it is deep when the muscle is relaxed on impact. Waterskiing accidents have an association with proximal, bony avulsions because the individual's knee is extended when the hip undergoes a violent, forceful flexion as he/she falls forward.

Related Medscape topics:

Resource Center Exercise and Sports Medicine

Resource Center Trauma

Specialty Site Orthopaedics

PreviousProceed to Clinical Presentation , Hamstring Injury

Sunday, February 9, 2014

Quadriceps Injury

Background

Several types of quadriceps injuries can occur, the most common being the quadriceps contusion, which is painful and disabling. The usual cause of the quadriceps contusion is a direct blow to the anterior thigh from an object or another person (eg, helmet, knee). Very rarely, this injury can be severe enough to progress to an acute compartment syndrome.

Because the quadriceps is in contact with the femur throughout its length, it is susceptible to compression forces. The rectus femoris is the most commonly injured portion of the muscle because of its anterior location. Minimally, impact causes cellular edema of the muscle, but complete capillary disruption with localized hemorrhage leading to a tense anterior compartment can occur. The muscle is more resistant to injury if it is struck while in a contracted nonfatigued state. Other quadriceps injuries range from simple strains to more complex and disabling muscle ruptures. See the image below.

Modified treatment of quadriceps contusion. Used wModified treatment of quadriceps contusion. Used with permission courtesy of John Aronen, MD.

Other types of quadriceps injuries include strains of the quadriceps tendon, complete and partial tears of the quadriceps tendon, and fascial rupture of the quadriceps muscle. Specific areas of the quadriceps are affected for each of these diagnoses. The classic quadriceps strain occurs at the conjoined muscle tendon junction (jumper's knee). The partial tear of the quadriceps most commonly affects the indirect (distal) head of the rectus femoris. Fascial rupture usually occurs anteriorly at the mid thigh and causes a muscle hernia.

NextEpidemiologyFrequencyUnited States

Although quadriceps strains are common, minimal information about the frequency with respect to specific sports is available. As for quadriceps contusions, the most detailed frequency data came from the US Military Academy at West Point,[1] and the distribution per year was reported as follows: rugby 4.7%, karate and judo 2.3%, football 1.6%, and all other sports fewer than 1%. Quadriceps muscle hernias are believed to be more common in soccer, basketball, and rugby.

The incidence of jumper's knee at the quadriceps insertion onto the patella is less common than patellar tendinitis. One study reported that of all tendinopathies affecting the extensor mechanism, the frequency of patellar tendinitis at its insertion was 65%, quadriceps tendinitis was 25%, and patellar tendinitis at its insertion into the tibial tuberosity was 10%.

Rupture of the quadriceps tendon is more common in both older patients and younger athletes. Several studies show that the mean age of patients with quadriceps rupture is about 65 years. However, in athletes, the mean age cited ranges from 15 to 30 years. Sports associated with quadriceps rupture are high jump, basketball, and weight lifting. Rupture is also not uncommon in patients with renal failure.

PreviousNextFunctional Anatomy

The quadriceps femoris acts as a hip flexor and knee extender. The quadriceps femoris is composed of the following:

Rectus femorisVastus lateralisVastus medialisVastus interomedialis

Origins/insertions of quadriceps components include the following:

Rectus femoris - Ilium/tibial tuberosityVastus lateralis - Femur/tibial tuberosityVastus medialis - Femur/tibial tuberosityVastus interomedialis - Femur/tibial tuberosity

The 3 thigh compartments are as follows:

Anterior - Quadriceps muscles, femoral nerve and arteryPosterior - Hamstring muscles, sciatic nerveMedial - Adductor muscles, cutaneous branch of obturator nervePreviousNextSport-Specific Biomechanics

The function of the quadriceps is primarily that of tibial (knee) extension. One electromyography (EMG) study showed that the maximum extension moment and maximum quadriceps EMG activity were early in the kicking action, as the initial flexion changes to extension. This moment occurs before the foot makes contact with the ball. The peak activity of the hamstring occurs after the quadriceps peak, shortly before the ball is struck. The largest extension moment in this study was 260 Nm; this corresponds to a calculated tensile force in the patellar tendon of 7 times body weight.

The mechanical properties of the quadriceps have been studied. The central aspect of 10-mm wide sections of the quadriceps was subjected to tensile loading and compared to a similar patellar tendon section. The ultimate load to failure of the unconditioned patellar tendon was higher (53.4 N/mm2) than the unconditioned quadriceps tendon (33.6 N/mm2). Strain at failure was also higher for the preconditioned patellar tendon (14.4%) than for the quadriceps tendon (11.2%).

Microscopic sections of human quadriceps tendon as it inserts into the patella show no crimping and no cement line. This is unlike other tendon insertion sites. The interdigitation between collagen fibers and the distinction between tendon and bone was least distinct along the anterior third of the patella.

A discussion of the biomechanics of specific injuries is as follows:

Strains, overuse, and rupture: The most common sites of injury correlate to the muscle tendon junctions both proximally and distally and to the muscle belly itself. Muscle strains are usually due to repetitive functional overload. Not surprisingly, quadriceps strains most commonly affect athletes who subject their knees to high levels of repeated loading of the extensor mechanism. The overuse trauma may range from microscopic failure of soft tissue with its associated inflammation or gross rupture. Gross rupture may be partial or complete. A large sudden load may cause the entire insertion to be compromised, leading to complete rupture. Repetitive loading, particularly eccentric loads, causes microfailure, usually at the muscle tendon junction. This microfailure can result in partial tears. Contusion: Direct trauma to the quadriceps may cause muscle fiber and connective tissue rupture and formation of a hematoma. Trauma to the quadriceps causes muscle fiber rupture, disruption of connective tissue, and hematoma formation. Inflammatory cells and macrophages enter the site of injury and begin clearing necrotic muscle cells. This process occurs over 2-3 days. Then, muscle cells attempt to regenerate at the same time scar tissue is being formed. A severe thigh contusion can lead to a compartment syndrome. Muscle hernia: The cause of this is not clear. It is usually associated with a sudden forceful kick, but it may be associated with a weakened or previously injured quadriceps fascia. PreviousProceed to Clinical Presentation , Quadriceps Injury

Saturday, February 8, 2014

Rotator Cuff Injury

Background

Rotator cuff injuries are a common cause of shoulder pain in people of all age groups. They represent a spectrum of disease, ranging from acute reversible tendinitis to massive tears involving the supraspinatus, infraspinatus, and subscapularis. Diagnosis is usually made through detailed history, physical examination, and often, imaging studies.[1, 2, 3, 4, 5]

A normal rotator cuff and rotator cuff tear are shown below.

