Chronic lameness in Akita Inu, two years after TTA
Dr. Vladislav Zlatinov,
Central Veterinary Clinic-Sofia, Bulgaria
Eri is a three years old male Akita Inu dog, weighing 39 kg. The dog was presented because of left hind leg lameness, lasting for about 4 months. A surgical treatment-Tibial Tuberosity Advancement (TTA) for cranial cruciate insufficiency had been done at the same leg, about 2 years ago. Eri is a pet dog, but has an active lifestyle- long walks (>8 kms) covered regularly.
ago, Eri was diagnosed and treated for stifle instability. Then, the
clinical signs had started sub acutely and had progressed to moderate
persistent lameness, not responding to NSAIDs therapy. The “Drawer” sign
was negative, but the cranial tibial compression moderately positive.
Stressed X- ray revealed femuro-tibial translation.
A surgical treatment by TTA was applied. The planning of the technique was based on classic method (not the common tangent); fork-less system and 12 mm titanium cage were used. During the procedure mini medial arthrotomy was done and the stifle explored. We found partially torn and fibrillated cranio-medial ligament bundle; the rest of the cranial cruciate looked intact. This part was not debrided (looking strong). Caudal cruciate ligament and both meniscuses were probed and appreciated as normal. Meniscal release was not done.
After the surgery, the dog showed fast clinical improvement with lameness disappearing within 2 weeks post op. A full osteotomy bone healing was confirmed on the 6-th week post op; the activity level was gradually increased to normal. The owner reported an excellent perceived quality.
One year later, Eri was presented to us with similar signs of the opposite, right leg. We found the right knee to suffer from identical pathology: partial cranial cruciate rupture with intact menisci. This time Cora Based Tibial Plateau Leveling Osteotomy (CBLO) was accomplished, again with fast clinical improvement.
In the recent months, Eri became symptomatic on the left leg again. The reported lameness was mild and intermittent, more pronounced after long walks. The owner noticed often weight shift to the right side of the body, when standing. The dog was responding to NSAIDs, but with overall lameness persistence.
During our examination we found very good athletic body condition. We distinguished intermittent mild (II/V) weight baring lameness and positive sit test on the left side. The musculature of the left leg was obviously weaker than the right one. During ROM testing, Eri was comfortable, but anxiety was elicited during stifle external and internal rotation in moderate flexion (“Mac Murray’s test”). Digital compression of the medial joint capsule was doubtfully appreciated as painful. There was slight decrease flexion ROM; the stifle was found grossly unstable: positive drawer test, but tibial compression test was negative. The patella was stable with maneuvers. Neurological tests were normal.
Orthogonal radiographs were made, revealing:
normal bony structure
several small osteophytes present
mild effusion/capsule thickening
mild mineralization area just next to extensor fossa
obviously mineralized structure in the cranial femuro-tibial joint (lateral view)
cloudy opacifications in the centro-medial and lateral compartment of the joint
on the depicted clinical history, clinical signs and X-rays, please
make a list of possible differential diagnoses, causing the lameness:
- Late intra-articular septic infection
- Progression to full cranial cruciate ligament rupture
- Rupture /luxation of the long digital extensor
- Suboptimal tuberosity advancement (continuously subluxating knee)
- Meniscus pathology
- Medial collateral instability
- Rupture of the caudal cruciate, caudal tibial thrust
- Patella baja
- Patellar ligament desmitis
- DJD progression
What would be your next diagnostic tests?
- Specific stress X- rays views
- Joint tap
- Stifle arthroscopy
- Exploratory surgery
- Nothing- will recommend physiotherapy
- What are common long-term clinical consequences after cranial cruciate ruptures?
- What are the chances that TTA prevents them?
- What are the first choice treatments for them, if diagnosed? Can they be managed conservatively?
- Can you build a precise diagnosis based on the clinical exam and radiographs?
Show right diagnosis and suggested treatment (only for VOG-Members)
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