Stifle Flashcards
Where does the cranial cruciate ligament arise from?
medial aspect of the lateral femoral condyle and inserts on the cranial aspect of the region between the condyles
Where does the Caudal cruciate ligament arise from?
lateral aspect of the medial condyle and inserts on the caudal aspect of the intercondylar region
What’s the relationship of the cruciate ligaments to the synovial lining of the joint?
They lie inside the the joint capsule but are actually outside the synovial lining of he joint. This is important because the synovial lining is an effective barrier between the collagen of the ligament and the immunoresponsive mechanisms of the joint. Thus a damaged cruciate ligament is a potent stimulus for ongoing inflammation, and thereby degenerative joint disease
What’s the function of the cranial cruciate ligament?
prevents internal rotation, hyperextension, and tibial thrust
Cranial Tibial thrust
A force that causes the tibia to slide cranially relative to the femur. Can also be used to indicate a positive tibial compression test
Why does cranial tibial thrust exists?
Cranial tibial thrust is generated any time there is compression between the femur and the tibia. This occurs any time there is weight applied to the limb, but can also occur artificially during a PE. Because the force of compression is applied at an angle to the relatively flat tibial plateau, the compression is converted to shear just as it would be in an oblique fracture. If the cranial ligament is intact, it opposes that cranial force.
Understand how cranial tibial thrust relates to cruciate ligament rupture
If the force of tibial thrust is greater than the breaking strength of the cruciate ligament, the obvious happens. It’s that simple. Sortof. As is discussed below, there is a big difference between simple traumatic rupture of the ligament and what happens in most of the cases of cruciate rupture that we see. Most cruciate ruptures are a result of normal tibial thrust forces applied to a cruciate ligament that is abnormally weak.
Understand the etiology of acute cranial cruciate ligament rupture
Acute CCL tears are usually traumatic. They result from excessive torsion (rotation of the limb at the stifle) or extension on a normal, healthy CCL. The result is usually pretty dramatic discomfort, and an affected dog will almost instantly be 3‐legged lame. It may present with the owner convinced their dog broke its leg. While this is a common presentation in human athletics (football, skiing, the classic “plant and pivot” injury), it is by far the least common in veterinary medicine – even when a dog presents with what appears to be an acute history, it is almost always an acute aggravation of a chronic process.
Understand the etiology of chronic cranial cruciate ligament disease
Chronic cruciate rupture is usually a result of a chronically weakened cruciate ligament. This ligament then cannot withstand the normal forces associated with weightbearing. Why this degeneration happens is discussed below. Because it is a degenerative process that occurs over a long period of time, it is common to refer to the condition as “chronic CCL disease” rather than “chronic cruciate rupture”. The disease term refers to the degenerative process that is frequently in place long before there are any clinical or radiographic findings. Part of chronic CCL disease is, of course, rupture of the CCL, but rupture refers specifically to breakage of the ligament. Note that with CCL disease the rupture also tends to be a chronic, progressive process, i.e., the ligament often does not tear all at once.
What is more common- chronic or acute cranial cruciate disease?
Totally chronic; The typical case of cruciate rupture occurs in a young adult (or older) medium‐ to large‐breed dog. In pretty much every case this will be a result of chronic degeneration of the ligament. Atypical cases, e.g., small and toy breeds or cats, are more likely to be traumatic in origin.
List the factors playing a role in the pathogenesis of chronic cruciate ligament disease
What we DO know is that there is a certain amount of degeneration that occurs with age, and that this degeneration tends to be worse in larger dogs (over 15kg). What we DON’T know is why so very many large dogs seem to have premature degeneration of the ligament. There are a number of factors that have been proposed: obesity, poor fitness, conformation, and excessive plateau angle. While they likely contribute to degeneration to some degree, none of them have borne out in the literature as directly causative.
Know the risk of contralateral disease with chronic cruciate ligament disease
While the precise number might vary depending upon the reference quoted, roughly 50% of dogs that blow one CCL as a result of chronic CCL disease will blow the other within 1‐2 years.
Describe the signalment of the typical dog with cruciate ligament disease
This is an acquired disorder, prevalent in adult, large to giant breed dogs. Female dogs are somewhat overrepresented in the literature. There have been a couple studies that indicated neutered dogs were more likely to be affected than intact dogs. These were retrospectives, though, so it’s difficult to draw too many direct conclusions from it.