Rotator cuff, normal anatomy. Rotator cuff, normal anatomy. Rotator cuff tear, anterior view. Rotator cuff tear, anterior view.

Often, younger individuals with rotator cuff injuries relate a history of repetitive overhead activities involving the rotator cuff or, less commonly, a history of trauma preceding clinical onset of symptoms. In contrast, older individuals usually present with a gradual onset of shoulder pain and, ultimately, after radiographic testing is shown to have significant partial or full rotator cuff tears without a clear history of predisposing trauma. Nonoperative or conservative treatment is usually sufficient to heal the problem in the vast majority of individuals, with a few exceptions that are discussed.[1, 2, 3, 4, 5]

For excellent patient education resources, see eMedicineHealth's patient education articles Rotator Cuff Injury and Shoulder and Neck Pain.

NextEpidemiologyFrequencyUnited States

The frequency of full-thickness rotator cuff tears ranges from 5-40%, with an increasing incidence of cuff pathology in advanced age. Cadaveric studies by Bigliani et al found that 39% of individuals older than 60 years had full-thickness rotator cuff tears with an even higher incidence of partial tears.[6]

PreviousNextFunctional AnatomyNormal shoulder motion

The shoulder complex is comprised of several joints, including the sternoclavicular joint, acromioclavicular joint, glenohumeral (GH) joint, and scapulothoracic (ST) joint or pseudoarticulation. These articulations work together to carry out normal shoulder motion. The majority of motion occurs at the GH and ST joints. A rhythm between these 2 areas of motion has been described.[1, 3, 7, 8, 9, 10, 11, 12]

The GH–to–ST motion ratio of total shoulder motion is 2:1 (ie, 180° of abduction, consisting of 120° of GH motion and 60° of ST motion). The 2:1 ratio is an average over the entire arc of motion. This ratio changes through the arc of motion (ie, the 2:1 ratio is not constant throughout the entire range of motion [ROM]). In the initial portion of abduction, GH motion predominates and the ratio is 4:1 (GH:ST). As the shoulder moves above 90° of abduction, this ratio becomes 1:1° GH to 1° ST motion.

The importance of the scapula in normal shoulder motion cannot be overstated. The scapula, with the glenoid as its contact point, forms the platform for humeral head articulation and motion. A stable platform is essential for normal shoulder biomechanics in everyday activities and is crucial for high-demand activities (eg, overhead sports or work).[13]

The scapula must glide along the chest wall as it protracts and retracts during normal shoulder movements. Scapular winging results in glenoid antetilting, which results in functional elevation of the humeral head and impingement of the rotator cuff. In addition, without scapular motion, the origin and insertion of the deltoid approximate each other, resulting in a decreased optimal length-tension relationship and a decrease in force as the shoulder abducts. Normal scapular motion allows the deltoid to maintain its length-tension relationship and generate adequate force.

Stabilizers of the shoulder

The shoulder is considered a ball-in-socket joint, although the glenoid fossa is flat. In addition, the surface area of the glenoid is much smaller than that of the contacting humeral head (25-30%). The cartilaginous labrum provides much of the socket function and increases the surface area of contact for the humeral head.

Together, these components provide a great amount of shoulder mobility with limited stability. Shoulder stabilizers can be grossly categorized as static or dynamic. Dynamic stabilizers require an intact neuromuscular system to function, whereas static stabilizers help maintain congruity.

The static stabilizers have been studied well in cadaver specimens to understand their stabilizing effects. Static stabilizers continue to function in the setting of neurologic or intrinsic muscle pathology in conditions such as hemiplegia, spinal cord injury, brachial plexus injury, suprascapular nerve injury, and myopathies. This is not true for the dynamic stabilizers (eg, rotator cuff muscles). With neuromuscular injury or intrinsic muscle damage, the dynamic stabilizers lose their ability to exert dynamic motor control of the humeral head, ultimately leading to GH laxity and shoulder pain.

Static stabilizers

Static stabilizers include the bony structures, labrum, GH ligaments, and joint capsule. Unlike the hip joint, the bony articulation of the shoulder offers little stability. This is due to the limited contact area of the glenoid with the humeral head, flattened architecture, and retroverted positioning. The labrum is a fibrous structure that attaches to the glenoid to increase the contact area and deepen the socket of the glenoid up to 50%, forming a concave surface. Three GH ligaments exist, as follows: superior, middle, and inferior. The inferior GH ligament is the most important for shoulder stability and has 3 components, anterior, inferior, and posterior, therefore, it is more appropriately referred to as the inferior GH complex.

Dynamic stabilizers

Dynamic stabilizers[14] include the rotator and scapular stabilizers (ie, teres major, rhomboids, serratus anterior, trapezius, levator scapula). The rotator cuff is composed of 4 muscles: the supraspinatus, infraspinatus, subscapularis, and teres minor. The supraspinatus is the principal supporting and kinetic muscle of the shoulder. The primary function of the rotator cuff muscles is to stabilize the GH joint so that the larger shoulder movers (eg, deltoid, latissimus dorsi) can carry out their function without significant motion of the humeral head on the glenoid. Increased movement results in shearing forces across the joint (to the labrum, in particular) and may result in humeral head migration and impingement upon the rotator cuff muscles and tendons.

