Hypothesis 2 Š Dystocia Š induced Limb Deformities

All of the hypotheses include the pertinent obvious injuries: there is a fracture in the 
metacarpo-phalangeal area that was produced from pulling the calf with the calf puller 
and obstetrical chains. It is also established that tissue / bone / joint damage allowed for a 
secondary infection to set into the joint and produce draining tracts. Finally, because of 
improper bandaging of the left front limb with casts and bandages, there was a large 
amount of tissue necrosis and tissue sloughing noticed when the bandages were removed.

This hypothesis includes the possibility that fetal-maternal disproportion exacerbated the 
malformations now seen in the bull calf. The following possibilities were considered.
There is certainly fetal-maternal disproportion, which led to dystocia. Fetal-maternal 
disproportion is seen often with embryo transfer calves, as the recipient cow does not 
contribute to the genetics of the calf. The embryos are usually very superior in genetics, 
and are often very large as newborn calves. In the large animal teaching hospital 95-
100% of the ET calves are delivered by C-section for the safety of the valuable calves 
and the large BW of the calves, which increases the likelihood of dystocia if born 
naturally.

Very large calves in dystocia cases are often in the pelvic canal for prolonged periods of 
time. With the dam pushing on the feet and head of the fetus, the blood supply to these 
areas is compromised. Calves delivered from dystocia are often edematous in the cranium 
and distal forelimbs as venous return is closed off and blood filled these areas. The soft 
tissue becomes tight with fluid and hydrostatic pressure pushes fluid into the interstitial 
spaces. The limbs become cyanotic, and tissue death may begin to occur.

There is a slight chance that congenital valgus deformities contributed to the lameness. 
This is unlikely because the history states that the valgus deformity wasnÕt noted until 
after the cast was removed. Therefore, the valgus deformity is due more to abnormal 
compressive forces placed on the distal limb with the improper reduction of the fracture.

Finally, it is possible that in addition to the aforementioned problems the calf was 
dysmature, and the bones of the distal metacarpus were not ossified completely, which 
made the lameness worse. The pathogenesis would have to include that while the calf 
was being pulled, an abnormal amount of force was placed on the left front limb (if the 
chains were attached to the calf puller incorrectly), which made the lameness apparent 
only on the left front limb. It seems that if there were deficiencies in bone ossification 
that you would see multiple limbs affected, but abnormal forces from the calf puller more 
easily injured the left front, and now the other limbs have had time to ossify. The 
possibility of a dysmature calf leads back to the extreme size is often seen with ET 
calves, and that crowding of the fetus inside the uterus stressed the calf and stimulated 
fetal cortisol release. This would convert the damÕs progesterone to estrogen, which 
would produce oxytocin receptors on the endometrium of the uterus. This would then 
cause the dam to begin labor before the calf was fully mature.