This is the eighth and final article in a series on canine hip dysplasia. What follows is written from the perspective that the readers of the series are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series, you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.
Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it is either genetically dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.
While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause inward side effects with megadoses.
Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic, neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most overdiagnosed and misdiagnosed conditions.
Sadly, no breed registry in the United States requires genetic screening of parents as a prerequisite for litter registration or even offers a "fitness for breeding" certification. The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the American Kennel Club-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders.
The two major methods of diagnosing canine hip dysplasia available to the fancy in the United States are that followed by the orthopedic Foundation for Animals and PennHIP. Both are diagnostic; however, the hip-extended protocol followed by OEA may produce false-negative results. The protocol followed by PennHIP has a prognostic capacity through the use of statistics and a carefully guarded data base that allows a prediction to be made with respect to the probability of phenotypic expression of canine hip dysplasia. No one has a clear quantification of the gray area between obviously clear and obviously dysplastic hips.
For many animals, canine hip dysplasia is a manageable condition, and they can lead relatively normal and active lives given that caution is exercised. Every dog is different in its response to pain and the treatment protocol needs to be tailored specifically to the particular animal. Only aspirin and phenylbutazone ("bute") are FDA-approved drugs for use in dogs, but they are not without serious side effects. Corticosteroids are dangerous and may require experimenting to find proper dosage levels and intervals. Favorable results have been reported from chiropractic, physical, drug and nutritional therapy.
Surgery is a viable option given the suitability of the candidate animal, the financial resources available, the expected activity level, longevity and the use and value of the animal. Choice of intervention, whether medical or surgical, and activity level depend upon the disease process. Problems with certain procedures may be associated with improper patient selection relative to the stage of the disease. To be fair, patient compliance, i.e., owner post-operative management, may also be a significant factor.
It is important to remember from the earlier articles in this series that canine hip dysplasia, as a degenerative joint disease, is a process, and that different interventions may be required at different stages in the process.
In this final article we will explore two surgical options not previously discussed. The first is an old standby that has relieved the pain and suffering of many a dysplastic dog over the years. It is radical and invasive surgery, but under the right circumstances has produced very acceptable results. The second is modern technology in a modular form that produces exceptional, though expensive, results. The beauty of this approach is that through careful selection of components, fit to the animal's skeleton can be optimized.
Surgical options for the treatment of canine hip dysplasia have, for the most part, been adaptations of human orthopedic procedures. In 1943, a Lancet article (British medical journal) described a surgery done in 1929 to relieve the pain caused by a tubercular hip joint in a human. This was possibly one of the first complete excisions of the femoral head and neck seen-- at least it was the first example we have been able to find in the literature. Since its inception, this procedure has been modified and used extensively by veterinary surgeons. Often considered an alternative to total hip replacement, the femoral head ostectomy is sometimes the only affordable surgical option available to many dog owners. While there is significant potential for long-term complications, femoral head ostectomy should be carefully considered within its narrow recommended parameters. A prolonged recovery, muscle atrophy and "bed sore"- type ulcers are frequent problems associated with this procedure. Best results are achieved and fewer complications are encountered when the dog weighs less than 50 pounds. Some clinicians feel that the procedure is most effective for dogs less than 35 pounds.
For dogs weighing more than 50 pounds, the femoral head ostectomy has been modified to include a muscle "sling" to support and cushion the femoral shaft. The sling is formed from the biceps femoris muscle (biceps muscle of the thigh). Two other options include using a part of the gluteal muscle (buttocks muscle) to pad the area between the excised femoral shaft and the pelvis, or using the joint capsule itself to accomplish this. These "pads" are sewn into place to fix their position. Over time, the muscle pad is transformed to a fibrous mass that is better able to absorb the impact of the forces exerted by the femor. Nothing will replace the near-frictionless and hydrostatic dampening of the cartilage of the original joint when it was in good condition, but if forces are limited, the muscle pad has been shown to serve well in this function in many cases.
Once the femoral head and neck have been removed, the surgeon takes the joint through a complete range of motion. This ensures that there are no obstructions to normal articulation. The muscle pad is sewn into place so it will attach securely to the acetabulum. The clinician also checks for crepitus, which is a dry, crackly sound. Ovary crepitus may indicate that not enough of the femoral neck was removed or that bony fragments are still at the excision site. Both conditions would cause loss of function and pain after surgery. It is much better to reduce the problem at the time of surgery than to have to go back into the joint a second time.