The rotator cuff muscles are associated and assist with some shoulder motion; however, their main function is to provide stability to the joint by compressing the humeral head on the glenoid. The supraspinatus assists in shoulder abduction by maintaining the humeral head centered on the glenoid, with the middle deltoid acting as the primary mover. These muscles act as force couples, because they work synergistically to carry out a particular movement.

Electromyography (EMG) studies have demonstrated a high degree of supraspinatus activity during the initial 30° of abduction. This has been misinterpreted to imply that the supraspinatus initiates shoulder abduction and acts to abduct the shoulder in the first 30°. In actuality, the supraspinatus fires to stabilize the GH joint as the deltoid abducts the arm.[15, 16, 17, 18, 19]

Increased EMG activity in the supraspinatus during the initial 30° is a reflection of increased firing requirements of this muscle to stabilize the GH joint as the deltoid is activated. The infraspinatus and teres minor muscles assist in external rotation of the shoulder and also provide an inferior pull upon the humeral head, assisting in its centering during overhead activity. The subscapularis muscle participates in this centering but also acts with the pectoralis muscles and latissimus dorsi as an internal rotator of the shoulder, serving as the main internal rotators of the shoulder.

Weakness or insufficiency of the rotator cuff muscles results in increasing demands on the static stabilizers. If these demands are long term or recurrent, static stabilizers may begin to fail. This can result in stretching or attenuation of the capsule, which results in even greater shoulder laxity and greater demands on the already weak rotator cuff muscles. Humeral head migration may occur with capsule laxity and result in rotator cuff impingement and pain. Pain may inhibit rotator cuff muscle firing, leading to disuse and further weakening of the dynamic stabilizers with greater demands placed on the static stabilizers.

Increased humeral head translation can also lead to shearing and injury to the glenoid labrum. Rotator cuff impingement, tendinitis, and labral pathology are commonly encountered injury patterns in athletes and workers who perform overhead motions. Focusing solely on the static stabilizers in treatment neglects the dynamic structures that probably initiate and perpetuate the cycle.

PreviousNextSport-Specific Biomechanics

A similar type of motion is involved in a number of overhead sports activities (eg, serving in tennis, spiking in volleyball, throwing a football or baseball). The baseball throwing motion has been studied in detail and can be divided into 5 stages.

Stage 1 is the wind-up phase. EMG studies have determined that the rotator cuff muscles are inactive during this initial stage.Stage 2 is the early cocking stage and involves shoulder external rotation and abduction supplied primarily by the deltoid.Stage 3 is the late cocking stage, which continues until maximal external rotation is achieved. The rotator cuff muscles are very active during this stage, especially the subscapularis, which eccentrically contracts and acts as a dynamic stabilizer. Stage 4 is the acceleration stage, which begins with internal rotation of the humerus and ends with release of the baseball. During this phase, the pectoralis major and the latissimus dorsi are very active, whereas the muscles of the rotator cuff are inactive. Stage 5 is the follow-through of the baseball pitch, where deceleration takes place. During this phase, the rotator cuff muscles and the posterior deltoid are most active. The supraspinatus eccentrically contracts to decelerate internal rotation of the limb.

Proper balance between the concentrically contracting muscles that generate force and the eccentrically contracting muscles that control movement is important. Imbalance between these opposing muscle groups results in overuse of muscles and, ultimately, overuse injuries of the shoulder. Note that a great deal of the force generated in overhead sports occurs in the trunk and lower extremity, and these areas should be targeted in any conditioning program for athletes who throw.

PreviousProceed to Clinical Presentation , Rotator Cuff Injury

Acromioclavicular Joint Injury

Background

Injuries in and around the shoulder are common in today's athletic society. Proper knowledge of the different problems and treatment options for shoulder disorders is necessary to get patients back to their preinjury state.

Acromioclavicular (AC) joint injuries are common and often seen after bicycle wrecks, contact sports, and car accidents. The acromioclavicular joint is located at the top of the shoulder where the acromion process and the clavicle meet to form a joint. Several ligaments surround this joint, and depending on the severity of the injury, a person may tear one or all of the ligaments. Torn ligaments lead to acromioclavicular joint sprains and separations.[1]

The distal clavicle and acromion process can also be fractured. Injury to the acromioclavicular joint may injure the cartilage within the joint and can later cause arthritis of the acromioclavicular joint.

This article discusses the anatomy of the acromioclavicular joint, the diagnosis of disorders of this joint, and the different treatment options.

For excellent patient education resources, see eMedicineHealth's First Aid & Injuries Center. Also, see eMedicineHealth's article on Shoulder Dislocation.

NextEpidemiologyFrequencyUnited States

Injuries to the acromioclavicular joint are the most common reason that athletes seek medical attention following an acute shoulder injury. Glenohumeral dislocations (see Shoulder Dislocation) are the second most common injuries seen. Men in their second through fourth decades of life have the greatest frequency of acromioclavicular joint injuries, which are most often incomplete tears of the ligaments.[1]

PreviousNextFunctional Anatomy

The normal width of the acromioclavicula joint is 1-3 mm in younger individuals; it narrows to 0.5 mm or less in individuals older than 60 years.

The acromioclavicular joint is made up of 2 bones (the clavicle and the acromion), 4 ligaments, and a meniscus inside the joint.

The acromioclavicular joint is surrounded by a thin joint capsule and 4 small ligaments. These ligaments mostly give joint stability to anterior and posterior translation, as well as provide horizontal stability to the joint.

Another set of ligaments also provides vertical stability to the acromioclavicular joint. These ligaments are called the coracoclavicular ligaments, which are found medial to the acromioclavicular joint and go from the coracoid process on the scapula to the clavicle.

Different injuries result in different tears of the 2 coracoclavicular ligaments (the conoid and the trapezoid). Torn acromioclavicular joint ligaments and/or torn coracoclavicular ligaments are seen in acromioclavicular joint sprains. The meniscus that lies in the joint may also be injured during sprains or fractures around the acromioclavicular joint. The acromioclavicular capsular ligaments provide most of the joint stability in the anteroposterior (AP) direction. The conoid and trapezoid ligaments aid in providing superior-inferior stability to the joint. Compression of the joint is restrained mainly by the trapezoid ligament.

