A strong, rounded muscle that runs along the back of the hind leg from the stifle joint to the hock (cannon bone), the gastrocnemius muscle (GM) helps with movement and stability. It is a key player in the horse’s balance and is innervated by the tibial nerve.
Foals that develop a rupture of the gastrocnemius muscle are often very lame and may not bear weight on the injured limb. Despite its importance, the gastrocnemius muscle is relatively poorly understood. This article focuses on the pathophysiology of gastrocnemius muscle injury in foals and how a simple diagnosis can improve the prognosis for these horses.
Difficulty during the birthing process, even in apparently normal cases, can cause an injury to a hind-leg muscle called the gastrocnemius muscle. A ruptured gastrocnemius is usually fatal in the horse, because it interrupts the horse’s ability to bear weight on its hind limb.
The GM is formed by two heads that terminate in the midcrus in a common tendon, the superficial digital flexor tendon (SDFT). A bursa, the calcaneal or intertendonous bursa, lies between the SDFT and gastrocnemius muscle, and a communication between these structures normally exists. Another small bursa, the subgastrocnemius bursa, lies cranial to the insertion point of the gastrocnemius tendon on the tuber calcanei.
These muscles are important for the control of walking, running and jumping. They are also involved in the formation of the equine thoracic girdle and in stabilizing the fetlock joint. The GM is composed of Type I and II fibres, with the deeper Type I fibres being more suited to aerobic, slower work such as joint stabilisation and Type II fibres being better suited to anaerobic, rapid bursts of work such as movement in a wide range of directions.
A group of Japanese researchers recently reported that a difficult or assisted birth can rupture the GM in some foals. The rupture is a devastating condition because the foals are unable to bear weight on their injured hind legs, and the resulting hematoma causes internal bruising and eventually leads to calcification.
In their study of 6 foals, the researchers found that gastrocnemius rupture is a significant cause of non-weight bearing in hind legs in these foals. The musculoskeletal injury was usually diagnosed as a contributing factor to dystocia or assisted delivery, and the most common clinical signs included inability to rise, disruption of the reciprocal mechanism, swelling of the caudal hind limb, and fluid in the stifle joint.
After initial stabilization of the injured limb in a sling, contracture of the flexor tendons developed, and the left foot was not able to support the body weight of the horse. A 4-cm heel-elevating pad was taped to the foot, and the flexor tendons were gradually stretched so that the horse could bear weight on the injured limb. After 8 days in the sling, the gelding was able to stand on three feet and was able to shift his weight from the right to the left hind limb.