When to Panic About That Fracture Repair
World Small Animal Veterinary Association World Congress Proceedings, 2008
John P. Graham, MVB, MSc, DVR, MRCVS, DACVR, DECVDI
Maitland, FL, USA

Primary Fracture Healing

Primary fracture healing occurs with rigid fracture fixation such as achieved by a DCP (dynamic compression plate) or sometimes an external fixator. Radiographically, it is characterised by minimal or no callus formation. Histologically, Haversian canals are seen to cross the gap if the fragments are closely apposed, anchoring the fragments together. If a small gap exists it is filled with lamellar bone which remodels in time to reorient to the original longitudinal structure.

Secondary Fracture Healing

Secondary bone healing is the more common type of fracture healing and occurs with less than completely rigid internal fixation (i.e., i/m pin), external coaptation or when no support is provided. The process may be divided into a number of stages:

 Fracture impact--force applied to the bone results in failure and a variable degree of soft tissue injury is also induced depending on the force applied.

 Induction--cells in the fracture area are induced to form bone. Factors involved include pH, oxygen tension and enzymes.

 Inflammation--this stage extends from the time of fracture until the formation of a bony callus. A haematoma forms at the fracture site between the fragments. The role of the haematoma is uncertain; it may form a scaffold for ingrowth of fibrous tissue and may provide some stability due to fibrin formation. The fracture results in a typical inflammatory reaction with release of lysosomal enzymes from the fracture ends and soft tissues. The bone at the fracture becomes necrotic with a hypoxic, acidic environment. Osteoclasts are mobilised and resorption of the fracture ends begins. Radiographically, the fracture ends become less opaque and their edges become indistinct.

 Soft callus--fibroblasts proliferate within a few days of injury. Osteogenic cells from the cambium layer of the periosteum and the endosteum proliferate and migrate into the fracture area forming an external and internal soft callus. The fibroblasts produce collagen, peaking at 7 days. Mucopolysaccharide and cartilage production also peaks at one week and declines over several weeks. Calcium uptake increases, peaking several weeks after injury, and remains high for months or years. This phase ends when the fragments are united by fibrous/collagenous tissue. The soft callus cannot be readily evaluated by radiographs and, at this point, the fracture may feel more stable clinically than it appears radiographically.

 Hard callus--during this stage the soft callus is gradually converted to woven bone by enchondral ossification if cartilage is present or mineralisation of new osteoid. Mineralisation is first visible radiographically at 1 to 3 weeks following injury, initially as poorly defined hazy mineralisations which coalesce to form a bony callus. Eventually, a trabecular pattern develops as the callus becomes more organised. This may take weeks to months and usually accompanies restoration of the endosteal and periosteal blood supplies.

 Remodelling--during this phase there is slow remodelling of the fracture callus to allow function and to restore normal or near normal strength.

Delayed Union

This is an intermediate stage in fracture healing which may either progress to union/malunion or nonunion. It is defined as 'failure of completion of fracture healing within the expected time period for a given fracture type and/or fixation technique'.

Nonunion

In this case there is failure of the fracture ends to unite and all healing has stopped. A number of classes of nonunion have been described.

Viable Nonunion

 Hypertrophic--'elephant foot'--abundance of callus with a well developed blood supply--flared fracture ends--closed sclerotic ends of medullary cavity--fracture gap filed with fibrocartilage--insufficient stabilisation and premature weight bearing

 Slightly hypertrophic--'horse hoof'--milder form of 'elephant foot'--usually due to resorption beneath a plate which does not adequately stabilise a fracture

 Oligotrophic--no evidence of callus--hypervascular fracture ends--ends may round off and demineralise--usually due to too much extension or poor apposition/reduction of fragments

Nonviable Nonunion

 Dystrophic--intermediate fragment with compromised blood supply--instability and poor blood supply result in inadequate osteogenesis

 Necrotic--numerous intermediate fragments--inadequate blood supply, such as a sequestrum

 Defect--loss of segment of bone

 Atrophic--end result of one of above categories--osteoporosis and muscle atrophy due to inactivity--loss of vascular supply--typically distal radius, toy breeds

Radiologic Assessment of Fracture Healing

A useful mnemonic for assessing fracture healing is ABCDs--which refers to alignment, bone, cartilage, device and soft tissues.

 Alignment: One should assess the fracture reduction, i.e., whether the fracture ends have been apposed and whether there is any abnormal angulation or rotational deformity at the fracture site.

 Bone: The bones should be assessed for evidence of lysis and for callus formation. New bone formation is normal, but in most cases should be confined to the fracture margins or surgical site. Extension beyond this may indicate osteomyelitis. The quantity of callus is also subjectively assessed to determine if it is appropriate or excessive. Excessive callus may indicate instability and/or infection.

 Cartilage: Cartilage refers to assessing the joints adjacent to or involved with the fracture. Degenerative joint disease is an almost inevitable sequel to articular fractures.

 Device: Following surgery, the implants used to repair a fracture should be assessed to determine if placement is satisfactory (engaged sufficient cortices, not within a joint etc.). As healing progresses, one should watch for implant failure or loosening.

 Soft tissues: Soft tissue swelling is to be expected immediately following a traumatic fracture and surgical repair. However, it should resolve within 7-10days. Swelling which persists or worsens indicates a seroma, abscess or cellulitis and may be the first indicator of developing osteomyelitis.