PreviousNextSport-Specific Biomechanics

When a person falls onto their shoulder, the force pushes the tip of the shoulder down. The clavicle is usually kept in its anatomic position, whereas the shoulder is driven down, which injures the different ligaments or causes a fracture. When the ligaments are injured they are either sprained or, in more severe cases, torn.

Acromioclavicular joint sprains have been classified according to their severity. In a type I sprain, a mild force applied to these ligaments does not tear them. The injury simply results in a sprain, which hurts, but the shoulder does not show any gross evidence of an acromioclavicular joint dislocation. Type II sprains are seen when a heavier force is applied to the shoulder, disrupting the acromioclavicular ligaments but leaving the coracoclavicular ligaments intact. When these injuries occur, the lateral clavicle becomes a little more prominent.

In type III sprains, the force completely disrupts the acromioclavicular and coracoclavicular ligaments. This leads to complete separation of the clavicle and obvious changes in appearance. The lateral clavicle is very prominent. A few more types of acromioclavicular joint sprains have been classified, but types I–III are the most common (see below).

Classification of acromioclavicular joint injuriesClassification of acromioclavicular joint injuries.

An acromioclavicular joint sprain is more common than a fracture after an injury. However, fractures of the distal clavicle and the acromion process may occur, so the healthcare provider must be aware of such injuries and ready to diagnose and treat them as well (see Clavicular Injuries).

PreviousProceed to Clinical Presentation , Acromioclavicular Joint Injury

Sunday, February 2, 2014

Sacroiliac Joint Injury

Background

Lower back pain is one of the most prevalent sports maladies, affecting athletes in nearly every sport. Diagnosing the cause of a back injury is quite difficult and challenging because multiple structures in the lower back region can cause pain. However, an accurate diagnosis is paramount to providing successful treatment of the spine injury.

Although still somewhat controversial, the sacroiliac joint (SIJ) is generally accepted as an anatomic structure within the lumbar complex that if injured can be a cause of lower back pain. Mechanical dysfunction, inflammation, infection, trauma, and degeneration all have been attributed to the SIJ. Once the diagnosis of SIJ injury is established, specifically directed treatment can lead to satisfying results. This article discusses the diagnosis, management, and rehabilitation of sacroiliac injuries and pain.

For excellent patient education resources, visit eMedicineHealth's Osteoporosis Center. Also, see eMedicineHealth's patient education articles Low Back Pain and Lumbar Disc Disease.

NextEpidemiologyFrequencyUnited States

The incidence of lower back pain in humans parallels the incidence of the common cold, with a lifetime rate approaching 95%. Goldwaith and Osgood first discussed the possibility that SIJ injury could cause low back pain as early as 1905.[1] In the decades since then, several attempts have been made to establish the prevalence of SIJ syndrome in persons with back pain, and the results of these reports vary widely.

Schwarzer et al remarked that "the prevalence of sacroiliac pain would appear to be at least 13% and perhaps as high a 30%" in patients with low back and buttock pain.[2] Bernard and Kirkaldy-Willis reported the prevalence rate to be 22.5% in 1293 patients with back pain.[3]

PreviousNextFunctional Anatomy

The SIJ is a true diarthrodial joint that joins the sacrum to the pelvis.[4, 5, 6] In this joint, hyaline cartilage on the sacral side moves against fibrocartilage on the iliac side. The joint is generally C shaped with 2 lever arms that interlock at the second sacral level. The joint contains numerous ridges and depressions, indicating its function for stability more than motion. However, studies have documented that motion does occur at the joint; therefore, slightly subluxed and even locked positions can occur.[2, 7]

Stability is provided by the ridges present in the joint and by the presence of generously sized ligaments. The ligamentous structures offer resistance to shear and loading. The deep anterior, posterior, and interosseous ligaments resist the load of the sacrum relative to the ilium. More superficial ligaments (eg, sacrotuberous ligament) react to dynamic motions (eg, straight-leg raising during physical motion). The long dorsal sacroiliac ligament can become stretched in periods of reduced lumbar lordosis (eg, pregnancy).

Many large and small muscles have relationships with these ligaments and the SIJ, including the piriformis, biceps femoris, gluteus maximus and minimus, erector spinae, latissimus dorsi, thoracolumbar fascia, and iliacus. Any of these muscles can be involved with a painful SIJ. As a true joint, the SIJ is a pain-sensitive structure richly innervated by a combination of unmyelinated free nerve endings and the posterior primary rami of L2-S3. The wide possibility of innervation may explain why pain emanation from the joint can manifest in so many various ways, with different and unique referral patterns for individual patients.

PreviousNextSport-Specific Biomechanics

The function of the SIJ is to dissipate loads of the torso through the pelvis to the lower extremities and vice versa. The pelvis acts as a central base through which large forces are accepted and dissipated. Although the main role of the joint is to provide stability, the SIJ has limited motion that allows it to dissipate and transfer significant loads and stresses. Studies by Weisel indicate that most movement occurs when rising from the sitting to the standing position. However, the amount of motion is small, making assessment of sacroiliac motion during physical examination quite difficult. Selvik suggested that hyperextension produces the greatest degree of motion (2° on average, with only minimal translation of 0.5-1.6 mm).

If the motion in the pelvis is asymmetric, then dysfunction can occur. Some conditions that cause asymmetric motion include leg-length inequalities, a unilaterally weak lower limb (eg, polio), tight myofascial structures (eg, iliopsoas), and scoliosis. Hip osteoarthritis can lead to leg-length shortening and SIJ pain.

Women may be at increased risk for SIJ problems because their broader pelvises, greater femoral neck anteversion, and shorter limb lengths lead to different, possibly predisposing, biomechanics. In addition, pregnancy often leads to stretching of the pelvis, specifically targeting the sacroiliac ligaments and possibly leading to dysfunction, hypermobility syndromes, and chronic pain.

