Sports Injuries Flashcards
Define “stress fracture”. How is a stress fracture treated in a normal person? What are the consequences of a stress fracture which is not treated? Why might a young woman with an eating disorder be at particular risk for a stress fracture?
A stress fracture occurs when a bone breaks microscopically after being subjected to repeated tensile or compressive stresses, ie cyclical loading, in which not one single load which would be large enough individually to cause the bone to fail. (A “normal host” is defined as a person who is not known to have an underlying disease that would cause abnormal bone fragility. ) That is, stress fracture is the granddaddy of “repetitive stress injuries”.
Here is an image to keep in mind:
As you know, bending a paperclip too much will break it. If a clip will break with 12 bends, at the 11th, it has a stress fracture.
A stress fracture is believed to develop with abrupt increase in the duration, intensity, or frequency of physical activity without adequate periods of rest.
Important risk factors for developing stress fractures include a history of prior stress fracture, low level of physical fitness, increasing volume and intensity of physical activity, female gender and menstrual irregularity, diet poor in calcium, poor bone health, and poor biomechanics.
A stress fracture is also called a “march fracture” as taking a 40 mile stroll with military gear on one’s back is a nice way to cyclically overload the bones
A bone scan, shown on the right, can help demonstrate the injury, as only an overt break would be seen on plain films. MRI can also make the diagnosis.
In addition to the tibia, the feet (5th metatarsal especially) are commonly involved.
Stress fracture is, fundamentally, an overuse injury and THE TREATMENT OF AN OVERUSE INJURY IS UNDERUSE . (That is, if the patient would only stop beating up the bone and just let it heal all will be well.)
Not listening to the instructions to stop is a sign of not being normal…If they don’t listen, a stress fracture can lead to “real” (separated) fracture.
A stress fracture of the superior femoral neck, shown here, can be a real disaster if not healed, as the fracture can displace and disrupt the blood supply to the femoral head.
By contrast, a stress fracture of the calcaneous, if it displaces, will collapse on itself and not separate.
Women with eating disorders are at particularly high risk for stress fractures because they typically lack adipose (a chemical precusor for many hormones) and thus do not have proper estrogen levels. Because osteoclasts are estrogen sensitive, these women have imbalanced bone remodeling –more eating, less building—and bad bone.
Eating disorders are one third of the so-called female athlete triad (eating disorders, amenorrhea, and osteoporosis).
What is the definitional distinction between grade I, II and III sprains? How would these various grades of injury present distinctly on examination?
A grade I sprain results from mild stretching of a ligament with microscopic tearing only. Patients have mild swelling and tenderness. There is no objective joint instability on examination. It is often a clinical (subjectively applied) diagnosis: if a patients says “I twisted my ankle and it hurts” and nothing is seen objectively, the diagnosis often applied would be “grade I” sprain. Many such patients have nothing wrong with them, giving rise to the incorrect notion that grade I sprain (when it truly occurs) is completely inconsequential injury. Signal change in the MCL indicates an injury (compare to ITB laterally (which is darker)), but the gross course of the ligament is unchanged.
A grade II sprain is a more severe injury involving an incomplete tear/macroscopic stretching of a ligament. Patients can have moderate pain, swelling, tenderness, and ecchymosis.
There is mild to moderate joint instability on exam with some restriction of the range of motion and loss of function. If a grade II sprain is found in the leg, weight bearing and ambulation are painful. Here is there is tearing within the ligament, but some fibers are in continuity. Think pulled taffy.
A grade III sprain involves a complete tear of a ligament. This is often the result of higher energy mechanisms, such as the valgus blow to the knee shown below (likely to injure the MCL). There is significant laxity perceived by the examiner. Patients might be unable to bear weight or ambulate. Paradoxically, perhaps, this may hurt less than a grade 2, as once the ligament is torn, it no longer is provoked with every step.
Note that a complete tear is the same as a grade III sprain.
OTHER POINTS:
There are proprioceptive nerves are within the ligament (informing the brain just how bent the joint is you might say) and therefore even a grade I sprain can cause proprioceptive disruption.
Also, there can be a chondral injury from impaction even with a grade I sprain (that’s the edema seen near the red asterisk, above). In all, Grade I injuries may be less benign than they might seem.
What is the function of the Anterior Cruciate Ligament (ACL) in the knee? How is the ACL torn? Along those lines, why might it be the case (as we suspect) that skiing-related ACL tears occur disproportionately after 2pm? How is an ACL tear detected on exam?
The main function of the ACL is restraint of anteroposterior translation of the tibia relative to the femur. It also acts as a secondary restraint to tibial rotation and valgus or varus stress.
The ACL courses from the anterior tibia to posterior femur at the knee.
(This sagittal view points out that the ACL is fairly vertical–not the most advantageous orientation to prevent anterior translation. Yet if the ligament were more horizontal (as I drew it below, with artistic license) the knee would not flex and extend normally)
The mechanisms of injury is typically a sudden deceleration or rotational maneuver with a force that sends the tibia one way and femur another (typically because the foot is planted and the body spins).
Not all such forces that exceed the strength of the ligament lead to a tear: often, the secondary restraints (the hamstrings mostly) can help resist a tear. When the secondary restraints are overwhelmed, the ligament can be exposed to forces it cannot bear.