Describe the history typical of chronic ligament disease
he typical history is that of a hindlimb lameness that is aggravated by activity or after rest. Especially early in the disease, the signs may be mild and episodic, with the lameness seeming to resolve between bouts. If you envision the diseased ligament as a weakened, braided rope, progression of the lameness occurs a bit like the fraying of the rope. It doesn’t rupture all at once; rather the individual fibers give way progressively. As the fibers give way the stifle becomes progressively less stable, the remaining ligament having to withstand the same forces with less substance and predisposing to further fraying. As the fibers give way the frayed ends are exposed to the joint and degenerative joint disease develops.
It is extremely common that, at some point during the course of this waxing/waning lameness, that a patient will be prescribed NSAID or other arthritis drugs. Typically the response to this sort of treatment is poor. That said, sometimes they will seem to respond pretty well. When this occurs, unfortunately it is the degenerative disease that is responding – which in turn simply means that the patient has fairly advanced disease.
Understand the relationship between acute signs of rupture and chronic disease
At some point, of course, the remainder finally gives way, resulting in a very severe to non‐ weightbearing lameness. For this reason the lameness may present as an acute problem. The presence of crepitus on physical exam and degenerative joint disease, however proves that the problem has been going on for quite some time – osteophytes take weeks to months to develop.
Describe the physical exam findings with cruciate ligament disease
Effusion is palpable just behind the patellar tendon. In a normal joint, you can identify the patella and then follow the patellar tendon distally. The medial border of the patellar tendon is distinctly palpable, and immediately caudal to that in a normal stifle there is a tiny “divot”. This will fill in with even a small amount of effusion, and the depression will disappear. Larger amounts of effusion will make the stifle more rounded, and obscure the normal “V” shape of the stifle. Persistent distension of the joint results in fibrotic change in the joint capsule, which is a compensatory mechanism.
Disuse leads to atrophy, as happens in any lameness. One can get an appreciation for atrophy by visually inspecting, or perhaps palpating, the circumference of the thigh muscles and comparing one side to the other. One can also use a tape measure to quantify the amount of atrophy present.Medial buttress is the accumulation of fibrosis along the medial collateral. Buttress is a very firm, almost bone‐consistency lump on the medial aspect of the joint right where the medial collateral is. Sometimes the buttress can get severe enough that it is grossly visible.
Crepitus indicates the presence of degenerative changes. In fact, there can be no crepitus without osteophytosis of the joint. Crepitus manifests as a light crackling or grating sensation, palpable by putting a hand over the stifle and putting the stifle through range of motion
What is the mainstay of the diagnosis of cruciate ligament rupture?
The mainstay of a diagnosis of cruciate ligament rupture, however, is the presence of instability in the joint. Instability (drawer motion, or tibial thrust, which will be described more completely below), if present, confirms that the cranial cruciate ligament is damaged.
Understand how the PE findings might differ with acute vs. chronic disease
Immediately after an acute, traumatic rupture, there will be some hemarthrosis. This stage is short‐ lived enough that it has usually resolved by the time the patient gets to surgery. An inflammatory response follows – a reaction to the joint trauma as well as the ruptured ligament. Thus effusion (whether it be hemarthrosis or the ensuing inflammation) is always the first sign of stifle disease. This is true of chronic ligament disease as well. At the very beginning of chronic cruciate disease, there is an inflammatory response which produces effusion. Effusion may be the only sign of disease, even before significant instability develops. It’s pretty rare to catch chronic disease that early, but it happens occasionally.
As the disease turns chronic, fibrosis and degenerative joint disease are seen. The more chronic the conditions, the more prominent all of the chronic changes (joint capsule fibrosis, muscle atrophy, medial buttress, and crepitus) become.
The hallmark of cruciate disease – instability – remains present whether the disease is acute or chronic. With acute rupture the instability is usually quite obvious and the stifle is very “loose”. The adaptive response to that instability is fibrosis, which will tend to limit the instability over time. Thus with chronic disease the instability becomes somewhat less dramatic, though it never will resolve completely.
Understand the meaning of the tibial compression test and cranial drawer test on orthopedic exam
The cranial drawer test and the tibial compression test are two ways to test for cranial cruciate ligament rupture. Detection of cranial translation of the tibia by either method is considered a positive test. A positive test by either method indicates cruciate rupture. Usually both tests will be either positive or negative in a given patient. Sedation may be required to elicit a positive response from either test.
