Trauma Flashcards
Describe the differences between primary and secondary bone healing.
The two mechanisms of bone healing are primary bone healing and secondary bone healing. (THIS IS JUST LIKE SKIN: you can sew it up or it can scab.)
Primary bone healing involves a direct attempt by the cortex to re-establish itself after interruption without the formation of a fracture callus.
Just like in skin, primary healing only works when the edges are touching exactly. And since touching edges are not common, primary healing is the less commonly seen type of healing.
In fact, this method is employed only after rigid surgical fixation, or in case with a partial crack in the bone, a so-callled “unicortical” fracture, where the remaining bone holds everything rigid.
The basic science, in brief: Primary bone healing is lead by the formation of a so-called cutting cone (consisting of osteoclasts at the front of the cone to remove bone and trailing osteoblasts to lay down new bone) across the gaps to form a secondary osteon.
Secondary bone healing involves the classical stages of injury, hemorrhage inflammation, primary soft callus formation, callus mineralization, and callus remodeling. This method of bone healing closely resembles endochondral ossification (which involves a cartilage template being replaced by bone).
This suggests that indirect bone healing results in re-formation of bone with essentially the same mechanical properties as the original bone, if not better.
Key point: healing in a sense recapitulates growth. So fracture healing can lead to completely new bone, not scar. (At the other extreme: cartilage: it heals poorly—it not only forms just scar, the scar is poor mechanical quality. Scientists among you: fix this!)
SCHEMATIC: SECONDARY BONE HEALING
1. Bone breaks
2. Hematoma (blood clot) forms at once.
3. From this hematoma, a primary callus forms
This is composed of granulation tissue
(fibroblasts and new blood vessels).
4. The cells in this soft callus make cartilage.
5. The cartilage is then mineralized,
producing “woven” or “lamellar”
ie disorganized, bone.
6. Last, the woven bone remodels
into normal bone (oriented in direction of load).
What are the necessary conditions for appropriate bone healing (leading to minimal functional residuals) and how may physicians optimize the chances for healing?
Successful bone healing requires:
adequate blood supply, relative mechanical stability, sterility and intact surrounding soft tissue.
Physicians may optimize chances of healing by promoting the proper mechanical and biological environment.
Specific measures include:
Reducing (aligning) the fracture; making sure the blood supply and soft tissue envelope are preserved or restored preventing or treating infection; minimizing edema (more for pain control and compartment syndrome prevention, but also to promote perfusion) and allowing just enough loading on the bone to stimulate bone growth but not so much to ruin the reduction or prevent hardening of the fracture callus. (gross motion at the fracture will lead to a so-called fibrous union: some tissue there, but not hard tissue)
Plating a fracture clearly disrupts the soft tissue envelope around a fracture. Why, then, is surgical plating ever used?
Here three types of surgical fixation devices seen in the femur: Plate, Intramedullary nail (rod), External fixator.
One famous orthopaedic surgeon said “fractures heal despite internal fixation, not because of it”.
Surgical implantation of bone plates increase risk of non-union. We use them nonetheless, because they likewise decrease the risk of mal-union (healed, but crooked). Plates can be used to restore alignment, especially near the joint line, where even slight deformities are poorly tolerated (ie, if the bone heals but the joint is not aligned, the patient is not helped).
Note: this question applies to plates which are a particularly disruptive form of internal fixation. Other means of fixation, such as intra-medullary rods, are less disruptive because they are inserted at a distance and funneled through the center of the bone (medullary canal).
Nails too are invasive of course; it is reasonable, then, for you to ask why they are ever chosen. Simply: because casting the bone in some instances would lead to too much immobilization. The nail seen above, for example, replaces a whole body cast.
The external fixator is probably the least desirable fixation device: it is held by pins, which connect the bone to the (dirty) outside world; and these pins (and the fixator itself) are not very rigid either. The external fixator chosen when no other option exists. In the photo shown, the patient had a gun shot wound with lots of soft tissue and vascular damage. The fixator holds the bone in place while those injuries are addressed. A patient with a gun shot wound with lots of soft tissue and vascular damage may have his fixator removed and replaced by a nail once the soft tissue issues are under control—that is, the fixator may be temporary.
Technical/Biological note: the periosteum, the lining of the bone, is the source of the cells that heal the fracture. Periosteal stripping at the time of surgery may make it easier to get the bone seen and the plate inserted, but will also prevent healing! Surgeons are taught to avoid getting hung up on achieving “perfect” looking xrays, especially at the cost of biological disruption.