(Why would the hamstrings be overwhelmed? Well, for one thing the knee may be extending at the very second of injury, a phase of motion where the hamstrings do not fire; alternatively, they could be too tired. While skiing, for example, at 10am your still-powerful hamstrings protect the ACL; at 2pm, when the tibia starts to subluxate, the hamstrings just acquiesce and let the bone subluxate, ultimately tearing the ligament.)
An ACL tear is suspected first by history. A “pop” heard by the patient, immediate pain and swelling after a twist are typical features.
To test for an ACL tear on physical exam one can use the anterior drawer and Lachman tests. The Lachman test is the gold standard because it is thought to isolate the ACL and not involve other stabilizing structures.
The Lachman test is performed by p attempting to produce anterior translation of the tibia. An intact ACL limits anterior translation and provides a distinct endpoint. Increased translation compared to the uninjured knee and a vague endpoint suggest ACL injury.
The anterior drawer is performed with the patient lying supine and the knee flexed at 90 degrees. The proximal tibia is gripped with both hands and pulled anteriorly, checking for anterior translation. Often the clinician sits on the foot while performing the test to provide stability. The test is positive if there is anterior translation.
In brief, if there is a good story on history; effusion; what you think is maybe a positive lachman or drawer then get MRI.
NOTE:
Knee aspiration can be a very important step in the initial management:
Here’s why:
If there is too much fluid you cannot sense laxity–the pressure of the fluid "stabilizes" the knee The pressure of the fluid hurts! It is simply kind and humane to relieve it BLOOD (as seen above) usually indicates a significant injury (MRI worthy to be sure!); if not an ACL then perhaps a chondral fracture, meniscal tear or patellar dislocation.
Why is it that a tear of the ACL typically requires surgical replacement whereas a grade III sprain tear of the medial collateral ligament of the knee can heal with immobilization and rehab?
“Suture repair of a torn ACL is generally unsuccessful—with a failure rate of 90 percent. As a result, the current standard treatment for an ACL tear is to remove the ligament and replace it with a tendon graft.”
“Dr. Murray and her team designed a series of experiments to define key biologic differences in healing between ligaments such as the medial collateral ligament (MCL) that heal and those such as the ACL that don’t.”
They first compared fibroblasts in the ACL with those in the MCL. They found that cells in both injured ligaments have comparable rates of proliferation, that each ligament was able to revascularize after rupture, and that collagen production in each ligament was comparable up to 1 year after injury. But in the injured MCL and other extra-articular ligaments, a provisional scaffold developed—something that was not seen in the ACL.
The synovial fluid that surrounds the ACL washed away the blood clot that forms as an early bridge between the two torn ends of the ligament. As a result, “there was no structure in place to rejoin the two ends of the ligament, no place for surrounding cells to invade and remodel into a functional scar tissue,” said Dr. Murray. The researchers hypothesized that the lack of a provisional scaffold between the two ends of the torn ACL was the key mechanism behind its failure to heal.”
What is the function of the meniscus in the knee? What is the consequence of tearing a meniscus? Why are most symptomatic meniscal tears removed and not repaired?
The medial and lateral meniscus together provide shock absorption, establish a broad base of contact surface and help provide stability to the knee.
It should be clear, even sans picture, that a wedge of cartilage helps absorb shock:
The meniscus also helps establish a broad base of contact surface. As shown below on the left, without a meniscus there is focal loading and higher pressure at the point of contact
Last, the meniscus is stabilizing – a so called “chock block” effect.
A lost meniscus (might) leads to
Pain with loading, such as jumping (because of lost shock absorption) Less anterior/posterior stability of the knee (because of loss of chock block effect) DJD (because lost broad base of contact surface leads to focal load bearing and increased pressure, P = F/A. High pressure stimulates bone formation and in turn a stiff, injury prone subchondral plate.
We remove menisci, in light of the above, only when we have to. And we usually have to remove symptomatic tears, because most tears don’t heal. In general, only tears at the periphery have healing potential, as the blood supply enters from the capsule. Also, if the meniscus is macerated, ie torn up, there is no point in repairing it.
The key clinical question (in light of the histological truth that menisci have no pain fibers) is whether the tear is causing the pain, or whether it is just part and parcel of an arthritic picture, or an incidental finding.
What is rotator cuff tendinitis? What are the consequences of labeling it (perhaps incorrectly) as an “—itis”? What are the consequences of labeling rotator cuff tendinitis as “impingement syndrome”?
Rotator cuff tendinitis is not an inflammatory condition (as “itis” would suggest); it is a degenerative wearing out of the tendon, owing to repetitive use, poor blood supply and aging. It should be treated with an anti-inflammatory only to the extent that the anti-inflammatory medicine is also a pain reliever.
The supraspinatus tendon, as you see, has to make a bit of a turn before inserting on the humerus, which might impair perfusion to the insertion site.
Accordingly, there is no evidence that we should surgically remove any “impinging” structures (though acromioplasty, the removal of “impinging” bone the acromion (and shown below), is among the most common operations we do) .
More troubling, perhaps, is that this is a question amenable to a randomized trial, yet such a study has not been done. Case series have shown that patients with no bone removal do as well as historical controls who did have bone resected.
