Hypothesis 2
Developmental

	The foal may have developed a deformity in the fetlock area, in which, at birth, the weight of the foal may have worsened the problem when trying to stand.  This deformity could in fact developed from the bone growing faster lengthwise rather than building up mass widthwise.  So with stress from standing could in fact lead to this lameness.  Tissue swelling probably occurred from acute damage to the fetlock when the foal tried to stand. Whenever tissue is stressed there is a stress leukogram response.  This response consists of increased leukocytes, therefore leukocytosis.  In addition, you'll see neutrophilia and monocytosis due to the decreased stickiness of the vessel's marginal surface.  All of these leukocytes would produce the increased swelling of the tissue.  So this could have been what we saw in the physical exam.  This is usually a local inflammatory response.  The pitting edema is most likely from the fluid accumulation from the acute rush of leukocytes to the stressed tissue.  One would not notice crepitance because of the increased fluid.
    

	This horse may have a congenital or acquired contracture deformity of the fetlock joint.  The cause of congenital contracture deformities is not known.  Congenital contracture deformities may result from nutritional imbalances in the pregnant mare, uterine malpositioning, teratogenic effects, genetic factors, and neuromuscular disorders.  Acquired contracture deformites usually involve either the metacarpophalangeal  or distal interphalangeal joint.  The cause of acquired contracture deformities is not known either.  Acquired contracture deformities may result from trauma or pain, leading to decreased weight bearing and resultant ligament, tendon and muscle contraction.  Acquired contracture deformities of the coffin joint are usually seen in foals and may develop acutely.  A relative shortening of the deep digital flexure musculotendinous unit is the primary abnormality seen in aquired contracture deformities.  This may lead to toe touching as the coffin joint is flexed due to the shortening of the deep digital flexor musculotendinous unit. Acquired contracture deformities of the fetlock joint may result from relative shortening of the superficial digital flexor musculotendinous unit, and result in knuckling at the fetlock with the foot remaining in normal alignment.  This may also account for the toe touching and lameness seen in the filly.  


	Another probable developmental problem may be angular limb deformity due to laxity of the periarticular structures of the fetlock joint.  This is a congenital problem in which many newborn foals will show weakened musculotendinous and ligamentous structures.  These weakened structures cannot support the joint i.e. fetlock. Therefore, upon standing or any stressful weight-bearing action, the joint could exhibit "laxity."   This laxity could produce traumatic stress to the joint, therefore, the joint will develop swelling and inflammation.  Whenever tissue is stressed there is a stress leukogram response.  This response consists of increased leukocytes, therefore leukocytosis.  In addition, you'll see neutrophilia and monocytosis due to the decreased stickiness of the vessel's marginal surface.  All of these leukocytes would produce the increased swelling of the tissue.  So this could have been what we saw in the physical exam.  This is usually a local inflammatory response.  The pitting edema is most likely from the fluid accumulation from the acute rush of leukocytes to the stressed tissue.  One would not notice crepitance because of the increased fluid.
  
Asymmetric growth of the metaphysis or epiphysis may also lead to the lameness seen in this filly.  Asymmetric growth of the metaphysis or epiphysis may be congenital or acquired shortly after birth.  Abnormal forces on the growth plates is the major cause of asymmetric growth.  Asymmetric growth of the meatphysis or epiphysis may lead to angular deformities that may present at birth, or develop within the first few weeks of life.  Intrauterine malpositioning and physeal fractures are other causes of asymmetric growth.