Lameness localized to the coxofemoral joint in large and giant breeds (e.g., Newfoundlands, Great Pyrenees, German shepherds, mastiffs, Labrador and golden retrievers) and chondrodystrophic breeds
(e.g., bulldogs, Shih Tzus and corgis) is most commonly attributed to coxofemoral dysplasia. Hip dysplasia is abnormal development
and growth of the coxofemoral joint resulting in abnormal laxity and incongruity of the joint. It's a polygenic, heritable
condition significantly influenced by environmental factors. Hip dysplasia and incongruity leads to laxity and subluxation
of the coxofemoral joint, resulting in cartilage damage, followed by progressive degenerative changes and osteoarthritis.
Photo 4A: A standard ventrodorsal hip-extended OFA view of the pelvis demonstrating bilateral coxofemoral subluxation and
early degenerative changes.
Hip dysplasia is considered a biphasic disease, with dogs demonstrating signs at two stages of life. Signs generally include:
- Bunny-hopping gait
- Reluctance to climb stairs, jump or exercise
- Stiffness after rest
- Poor hindlimb musculature
- Popping or clicking sound when sitting or rising.
Signs of hip dysplasia in juvenile dogs are due to hip laxity, subluxation of the femoral head, joint inflammation, effusion
and pain. Signs in adults are from decreased range of motion, cartilage loss and remodeling, osteoarthritis, joint inflammation
Photo 4B: A standard PennHIP compression view of the pelvis.
In juvenile dogs, positive Ortolani or Barden signs are consistent with joint laxity and subluxation. Radiographs (OFA hip
extended and PennHIP views) of the pelvis can confirm the diagnosis (Photos 4A-4C).
Conservative treatment of hip dysplasia includes weight control, low-impact exercise, nonsteroidal anti-inflammatory agents,
analgesics and chondroprotectives. Successful surgical treatments depend on an animal's age and degree of arthritis; a full
explanation is beyond the scope of this article.*
Photo 4C: A standard PennHIP distraction view of the pelvis.
This condition should be considered when lameness is localized to the coxofemoral joint in small breeds, especially toy breeds
and terriers. The pathophysiology of Legg-Calvé-Perthes disease (LCP) is not completely known, but it is characterized by
ischemic damage to the femoral head and neck resulting from vascular compression. Normal weight-bearing activities then cause
compression and malformation of the head and neck.
An autosomal recessive gene linked to LCP has been identified. Clinical signs of LCP include hindlimb lameness, pain with
manipulation of the coxofemoral joint and muscle atrophy. Diagnosis is based on signalment, clinical signs and radiographs
(Photo 5). The treatment of choice is femoral head ostectomy.
Photo 5: A ventrodorsal view of the pelvis demonstrating Legg-Calvé-Perthes. Note the apple core appearance and irregularity
of the right femoral head and neck.
Lameness in juvenile canines can have myriad causes but most commonly can be attributed to the conditions discussed in this
two-part article series. Remember: The key to diagnosis of lameness is localization.
*For more on this topic, see: Henry WB. Surgery STAT: Diagnosis and treatment of juvenile canine hip dysplasia. DVM Newsmagazine Oct. 2009.
Dr. Janice Buback is a surgeon with Lakeshore Veterinary Specialists in Port Washington, Glendale and Oak Creek, Wis.