Innervation

The nerve supply of the SIJ originates from multiple lumbosacral root levels with partial innervation from L2 (anterior joint) to S3 (posterior joint). Because the root innervation can vary so widely, the pain referral patterns from primary sacroiliac pain can also vary. Fortin et al interviewed multiple patients documented to have sacroiliac pain by anesthetizing the joint with lidocaine injections under fluoroscopic guidance.[8, 9] He found referral patterns ranging from localized buttocks pain to frank radicular leg pain and many other descriptions in between.

PreviousProceed to Clinical Presentation , Sacroiliac Joint Injury

Sunday, January 26, 2014

Anterior Cruciate Ligament Injury

Background

Based on statements found in the recent Orthopaedic Knowledge Update regarding the increased incidence of knee ligament injuries, the author proposes that this incidence may be associated with the current emphasis on fitness. These injuries are most often a result of low-velocity, noncontact, deceleration injuries and contact injuries with a rotational component. Contact sports also may produce injury to the anterior cruciate ligament (ACL) secondary to twisting, valgus stress, or hyperextension all directly related to contact or collision.

The MRI image below shows a rupture ACL:

MRI displaying a ruptured anterior cruciate ligameMRI displaying a ruptured anterior cruciate ligament.

When matched for activities, a greater prevalence for ACL injury is found in females compared with males. Approximately 50% of patients with ACL injuries also have meniscal tears. In acute ACL injuries, the lateral meniscus is more commonly torn; in chronic ACL tears, the medial meniscus is more commonly torn. The only study on the prevalence of ACL injuries in the general population has estimated the incidence as 1 case in 3,500 people, resulting in 95,000 new ACL ruptures per year.

The importance of the ACL has been emphasized in athletes who require stability in running, cutting, and kicking. The ACL-deficient knee has also been linked to an increased rate of degenerative changes and meniscal injuries. For these reasons, approximately 60,000-75,000 ACL reconstructions are performed annually in the United States.

For restoration of activity and stability, the expected long-term success rate of ACL reconstruction is between 75-95%. The current failure rate is 8%, which may be attributed to recurrent instability, graft failure, or arthrofibrosis.

Treatment options must be tailored to a patient's preoperative level of activity. The following activity levels are based on the International Knee Documentation Committee:

level I includes jumping, pivoting, and hard cutting.level II is heavy manual work or side-to-side sports.level III encompasses light manual work and noncutting sports (eg, running, cycling).level IV is sedentary activity without sports.

Nonsurgical treatment may be considered for patients who participate in level III or IV activities; all others should be considered as candidates for surgery. In addition, consider surgical consultation on any young athlete due to potential complications from recurrent instability.[1, 2, 3, 4, 5, 6]

Recent studies

A recent randomized, prospective study by Wipfler et al comparing bone-patella-bone (BTB) autografts to hamstring tendon (HT) grafts at 9 years demonstrated significantly better International Knee Documentation Committee (IKDC) scores in the HT group, with no significant differences in laxity, tunnel widening, or any other parameters.[7]

Leys et al also found equivalent IKDC scores and better long-term outcomes (radiological evidence of osteoarthritis, level of activity, knee motion and single leg hop test) in HT versus BTB in a long-term cohort study following patients for 15 years postoperatively. The HT group had higher ipsilateral graft rupture rates (17% versus 8%), but lower contralateral ACL injury (12% versus 26%).[8]

One study compared the clinical outcomes of ACL reconstruction with hamstring tendon autograft versus irradiated allograft. The results found the rate of laxity with irradiated allograft was higher than that with autograft (32.3% vs 8.3%, respectively) in the 67 patients studied. Statistically significant differences were noted between the groups in the Lachman test (P = .00011), anterior drawer test (P = .00016), pivot-shift test (P = .008), and KT-2000 arthrometer assessment (P = .00021); the anterior and rotational stabilities decreased significantly in the irradiated allograft group. No significant differences were found between the 2 groups in functional and subjective evaluations, and activity level testing; however, patients in the irradiated allograft group had a shorter operative time and a longer duration of postoperativefever.[9]

Another study evaluated the outcome of anatomic double-bundle anterior cruciate ligament reconstruction with hamstring tendon autografts in both women and men. After a 2-year postoperative evaluation, the results noted that the assessment results for ligament laxity were approximately identical in both groups.[10]

The results from another study noted that 11 years after anterior cruciate ligament reconstruction, both hamstring and patellar tendon autografts provided good long-term outcomes and stability. However, a positive result on the pivot-shift (1+) test was significantly more frequent in the patellar tendon group, as was the rate of osteoarthritis.[11]

Geib et al compared intermediate-term outcomes of ACL reconstruction by bone-patellar tendon-bone (BPTB) with the outcomes associated with quadriceps tendon with a bone plug (BQT) and quadriceps tendon without a bone plug (QT). They found that QT and BQT produced results equivalent to those of BPTB autograft in arthroscopically assisted ACL reconstruction. When compared with BPTB autograft, the quadriceps tendon autograft showed significantly better results, with less anterior knee pain (4.56% vs 26.7%), less anterior numbness (1.5% vs 53.3%), a higher percentage of arthrometer measurements showing a side-to-side difference of 0 to 3 mm (88% vs 68%), and better extension (mean loss, 0.55º vs 2.77º).[12]

According to the results of a study by Marchant et al, computed tomography is the most reliable imaging modality for evaluation of ACL bone tunnels, as proven by superior intraobserver and interobserver testing results, when compared with results obtained with MRI and radiographs. According to the authors, radiographs and MRIs were not reliable even for identifying the presence of a bone tunnel. Intraobserver kappa scores for tibial cross-sectional area using CT, radiographs, and MRI were 0.66, 0.5, and 0.37, respectively. Interobserver kappa scores for tibial cross-sectional area using CT, radiographs, and MRI were 0.65, 0.39, and 0.32, respectively.[13]