Suggest how a femoral shaft fracture can be lethal.
A femoral shaft fracture in isolation should not cause death. Yet a patient with a femoral fracture can die from this injury.
Recall that bone is vascular and fractures let marrow contents (fat especially) out into the circulation. Fat could embolize to the brain or the lungs.
These marrow contents are inflammatory in the lungs, and thus, after a femoral fracture, some patients develop ARDS (adult respiratory distress syndrome). Also, the marrow contents are thrombogenic. Patients with fracture, especially if immobilized can get extremity venous clots, and when a clot embolizes to the pulmonary artery unhappiness is the result.
Other serious co-morbidites of femoral shaft fractures include shock from significant blood loss and visceral injuries from the initial injury force that broke the bone.
In this CT angiogram a pseudoaneurysm of medial branch of the profunda femoral artery is seen. Bleeding from this location is not apt to be lethal, but the picture should remind you of the interplay between vascular injury and bone fracture
What is compartment syndrome and how is it prevented, diagnosed, and treated? What are the consequences of not treating a compartment syndrome and over-treating a suspected compartment syndrome?
Compartment syndrome is the clinical condition of increased pressure within an enclosed fascial space, leading to muscle and nerve death from ischemia.
The leg is a typical location because of its well defined (and not very roomy!) compartments, as shown
Compartment syndrome could occur from tibia fractures (bleeding), compressive devices (casts, ace wraps), IV infiltration or burns. (Reprofusion after vascular repair is a non-musculoskeletal cause too.)
The hallmark of compartment syndrome is severe pain that is out of proportion to what is expected from the given injury/situation. One clue what is “out of proportion to what is expected” is pain that increases over time (by contrast, a patient with a splinted fracture should start hurting less once immobilized).
The patient controlled analgesia machines (by which the pain medicine is self-dosed) can give a clue as to the patient’s pain.
In more advanced cases, symptoms may also include decreased sensation, pale skin, and weakness of the affected area.
Physical exam will reveal tensely swollen and shiny skin, and pain when the compartment is squeezed.
Confirming the diagnosis of compartment syndrome involves directly measuring the pressure in the compartment, which is done by inserting a needle attached to a pressure meter into the compartment—or treating empirically if needed.
Treatment is a surgical procedure, fasciotomy, where long surgical cuts are made in the fascia to relieve the pressure. The incisions are generally left open to be closed during a second surgery about 48-72 hours later.
If compartment syndrome is not prevented, permanent nerve injury and loss of muscle function can result and in severe cases amputation may be required. Performing a fasciotomy can potentially increase the risk of infection but overall the risk of not operating is considerably higher…
Define Joint dislocation, subluxation and reduction.
Joint Dislocation (also known as luxation) occurs when the joint surfaces become completely disengaged. A dislocation always damages the ligaments.
Joint subluxation is an incomplete/partial dislocation of a joint.
Joint Reduction is the process by which a structure is brought back into its normal anatomic position. (This term also applies to the bones in the case of fracture.)
Reduction can be spontaneous—ie, the joint simply “pops back into place”. This process of spontaneous reduction, as you might imagine, is more common in joints that are not particularly stable, such as the patello-femoral joint. (Makes sense: easy out; easy in.)
And now think about the structural damage: with a dislocation, there could be a bone contusion where there is abnormal contact (shown below as the green “kissing contusion”); and the ligaments can either rip (as shown) or get really stretched. (A subluxation can cause a bone contusion or stretching of the ligaments; a full tear is less likely.)
Why is a traumatic hip dislocation typically worse than a shoulder dislocation? Contrast the mechanisms which prevent the normal shoulder from dislocating with those of the hip joint, and consider what structures must be damaged when the joint comes out of place.
In brief, the shoulder is a loose joint: the humeral head held in place, adjacent to (but not technically “in”) the glenoid, by soft tissue, not bone. This arrangement allows for more range of motion yet less inherent stability. The hip is held in place, by contrast, via bony congruity: the femoral head sits within the acetabulum.