From a physics standpoint, envision the femur and tibia as two wedges connected by a short string to symbolize the cranial cruciate ligament. The cranial drawer test is a bit like trying to pull the wedges apart. If the wedges separate, then there is positive cranial drawer. The tibial compression test is like pushing the wedges together to see if they slide past each other more than the string would allow. If they do, that is a positive test.
What is the difference between cranial drawer and tibial compression test?
The difference between the two tests is that the cranial drawer test is testing the cranial cruciate ligament passively, i.e., without any effort from the patient. The tibial compression test is testing the cranial cruciate actively, i.e., by simulating weightbearing. It kindof doesn’t matter whether the stifle is unstable when the dog is not weightbearing. It only matters when there is weightbearing, because that is when tibial thrust (the force) is generated. This is a distinction between the extracapsular techniques and the osteotomy techniques. The extracapsular techniques are aimed at restoring both passive and active stability to the joint. The osteotomy techniques only address the active portion. In other words, a dog treated by TPLO or TTA should have a negative tibial compression test, but will have a positive cranial drawer test.
Is sedation required for a cranial drawer or tibial compression?
Yep. It is. Many dogs with cruciate disease will have instability that is detectable on awake exam. In those cases you don’t really need sedation – if it’s there, it’s there, and sedation won’t change anything. However if you don’t feel instability on an awake exam and you suspect cruciate disease you must sedate the animal to be sure.
What is puppy drawer?
Very young animals may have a limited amount of drawer, though the characteristics of the drawer are quite a bit different. Puppy drawer has an abrupt stop, where “standard” drawer has a softer, less well‐ defined stop. This drawer can be a normal finding in a young patient. After about the age of 6 months, significant puppy drawer becomes much less likely.
Understand the functional divisions of the CCL
Looking at the function of the cranial cruciate ligament, it can be divided into two subdivisions, the craniomedial band and the caudolateral band. There is a slight difference in function between them, in that the craniomedial band is taut throughout the entire range of motion, where the caudolateral band is taut only in extension. The caudolateral band is lax in flexion.
Note that these are divisions in the function of the cruciate ligament. There is no clear anatomic division, which is why you might not have been told about this in anatomy.
Understand how disruption of one band affects the palpation findings with partial vs. complete tears of the cruciate ligament
With a partial tear, it is the craniomedial band that ruptures. In this situation there will be a positive cranial drawer or tibial thrust, but ONLY when the joint is in partial flexion. When the stifle is in extension, it will appear stable.
Understand how treatment of a partial tear differs from treatment of a complete tea
A partial tear still has instability and still results in wear and tear on the cartilage. Most importantly, a dog with a partial tear has discomfort. For all of those reasons, the surgical recommendations for a dog with a partial tear are no different from those for a dog with a complete tear. There is no reason to delay surgery. In fact, in general the earlier the surgery is done the better off the patient will be – there will be less arthritis and less atrophy earlier in the process. The atrophy is reversible with surgery, though takes longer to restore muscle mass if there’s more atrophy. Arthritis, once present, is not reversible.
Understand the function of the menisci
Primarily, the menisci are shock absorbers. As fibrocartilage, they are compressible and thus act as padding between the femur and tibia. As an interface between the two bones, they increase the surface area of load transmission, which reduces the stress on the cartilage. The circular shape of the menisci helps dissipate the force of weightbearing by converting it to a different directional force.The secondary function of the menisci is to improve stability of the joint. The round femoral condyles nestle into the concave shape of the menisci, which helps to contain them and thus prevent subluxation of the joint that occurs when the cranial cruciate is damaged.Sagittal image of a cadaver sectioned through the medial tibial and femoral condyles, illustrating the shape of the meniscus and the interface it forms between the femur and tibia. Because it is a cadaver specimen, the space between the meniscus and tibia is greater than it normally would be. Image: Tobias, Veterinary Surgery Small Animal, 2012
Know the frequency of meniscal injury
60‐70% of dogs with cruciate rupture will have some amount of meniscal disease. The published numbers vary widely, but that’s the sort of number that most people quote. The point is that if the cruciate is injured, there is an excellent chance that the meniscus is injured as well.
Know which meniscus is most commonly damaged
It’s the medial one.
