AAOS Comprehensive Orthopaedic Review

Section 5 - Sports Medicine

Chapter 45. Overuse Injuries

I. Stress Fractures

A. Epidemiology


1. Stress fractures are not uncommon in highly committed athletes.


2. Stress fractures have a predilection for certain bony locations; the vast majority are in the lower extremity, with the tibia and metatarsals being the most common.


3. Stress fractures do occur in the upper extremity; these tend to heal well with relative or absolute rest.


4. Stress fractures fortunately occur in <1% of the general athletic population, but running track athletes can have an incidence of 10% to 20%. The rate of recurrence may be approximately 10% for all athletes, but as high as 50% in runners.


B. Pathophysiology


1. The concept of a stress fracture was first described by Breithaupt in the 1850s, who called it a "march fracture" because it was observed in the metatarsals of marching soldiers.


2. Stress fractures can be considered a fatigue failure of bone; they result from the accumulation of microdamage that occurs with repetitive loading of bone.


3. Fatigue failure starts in an area of stress concentration and is termed "crack initiation."


4. If this initial microscopic crack is not repaired and repeated loading of the bone continues, the crack extends; this is referred to as "crack propagation."


5. Ultimately, if enough microdamage accumulates, the bone will fail macroscopically.


6. In vivo, bone responds to crack initiation and propagation with a reparative biologic response; this response appears to be dependent on age, nutritional status, hormonal status, and possibly genetic predisposition.


7. A dynamic balance exists between accumulation of microdamage and host repair processes.


a. When microdamage accumulates in excess of the reparative response, the result is a stress fracture.


b. Any factor that disrupts this dynamic balance can increase the risk of stress fracture.


c. Theoretically, any factor that increases stress on a bone will cause an increase in microdamage accumulation with each loading episode.


d. Likewise, any factor that impairs the reparative biologic response, such as poor vascularity or an altered hormonal milieu, may also increase the risk of developing a stress fracture.


C. Evaluation


1. Stress fractures typically present with an insidious onset of pain, but they may present with acute onset of pain.


2. A history of either a prolonged level of high activity or a recent rapid increase in activity level is usually present.


3. Without a history of significant repetitive loading episodes, an insufficiency fracture or pathologic fracture must be considered.


4. Physical examination may reveal pain to direct palpation or mechanical loading of the affected site.


5. Radiographs, bone scan, CT, and MRI are the imaging techniques of choice to evaluate stress fractures. Each has advantages.


a. Radiographs are frequently unremarkable or have very subtle findings; this is especially true early in the course of the fracture.


b. Bone scans are very sensitive in identifying the presence and location of stress fractures, but they do not reveal macroscopic fracture lines in the bone.


c. MRI can identify the bony edema associated with early stress fracture as well as reveal the presence of a fracture line. MRI has the additional advantage of showing the surrounding soft tissues.


d. Delineation of the location and extent of a fracture line is best achieved with CT.



Table 1. Locations of High-Risk Stress Fractures]

D. Classification


1. Stress fractures at certain locations have a poor natural history and are termed high-risk stress fractures (Table 1).


2. Delayed recognition or undertreatment of high-risk stress fractures tends to result in fracture progression, nonunion, the need for surgery, and refracture.


3. Other fractures have a more benign natural history and are referred to as "low-risk" stress fractures; these fractures tend to heal with activity modification.


4. Recognizing the class of stress fracture is important for optimizing treatment (

Table 2).


a. Delayed recognition or undertreatment of a high-risk stress fracture can result in a prolonged recovery, surgery, or season/careerending sequelae.


b. Overtreatment of a low-risk stress fracture can result in undue loss of playing time and deconditioning.


5. One MRI classification of stress fractures is correlated with time to return to play.


E. Treatment principles


1. Treatment must alter the biomechanical and biologic environment such that the reparative processes exceed the accumulation of microdamage at the fracture site.


2. An evaluation of the athlete's biologic bone-healing capacity should be performed. This includes review of the athlete's nutritional, hormonal, and medication status.


[Table 2. Classification of Stress Fractures]

3. The "female athlete triad" (amenorrhea, disordered eating, and osteoporosis) must be considered in any female athlete with stress fractures; appropriate evaluation/treatment should be initiated.


4. The fracture site must also be protected from future strain episodes through relative rest, absolute rest, bracing, technique modification, or surgical fixation.


a. Relative rest involves decreasing the frequency or magnitude of strain episodes at the stress fracture site by modifying the athlete's training volume (intensity, duration, and frequency), technique, and equipment; through the use of a brace or orthosis; or by cross-training.


b. Absolute rest removes all strain episodes from the fracture site. This is often done by making the athlete non-weight-bearing.