As mentioned before, femoral head excision tends to be more effective and fewer complications are encountered when the dog weighs less than 50 pounds. A study published in 1988 evaluated the use and efficacy of the biceps femoris muscle sling. Sixteen dogs with normal hips were given the biceps femoris muscle sling surgery and six normal dogs were given the conventional excision of the femoral head and neck. While both control and treatment animals had similar post-surgical limb functions, there was marked edema and swelling of the affected limb in half of the dogs with slings and not in the control dogs. Four of the sling dogs developed post-operative infection and all of the treatment animals had elevated temperatures after the procedure. Their results indicated that the added risk of infection and complications was not justified and that further clinical trials needed to be run before the efficacy of this adjunct treatment could be established.
For those considering this type of surgery, it should be noted that this is a strictly end-stage salvage procedure. Only those animals demonstrating severe bony changes in the coxofemoral joint and clinical signs of pain should be considered for this procedure. Also, excisions without adding a prosthesis shortens the leg, which affects the gait, and the biceps sling can cause a slight adduction (drawing in toward the center line) of the affected limb during exercise. On the positive side, this procedure has worked well over the years and is still the standby short of total hip replacement.
The first human total hip replacement was performed in 1891 using an ivory ball-and-socket joint that was attached to the bone with nickel-plated screws. After this pioneering effort, replacement of just the femoral head or the acetabulum (unipolar) was the accepted practice until the 1950's. Later, the bipolar procedure (replacing both the femoral head and the acetabulum) was adopted as the preferred way to achieve long-term success. Better results were obtained, too, after the advent of polymethylmethacrylate (PMMA, or bone cement, which was approved by the FDA in 1967. Not only was the prosthesis stabilized by the cement, but its use was effective in preventing bone resporption where metal contacted bone. Orthopedic surgery has never been the same since.
In 1953, the first unipolar arthroplasty performed on a canine was described by R.E. Brown. His procedure replaced just the femoral head with a stainless-steel prosthesis. It was not until 1957, though, that H.A. Gorman did the first total bipolar hip replacements on 53 military working dogs. Much of the work done today is based on Gorman's truly pioneering efforts.
Besides the secondary osteoarthritis associated with canine hip dysplasia, total hip replacement is indicated for failed femoral neck and head excisions, irreparable femoral head and neck fractures, non-reducible chronic hip luxations, avascular necrosis of the femoral head and repair of a failed total hip arthroplasty. Major surgical failure lead directly to a requirement for total hip replacement. In a nutshell, when all else has failed, especially surgical procedures, total hip replacement may be the solution to restoring function and a pain-free quality of life.
The ideal candidate must have obtained adult growth, usually between 9 to 12 months of age, and must have obtained at least 30 pounds lean weight (no fat little dogs need apply). Other contraindications include infection anywhere in the body, anemia, neurological disease and concurrent orthopedic problems. A dog with arthritic hips and pain-free normal function is not a candidate for total hip replacement.
The most recent innovation developed for this type of surgery is the use of modular components in a sort of "mix and match" attempt to optimize the fit of the prosthesis. In June 1990, a canine modular hip prosthesis and instrument system was introduced at Ohio State University and marketed under the name of BioMedtrix. This system has the obvious advantage of being able to customize the fit of the various prosthesis components to better match the dog's original skeletal conformation. Thus femoral neck lengthening can be accomplished through choosing a particular femoral head and a particular femoral shaft. Note from Figure 1 that there is a set of prosthetic hip components for virtually any dog; specifically there are five-stem sizes, four standard and one nonstandard, acetabular cup sizes and three neck lengths\ offsets. Figure 2 shows an example of the prosthetic acetabulum, femoral head and neck. Figure 3 shows a "junk" hip on a 1 and a half year old Labrador Retriever. Figure 4 shows the same animal eight years and one month post-surgery. This ought to dispel doubts as to the length of benefit to be derived from total hip replacement. Look at the X-rays for a while. This is a good result, and it shows what can be expected from the technology.
Although expensive (our quick, non-statistical survey revealed $1,300 to $1,600 per hip was common), replacement of the arthritic hip with the appropriately sized mix of prosthesis components allows early if not immediate post-operative use of the limb. Most dogs are able to resume their normal level of activity within two months after surgery. Where there is clear indication that conditions will only worsen with time, a total hip replacement may make social and economic sense consistent with the age, purpose and value of the animal and the financial condition of the owner. We found that though results are not guaranteed, they tend to be consistently good to excellent, as supported by reports in the medical literature.
