Understanding strain theory and working length and how this applies to fracture repair
Created with the help of Dr Lucas Beierer, specialist surgeon at QVS. Thank-you Dr Beierer.
This is a topic I really struggled to get my head around for my specialty fellowship examinations. I hope by sharing my confusion, it can help to mitigate others.
Let's start with some definitions and concepts.
Strain: Essentially, strain is the amount of movement. It is expressed as a percentage of movement i.e. movement of gap / original fracture gap.
How does this apply to fractures?
If you have a fracture gap, and the fracture ends touch when you apply a force, this will result in 100% strain. It also means if you have one small gap, any force and subsequent movement is concentrated at this one fracture gap. If you have a comminuted fracture, the several gaps equate to one large fracture gap. This results in inherently lower strain (see the above equation, the denominator will be larger).
Stress: Stress is the force experienced by an object, and it is expressed as force per area or Force/Area.
Working length: This is the inner most section of the construct as it passes across the gap. If a plate is compressed against the bone (dynamic compression plate), the working length is the distance between the bone ends. If not, which is often the case for locking plates, the working length reflects the distance between the innermost screws.
In simple terms, I found it helpful to think of strain as movement and stress as force.
Tomorrow, we discuss plate strain, interfragmentary strain and stiffness.
Plate strain: - This is the strain (movement) experienced by a plate. More specifically, it is the amount the plate moves with a certain force (proportional to the original length). Areas of high strain, are areas of high stress (see the stress, strain curve for this direct relationship).
We don't want high plate strain, because small increases in stress on a plate DECREASE the fatigue life of an implant. The majority of implant failures in the veterinary world are fatigue failures.
Inter-fragmentary strain: - This is the strain (movement) experienced at the fracture gap. The fracture gap can widen, compress or twist, depending on the type and direction of force on the bone. This is important to understand, because if you have a biomechanical study that looks only at one force (e.g. tension bending i.e. the force generally seen with compression or weight bearing - imagine pushing the two ends of the plate together), this might not reflect the real life situation where we know there are different directions of force with weight bearing. Forces include torsion, compression bending and tension bending. Forces change orientation during loading and un-loading of a limb.
As you can imagine, if the plate is more flexible/bendy ie. higher plate movement and higher plate strain, the inter-fragmentary strain is also going to be greater. This makes sense - the plate has more movement, the fracture gap has more movement. More movement = more strain.
Stiffness:
Stiffness can be thought of as how much something moves when a force is applied (it is the slope of the stress/strain curve). If something is stiff, it doesn't want to move when you apply a force. One of the determinants of stiffness is working length. If you increase working length, you decrease stiffness. This means more movement of the plate and higher stress (remember higher strain is higher stress).
So why are these concepts important? - If you increase strain and stress on implants, you decrease the fatigue life of a plate. If you reduce the fatigue life of a plate from 100,000 cycles, to 10,000 cycles this could be the difference between the fracture healing prior to implant failure and catastrophic failure requiring revision.
What else do we know about strain?
We know that strain/movement at the fracture gap needs to be within the tolerable levels for tissues. Fracture stability dictates the type of healing that will occur. With strain below 2%, primary bone healing can occur, whereas at 100% strain the only tissue that can form is granulation tissue. This is the initial tissue at the fracture site. The tissue then progressively stiffens until cartilage can form. Cartilage has a strain tolerance of around 10%. In vitro data suggests that callus is stimulated at strains of around 5-10% and bone is stimulated at strains between 1 and 5%. Bone formation starts in lower strain zones at the periphery prior to spreading inwards across the entire fracture gap.
When I was reading through the literature, I realised why I had become confused about whether increasing working length protected a plate against fatigue fracture and also whether having increased flexibility of a plate sped up fracture healing and reduced complications. What led to my confusion? I have created a list, which starts with ‘Stoffels Paper’.
1 - Stoffels paper.
