Equine Lameness and Diagnostics Flashcards

A 12-year-old Warmblood sport horse presents with subtle right forelimb lameness that worsens significantly after palmar digital nerve blocks but does not improve with abaxial sesamoid blocks. Radiographs of the foot are unremarkable. Which diagnosis best explains this paradoxical worsening?

Answer: Neurectomy effect unmasking proximal limb pain

Paradoxical worsening after a distal nerve block occurs when the blocked region was providing some compensatory proprioceptive input or the horse was guarding against distal pain in a way that partially stabilized a more proximal lesion. By abolishing the distal pain signal, the proximal pathology (which the abaxial sesamoid block does not reach) becomes the dominant pain source and lameness worsens. This 'unmasking' phenomenon is a recognized pitfall in sequential perineural diagnostic analgesia.

During dynamic evaluation of a horse on a lunge circle, the examiner notices that forelimb lameness is most pronounced on the OUTSIDE limb when tracking left on a firm surface, but this pattern reverses on soft footing. Which pathological process is most consistent with this footing-dependent reversal?

Answer: Medial collateral ligament desmitis of the coffin joint

Collateral ligament desmitis of the distal interphalangeal (coffin) joint produces mediolateral loading-dependent lameness. On firm footing, the inside limb bears greater concussive medial load, but on the outside limb the lateral collateral structure is loaded via centrifugal ground reaction force. Soft footing attenuates peak impact loading and shifts the dominant force vector, reversing which limb appears lame. MRI is the gold standard for confirming collateral ligament lesions that are often missed on radiographs.

A 7-year-old Quarter Horse cutting horse has a 2/5 right hindlimb lameness. Intra-articular analgesia of the tarsometatarsal and distal intertarsal joints produces 50% improvement. A subsequent high plantar nerve block produces complete resolution. MRI is unavailable. Which additional diagnostic step is MOST likely to differentiate proximal suspensory desmitis from a cunean tendon lesion as the remaining pain source?

Answer: Ultrasound of the proximal third metatarsal region in both transverse and sagittal planes

After confirming the pain source is proximal to the plantar nerve block level (consistent with the high plantar block resolving lameness) and ruling out a tarsal joint contribution, ultrasound of the proximal suspensory ligament (PSL) in both transverse and sagittal planes is the most practical next step. PSL desmitis in hindlimbs frequently occurs without obvious fiber disruption and requires systematic probe placement on the palmaroproximal metatarsus. The cunean tendon runs superficially and can be distinguished from the PSL by its more medial course and distinct echogenic envelope. CT and scintigraphy provide complementary data but are less accessible and not the first-line differentiation tool.

A 5-year-old Thoroughbred racehorse presents with acute-onset bilateral forelimb lameness, a classic sawhorse stance, and refusal to move. The trainer reports the horse received a phenylbutazone injection yesterday for a minor muscle strain. Careful examination reveals bilateral forelimb digital pulses of 4/4 and marked heat in all four feet. Which diagnostic finding would most strongly support laminitis secondary to phenylbutazone toxicosis rather than sepsis-induced laminitis in this horse?

Answer: Protein-losing enteropathy with hypoalbuminemia on chemistry panel

NSAID toxicosis (right dorsal colitis or gastric ulceration) causes protein-losing enteropathy through mucosal damage, resulting in hypoalbuminemia. This decreased oncotic pressure promotes digital lamellar edema and precipitates laminitis via a distinct vascular mechanism separate from inflammatory cytokine cascades. Hypoalbuminemia on a chemistry panel, combined with the recent NSAID exposure and absence of a septic focus, strongly implicates phenylbutazone-induced colitis as the trigger. Elevated SAA suggests systemic inflammation but is nonspecific. Radiographic rotation is a consequence of laminitis, not a cause-differentiator. Fecal alpha-1 PI elevation confirms enteropathy but is more useful for chronic protein loss confirmation.

Kinematic gait analysis of a Warmblood dressage horse reveals a decreased protraction arc of the right forelimb with a shortened cranial phase of the stride but a normal caudal phase. Flexion tests are equivocal. Diagnostic analgesia of the coffin and pastern joints is negative. Which anatomical structure's pathology BEST explains decreased protraction with preserved caudal phase?

Answer: Infraspinatus muscle contracture limiting shoulder abduction and cranial advancement

Infraspinatus muscle contracture or fibrotic myopathy produces a characteristic limitation of shoulder abduction and external rotation, mechanically restricting cranial limb advancement (protraction). Because the caudal phase depends primarily on the stay apparatus and caudal muscle groups — which are unaffected — the stride has a normal push-off but a clipped cranial arc. This is distinct from elbow or carpal lesions and from foot pain. Diagnosis is confirmed by palpation of a firm, fibrous infraspinatus body, asymmetric shoulder abduction, and circumduction gait. It is an under-recognized cause of 'subtle' forelimb gait asymmetry in sport horses.

A 10-year-old Andalusian stallion used for breeding has a 6-month history of insidious right hindlimb lameness. Rectal palpation reveals firm enlargement of the right sacroiliac region. Intra-articular sacroiliac injection under ultrasound guidance produces 70% improvement. Bone scan shows focal increased radiopharmaceutical uptake at the right sacral wing. Which additional finding on standing MRI of the pelvis would MOST specifically confirm active sacroiliac joint disease versus sacral stress fracture as the primary lesion?

Answer: Disruption of the interosseous sacroiliac ligament with periarticular edema on T2-STIR

Disruption or thickening of the interosseous sacroiliac ligament with periarticular soft tissue edema on T2-STIR sequences is specifically diagnostic of sacroiliac joint disease (sacroiliitis or desmopathy), distinguishing it from a primary sacral stress fracture. T2-hyperintense signal in cancellous bone is consistent with bone marrow edema from either a stress fracture or joint disease. Cortical irregularity of sacral foramina and gluteal atrophy are indirect, nonspecific findings. The interosseous ligament finding directly localizes pathology to the joint interface, correlating with the analgesia response and scintigraphic uptake pattern.