Complication due to infection is the most common occurrence associated with hip replacement and is directly related to the number of surgeries and the duration of the procedure. In dogs, blood-borne infections have been reported at 22 to 28 weeks after surgery. Infection rates in the 1970s ranged from 7.7 to 11 percent. More recently, infection rates of 1.5 to 3 percent have been reported.
Another complication that occurs with this surgery is a condition called "cement disease" or aseptic loosening. A fibrous membrane normally develops between the bone and the cement. With cement disease, however, a synovial like membrane containing particulate debris develops that produces large amounts of bone resorbing factors such as prostaglandin E2, collagenase, interleukin-1 and tumor necrosis factor. Newer techniques using a cement gun to introduce PMMA under pressure have decreased the incidence rate of cement disease. Mixing gentamyacin and the cephalosporins in the cement has also reduced the rates of infection. Another complication due to the use of cement is sciatic neuropraxia (the inability of the nerve to conduct impulses). Nerve contact with PMMA during its exothermic or heat-generating reaction has been implicated.
How well does a total hip replacement work? Very well, indeed. Olmstead, Hohn and Turner (1983) did follow-ups on 221 total hip replacements done between 1976 and 1981. After a four-week convalescent period, 216 cases (91.2 percent) had satisfactory function. A follow-up study of 174 THRs was done with 95.2 percent of the cases being restored to satisfactory function. We conclude that the total hip replacement, in suitable candidates, provides exceptional results. Olmstead boasts, as well he should, that one of his THRs won an international field trial. Total hip replacement restores function and relieves pain. Be aware that surgery cannot undo generations of genetic makeup, or prevent that which is predisposed. Total hip replacement is not prophalaxis to the problem; it is but a band-aid to the underlying genetic problems.
Femoral head and neck ostectomy and total hip arthroplasty are two of the major surgical options available to the owner of a dysplastic animal. If economically feasible, the THA/THR option is the more viable in terms of predictable outcome in larger animals. In smaller animals, favorable results have been reported with the femoral head and neck ostectomy, though obviously, somewhat less than total function is restored. With the advent of the use of PMMA and adjunct of antibiotic therapy, infection and "cement disease" rates have dropped remarkably during the past decade to the extent that they should be viewed as manageable concerns.
There is no substitute for genetic screening and refraining from breeding, no matter how attractive a particular breeding might be unless there is a clear indication that the parents, their siblings and get are free of hip dysplasia. To that end, we support the concept of open registries and place the blame for much of the genetic disease we find in the fancy today squarely on the shoulders of the various registries that have the power to make a difference. Until the time that the genetic disease aspect is recognized and successfully handled, there will a continued necessity for the surgical option.
We, the authors, wish to thank those professionals and caring veterinarians and researchers who have provided much of the information, without which this series would have been impossible. They not only gave generously of their time, but even shared unpublished manuscripts and unpublished manuscripts and unpublished insights to the various procedures. The result has been a survey of the recent literature with comments extracted from those at the very forefront of technology. Controversy has raged throughout the research process as the many professional opinions struggle for primacy. We have attempted to present not only the mainstream but also the fringe where there was adequate documentation of beneficial results.
Special acknowledgment goes to Doctors of Veterinary Medicine Marvin Olmstead, Gail Smith, Barclay Slocum, William Inman, Daniel Richardson and Terry Braden, all of whom we found to be genuinely concerned with the welfare of their animal charges. They are truly pioneers in the treatment of canine hip dysplasia.
Special thanks go to Doctors of Veterinary Medicine Rachel St. Vincent and Veronika Kiklevich of the Washington State Veterinary School.
For more information about PennHIP contact International Canine Genetics Inc., 271 Great Valley Parkway, Malvery, Pa. 19355; (800) 248-8099.
Special dedication goes to author Susan Thorpe-Vargas' dog-- call name "Smash," or if we're being more formal, Belaya Sobaka's Simply Smashing-- a Samoyed who touched our hearts as we wrote this series.
Last, but not least, we thank the readers who steered us in the right directions to those important researchers mentioned above and sincerely appreciate how DOG WORLD Editor Donna Marcel and her staff went out on a limb to approve and schedule this long series of eight articles.