Group 13	

DIAGNOSIS

Multiple fractures of the hind limbs; abdominal hemorrhage.


Manifestation of complete diaphyseal fractures of the left femur and right tibia is evident.   
Upon physical exam, palpable instability of the right tibia is apparent.  There is also 
questionable continuity of the left femur due to the presence of crepitus and abnormal 
movement of the leg.  Radiographically, we see a  mid-diaphyseal, complete, 
comminuted fracture of the left femur.  Severe swelling of the proximal part of the left 
leg is indicative of soft tissue damage consistant witb the fracture of the femur.  This 
swelling is caused by the normal healing response to bone and soft tissue after injury.  
The first phase in the healing process is inflammation.  With the tearing of the soft tissues 
surrounding the fracture site and the disruption of the periosteum, we get hematoma 
formation at the ends of the bone and within the medullary cavity.  The osteocytes at the 
location of the fracture become deprived of blood and die. This provides the appropriate 
environment for inflammation.  Vasodilation causes leakage of plasma into the interstitial 
spaces surrounding the fracture site which manifests as the acute edema seen.  
Inflammatory cells are also leaving the intravascular space to clean up the necrotic 
osteocytes and other tissue.  Upon radiographing the right leg, we see a mid-distal 
diaphyseal, comminuted fracture of the tibia and fibula.  This fracture is consistant with 
the swelling of the right leg distal to the stifle.  The same stage of the healing process is 
present in this leg as well.  The hematoma that is formed during this stage becomes 
infiltrated with fibroblasts.  The fibroblasts produce fibrous connective tissue providing a 
framework for cartilage deposition.  This cartilage mineralizes to become immature bone.  
This is known as the callus.  The presence of a callus indicates union of the fracture.  
From this point, various stages of remodeling occur until the callus becomes completely 
mineralized.


Evidence of the fractures was present in the clinical pathology results.  A marked 
increase in alkaline phosphatase suggests an increase in bone osteoblast activity.  The 
margin of ALP increase does not appear to be large.  However, because there are a 
number of ALP isozymes in the body, a modest increase may be present in the face of a 
severe bone problem.

This animalŐs hematocrit is very low.  A decrease in the hematocrit illustrates a loss of 
red blood cells from the circulation.  A likely reason for this loss is hemorrhage.  More 
specifically, hemorrhage into the abdomen as a result of being hit by a a car.  The normal 
total protein, albumin, and globulin values suggest that hemorrhage is NOT evident, 
however.   The normal blood protein values can be explained by the decreased Na and Cl 
values, which point to hemoconcentration as a result of dehydration.  In other words, 
although the blood protein levels suggest that hemorrhage is not present, dehydration and 
resultant hemoconcentration may falsely increase their values to a normal level.  
Additionally, because of this hemoconcentration, it is likely that the hemorrhagic anemia 
is more severe than the hematocrit value suggests.

It is unknown as to whether or not the hemorrhage is accompanied by inflammation.  
Although the white blood cell percentages do not suggest an abnormality, the animal may 
in fact have severe neutropenia.  This is because the WBC counts are given as 
percentages, not absolute counts.

It is unlikely that the liver has been damaged.  The presence of bilirubin and bilirubin 
crystals in the urine are the result of the hemorrhage, cholestasis or liver insufficiency.  
With hemorrhage, the extravascular destruction of red blood cells causes the release of 
hemoglobin, which is metabolized into bilirubin by macrophages and the liver.  Also, the 
liver enzyme ALT level is normal, and the liver is conjugating bilirubin into 
urobilinogen.