According to a study of National Football League players by Brophy et al, a history of meniscectomy, but not ACL reconstruction, shortens the expected career of a professional football player, but a combination of ACL reconstruction and meniscectomy may be more detrimental to an athlete's durability than either surgery alone. In their study, 54 athletes with a history of meniscectomy, 29 with a history of ACL reconstruction, and 11 with a history of both were identified and matched with control subjects. Isolated meniscectomy reduced the length of career in both years (5.6 vs 7.0; P = .03) and games played (62 vs 85; P = .02). Isolated ACL surgery did not significantly reduce the length of career in years or games played. Athletes with a history of both surgeries had shorter careers in games started (7.9 vs 35.1; P [14]

Lyman et al found that although ACL reconstruction appears to be a safe procedure, the risk of a subsequent operation on either knee is increased among younger patients and those treated by a lower-volume surgeon or at a lower-volume hospital. According to the authors, patients were at increased risk for readmission within 90 days after surgery if they were older than 40 years, sicker (eg, had a preexisting comorbidity), male, or operated on by a lower-volume surgeon. Predictors of subsequent knee surgery included being female, having concomitant knee surgery, and being operated on by a lower-volume surgeon. Predictors of a subsequent ACL reconstruction included age less than 40 years, concomitant meniscectomy or other knee surgery, and surgery in a lower-volume hospital.[4]

NextEpidemiologyFrequencyUnited States

An estimated 200,000 ACL-related injuries occur annually in the United States, with approximately 95,000 ACL ruptures. Approximately 100,000 ACL reconstructions are performed each year. The incidence of ACL injury is higher in people who participate in high-risk sports such as basketball, football, skiing, and soccer. When the frequency of participation is considered, a higher prevalence of injury is observed in females over males, at a rate 2.4-9.7 times greater for females.

PreviousNextFunctional Anatomy

The knee joint develops as a cleft between mesenchymal rudiments of the femur and the tibia. This occurs around the eighth week of fetal development. The cruciate ligaments appear as condensations of vascular synovial mesenchyme at the same time.

By 14weeks' gestation, the ACL and posterior cruciate ligament have divided; both have a functional blood supply, which is mainly derived from the middle geniculate artery. The inferomedial and lateral genicular arteries also provide blood supply through the fat pad.

The ACL is composed of densely organized, fibrous collagenous connective tissue that attaches the femur to the tibia. The ACL is composed of 2 groups, the anteromedial and the posterolateral bands. During flexion, the anterior band is taut, while the posterior band is loose; during extension, the posterolateral band is tight, while the anterior band is loose.

The ACL attaches to bone through a transitional zone of fibrocartilage and mineralized cartilage. On the femur, the ACL is attached to a fossa on the posteromedial edge of the lateral femoral condyle. The tibial insertion is located in a fossa that is anterior and lateral to the anterior tibial spine. The tibial attachment is noted to be somewhat wider and stronger than the femoral attachment.

The ACL is intracapsular and extrasynovial. It courses anteriorly, medially, and distally as it runs from the femur to the tibia.

The ACL receives nerve fibers from the posterior branch of the posterior tibial nerve. The main function is believed to be proprioception, providing the afferent arc for postural changes during motion and ligament deformation.

PreviousNextSport-Specific Biomechanics

The ACL is the primary (85%) restraint to limit anterior translation of the tibia. The greatest restraint is in full extension.

The ACL also serves as a secondary restraint to tibial rotation and varus/valgus angulation at full extension. Since the relationship between the tibia and femur provides little bony stability, the ligamentous structures must provide stability. When the ACL is injured, a combination of anterior translation and rotation occurs.

The average tensile strength for the ACL is 2160 N. This is slightly less than the strength of the posterior cruciate ligament and approximately half as strong as the medial collateral ligament (MCL).

PreviousProceed to Clinical Presentation , Anterior Cruciate Ligament Injury

Saturday, January 25, 2014

Medial Collateral Knee Ligament Injury

Background

Medial collateral ligament (MCL) injuries of the knee are very common sports-related injuries. The MCL is the most commonly injured knee ligament. Injuries to the MCL occur in almost all sports and in all age groups.

NextEpidemiologyFrequencyUnited States

The incidence of MCL injuries is impossible to determine because of the wide spectrum of injury severity. Many MCL injuries are minor and may never be evaluated by a physician.[1]

PreviousNextFunctional Anatomy

The medial aspect of the knee has been divided into 3 distinct layers based on cadaver dissection. The first layer is the deep fascia, which consists of the sartorius fascia anteriorly and a thin fascial layer posteriorly. The thin posterior fascia covers the popliteal fossa and the heads of the gastrocnemius muscle. The second layer includes the superficial MCL, also known as the tibial collateral ligament. This ligament attaches proximally to the medial femoral epicondyle and to the tibia distally, approximately 4-5 cm distal to the joint line. The parapatellar retinaculum and patellofemoral ligament are within this layer.

The third layer is the knee joint capsule, which attaches proximally and distally at the articular margins. The capsule is divided into thirds from anterior to posterior. The anterior third of the capsule is the thinnest portion. It is attached to the anterior horn of the medial meniscus and is reinforced by the medial retinaculum. The middle third of the capsule consists of the deep medial collateral ligament. It is firmly attached to the mid body of the medial meniscus. Proximal to the meniscal attachment, it is termed the meniscofemoral ligament. Distal to its meniscal attachment, it is termed the meniscotibial ligament. The posterior third of the capsule includes the posterior oblique ligament (POL) and the oblique popliteal ligament. The POL has 3 arms, the superficial, tibial, and capsular.

See the figure below.

The medial and lateral collateral ligaments of theThe medial and lateral collateral ligaments of the knee. Courtesy of Randale Sechrest, MD, CEO, Medical Multimedia Group PreviousNextSport Specific Biomechanics

The superficial MCL has been shown through serial cutting studies to provide the primary restraint to valgus loads at all degrees of flexion. It is also an important restraint to anterior tibial translation when the anterior cruciate ligament is injured. The superficial MCL acts as a primary restraint to external rotation of the tibia.

