These conditions are not always painful so will not block out. Being able to identify them will save you time and trouble!
Etiology: Atrophy of the shoulder muscles: this allows the shoulder to luxate since there are no collateral ligaments of the shoulder joint. Muscles such as supra- /infraspinatus, subscapularis are so called “active collateral ligaments”. In the past, this was associated with cart horses and pressure on the suprascapular nerve. Now it is most often associated with trauma to the shoulder: eg a kick or fracture that damages the nerve or running into a gate or fence post.
Clinical signs : Shoulder joint moves outward from the scapula. Can also see this with damage to the muscles : torn or stretched muscles
Treatment : rest, anti-inflammatory drugs, surgery to decompress the nerve
Surgery is not usually performed until after 3 months of rest and waiting to see if the muscles will regain tone
Prognosis : guarded to poor for return to normal function
Upward fixation of the patella
Etiology : lack of tone in the quadriceps, allowing the patella to lock in place. This is most common in young horses and those that have been out of training for awhile
Clinical signs : stiff extended leg, particularly when the horse is backed up. May be bilateral . When the stifle “unlocks” horse moves forward normally. May be able to manually move patella into locked position fairly readily
Treatment: old treatment was to cut the medial patellar ligament, thereby preventing the locking. However, normal horses that have this surgery have a strong tendency to develop arthritis in the stifle joint. Now we recommend exercise to strengthen the quads : hill work, over culverts, etc. Other treatments include tendon splitting, irritants injected around the medial patellar tendon to tighten it up, and hormone injections to change the amount of ligamentous/tendinous relaxation.
Prognosis : good if no other problems with the stifle joint
Etiology : trauma to the semitendinosus muscles (injection, injury)
Clinical signs: restricted forward motion to hind limb action at a walk. Limb moves forward only so far and then is slapped to the ground due to the restricted muscle action. Cannot be seen at faster gaits
Treatment : old treatment was to resect the scar tissue but this made more scar tissue. Now most people either ignore it, transect the tendon of insertion of the semitendinosus muscle, or cut some of the restrictive areas under local anesthesia in the standing horse.
Prognosis: there are complications associated with the treatment; If it is mild, it may be best to avoid surgery
Peroneus (fibularis) tertius rupture
Etiology: overextension of the hind limb such as when it is caught in or under something. It may also be iatrogenic during recovery from anesthesia when the leg is in a full limb cast. This occurs because the cast makes the hock more immobile than the stifle joint.
Clinical signs: loss of reciprocal apparatus — the hock can be extended when the stifle is flexed and the hock does not flex much when the horse is moving (straight leg)
Treatment: rest and anti-inflammatory drugs
Etiology: thought to be neuronal dysfunction or adhesions around the lateral digital extensor tendon; plant toxin in Australia
Clinical signs: overflexion of the limb during the forward phase of the stride –the hind limb is pulled up in an exaggerated motion and may even hit the ventral abdomen; may be bilateral
Treatment : can try lateral digital extensor tenotomy If acute lesion, try anti-inflammatory drugs and physical therapy to prevent adhesion formation
Prognosis : guarded for full recovery
Etiology : neuromuscular disease that likely involves an abnormality in the feedback loop between afferent and efferent nerve fibers
Clinical signs : involuntary jerky flexion of the pelvic limb (and testicles) as well as extension of the tail : leg is held off the ground in a flexed position and muscles of hind limb and tail may quiver. Mild cases may be intermittent. Generally noted when horse is backed, turned, or made to step over an object. Most common in draft breeds.
Treatment : none
Prognosis : slowly progressive; overall prognosis is poor;
It is important to determine that the signs aren’t caused by PSSM (polysaccharide storage myopathy) as that disease is very treatable
Etiology : Foals may develop gastrocnemius rupture during dystocia and with assisted delivery. Rupture of the gastrocnemius muscle occurs when the stifle is forced into overextension while the tarsus is flexed. Adult horses may develop gastrocnemius rupture during exercise (in humans, this is generally with twisting; in horses with strenuous stopping).
Clinical signs: Dropped tarsus with extended stifle. inability to straighten the hindlimb. Mild to severe swelling in the upper limb. If the rupture is complete, the horse is unable to bear weight on the affected limb. Bilateral hindlimb gastrocnemius ruptures will result in recumbency due to the inability to stand. Ultrasound, radiographs (calcified injury area) and CT have been used to confirm incomplete ruptures.
Treatment : stall rest, fixation of the affected limb by a full limb cast and/or Robert Jones bandage and administration of anti-inflammatory agents have been used with varying success. Lack of stabilization of the limb makes casts challenging as rub sores are almost inevitable. Affected foals have been reported to return to full function without bandaging or splinting. Intensive supportive care is needed to ensure the foal can stand to nurse. The contralateral limb is at risk of developing angular limb deformities (foals) or laminitis (adults) due to increased weight bearing.
Prognosis : fair if incomplete, guarded to grave if complete rupture