The differential diagnosis for a patient presenting in an outpatient clinic with hip pain is relatively narrow. It’s been said that when you hear hoofbeats, think horses, not zebras. In other words, those hoofbeats you’re hearing are more likely to be coming from common things (horses) than uncommon things (zebras). That makes good sense and is practical, but just to be safe, we will cover both the “horses” and the “zebras” in this chapter. The horses (common conditions) are hip arthritis, greater trochanteric bursitis, and hip pain that is actually pain radiating down from the lumbar spine. These three hip conditions account for over 90% of the hip pain you are likely to encounter in an outpatient setting. The occasional patient with avascular necrosis (AVN) or a form of femoral-acetabular impingement (FAI), make up the other 10%—these are the zebras.
Let’s start with hip arthritis. As discussed in Chapter 1, in orthopedics, we consider arthritis to be a disease of the articular surfaces of the joint. Figure 3-1 shows a hip joint that has been dislocated to show the head of the femur and acetabular socket better. In a normal hip, both the surface of the femoral head and the surface of the socket are coated with a 2- to 4-mm thick layer of slick, numb articular cartilage. Most patients are familiar with this material because they have seen it on the ends of chicken bones (see the sidebar in Chapter 1, for more details). In arthritis, this material wears thin or, in some instances, is gone completely, exposing the underlying bone. Bone is not slick and slippery; it is rough and abrasive. It isn’t numb like articular cartilage either. It has a rich nerve supply and, as a result, is very sensitive and a poor bearing surface for a weight-bearing joint. Figure 3-2 shows an arthritic femoral head with a large area of worn cartilage and exposed bone.
The most common cause of hip arthritis is osteoarthritis. In osteoarthritis, the articular cartilage simply wears away with time and use. For this reason, most patients with osteoarthritis of the hip are older. A history of “high mileage” is probably the single most important factor in a patient’s history that predicts osteoarthritis. High mileage can mean many decades of normal use or a few decades of heavy use. Patients with hip arthritis usually complain of groin pain and will often remark that they have trouble getting their shoes and socks on due to hip pain and stiffness.
The hip joint capsule (Figure 3-3) is an envelope, or membrane, of firm but flexible tissue that surrounds the joint. It is attached to the rim of the socket on the acetabular side and the neck of the femur just below the femoral head on the femoral side. Hip joint fluid is contained within the capsule, and the capsule helps hold the ball inside the socket.
When the hip is inflamed, the synovial cells overproduce joint fluid, and the capsule becomes tense and distended. Some of the pain and stiffness that patients with hip arthritis have is from the pressure that develops in the overdistended hip joint capsule. If the hip joint is flexed 90 degrees, as it is when the patient is seated on the exam table, and we internally and externally rotate the femur, we greatly increase the pressure inside the overdistended capsule (sort of like wringing out a washcloth). Typically, the patient will complain of pain, and we will find that the arthritic hip does not rotate as freely or through as great a range of motion as the asymptomatic hip. This physical exam test (internal and external rotation of the hip in 90 degrees of flexion) is called the “windshield wiper test” and is illustrated in Figure 3-4.
The best diagnostic tool for detecting hip arthritis is a plain anteroposterior (AP) pelvis x-ray. Since the cartilage coating on the surface of the ball and socket are invisible on x-ray, a normal hip joint with a healthy layer of articular cartilage surface appears to have a gap between the surface of the ball and the surface of the socket. This gap is sometimes referred to as the joint space, but technically speaking, there is no space. The cartilage on the surface of the ball is resting directly on the cartilage surface of the socket; it is just that these surface materials are not visible on the x-ray, so there appears to be a space. Figure 3-5 is an AP pelvis x-ray. The hip on the patient’s left (our right) is normal and has no significant narrowing of the apparent joint space. The patient’s right hip has lost all of the cartilage on both the femoral head and the acetabular socket in the area marked by the arrow. In this part of the patient’s right hip joint, the bone of the ball is resting directly on the bone of the socket. This is what is termed bone-on-bone arthritis. Less-advanced cases of hip arthritis will have joint spaces that are narrower than the asymptomatic side but are not yet down to bone on bone.
Figure 3-5.
An AP pelvis x-ray showing a patient with a normal left hip joint and right hip bone-on-bone arthritis. Note the dark, radiolucent “gap” between the ball and the socket on the healthy left hip (white arrow). The dark space between the ball and the socket is full of healthy cartilage. There is an area where there is no cartilage between the ball and socket of the patient’s right hip (yellow arrow).
SEEING ARTHRITIS ON AN X-RAY
The following are the four radiographic signs of arthritis (Figure 3-A):
Narrowing of the apparent joint space. The loss of radiolucent articular cartilage narrows the space between the two bones.