Dr Mark Glyde gave an excellent AO webinar and highlighted that part of the confusion came from the Stoffel paper. Why did this cause confusion? Because Stoffel found that in the situation of a 1mm fracture gap, the strain experienced on the plate in tension bending was lower with a long working length. However - try to imagine a bendy plate. If you have a bendy plate, the fracture ends touch and suddenly you get load sharing, therefore less movement and lowered strain, however ONLY in tension bending. This is versus a stiffer implant, where you don't get the plate bending in tension bending.
This is what Dr Glyde called the 'strain paradox'. Basically, in the situation of a 1mm gap, strain was paradoxically decreased with a longer working length. However, this was only because the fracture ends touched preventing further movement of the plate in the 'in vitro' situation.
The talk, called 'How Surgical Choices Affect Biomechanical Performance of Fracture Repairs' is an absolute must watch for anyone studying for fellowships and has some excellent diagrams that explain the strain paradox in detail. This is available on the AO website.
2 - Micromotion.
The concept of micromotion led to me becoming confused around whether we should try to have a less stiff implant such that we allow a little bit of movement i.e. micromotion. However, when looking carefully at the literature around 'micromotion', it refers to a specific type of motion which is axial micromotion. Axial micromotion can be created with circular external skeletal fixators (because the wires allow motion at the fracture site that is axial in direction), with some configurations of inter-locking nail and with special plate designs. However, the theory of micromotion should not lead one to believe that we should use less stiff implants in general. When we use a locking plate with a long working length, the motion at the fracture site is multi-directional and not just axial.
3 - Implants that are 'too stiff' delay healing, as callus can't form as strain conditions are too low. Therefore, we should be paranoid about implants being too stiff.
If you have a situation where strain is 0%, potentially this could delay healing. However, it is an unlikely situation in our animal patients that run around on our implants despite our best advice. Running = force = stress = movement and strain. Under-engineered repairs are of greater concern in the veterinary patient and often delayed and non-unions are a consequence of inadequate mechanics or poor biology versus too stiff implants. Low strain environments created by stiffer implants facilitate harversian canals and bone formation.
‘Too stiff’ constructs are more common in the human counterpart and there is more discussion in the human literature.
4 - The concept of elastic osteosynthesis - this is a situation where we choose a long working length / 'bendy plate' on purpose.
This is something that is very specific to juveniles less than 4 months of age. Juveniles have thin cortices but robust periosteum. If you use overly rigid fixation in juveniles, this can lead to concentrated forces at the screw-bone interface. In the situation of a cortical screw, in this poor quality soft juvenile bone, this could result in poor screw purchase, screw loosening and subsequent implant failure. This situation is less common with locking screws, as for a locking screw to fail it needs to 'slice' through the bone.
5 - Toy breeds. Toy breeds are another special case that have led to confusion over working length and stiffness. The thing to remember about toy breeds, is that any implant has the potential to lead to stress protection. This doesn't mean that for toy breeds we should use flexible implants. For the same reasons as above, implants without the appropriate stiffness will fail in the same way as for any dog. There are other ways to reduce the risk of complications in toy breeds, however this is for another post.
6 - Minimally invasive plate osteosynthesis. This is a situation where we often end up with a long working length, however this is because we have chosen to sacrifice the mechanics of our implant, to preserve the biology. This approach can be appropriate, however it should be undertaken with knowledge that that the increased working length decreases the stiffness (and therefore 'life' of the plate). We therefore rely on the biology to speed up healing so our plate doesn't prematurely fail due to fatigue failure. Further advancements with intra-operative imaging such as fluoroscopy, has meant that we can maximise biology and also place implants with a smaller working length. This is possible via small stab incisions.
Summary:
- More flexible implants increase strain at the fracture site. An increase in working length, creates a more flexible implant.
- If you increase strain and stress on implants, you decrease the fatigue life.
- Strain needs to be at the tolerable levels for bone formation and this tends to be very low.
- There are multiple concepts that have led to confusion around strain theory. I have outlined how the strain paradox, the concept of micromotion, the fear of 'too stiff' implants, the concept of elastic osteosynthesis in juveniles, fracture healing in toy breeds and minimally invasive plate osteosynthesis led to confusion for me.
I hope that the creation of these posts has helped to explain these concepts further. Dr Lucas Beierer and myself would be happy to answer any questions.
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