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There isn't as much deception with joint replacement surgery as there is with outpatient arthroscopies (see What Your Doctor May Not Tell You About Knee Pain and Surgery, Warner Books, 2002). If your doctor has suggested a joint replacement, you are probably a reasonable candidate for the procedure. The only thing to quibble about is timing. Do you really need it now? During an arthritic flare-up, you'll agree to just about anything, including major surgery. Of course, this flare-up will quiet down, especially if it's one of the first. The unscrupulous doctor may quickly sign you up for surgery without informing you that arthritis pain typically waxes and wanes.
Here is a tip: If the doctor looks at your X-ray, throws a doleful look your way, and advises you of the need for a joint replacement, run out of there as fast as your arthritic legs can carry you! A good doctor treats patients, not X-rays! I'm reminded of the ninety-two-year-old man who came to see me a few years ago. He walked in and plopped his X-rays on my desk. They showed some of the worst arthritis I'd ever seen. The bones were so close together that I couldn't quite tell where one started and the other ended. I started to think about the risks associated with performing knee replacement surgery on a nonagenarian. Then he started his story: "Doc, I carry my own golf clubs, and after nine holes my knees are achy ..." This man obviously enjoyed a great quality of life and didn't need any surgery. So much for the knee replacement. On the other hand, some people whose arthritis is barely visible on X-rays are in severe pain. So once again, I tell my students to "treat patients, not tests." Joint replacement surgery is indicated for patients who suffer from either arthritis or avascular necrosis, also known as osteonecrosis. Certain types of hip fractures are also best treated with a hip replacement.
Like bursitis and tendinitis, the word arthritis is bandied about rather loosely. But it has a specific definition: the wearing out of the articular cartilage covering the ends of a bone. Look at a chicken bone. The shiny white material at the end of the bone is the articular cartilage. It is very, very smooth. Two pieces of articular cartilage gliding along each other exhibit a coefficient of friction eight times lower than two pieces of ice! When cartilage wears out, bone is exposed the way the concrete of a skating rink is laid bare by a spring-time melt. This wearing off of cartilage can be painful but, interestingly, not automatically so. People can live with arthritis for years without a day of pain. And then, one day, some event triggers the pain. Blunt trauma (hitting the knee against a hard object), for example, or a seemingly innocuous twisting injury. The triggering event isn't always obvious. You might come across the term arthrosis. For the purposes of this discussion, the term is synonymous with arthritis.
Not everybody with arthritis requires joint replacement surgery. A number of nonoperative treatment options exist, especially for the knee. And remember: As noted above (and yes, it does warrant repeating), arthritis pain flares up and quiets down. Joint replacement surgery is not indicated until the flare-ups are lengthy and frequent.
OSTEONECROSIS, AKA AVASCULAR NECROSIS (AVN)
It's easy to think of bone as a piece of wood. That's because the only bone you've ever seen (presumably) is on your dinner plate. But bone is a very living tissue. It is richly supplied with blood vessels and it is constantly being broken down and built back up.
When blood is unable to reach part of a bone, that part literally dies. That is because bone is made of cells like any other human tissue, and when cells are deprived of oxygen, they die. This is akin to the bone having suffered a stroke. The term osteonecrosis literally means "bone death." The term avascular necrosis is not as helpful. It is actually a redundancy because the word necrosis already implies death due to a lack of blood supply.
Nevertheless, its abbreviation AVN is commonly used, probably because it is less of a mouthful than osteonecrosis or avascular necrosis. AVN, avascular necrosis, and osteonecrosis all denote the same condition.
For reasons that are not always completely understood, there are bones in the human body that are subject to seeing their blood supply interrupted. In the case of the thighbone (femur), it's not the whole bone that is at risk, just the two ends: the femoral head at the hip and the femoral condyles at the knee.
Sometimes there exists a clear-cut risk factor for a person to develop AVN: At particular risk are patients with sickle cell anemia and Gaucher's disease (a congenital "lipid storage" liver condition that allows large, vessel-clogging molecules to form), patients who have taken steroid medications (not including injections into tendons and joints), patients who ingest more than moderate amounts of alcohol, deep-sea divers who come up too quickly, and patients who have sustained specific types of trauma.
Some of these risk factors are relatively easy to understand: In sickle cell anemia the red cells clump together and clog small arteries called arterioles. If these arterioles represent the only source of blood for a particular section of bone, it's going to be a bad day for that piece of bone when those arterioles become clogged. The use of steroids is thought to increase the amount of tiny fat globules in the bloodstream, and these tiny globules can block an arteriole just like a clump of red cells.