Subchondral sclerosis. Bone density increases when bone is subjected to increased forces. Joints with little or no articular cartilage left articulate with greater friction and compression forces, so the bone just beneath the surface of the joint (known as the subchondral bone) becomes more dense and radiopaque.
Subchondral cysts. Small foci of bone necrosis on the surfaces of arthritic joints create small, lucent lesions known as subchondral cysts.
Osteophytes. For some reason, perhaps in an attempt to distribute increased joint forces over a larger area, arthritic joints grow extra bone along their articular margins. These “bone spurs” are referred to as osteophytes. Because they have a sharp, pointed appearance, patients often believe that these osteophytes are what cause the pain of arthritis, and that, if the bone spurs could be removed, their pain would improve. Unfortunately, surgically removing osteophytes from an arthritic joint has not been shown to significantly decrease joint pain. The pain is more likely the result of direct stimulation of the nerves in the exposed bone surfaces and pain from over distension of the joint capsule, both of which are still present after the osteophytes are removed.
Since a portion of the joint pain and stiffness in an arthritic hip is due to excess fluid within the joint capsule, medications that “deflate” the capsule by decreasing the production of inflammatory fluid tend to help. Nonsteroidal anti-inflammatory drugs (NSAIDs) most likely work in this way. Similarly, an intra-articular cortisone injection may help as well. These injections are usually given using image guidance, and a technique for administering an intra-articular hip cortisone injection is outlined in Chapter 9. Though anecdotal evidence exists to support the use of nutritional supplements (glucosamine, chondroitin sulfate, MSM [methylsulfonylmethane], etc.) to treat arthritis, the results of large, randomized, prospective, blinded trials have not shown these treatments to be effective. Strategies to decrease joint compressive forces include weight loss and the use of assistive devices such as a cane, crutches, or a walker. Physical therapy can help by increasing the flexibility and compliance of the joint capsule, allowing it to accommodate swelling better.
The surgical treatment for hip arthritis is a hip replacement. In this operation, the acetabular socket is resurfaced with a layer of low-friction material (usually polyethylene plastic), and the rough, worn femoral head is replaced with a smooth, polished ball made of either metal or ceramic (Figure 3-6). To secure the ball to the shaft of the femur, the ball is connected to a titanium stem that fits inside the hollow marrow cavity of the femur bone. Early designs were bonded to the bone with bone cement (a technique that is still used if the bone is very osteoporotic), but more modern devices have a porous texture on the surfaces of the stem that allows bone to actually grow to the implant. The polyethylene plastic socket is contained in a metal shell that has a similar coating that allows it to bond to the bone of the acetabulum. As an operative procedure, the hip replacement operation has been a tremendous success. Few surgical procedures can match its track record for safety and patient satisfaction.
TWO CRUMMY OPERATIONS …
Late in the second half of the 19th century, physicians were starting to experiment with the concept of hip joint replacement. At that time, a common procedure was to surgically excise the ball and neck of the arthritic hip, then allow the void to fill with blood, which would later harden into scar tissue and form a dense scar “spacer” between the femur and the acetabulum. The result was what is called a resection arthroplasty. The operation was feasible because it was fast. There was no anesthesia at that time, so only short procedures were practical. The operation eliminated the pain from bone grinding against bone in the joint, but the resulting scar articulation wasn’t as strong or stable as a normal hip. Innovators in the field started experimenting with materials that could be interposed between the femur and acetabulum. Glass, gold foil, and pig bladder were some of the materials that were used, but none worked well. Figure 3-B shows an x-ray of a resection arthroplasty performed on a patient who had right hip arthritis. Note the “empty socket.” The resection arthroplasty operation is also known as a Girdlestone procedure.
The other procedure that was used to treat hip arthritis was called a hip fusion, or arthrodesis. In this procedure, the raw, exposed bone on the surface of the femur is screwed to the raw, exposed bone on the surface of the socket. As is the case with a fracture, the two exposed bone surfaces will heal together if held still and in close apposition for 6-8 weeks. The result is that the pelvis and femur become one solid bone. Like the resection arthroplasty, this operation eliminated the pain from bone rubbing against bone, and it had the advantage of being more stable. But, the pain relief that this procedure afforded patients came with a price: the joint could no longer move.
HOW LONG WILL IT LAST?
A modern hip replacement is a wonderful operation, with low complication rates and high patient satisfaction scores, but like all human-made devices, the implants will inevitably wear out over time. The components themselves are actually fairly durable. As you would expect, the weakest link in the system, in terms of wear, is the plastic socket liner. But, even these wear relatively slowly. The plastic of a modern hip replacement socket wears at a rate of less than a tenth of a millimeter a year. Given that the plastic is usually on the order of a centimeter thick, it would take 100 years for a patient to wear all the way through one. Why is it, then, that our total hip replacements don’t last the patient’s lifetime?
