9 mo. f/s rotty-large breed, not yet mature
History
Awkward gate of several week duration-chronic problem
Primarily rear legs-localizes the problem
Right leg may be worse than left-bilateral lameness that affects one leg more than the other 
Worse in morning and after exercise-stiffness associated with pain,  exercise induces pain
Unable to climb stairs for 2 weeks-chronic, severe enough to inhibit ability to climb stairs
Currently on rimadyl 10mg/kg orally as needed
no response noticed to rimadyl- pain and inflammation severe enough that drug 
does not eliminate pain
No history of trauma- less likely to be traumatic injury
Free choice food-free choice feeding predisposes to developmental orthopedic disease

PE
Disproportionate weight carried on front legs-indicates pain in back legs
Grade 1/4 lameness in right hind-tells degree of lameness therefore most likely not due to acute trauma or grade would be reflected as more severe.
Painful on palpation of hip joints-indicates primary problem in hip joint
Hip range of motion reduced to 100 degrees-indicates pain in hip area
Ortolani positive on left-indicates hip laxity


Hypothesis

Hypothesis 1-joint malformation
	Joint malformation can be due to genetic predisposition and environmental factors which lead to: abnormal conformation, laxity in joint and surrounding tissues, lack of congruity between articular surfaces, femoral head subluxation, limited contact of femoral head with acetabulum, increased pressure of femoral head on the acetabulum between 10-2 o'clock, tissue fatigue and loss of elasticity, microfracture of acetabulum, pain associated with tearing of periosteum, and osteophyte formation on the acetabulum and femoral neck.

Hypothesis 2- Cartilage malformation/damage
	Cartilage malformation/damage due to genetic predisposition traum and environmental factors, such as high plane of nutrition. Combined these factors lead to disruption of endochondral ossification which causes a thickening of the cartilage. The cartilage cells closest to the subchondral bone have decreased nutrition causing them to degenerate and fissures to form.  When a fissure reaches the joint surface, necrotic debris enters the joint, resulting in inflammation. This inflammation causes joint pain.  The fissure may encircle the thickened zone of cartilage, causing it to dislodge and become a joint mouse. The joint mice and chronic inflammation lead to degenerative joint disease.

Hypothesis 3-vascular damage
	Genetic predisposition, infection releasing cytotoxic factors,  trauma, or emboli could result in vascular damage to the coxofemoral joint.  The interuption in blood supply could result in death of the osteocytes and bone resorption. This decreases the cross-sectional area producing a location of stress concentration.  Stress concentration at the periphery produces a fracture through the cancellous bone that follow the junction of living "repair bone" and devascularized trabeculae. Fibrous tissue or fibrocartilage fills the fracture gap and begins to replace the remaining devascularized bone within the femoral head. These portions of the femoral head are mechanically weak and may collapse under loads producing articular incongruities and pain.

Plan of Action: 

1. Recommend radiographic evaluation of the coxofemoral joints. 
2. If inconclusive, MRI evaluation of the same area.
3. Restrict activity until results returned.
4. Client education regarding proper nutritional management