It is important here to distinguish between different types of steroids. The steroids that can cause AVN are steroids taken by mouth or by injections into muscles (IM injections).
Such steroids are given for a multitude of medical conditions including asthma, inflammatory arthritis (see above), organ transplants, head trauma, and chronic pain. Prednisone is typical of this category. Prednisone and related steroids are very different from the steroid preparations injected directly into a joint, such as Kenalog, Depo-Medrol, and Celestone. The latter are designed to work specifically on the joint that has been injected. They are not supposed to have so-called systemic effects, i.e., effects throughout the entire body. Sure, a small amount is certainly absorbed from the joint into the rest of the body, but by and large this small systemic dissemination has little effect. So with this second type of steroid you don't see the common side effects of prednisone such as swelling of the face, raising of blood sugar, and osteoporosis.
Most significantly, you don't develop AVN from injections into a joint, assuming the injections are given at a reasonable frequency (for most patients three injections per year in a given joint would be considered reasonable).
Alcohol can affect the liver's ability to metabolize fats and it has been postulated that this can also lead to clogging of certain bone arterioles. Fractures can occasionally damage the arteries feeding a certain section of bone. This is particularly true of certain hip fractures. Divers who surface too quickly suffer from a condition called the bends. Nitrogen comes out of solution and forms bubbles. These bubbles, like clumped red cells and fat globules, can also clog arterioles.
But for half the patients suffering from AVN, there is no discernible cause. It just happens. When doctors cannot explain where a condition comes from, they term the condition idiopathic. If the doctor says you have idiopathic AVN, it means he or she can't identify any risk factor that would have caused your bone necrosis. Note that as more risk factors are identified, fewer people with AVN will be said to have the idiopathic variety. For example, I'm willing to bet that in the not too distant future we'll identify a certain gene that predisposes someone to the condition.
Investigators have noted that a bone with AVN builds up abnormal amounts of pressure. It remains to be determined whether this is the result or partly the cause of AVN. How old are patients with AVN? Patients with AVN of the hip tend to be on the younger side, the average age being close to forty. Patients developing AVN of the knee are in their sixties or early seventies. Interestingly, though AVN can take months or years to develop, the pain often comes on precipitously, especially about the knee. Patients report pain coming out of the blue, a lightning bolt out of the sky. Hip AVN is much more common in men, but knee AVN is more common in women.
The natural progression of AVN. Sometimes the part of the bone that is affected by AVN is tiny. Bone being living tissue, it gobbles up the tiny dead part and replaces it with healthy, living bone. You may never have had a day of pain. If the part of the bone that is affected is bigger, you may develop pain, but the body may still be able to heal itself. Once it reaches a certain size, though, the condition progresses: Parts of the bone become rock hard, other parts become soft as the body tries to introduce new bone, and certain areas literally collapse. The collapse usually takes place near the surface-in other words, near the articular cartilage. This is referred to as subchondral collapse. In the hip joint, the bone, instead of being convex, appears concave over the affected area.
This is called the crescent sign. Over time the cartilage deteriorates, and the bones on both sides of the joint rub together, producing a frankly arthritic picture.
The "staging" of AVN. AVN exists in varying degrees of severity. A number of staging classifications have developed over time to assist in communication and treatment. For example, your doctor might indicate in his report that you have Stage III AVN, thus communicating to any orthopedist the extent of your condition. There are four commonly accepted stages for AVN of the hip:
In Stage I, the AVN is not visible on the X-ray but is already visible on an MRI.
In Stage II, the dead bone is now apparent on the X-ray, being whiter than the surrounding bone.
In Stage III, the bone no longer has a smooth, round, convex shape. It has collapsed at the edge-the so-called crescent sign on a hip X-ray.
In Stage IV, the bones on either side of the joint have come together as the cartilage has deteriorated. To say that someone has Stage IV AVN is tantamount to saying that they now have arthritis.
Other classifications featuring groups and subgroups have been devised, but the stages I've outlined above are considered classic.
The treatment of AVN. Since we don't always know where AVN comes from, it isn't always easy to come up with a rational plan, and because there are multiple causes of AVN, it would make sense for the medical community to come up with a treatment specific to each cause. It hasn't happened yet.
The normal femoral head is round. Note here how the bone has collapsed and the femoral head is no longer a smooth, round structure. Choices include using crutches to alleviate pain and to allow the bone to heal itself without collapsing, making holes in the bone (more on this shortly), bone grafting (bringing bone from elsewhere), applying electrical stimulation to the affected area, and replacing the joint.
The drilling of holes in the hip is called a core decompression since you take a core of bone out to decompress it. The concept of making holes in the bone comes from the observation that abnormal pressures build up in bones with AVN. This pressure causes pain and can contribute to cell death.