5. An assessment of biomechanical risk factors such as malalignment should be performed as well.


6. The use of biophysical enhancement technologies such as pulsed ultrasound and electrical stimulation in stress fractures is still under investigation.


7. With these principles in mind, the management of stress fractures depends on classifying each fracture as either high or low risk. This is summarized in

Figure 1.


a. High-risk stress fractures are typically treated with absolute rest or surgery.


b. Serious consideration of risk must be done prior to allowing patients with high-risk stress fracture to continue to play; however, patients with low-risk stress fractures may do so with activity modification.


[Figure 1. Treatment algorithm for management of lower extremity stress fractures. BS = bone scan, NWB = non-weight-bearing.]

II. Exercise-Induced Leg Pain and Compartment Syndrome

A. Epidemiology


1. It has been estimated that "shin splints" account for 10% to 15% of all running injuries.


2. Shin splints may account for up to 60% of leg-pain syndromes.


B. Etiology and differential are listed in

Table 3.


C. Medial tibial stress syndrome


1. Definition—Tenderness over the posteromedial border of the tibia and dull aching to intense pain


[Table 3. Etiology and Differential of Exercise-Induced Leg Pain and Compartment Syndrome]

   that is alleviated by rest, in the absence of any neurovascular abnormalities.


2. Imaging


a. If the diagnosis is not clear, bone scan or possibly MRI should be diagnostic.


b. Periostitis has a distinct scintigraphic/MRI appearance, with increased uptake along the posteromedial border of the tibia.


3. Treatment


a. Nonsurgical


i. Modification of activities


ii. Modalities to decrease inflammation


(a) Nonsteroidal anti-inflammatory medication


(b) Local phonophoresis with corticosteroids


(c) Ointments


(d) Leg wraps


iii. If pes planus needs correction, orthoses may help.


iv. A dedicated program of strengthening of the invertors and evertors of the calf is very important in preventing recurrence; recurrence is common after patients resume heavy activity.


b. Surgical


i. The results of surgery are variable given the absence of rigid diagnostic clinical criteria and variability in the surgery performed.


ii. If nonsurgical treatment fails and the patient remains symptomatic, a fasciotomy of the deep posterior compartment with release of the painful portion of periosteum is recommended.


D. Exertional compartment syndrome


1. Overview


a. Anterior compartment involvement is more common and accounts for approximately 70% to 80% of cases.


b. Posterior compartment involvement is less common and has been associated with less predictable surgical outcomes.


2. Pathophysiology


a. Experimental evidence has been unable to demonstrate a decrease in blood flow despite documented elevated compartment pressure and a consistent clinical presentation.


b. MRI, MRI spectroscopy, and nuclear medicine blood flow studies all have been used with limited success.


c. Muscle biopsies have provided conflicting results regarding the role of muscle ischemia in the generation of pain.


3. Diagnosis—Although the diagnosis has long been considered to be one of exclusion, with a better understanding of the presentation the diagnosis is usually readily apparent.


a. The patient characteristically has a normal physical examination, no pain at rest, and reproducible exercise-induced leg pain that is completely relieved by cessation of the offending activity.


b. Investigation—Intracompartmental pressure measurements, rather than extensive imaging studies, are used to confirm the diagnosis.


c. Measuring intracompartmental pressure


i. Resting pressure, immediate postexercise pressure, and continuous pressure measurements for 30 minutes after exercise are most important for confirming the diagnosis.


ii. A study is considered positive if the insertional pressure is ≥15 mm Hg, the immediate postexercise pressure is ≥30 mm Hg, or the pressure fails to return to normal or exceeds 15 mm Hg at 15 minutes postexercise.


4. Treatment


a. Nonsurgical


i. Intracompartmental pressure normally rises and falls with activity; therefore, nonsurgical modalities do not affect pressure.


ii. Physical therapy, anti-inflammatory medications, and orthoses have generally been ineffective.


b. Surgical—Indicated for patients who have appropriate clinical presentations with confirmatory pressure measurements and are unwilling to modify or give up their sport.


E. Fascial hernia


1. Pathophysiology—A hernia can become symptomatic because of chronic exertional compartment syndrome, a compressive neuropathy, or ischemia of the herniated muscle tissue.


2. Evaluation—A hernia at the exit of the superficial peroneal nerve or of one of its branches is common in "chronic compartment syndrome."


3. Treatment


a. Patients with asymptomatic hernias require no treatment.


b. Symptomatic hernias should be managed initially with education, activity modification, and, possibly, use of support hose.


c. Failure of these modalities may be an indication for decompressing the entire compartment with fasciotomy.


d. Closure is contraindicated.