Stability of the medial side of the knee is provided by dynamic and static restraints. The static restraints are the superficial MCL and the joint capsule, including the deep MCL and the POL. The semimembranosus muscle, the pes anserine muscles, and the vastus medialis muscle provide dynamic stability. The muscles of the pes include the sartorius, gracilis, and semitendinosus. These muscles flex and internally rotate the tibia. The semimembranosus has 4 attachments: direct, tibial, inferior, and capsular.[2, 3]

PreviousProceed to Clinical Presentation , Medial Collateral Knee Ligament Injury

Friday, January 24, 2014

Lateral Collateral Knee Ligament Injury

Background

Lateral collateral ligament (LCL) injuries result from a varus force across the knee. A contact injury, such as a direct blow to the medial side of the knee, or a noncontact injury, such as a hyperextension stress, may result in a varus force across the knee injuring the LCL. In terms of functionality, the LCL has often been grouped with the popliteofibular ligament and the popliteus tendon as the posterolateral corner (PLC).

See the figure below.

The medial and lateral collateral ligaments of theThe medial and lateral collateral ligaments of the knee. Courtesy of Randale Sechrest, MD, CEO, Medical Multimedia Group NextFunctional Anatomy

The LCL is a round ligament that originates close to the lateral epicondyle and inserts onto the fibular head.

PreviousNextSport-Specific BiomechanicsVarus stress

The LCL is the primary restraint to varus stress across the knee.

External tibial rotation

The PLC, which includes the LCL, popliteofibular ligament, and popliteus tendon, is the primary restraint to external rotation stress across the knee.

PreviousProceed to Clinical Presentation , Lateral Collateral Knee Ligament Injury

Wednesday, January 22, 2014

Acromioclavicular Joint Injury

Background

Injuries in and around the shoulder are common in today's athletic society. Proper knowledge of the different problems and treatment options for shoulder disorders is necessary to get patients back to their preinjury state.

Acromioclavicular (AC) joint injuries are common and often seen after bicycle wrecks, contact sports, and car accidents. The acromioclavicular joint is located at the top of the shoulder where the acromion process and the clavicle meet to form a joint. Several ligaments surround this joint, and depending on the severity of the injury, a person may tear one or all of the ligaments. Torn ligaments lead to acromioclavicular joint sprains and separations.[1]

The distal clavicle and acromion process can also be fractured. Injury to the acromioclavicular joint may injure the cartilage within the joint and can later cause arthritis of the acromioclavicular joint.

This article discusses the anatomy of the acromioclavicular joint, the diagnosis of disorders of this joint, and the different treatment options.

For excellent patient education resources, see eMedicineHealth's First Aid & Injuries Center. Also, see eMedicineHealth's article on Shoulder Dislocation.

NextEpidemiologyFrequencyUnited States

Injuries to the acromioclavicular joint are the most common reason that athletes seek medical attention following an acute shoulder injury. Glenohumeral dislocations (see Shoulder Dislocation) are the second most common injuries seen. Men in their second through fourth decades of life have the greatest frequency of acromioclavicular joint injuries, which are most often incomplete tears of the ligaments.[1]

PreviousNextFunctional Anatomy

The normal width of the acromioclavicula joint is 1-3 mm in younger individuals; it narrows to 0.5 mm or less in individuals older than 60 years.

The acromioclavicular joint is made up of 2 bones (the clavicle and the acromion), 4 ligaments, and a meniscus inside the joint.

The acromioclavicular joint is surrounded by a thin joint capsule and 4 small ligaments. These ligaments mostly give joint stability to anterior and posterior translation, as well as provide horizontal stability to the joint.

Another set of ligaments also provides vertical stability to the acromioclavicular joint. These ligaments are called the coracoclavicular ligaments, which are found medial to the acromioclavicular joint and go from the coracoid process on the scapula to the clavicle.

Different injuries result in different tears of the 2 coracoclavicular ligaments (the conoid and the trapezoid). Torn acromioclavicular joint ligaments and/or torn coracoclavicular ligaments are seen in acromioclavicular joint sprains. The meniscus that lies in the joint may also be injured during sprains or fractures around the acromioclavicular joint. The acromioclavicular capsular ligaments provide most of the joint stability in the anteroposterior (AP) direction. The conoid and trapezoid ligaments aid in providing superior-inferior stability to the joint. Compression of the joint is restrained mainly by the trapezoid ligament.

PreviousNextSport-Specific Biomechanics

When a person falls onto their shoulder, the force pushes the tip of the shoulder down. The clavicle is usually kept in its anatomic position, whereas the shoulder is driven down, which injures the different ligaments or causes a fracture. When the ligaments are injured they are either sprained or, in more severe cases, torn.

Acromioclavicular joint sprains have been classified according to their severity. In a type I sprain, a mild force applied to these ligaments does not tear them. The injury simply results in a sprain, which hurts, but the shoulder does not show any gross evidence of an acromioclavicular joint dislocation. Type II sprains are seen when a heavier force is applied to the shoulder, disrupting the acromioclavicular ligaments but leaving the coracoclavicular ligaments intact. When these injuries occur, the lateral clavicle becomes a little more prominent.

In type III sprains, the force completely disrupts the acromioclavicular and coracoclavicular ligaments. This leads to complete separation of the clavicle and obvious changes in appearance. The lateral clavicle is very prominent. A few more types of acromioclavicular joint sprains have been classified, but types I–III are the most common (see below).

Classification of acromioclavicular joint injuriesClassification of acromioclavicular joint injuries.

An acromioclavicular joint sprain is more common than a fracture after an injury. However, fractures of the distal clavicle and the acromion process may occur, so the healthcare provider must be aware of such injuries and ready to diagnose and treat them as well (see Clavicular Injuries).