Osteomyelitis

Unfortunately, surgical intervention is probably the most common cause of osteomyelitis in companion animals. When assessing a fracture for suspected osteomyelitis the presence of soft tissue changes, type of fracture, method of fixation and extent of bone lysis or production should be considered. Open fractures or fractures with extensive soft tissue injuries are more likely to become infected. Some types of fixation may predispose to complications. For example, the use of large intramedullary pins in immature animals may disrupt the endosteal blood supply and cause sequestration of a segment of a bone.

The body's response to infection is limited to bone production and lysis, both of which we expect to see in the course of normal fracture healing. Infection should be suspected if the degree of new bone formation is greater than expected for the fracture type and fixation technique. New bone which extends some distance from the surgical site also suggests infection. However, in juveniles, the periosteum is frequently elevated from the underlying cortex for some distance from the facture. New bone formation should be assessed to determine its degree of chronicity and activity. Bone production usually occurs on the periosteal surface of the cortex in response to lifting or tearing of the fibrous periosteum. Periosteal new bone should be evaluated for shape, margination and definition. Lamellated new bone consists of multiple layers, much like a cross section of an onion and is usually chronic and the result of repeated insults. It may be seen at the edge of an expansile lesion where repeated growth spurts lift the periosteum from the original cortex and then the new bone forms in layers. A palisade type of new bone formation has a ragged margin and resembles a picket fence in appearance. This is associated with a lesion which is at least moderately aggressive and is a common finding in osteomyelitis. Solid, homogeneous periosteal new bone indicates a chronic and probably inactive process, such as a healed callus. The so-called 'sun burst' pattern of new bone formation is relatively uncommon. This appears as radiating spicules of poorly defined new bone.

The degree of mineralisation of new bone is a useful and reliable indicator of age of a lesion and to a lesser extent of the degree of aggression. Very poorly mineralized new bone is almost always recently formed. In adult animals it takes approximately 10 days for mineralized new bone to become radiographically visible. In juvenile animals this may happen more quickly and new bone formation may be visible 5 to 7 days after an insult. Acute periosteal new bone may be so poorly mineralized that it will not be visible without using a hot light. A relatively underexposed film may be helpful in detecting very poorly mineralized new bone. If the degree of mineralisation of new bone is comparable to the original underlying cortical bone this indicates a chronic process.

The shape and definition of the margin of the new bone should also be evaluated. A useful rule of thumb is that if one cannot trace the outline of the new bone with a sharp pencil then it is classified as poorly defined and should be considered recent and active in nature. If the edge is well defined this indicates a chronic process. A smooth margin indicates a chronic lesion which is completely remodeled and probably inactive. A well defined irregular margin suggests a lesion which is chronic but probably active and is likely to be mildly to moderately aggressive. Productive lesions often include both active and inactive areas of bone formation and, in such cases, one should classify the lesion based on the most aggressive new bone. The rate of change of a lesion is a very useful indicator of the degree of aggression or malignancy. Serial radiographs obtained at 7- to 14-day intervals can be used to evaluate suspicious lesions, especially where the initial findings are equivocal. Aggressive lesions usually show a rapid rate of change with clear evidence of progression of osteolysis and bone formation over a relatively short period of time. If serial radiographs demonstrate no change over a period of 4 to 6 weeks, the lesion is almost certainly non-aggressive.

Fracture Instability

The major differential diagnosis consideration for osteomyelitis is fracture instability either due to implant loosening, inadequate fixation or failure by the owner to enforce exercise restrictions. In some cases, both processes are combined, when infection causes implants to loosen which in turn results in instability. Healing of unstable fractures is characterized by exuberant callus formation. At first this new bone may appear poorly defined and poorly mineralized, which simply indicates that it is new and active rather than aggressive. Over time, the bone should remodel and appear more organized. New bone which has a persistently active appearance suggests infection. Excessive callus formation due to instability is usually confined to the immediate fracture area. Extension some distance from the fracture should lead one to consider infection. The presence of soft tissue swelling in combination with excessive new bone formation and bone lysis supports a diagnosis of osteomyelitis. Clinical signs may also be helpful and may have indicated the diagnosis before the radiographs were obtained. Resolving osteomyelitis is characterized by remodeling of the new bone which eventually becomes smooth, much as healed callus. However, such new bone may be seen with chronic lesions where the new bone walls off the septic focus, a classic example is the bone formed around a sequestrum.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

John P. Graham, MVB, MSc, DVR, MRCVS, DACVR, DECVDI
Maitland, Florida, USA


MAIN : Diagnostic Imaging : Fracture Repair
Powered By VIN

Friendly Reminder to Our Colleagues: Use of VIN content is limited to personal reference by VIN members. No portion of any VIN content may be copied or distributed without the expressed written permission of VIN.

Clinicians are reminded that you are ultimately responsible for the care of your patients. Any content that concerns treatment of your cases should be deemed recommendations by colleagues for you to consider in your case management decisions. Dosages should be confirmed prior to dispensing medications unfamiliar to you. To better understand the origins and logic behind these policies, and to discuss them with your colleagues, click here.

Images posted by VIN community members and displayed via VIN should not be considered of diagnostic quality and the ultimate interpretation of the images lies with the attending clinician. Suggestions, discussions and interpretation related to posted images are only that -- suggestions and recommendations which may be based upon less than diagnostic quality information.

CONTACT US

777 W. Covell Blvd., Davis, CA 95616

vingram@vin.com

PHONE

  • Toll Free: 800-700-4636
  • From UK: 01-45-222-6154
  • From anywhere: (1)-530-756-4881
  • From Australia: 02-6145-2357
SAID=27