F. Peripheral neuropathy


1. Pathophysiology


a. The superficial peroneal nerve is a branch of the common peroneal nerve.


b. The nerve is most commonly compressed as it exits the deep fascia to become subcutaneous, a point where localized tenderness may be encountered.


c. In addition to muscle herniation, the nerve can also be compressed by the fascial edge or be subjected to repeated traction by recurrent inversion ankle sprains; 25% of patients note a history of trauma, particularly recurrent ankle sprains.


2. Evaluation


a. Patients may have activity-related pain and neurologic symptoms in the distal third of the leg or the dorsum of the foot and ankle.


b. Weakness is not expected because the innervation of the peroneals is proximal to the site of compression.


3. Treatment—If the neuropathy is caused by muscle herniation or compression on fascial edge, decompression can be performed.

III. Soft-Tissue Overuse

A. Pathophysiology


1. Clinically, tendinosis is an overuse injury with recalcitrant symptoms of pain with activity.


2. Histologically, tendinosis is a chronic intratendinous degenerative lesion of tendon.


3. Puddu used the term tendinosis in 1976, noting it was troublesome in athletes.


4. Tendinosis is not a failed healing response; there is no overt acute injury and no inflammatory phase as has been so well described in classic healing responses.

5. Neovascularization has been described as a very early histologic finding in tendinosis.


6. Tendon strain up to 6% is physiologic; strain in the 6% to 8% range can result in overuse injuries; and strain >8% can cause complete rupture of the tendon.


7. In tendinosis, instead of the normal constructive adaptive response of repeated loading, the tendon no longer responds in a positive fashion, but starts to accumulate increasing amounts of poorly organized and dysfunctional matrix; it is this degenerative tissue that is the hallmark of tendinosis.


8. Tendinosis occurs most commonly in the rotator cuff, patella tendon, Achilles tendon, posterior tibialis tendon, and common extensor origin at the elbow.


B. Classification—Blazina grading system of tendinitis:


1. A grade I lesion on the Blazina scale is characterized by pain that occurs only after the activity.


2. A grade II tendinitis lesion is characterized by pain that occurs during activity but does not affect performance.


3. A grade III lesion is characterized by pain that occurs during the activity and affects performance, such that the athlete cannot train and perform at the desired level.


C. Treatment


1. Nonsurgical


a. Traditionally, initial treatment consists of rest and physical therapy. Many nonsurgical interventions have been advocated, including hyperbaric oxygen, nitric oxide, sclerotherapy, and extracorporeal shockwave, to name a few.


b. Few controlled studies have been done.


c. Eccentric exercises were shown in one controlled trial to be as effective as surgical debridement in treating patellar tendinopathy.


2. Surgical


a. If nonsurgical measures fail in a grade 3 lesion and the tendinosis lesion is well established on MRI, surgery can be considered.


b. Surgical intervention falls into two broad categories.


i. The "excise and stimulate" group includes the open marginal or wide excision techniques.


ii. The "stimulate a healing response" group includes using percutaneous needling, or open multiple longitudinal tenotomies.


c. Both seek to induce a healing response in the tendinosis lesion by inflicting an acute traumatic event. This induced acute healing response will hopefully result in a repair of the degenerative lesion.


D. Results


1. Improvement in the patient's ability to perform activities of daily living is typical.


2. Unfortunately, relapse after the athlete returns to aggressive loading activity levels is not uncommon.


3. A randomized controlled trial found eccentric exercise as effective as surgery in treatment of patellar tendinopathy.

Top Testing Facts

1. The tibia and metatarsals are frequently affected with stress fractures.


2. Stress fractures result from "crack propagation" that exceeds the bone's reparative biologic response.


3. High-risk stress fractures usually involve the tension side of bone, have a poor natural history, and are aggressively managed, including with surgery.


4. Shin splints (medial tibial stress syndrome) are responsible for 10% to 15% of all running injuries.


5. The anterior compartment is most commonly involved in exertional compartment syndrome.


6. The diagnosis of exertional compartment syndrome can be made if the patient has both reproducible exercise-induced leg pain and an immediate postexercise intracompartmental pressure ≥30 mm Hg.


7. The treatment for athletes with exertional compartmental syndrome who are interested in returning to sport is surgical release of the involved compartment.


8. Tendinosis, a soft-tissue overuse injury, is considered a failed adaptive response.


9. The Blazina grading system uses a pain scale to stage tendinitis as well as functional limitation into three grades.


10. A randomized controlled trial found eccentric exercise as effective as surgery in treatment of patellar tendinopathy.


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