Conceptually, the hip is a “ball in socket” joint whereas the shoulder joint is more like a ball sitting on a golf tee. These anatomical differences explain why a traumatic hip dislocation is typically worse than a shoulder dislocation:
A hip dislocation requires more force to get the joint out of place. And as a higher energy injury, a hip dislocation is more likely to be associated with other structural damage, such as a pelvic fracture or visceral injury (such as a urethral or bowel tear). Because the shoulder has so much natural freedom, the soft tissues are not tethered tightly and typically have fairly wide excursion. Specifically, the axillary artery must naturally be allowed to move as such motion occurs during normal use of the arm. On the other hand, the femoral circumflex arteries on the femur ordinarily do no move much relative to the pelvis, and when a dislocation "demands" them to move, they are less able to comply. As such, when the hip is dislocated, it is correspondingly more likely that the blood vessels (and nerves) are apt to be damaged.That said, a shoulder dislocation can, under the right (or should we say "wrong") circumstances be associated with a neurovascular injury as well---it is just that there is more margin for error.
What is osteonecrosis? (also known as “avascular necrosis” or “AVN”) How does hip dislocation lead to avascular necrosis? How does avascular necrosis lead to end stage arthritis?
Avascular necrosis is the death of bone, secondary to loss of blood supply and resultant ischemia as seen on the right.
ip dislocation can cause disruption of the blood supply to the head and thus lead to AVN
Recall that bone is alive. Hence:
If bone (like all living tissue) is deprived of its blood supply, ie gets ischemic, it will die. If bone dies, it does not remodel (you remember this...). If bone does not remodel, micro-damage does not get repaired just as a ship that does not get painted with rust. If enough damage accumulates, the bone loses its normal material properties (strength and compliance). It will break, not bend Specifically, the sub-chondral bone will collapse, as shown here.The bone is literally not supporting the surface, which then too will collapse If the sub-chondral bone collapses, the joint surface of course becomes irregular and no longer smooth If the joint surface is not smooth it will damage its rival surface.
This is not a histology slide–it’s a picture of sandpaper. The effect of a rough surface on a smoother one is to make the smooth rough
Note: although you can detect muscle fairly quickly (within hours after an infarct, certainly), acutely dead bone (within hours after an infarct, say) would look normal if examined histologically. That is because for bone, the blood supply primarily serves maintenance, not sustenance. By (poor) analogy: if you can’t get water to drink (sustenance) in three days, you die; whereas if you can’t get water to shower (maintenance) in three days, you don’t start stinking immediately, but stink you will eventually.
Besides osteonecrosis, what other mechanisms may enable a dislocation to cause arthritis?
Recall this picture: dislocation can be associated with an impaction injury to the joint surface, and torn or stretched ligaments.
The MRI of the knee above shows a so called “kissing contusion”—the two high signal areas were impacted against each other. Although the MRI does not show the articular surface very well, we can infer from the appearance of the bone that there was also an impaction injury to the cartilage, with possible irreparable damage inflicted.
Further, if the ligaments heal loosely, if at all, the joint may be unstable, and an unstable joint may be subject to repetitive “micro-trauma”, as the talus (in the example above) rattles around in the joint. (This is the same mechanism by which a loose lug nut on your car may cause your tire to wear out prematurely.) Because of instability the forces in the joint are not applied across a broad area, but rather focally. And because P=F/A, a smaller area for a given force results in higher pressure.
A patient falls on his outstretched hand and has normal appear xrays but tenderness in the “anatomic snuff box” (between extensor pollicis longus and abductor pollicis longus/extensor pollicis brevis).
Why might such a patient be placed in a cast despite the normal x-ray?
A fall on an outstretched hand can fracture the scaphoid bone.
Yet (probably owing to the scaphoid’s geometry and location), a non-displaced fracture of this bone may not be discernable on a plain x-ray.
A patient with a fall and snuff box tenderness may have a non-displaced fracture.
In the event of a suspected scaphoid injury, it is imperative to prevent displacement of the fracture and disruption of the blood supply.
Blood supply to the scaphoid bone is tenuous as most of the scaphoid surface is cartilage–this leaves only a small area for arterial blood supply to enter the bone from the dorsal carpal branch of the radial artery and feed the bone in retrograde fashion.
If the fracture displaces, the blood supply may be interrupted and avascular necrosis of the scaphoid may result.
Preventative casting (to prevent fracture displacement) and follow up radiograph imaging is the standard of care following a scaphoid injury. (In the alternative, an MRI may be used to exclude a non-displaced fracture as shown above. This indeed may be cheaper in the long run, to say nothing of kinder: an unnecessary cast is a burden).
