Diagnosis

We believe that TitanÕs problems originated with congenital malformations. Small 
breed 
dogs are more prone to medial luxations of the patella due to several factors. 
Usually 
abnormalities are present at birth; however clinical problems do not usually 
present until 
later due to other outside stimuli that caused joint instability. Abnormalities 
that may be 
present include: Coxa vera (reduction of the inclination of the femoral head and 
neck to 
the long axis of the femoral shaft), distal third of femur may be bowed medially 
( genu 
varum), a shallow trochlear sulcus with poorly developed or absent medial ridge. 
None of 
these abnormalities were definitively seen radiographically; however, we felt 
there may 
have been some slight bowing of the distal femur. We are unsure as to whether 
one can 
truly assess the depth of the trochlear sulcus radiographically.
Up until a year ago, there was no previous history of lameness. This is fairly 
typical of 
this condition as many animals may be asymptomatic, or at least unnoticed to the 
owner, 
for life. Lameness, even then may be intermittent and not necessarily reported 
by the 
owners.  Signs may worsen as the animal gains weight, there is erosion of the 
cartilage, 
or if the luxation becomes permanent, the cruciate ruptures or if the hip is 
luxated
A year ago when Titan fell of the bed, we suspect he may have partially  or 
totally 
ruptured the cranial cruciate ligament which is a likely sequalae to a patellar 
luxation. We 
do not suspect it is a patellar ligament or caudal cruciate ligament rupture 
because those 
are rare and usually due to something more traumatic than falling off the bed. 
TitanÕs 
lameness resolved a month after the fall.  In the ÒnormalÓ pathophysiology of 
cruciate 
tears in small animals, the joint tends to Òself-stabilizeÓ. This appears to the 
what 
happened in this case since medial buttressing was noticed on the right stifle 
joint. Medial 
buttressing indicates fibrosis of the joint capsule which provided some 
stability for the 
joint for the next several months until Titan presented again with lameness.  
This second 
bout of lameness was most likely due to the wearing of the meniscus over that 
time 
period. This is a fairly classic presentation for cruciate tears in small 
animals: to be lame 
for about a month, then appear normal, and then reappear with sudden decline and 
lameness. ON this exam, there was definite medial luxation of the patella on 
extension of the joint. This was our ÒbiggestÓ clue that the animal probably had 
some predisposing (congenital ) factors that would lead to luxation post trauma.
On this examination the cranial drawer test was negative. This does not mean 
that the 
cruciate was not torn at some point. First of all, itÕs been a year since the 
trauma and with 
the Òself-stabilizationÓ there may not be as noticable joint laxity. Secondly,  
a positive 
cranial drawer depends on which part of the cranial cruciate ligament was 
damaged (the 
small craniomedial band versus the larger caudolateral band).  The pain the 
animals is 
feeling is most likely due to subsequent meniscal damage due to the joint 
instability ( 
despite the joint capsule fibrosis).  Definitive diagnosis of meniscal damage 
can only be 
done with arthrotomy.  The orthopedic examination under sedation only confirmed 
pain 
on the right side and radiographs did not show any evidence of degenerative 
changes.  
Radiographs are not useful for diagnosing ligament or meniscal damage. This can 
only be 
confirmed with exploratory surgery of thejoint.
So what we have here is an animal that most likely is predisposed to patellar 
abnormalities. We can not prove this until surgical exploration ( the only 
possibly seen 
abnormality was slight bowing of the femur, trochlear sulcus depth is not 
determined 
radiographically) . We believe the trauma to the joint caused the clinical signs 
associated 
with patellar luxations to become evident. Again, we can not prove the torn 
ligament or 
meniscal damage with out exploration.  Our pathophysiology of this condition is 
rather 
hypothetical since we can not prove anything until surgery. We are basing our 
assumptions on the breed of the animal and the animalÕs presentation with 
trauma, a 
period of normalcy, and then sudden lamenss again.