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Toronto,
ONHistorically,
it was generally accepted that once a diabetic patient developed
a foot ulcer the next surgical intervention was a below-knee amputation.
This is no longer the accepted standard of care, said Tim
Daniels, MD, assistant professor, University of Toronto, and an
orthopedic surgeon specializing in the foot and ankle, St. Michaels
Hospital.
If the blood supply is sufficient, there are many things that
can be done to provide the patient with an ulcer-free foot and a
functional leg for many years.
In addition to glucose management and wound debridement, pressure
offloading is essential to healing the pressure ulcer. Offloading
technique depends on the etiology of the pressure ulcer.
Peripheral neuropathy leads to loss of protective sensation.
Eighty-five per cent of diabetics with a neuropathic ulceration
have lost their protective sensation. Its not the only factor,
but its an important factor, Dr. Daniels said at the
annual meeting of the Canadian Association of Wound Care.
Two current theories for the development of diabetic neuropathic
foot disease are:
Increased sorbitol levels decrease the potential for detoxification,
altering fatty acid metabolism, and causing permanent damage of
axonal transportation in the nerves; and
Since tissues are continuously bathed in abnormally high
glucose, glucose byproducts attach to areas they should not, leading
to altered crosslinking of collagens.
As well as loss of protective sensation, peripheral neuropathy can
cause muscle contractures that lead to gait changes. For example,
a tight heel cord commonly occurs. This causes the heel to leave
the ground earlier in the gait cycle and increases the pressure
at the toes. The abnormal pressure can lead to callouses and pressure
ulcers.
There are many ways to reduce the forces and pressures that can
lead to foot ulcers or sores (off- weighting). It may be as simple
as checking the shoe. Poor-fitting or worn out shoes can lead to
increased pressures on the foot. Callous reduction or debridement
is another form of pressure reduction.
Callous debridement
Callouses on the feet of diabetics are thicker than normal. This
is due to nonenzymatic glycosylation. It gets to a point where
its starting to cut off the blood supply to the tissues between
the bone and the skin. Normally this would be painful, but in a
person with diabetes and neuropathy there is no pain, so the individual
keeps walking, said Tim Kalla, DPM, clinical instructor, University
of British Columbia, Vancouver, and an operative podiatrist and
diabetic foot specialist, Foot and Ankle Clinic, Providence Health
Care.
Continued walking on the thick callous damages the deeper tissues
and fluid starts to form under the skin. The fluid needs to drain
and usually it bursts out through the skin. Once this happens bacteria
can get in through the drainage hole. If the broken callous (ulceration)
is not debrided or cleaned up properly at this point, skin may form
over the surface of the wound, sealing in the bacteria and starting
an infection. Furthermore, callous debridement reduces pressure
on the tissue of the foot, allowing the ulcer to heal. The
rule of thumb is to debride the callous twice as wide as it is deep,
Dr. Kalla said. Studies have demonstrated that debridement of the
callous can decrease the pressure to that area by 30 per cent, Dr.
Daniels said.
Pressure offloading
Rocker-soled (rigid-soled) shoes and total contact casting both
allow the diabetic patient to approximate a normal gait, redistributing
pressure evenly while walking. It is very important that the upper
part of the rocker shoe is straight, Dr. Kalla said. Ive
seen some rocker-soled shoes where the sole is very rockered, but
so is the upper. The whole thing is bent like a banana. If the foot
is as stiff as it is, the foot will never fit into the shoe, and
the shoe will cause the patient more harm.
Total contact casting combines protection of the limb/foot from
outside trauma with gait correction. Casting to heal a diabetic
foot ulcer is almost the same as casting for a broken ankle, said
Gord Jones, registered orthopaedic technologist, St. Michaels
Hospital. Find the person who puts on broken ankle casts and
tell them they can do total contact casting now. If they want to
know what the subtle differences are, give them my phone number.
I can teach them on the phone, Mr. Jones said. He noted the
main differences in casting to correct diabetic foot ulcers:
Casts should have a minimum of padding;
Casts should extend beyond the toes on the bottom and be
cut back on top so that the patient can monitor circulation or the
general condition of the foot;
There is a 30 per cent chance that the limb is disvascular,
so the limb must be palpated for a pulse. A cast is only appropriate
on a limb with a good blood supply.
Extreme care should be taken to ensure that the cast does
not put too much pressure on any part of the foot or limb. The patient
does not know if there is too much pressure because he cannot feel
the pain.
Surgery
Bunions or bone mass can be removed, and the heel cord can be lengthened.
Dr. Kalla described a patient with a metatarsal amputation who subsequently
developed a stump ulcer with new bone formation on the stump. Some
amputees develop stump ulcers because bone deposits at the site
of the surgery, increasing pressure on the soft tissue. In this
case, Dr. Kalla did not remove excess bone mass because the problem
was a stiff ankle joint. The joint was probably tight to begin
with secondary to the glycosylation of collagen (Achilles tendon),
so the patient developed equinus contracture of the ankle.
In addition, the amputation severed the extensor tendons (primary
dorsiflexors) that counterbalance the Achilles tendon. The heel
cord was lengthened so the foot could rest flat on the ground. A
month after heel cord lengthening, the ulcer at the front part of
the foot healed up nicely.
One study showed the risk for neuropathic diabetic foot ulcer recurrence
is 75 per cent less at seven months and 52 per cent less at two
years for heel cord lengthening versus casting alone (J Bone
Joint Surg Am 2003 Aug;85-A(8):1436-1445).
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