Diagnosis: Trauma/HBC

The pathophysiology of the initial trauma is somewhat speculative. Based on the 
anatomic areas of fractures we suspect that Ramon was hit on the Right side initially 
causing the tibial fracture.  The impact of the car probably threw Ramon onto his Left 
side resulting in the Midfemur fracture and diffuse swelling of the left leg.  Due to the 
force of the car hitting Ramon and the following impact on the ground the soft tissues 
surrouding the impact areas were affected.  Again we speculate that the swelling was 
more focal on the right side due to the direct hit, whereas the swelling on the left side is 
more diffuse due to the impact of the whole left side with ground.  The forces of both of 
these impacts was enough to cause direct soft tissue damage ( bruised muscle) and 
breakage of blood vessels leading to subcutaneous fluid accumulation.  The swelling 
could be due to hemorrhage ( supported by the decrease in PCV-22%, with no evidence 
of concurrent internal hemorrhage, although this was difficult to rule out since abdominal 
and chest radiographs were not provided) and inflammatory mediated vasodilation and 
subsequent leakage of intravascular fluid into the subcuitis.  Besides the torn soft tissues 
and vessels, the disrupted periosteum also lead to hemorrhage as well.  With severe soft 
tissue trauma, fracture repair may need to be delayed until some of the 
swelling/hemorrhage is resolved.  Since it has been 3 days since Ramon was hit by the 
car, he is probably still in the inflammatory stage of healing ( again, besides the phyical 
indicators of swelling/hemorrhage, this is difficult to assess according to the CBC 
because only percentages of each of the white blood cell types was given, rather than 
absolute values).  The environment in the inflammatory phase consists of the torn soft 
tissues, the periosteum and vessels.. There is a hematoma within the medullary canal and 
surroudnign the fracture ends.  The hematoma serves as a clot.  The osteocytes within the 
lacunae  of bone ends are deprived of blood supply and dies as far back as the collateral  
channels.  The immediate fracture ends are dead ( contain no living cells).  There is the 
presence of much necrotic material.   In response to all of this there is vasodilation and 
plasma exudation leading to acute edema ( the diffuse and local swelling noted on 
physical exam).
	The presence of superficial and deep pain indicate that there was not 
severe/irreversible spinal cord damage. The nonrepeatable reflexes may be due to the 
pain and decrease in motor response.  These should be re-evaluated in a few days.  
	The blood work indicates that Ramon is anemic, most likely due to hemorrhage at 
the fracture sites.  The other values do not seem to be too skewed from normal (although 
there was no reference range made available ).  The chloride and sodium may be low due 
to the hemorrhage as well.  It is difficult to evaluate this fully without reference intervals 
for a young dog.  

Most likely in the the next few days there will be organization of the hematoma which 
plays a minor role in fracture stabilization and serves as a fibrin scaffold for reparative 
process to occur.  Mesenchymal cells will migrate primarily from surrounding vessels, 
linked with ingress of capillary buds.  There will be an increase in the vascular bed 
surrounding the soft tissues, but this lasts only til normal circulation is restored in the 
surrounding soft tissue.   Internal, external and intercortical calluses will form. Cells 
invade the hematoma and produce fibrous tissue. This turns to cartilage and then 
immature fiber bone.   This causes an increase in stability ( clinical union). This whole 
process is influenced by intrinsic and extrinsic stability.

The next stage is remodeling.  There is reorganization  of bony architecture ( bone 
resorption, bone deposition) according to mechanical stress .   This will occur over a long 
period of time.  

Depending on how well the surgical fracture stabilization goes there may be gap healing 
or contact healing.   In gap healing there is filling of a fracture gap by primary bone 
formation with organization of new bone transverse to the long axis of the diaphysis.  
"Cutting cones" ( osteoclasts followed by a thin walled capillary loop running within the 
resorptive cavity, surrounded by osteoclast precursors which  differentiate into 
osteoblasts and produce osteoid on the surface o fthe resorptive cavity ( mineralization of 
osteoid occurs; the resorption cavity will fill entirely with connective layers of new bone 
and become and osteon) and advance thru the new bone.  In this way the gap is healed.  
This would occur if not all fragments were able to be placed in their original fragments.

IN contact healing, the bone ends are held tightly in contact by compression. There is no 
gap to fill, therefore normal Haversian remodeling begins immediately with cutting 
cones.

Conditions that will influence the fracture healing include local factors such as the degree 
of local trauma, the degree of bone loss, and type of bone involved, the degree of 
immobilization, and if there is infection present.  Pathologic conditions can also affect 
but this does not appear to be a factor in this particular case.  Systemic factors such as age 
( this is a young patient so is expected to heal faster/better), hormones, and exercise. 
Rest/leash walking will be critical points in client communication.