While a few hip replacements will fail as a result of unusual complications such as infection and dislocation (each accounting for about 1% of total hip failures), most will fail because the bond between the replacement part and the bone fails. Like a crown that comes off of a tooth, the bonded interface between the socket or stem and the bone loosens over time, and when it finally fails, the hip replacement components are no longer affixed to the skeleton, and they move or shift a tiny bit when the patient walks. This motion of the device against the adjacent bone is painful.
One of the factors that can hasten the process of component loosening is wear debris. It turns out that, as the ball rubs against the plastic socket liner, the liner sheds tiny, submicron particles of plastic into the joint fluid. These particles are about the same shape and size of bacteria, and they elicit a robust immune reaction. That immune reaction attacks both the plastic particles and the bone/prosthesis interface, and this weakens the bone near the implant, which leads to loosening. Once the association between polyethylene plastic wear debris and component loosening was recognized and confirmed by multiple investigators at multiple institutions, the goal became to limit or eliminate these particles. The “gold standard,” a metal ball articulating against a traditional plastic socket liner, generated the highest volumes of polyethylene plastic debris. The first innovation was to strengthen the plastic of the socket liner by a process called cross-linking. This step alone led to an order of magnitude decrease in polyethylene debris. Other bearing surface combinations were also tried. A metal ball articulating with a metal socket liner was attractive because it yielded no plastic particles at all. Unfortunately, the particles that metal on metal bearings shed, cobalt and chromium metal ions, appear to have a toxic affect locally in the hip joint and systemically throughout the body. For this reason, metal-on-metal bearings have fallen out of favor among hip replacement surgeons. Another interesting bearing material is ceramic. Ceramic ball-and-socket liners provide articulations that do not shed any plastic particles. In fact, the ceramic material is so hard, so smooth, and so wear resistant that it is hard to measure any wear debris of any kind in these joints. The problem with ceramics turned out to be chipping, cracking, and fracture, as well as high manufacturing costs. A bearing surface combination that remains an attractive choice, especially in young patients, is a ceramic ball in a cross-linked polyethylene plastic socket liner. Because the ceramic is smoother than metal, a decrease in wear debris of over two orders of magnitude can be achieved when compared to a metal ball in a traditional plastic socket. Because the plastic liner is softer than a ceramic liner, chipping, cracking, and fracturing are less common as well.
HIP JOINT DISLOCATIONS
One of the potential complications of total hip replacement surgery is dislocation (Figure 3-C). A natural hip has a strong but flexible ligament connecting the ball to the socket of the joint. This ligament, the ligamentum teres, prevents the ball from coming out of the socket (see Figure 3-15). Though a few designs have been considered, no hip replacement has ever been manufactured with a connector like this. Metal chains and cables scratch the bearing surfaces of the ball and socket, and other, softer materials aren’t durable enough. We have had to omit this important ligament, and, as a result, human-made hip joints are inherently more prone to dislocating than mother nature’s original design. Fortunately, dislocation is an infrequent complication of artificial hips, occurring in only about 1% of patients.
WHAT’S THE BEST WAY TO GET THERE?
If you are planning to climb a mountain peak, you must first choose a route. Chances are, several routes to the top of that peak exist, each with their own advantages and disadvantages, and every so often, an innovative thinker will discover a clever new route that no one else has thought of. The same is true regarding the surgical approach used to perform a total hip replacement. We can approach the hip joint from the back (a posterior approach), the side (a lateral approach), or the front (a direct anterior approach). All of these approaches can be used to get the job done, and all have been used successfully in legions of patients, but the direct anterior approach is gaining widespread popularity because fewer muscles are injured in this approach, resulting in faster healing times and shorter hospital stays.
Another common cause of hip pain is greater trochanteric bursitis. Figure 3-7 shows the bony prominences created by the greater trochanters of the proximal femur bones. The greater trochanters are usually palpable on the lateral sides of the hip joints. The iliotibial band (IT band or ITB) originates from the ilium of the pelvis and inserts on the lateral tibia just below the knee joint. This dense strap of connective tissue is the tendon of the gluteus maximus and tensor fascia lata muscles, and it passes back and forth over the greater trochanter like a windshield wiper when we walk. The relationship between the IT band and the greater trochanter is shown in Figure 3-8. If the IT band becomes too tight and rubs against the trochanter with too much friction, it can cause swelling in the greater trochanteric bursa and create a focus of inflammation known as greater trochanteric bursitis.
Figure 3-7.
The greater trochanters (arrows) are bony prominences on the lateral side of the proximal femur.
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