Rethinking orthopaedic and forefoot surgery.

This post continues the page Stop! Wrong way! in relation to orthopaedic management

Deformities of the forefoot. These include “bunions”, Morton’s “neuroma”, clawed toes and “flat foot” (whatever that is intended to mean). It is unlikely that any group of elective procedures has been performed, in total ignorance of the causative factors, more often, by more people, in more ways, than various forms of surgery to the forefoot.

Fractures being “set” as soon as possible after the injury. This damaging policy produces significant, irreversible, complications. It will be addressed in a separate post on this site at a later date.

Finger-tip injuries. These common injuries produced a plethora of surgical treatments, from skin grafts and”rotational flaps” to “cross-finger flaps”. These required not-inconsequential surgery, sometimes under general anaesthetic, were expensive and incapacitating for various periods, and unnecessary. Harvest was taken from uninjured areas of the palm and other fingers, scarring those. The best results however have been shown to be obtained by doing nothing beyond usual wound care! The body’s capacity to heal itself at that site is not unexpected, being as easily and frequently injured as the fingers are.

“Traction” for so called “slipped discs” (mostly that diagnosis was incorrect, in the event). Tens of thousands of patient-days were lost by placing these unfortunates in hospital and attaching weights by cords to their legs, literally tethering them to their bed for days or weeks. This was entirely ineffective since the friction of the legs prevented transmission of any “traction” to the discs. The management was adversely effective, since most low back pain improves more rapidly with movement (ideally in water). Deep vein thrombosis would be expected to be increased by this form of immobility. I wonder how many died of resulting pulmonary embolisms.

 Osteomyelitis. Antibiotic usage and aggressive resection of bone is often counter productive and dangerous. The loss of the limb might result from some current management policies. This is addressed in a separate post on this site.


Broken leg!

Breakages of the tibial shaft are often tragic injuries. Relatively common, they often occur in the young and active, often the bread-winner with a young family. The convalescence is long, often harrowing and at times results in the loss of a leg.
It is only the shaft breaks which are so distinctly different. Breaks of the tibia near the knee or ankle, although challenging to the surgeon, nevertheless follow the relatively predictable course of other breakages. Tibial shaft breakages are different from other long bone breaks and are notorious for the following triad of serious complications.:

1. The bone easily breaks through the skin because of the closeness to the skin.
2. These breaks are prone to develop infection (osteomyelitis).
3. These breaks are prone to delayed union, or fail to unite.
“Conventional wisdom” has traditionally sought to explain the behaviour of tibial breakages as follows:
1. The skin breaks easily, therefore the wounds become contaminated at the time of the accident
2. Contaminated wounds cause infections.
3. Infections cause the delayed union or non union.
This “wisdom” then dictates that the contamination requires immediate treatment, and it is claimed that if the infection is prevented or treated early enough, all will be well. Is this true? Why then is there such a problem, and why are limbs still lost?

The management is often less than optimal because this “authoritatively” held rationale is fallacious. This is demonstrated by the following:
1. Tibial breaks in which the skin is not damaged also become infected. This is contrary to the normal resistance of non-injured bone which, in the adult, is remarkably immune to infection.
2. Impaired union also occur without infection.
Therefore there must be another explanation, and an additional factor operative.

In fact there is, something that has been long known, but now not considered by some. This is the unique blood supply to the tibia. Because the cortex is so thick and dense, the major part of the bone of the distal tibial shaft is supplied by “endosteal” vessels. Usually only a single artery gains entry through one (occasionally more) “nutrient foramen” into the marrow cavity. This is a small hole in what is otherwise a solid and strong bone. When the tibia breaks it might do so through that perforating tunnel (not unexpectedly since it is a potential weakness in the bone) the site of the nutrient artery. The fragments displace, and this vulnerable vessel is easily torn. Once this happens a large part of the tibia is deprived of its blood supply and could die.
Well known analogies are breakages of the scaphoid and femoral neck, where the blood supply is often damaged with resulting impairment of union.
In addition to the endosteal supply tibia has a lesser blood supply from the surface (not the marrow) of the bone, via “periosteal” vessels. However these, also, can be damaged directly by trauma or indirectly by “compartment syndromes”, or (tragically) ill designed surgery. The analogy here is with injudicial surgical “stripping” (destruction) of the periosteum in the process of plating the bone. This also causes bone death, which is followed by loss of resistance to infection and loss of capacity to unite.

It is this dead bone, like all dead organic matter, is then becomes vulnerable to becoming infected by organisms which are in or on the body, and which might be transported by the blood stream. Certainly some infections are introduced by breaks in the skin, but it is the death of the bone which allows the infection to become established, and resistant to treatment. That will explain why the infections in broken tibias can occur after a delay, sometimes a considerable delay. It also explains why non union occurs, which is because dead bone does not have the vitality to unite. Natural healing tendencies do cause new blood vessels and new bone to try to grow into the dead skeleton and so re-vitalised it. Therefore, at times, even when the tibia is dead, and perhaps infected, union might eventually occur.

However the absence of early radiological evidence is not surprising; unless there is a blood supply the calcium and other minerals cannot “wash-out” and become radiologically identifiable. But once bone regeneration occurs (usually via the periosteum provided this has not been destroyed surgically) new bone becomes apparent radiologically and the well recognized “involucrum” can be seen. As newer blood vessels invade the dead bone, then the mineral is resorbed, fragmentation becomes possible and this dead bone separates as a “sequestrii”. At some stage after a tibial break spicules of bone (caused by the break or perhaps surgical reaming) can, not unexpectedly, be expelled, as reparative secretions tend to wash out inert debris.

What is the evidence for this hypothesis?
1. The vulnerability of the blood vessels is supported by long established anatomy.
2. The portions of the tibia near the knee and ankle have a different, less vulnerable blood supply, and do not have these complications.
3. Dead bone is demonstrable at surgery.
4. In order to produce osteitis experimentally in animals it is usually necessary to introduce a “sclerosant” to kill the bone at the time of inoculation with the bacterial infection. Living bone effectively resists infection.
5. Radioisotope labels do not label dead bone, and this has been shown to be the case with infected and non-uniting tibial shafts
6. Radio isotope labeled white cells can be shown to attach to infected or non-uniting tibial shafts, reaching the bone, not through the blood supply, but by migration.
7. Intravenous antibiotics are less effective in the management of tibial infections (because of poor blood supply) than antibiotics administered by lavageing fluids, an alternate route.
8. Compartment syndromes, common in tibial injuries, are known to interfere with the periosteal blood supply, which could otherwise supplement insufficient endosteal supply.
9. Surgical “reaming” for fixating intermedullary nails has been shown to cause a higher infection rate. This is because the endosteal vessels are further damaged, and aggressive reaming can burn the tibia with further death of bone.
10. The analogies with other bones.

Recognizing that the primary cause of the complications of tibial shaft fractures is a failure of the blood supply has important relevance to the treatment of tibial shaft fractures, particularly where infection and delayed union develop