PreviousProceed to Clinical Presentation , Acromioclavicular Joint Injury

Tuesday, January 21, 2014

Atlantoaxial Injury and Dysfunction

Background

Disability and instability of the unique atlantoaxial joint result in controversies regarding the management of acute trauma and also the screening evaluation of particular at-risk individuals. The purposes of this article are to define atlantoaxial instability (AAI); describe the relatively rare symptomatic lesions with significant morbidity and mortality; and, finally, discuss the rationale for and against screening and restricting the activities of at-risk individuals.

Definition

AAI, also known as atlantoaxial subluxation, is radiologically identified increased mobility or laxity between the body of the first cervical vertebra (atlas) and the odontoid process of the second cervical vertebra (axis) (see the image below).[1, 2, 3, 4, 5] The subluxation can be anterior, posterior, or lateral, and symptoms occur as a result of cervical cord impingement.

Medial-sagittal cross-sectional view of the atlas Medial-sagittal cross-sectional view of the atlas (C1) and the odontoid process of the axis (C2). Epidemiology

Although traumatic lesions involving the atlantoaxial region are relatively rare, certain disease states and conditions present a higher theoretic risk of instability due to increased atlantoaxial joint laxity.

Surveys indicate 10-25% of patients with trisomy 21 have AAI.[6, 7] Two thirds of these cases are due to laxity of transverse ligament, whereas one third are due to abnormal odontoid development. Although this association has been depicted on radiographs, the clinical incidence of serious cervical spine injury is not increased in this population compared with other populations.

About 25% of patients with rheumatoid arthritis have atlantoaxial instability, which is thought to be due to chronic inflammation.[8] Congenital skeletal dysplasias may cause resultant odontoid hypoplasia. Marfan syndrome may involve ligamentous laxity, and acute inflammatory processes can affect the retropharyngeal, neck, or pharyngeal spaces.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education article Neck Strain.

Related Medscape topics:

Marfan Syndrome

Skeletal Dysplasia

Related Medscape resources:

Resource Center Exercise and Sports Medicine

Resource Center Genomic Medicine

NextEpidemiologyFrequencyUnited States

Approximately 15-25% of all patients with trisomy 21, and about 25% of patients with rheumatoid arthritis have atlantoaxial injury or dysfunction.[6, 7, 8]

PreviousNextFunctional Anatomy

The articulation of the odontoid process of C2 (axis) with the anterior arch of C1 (atlas) allows for 50% of cervical lateral rotation. The transverse and alar ligaments maintain joint integrity and limit posterior motion of the odontoid process relative to the C1 anterior arch. Abnormal posterior translation (or subluxation) can cause cervical cord impingement with the potential for significant neurologic compromise and even death.

PreviousNextSport-Specific Biomechanics

During extremes of cervical flexion or extension, competent transverse and alar ligaments limit posterior translation of the odontoid process. Incompetent ligaments or a damaged odontoid process can allow for significant translation and potential damage in cases of cervical hyperflexion or hyperextension in which axial compression is delivered to the head and cervical spine. Given the potentially serious sequelae of significant atlantoaxial dysfunction, patients with defined instability are restricted from participating in contact sports and in sports requiring significant cervical flexion or extension.[1, 4, 9]

PreviousProceed to Clinical Presentation , Atlantoaxial Injury and Dysfunction

Friday, January 10, 2014

Talofibular Ligament Injury

Background

Ligamentous injuries of the ankle are common among athletes.[1, 2] Inversion injuries of the ankle account for 40% of all athletic injuries. The anterior talofibular ligament (ATFL) and the calcaneofibular ligament (CFL) are sequentially the most commonly injured ligaments when a plantar-flexed foot is forcefully inverted. The posterior talofibular ligament (PTFL) is rarely injured, except in association with a complete dislocation of the talus.[3, 4, 5]

Ligamentous injuries of the ankle are classified into the following 3 categories, depending on the extent of damage to the ligaments:[6, 7, 8, 9, 10]

Grade I is an injury without macroscopic tears. No mechanical instability is noted. Pain and tenderness is minimal.Grade II is a partial tear. Moderate pain and tenderness is present. Mild to moderate joint instability may be present.Grade III is a complete tear. Severe pain and tenderness, inability to bear weight, and significant joint instability are noted.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Ankle Sprain and Sprains and Strains.

Related Medscape Reference topics:

Ankle Impingement Syndrome

Ankle Sprain

Ankle Taping and Bracing

Related Medscape resources

Resource Center Exercise and Sports Medicine

Resource Center Joint Disorders

Specialty Site Orthopaedics

NextEpidemiologyFrequencyUnited States

Approximately 3600 cases of talofibular ligament injury per 100,000 people are reported per year.

PreviousNextFunctional Anatomy

The lateral articular capsule of the ankle can be divided into anterior and posterior segments. The anterior segment attaches proximally to the anterior portion of the distal tibia superior to the articular surface and to the border of the articular surface of the medial malleolus. The posterior segment attaches distally to the talus just posterior to its superior articular facet and attaches laterally to the depression in the medial surface of the lateral malleolus.[3, 4, 5]

The ATFL is intracapsular and attaches anteriorly to the anterior border of the distal fibula and laterally to the neck of the talus. The PTFL attaches posteriorly to the digital fossa of the fibula and laterally to the lateral tubercle on the posterior portion of the talus.

PreviousNextSport-Specific Biomechanics

The talofibular ligaments along with the CFL are components of the lateral ligament complex. This complex becomes stressed when the ankle is inverted and plantar flexed.[11] Supination of the foot in neutral flexion usually results in injury of the CFL. Supination and adduction injuries tear both the ATFL and the CFL.

The PTFL is the strongest of the lateral ligaments, and extreme inversion with plantar flexion is required to place the PTFL under stress; as a result, the PTFL is less commonly injured.[11] Transient subluxation or dislocation of the talus from the tibial mortise usually results in injury of all 3 lateral ligaments. Prevention of anterior displacement of the talus is primarily a function of the ATFL. Little additional motion occurs when the CFL also is damaged. Instability to inversion is greater when both the CFL and the ATFL are injured than when either ligament is injured alone.

PreviousProceed to Clinical Presentation , Talofibular Ligament Injury