Drilling holes in the affected area lowers the pressure. It may also stimulate the bone to remove the dead bone and replace it with healthy bone. At least so goes the theory. Since new bone is soft bone and soft bone is more prone to collapse, do you really want a large area of fresh, soft bone? Orthopedists have been debating this for years. There is no risk of aggravating the AVN by performing a core decompression, and so it is a commonly accepted procedure.
But by making a hole in the shaft of the femur to gain access to the femoral head, the surgeon creates an area of weakness in the bone. This weakness predisposes you to a serious hip fracture should you take a misstep. Your surgeon will, therefore, have you walk with crutches for six to twelve weeks. Yes, back to the crutches. Cynics say that the core decompression is just a way of enforcing crutch walking that would otherwise be unacceptable to the patient.
Having made a hole in the bone, most surgeons are content to leave that hole unfilled. Another approach, though, is to fill the hole. Some surgeons have used a piece of fibula, the little bone that runs along the lower leg. But that piece of bone dies as soon as it is separated from its blood supply-that's what happens anytime you take a piece of bone out of someone.
Other investigators have, therefore, harvested the fibula along with the main blood vessels feeding it. The vessels are then connected to arteries about the hip joint, thus maintaining the fibular graft alive. This is a relatively complex and time-consuming operation, but at least there is now a live piece of bone inside the femoral head. The extent to which this technique represents an improvement over the straightforward core decompression remains to be determined.
Electromagnetic stimulation was tried in the 1980s. The theory was that coursing a specific electromagnetic field across the affected hip would stimulate the healthy bone to replace the dead tissue. This was not as far-fetched as it seems, since electromagnetic stimulation has been shown to assist in the treatment of hard-to-heal fractures. Some investigators reported success early on, but this success has not been duplicated.
When all else fails and the AVN has reached Stage III or IV, a hip or knee replacement can be contemplated. The question that comes up in orthopedic circles is whether both sides of the hip joint need to be replaced. In other words, in addition to removing the afflicted femoral head, should the surgeon remove the articular cartilage covering the acetabulum and replace it with a cup? Here are the two sides of the argument: Only the femoral head is diseased, so why mess with the healthy cartilage on the acetabular side? Why not simply implant a partial hip replacement, a so-called hemiarthroplasty, the literal translation of which is "half" a replacement?
In a hemiarthroplasty, the femoral head is replaced with a metallic ball that matches the size of the bone that was just removed. This differs from a total hip replacement in two significant ways:
1. The acetabulum is left intact. No cup is implanted. The operation, therefore, takes less time than a total hip replacement.
Excerpted from What Your Doctor May Not Tell You About Hip and Knee Replacement Surgery by Ronald P. Grelsamer Copyright © 2004 by Ronald Grelsamer, M.D.. Excerpted by permission.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.
|Introduction: Why You Need This Book||ix|
|Part I.||An Overview|
|Chapter 1||Who Needs a Joint Replacement? Arthritis, AVN, and Femoral Neck (Hip) Fractures||3|
|Chapter 2||Nonoperative Alternatives||25|
|Chapter 3||Operative Alternatives to Joint Replacement Surgery||43|
|Chapter 4||What Exactly Is a Joint Replacement?||48|
|Chapter 5||Getting Ready for Surgery||64|
|Part II.||The Hip|
|Chapter 6||The History of Hip Replacement Surgery||83|
|Chapter 7||The Anatomy of the Hip||95|
|Chapter 8||How Surgery Is Performed--The "Routine" Hip Replacement||100|
|Chapter 9||How Surgery Is Performed--The Difficult Hip Replacement||122|
|Chapter 10||Your Hospital Stay, Day by Day||134|
|Chapter 11||Going Home After Hip Replacement Surgery||144|
|Part III.||The Knee|
|Chapter 12||The History of Knee Replacement Surgery||153|
|Chapter 13||The Anatomy of the Knee||160|
|Chapter 14||How Knee Replacement Surgery Is Performed||163|
|Chapter 15||Your Hospital Stay, Day by Day||171|
|Chapter 16||Going Home After Knee Replacement Surgery||182|
|Part IV.||Controversies and Admonitions|
|Chapter 17||Do's and Don'ts After Surgery||191|
|Chapter 19||Do You Really Want the Latest Implant? The Mini-incision, Partial Knee Replacements, and Other Controversies||225|
|Chapter 20||The Economics of Joint Replacement Surgery||236|
|Chapter 21||How to Choose a Surgeon||243|
|Chapter 22||Answers to Common Questions||250|