Mechanism of Anterior Cruciate Ligament Injuries

Our posts for the next few months will be a series on our understanding, philosophy and rationale for surgical treatment, progression from ipsilateral to contralateral patellar tendon graft and rehab progression for treating anterior cruciate ligament (ACL) tears. To start, one must have a good understanding of how the ACL tears. Dr. Donald Shelbourne published a paper regarding this topic in December of 2016.⁶

“In general, non-contact ACL injuries occur in sports involving jumping, landing and pivoting where the athlete generates forces upon sudden deceleration that are greater than the ACL can accommodate."⁶ Over the years, there have been many theories on the exact mechanism of ACL tears but it is impossible to do a randomized controlled study on the exact mechanism. However, if we take time to listen to the patients describe their injury in detail, watch videos of the injury in slow motion, and then look at X-rays and MRI scans, our office could make a very strong case for the correct mechanism of injury. By understanding this mechanism of injury, you then also have to question if the ACL prevention programs that have been marketed so heavily are really doing what they intend.

BACKGROUND RESEARCH

In 2004, DeMorat et al.⁴ reported that a 4500N, quadriceps contraction to a fixed femur and the knee in nearly full extension was enough force to cause an ACL tear. In 2003, Elias et al.⁵ found that the combined forces of the gastrocnemius and soleus caused anterior translation of the tibia. Boden et al. reported in 2000 that occurred during foot strike with the knee close to full extension.¹ There were two other studies that looked at videotape of noncontact ACL injuries and they concluded that the majority of injuries occurred when the athlete was in close proximity to an opponent.^2,3

“When playing sports, athletes generate both quadriceps and hamstring muscle contraction in anticipation of changing directions or landing from a jump. The quadriceps muscle must generate greater forces than the hamstring muscles in order to absorb the landing forces and to keep the knee from being flexed too quickly. Furthermore, the gastrocnemius and soleus muscles are contracted to avoid unopposed dorsiflexion of the ankle. These muscle contractions are performed thousands of times during athletic practice and competition. When the timing of the foot plant is miscalculated, however, the foot is planted a split second after the anticipated landing."⁶

When you look at acute tears on an MRI scan, there are bone bruises present on the lateral femoral condyle and the posterolateral tibial plateau. One has to ask, how do the bone bruises get in these locations? After listening to several thousand patients’ histories, watching videotape of their injuries and looking at MRI scans, Dr. Shelbourne proposed that the injury occurs from a mistimed foot plant. When the athlete is reacting to an opponent quickly, the athlete mistimes a landing by planting the foot a split second after expected, and after the maximum quadriceps and the gastrocnemius muscle contractions have already occurred pulling the tibia so far forward before the foot has made contact with the ground. At the time of the actual foot plant, the tibia is anteriorly translated upon contact with the ground compression forces and the terminal sulcus of the femur comes in contact with the posterolateral tibial plateau. The compression of the lateral compartment and the lateral meniscus caused an indentation on the lateral femoral condyle. When the muscles contract after the injury, they pull the knee back together and the lateral meniscus gets caught in the dent of the lateral femoral condyle. MRI scans indicate that the tibia is shifted anteriorly at the time of impact with the ground. It is when the tibia is already in an anterior position on the femur, the blow of the femur on the posterior aspect of the tibia causes the knee to be forced into further flexion therefore causing the ACL to be stretched to the point of tearing; somewhat like a crow bar motion.

Getting a good detailed subjective history of the mechanism from the patient is critical and, if able, watching video of the injury in slow motion is also very helpful. Most patients’ injuries will typically occur in a game situation and they will describe it as “my knee gave out to the inside.”

References

1. Boden BP, Dean GS, Feagin JA, Garrett WE, Mechanisms of anterior cruciate ligament injury. Orthopaedics. 2000;23:573-578.
2. Krosshaug T, Nakamae A, Boden BP, Engebretsen L, Smith G, Slauterbeck JR, et al. Mechanisms of anterior cruciate ligament injury in basketball: video analysis of 39 cases. Am J Sports Med. 2007; 35: 359-367.
3. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004; 32: 1002-1012.
4. DeMorat G, Weinhold P, Blackburn T, Chudik S, Garrett W, et al. Aggressive quadriceps loading can induce noncontact anterior cruciate ligament injury. Am J Sports Med. 2004; 32:477-483.
5. Elias JJ, Faust AF, Chu YH, Chao EY, Cosgarea AJ. The soleus muscle acts as an agonist for the anterior cruciate ligament. An in vitro experimental study. Am J Sports Med. 2003; 31: 241-246.
6. Shelbourne KD. Proposed mechanism for noncontact anterior cruciate ligament injury. Ann Sports Med Res. 2016;3(8):1095.