DIABETIC FOOT CARE

The primary goal in the management of DFI is to maintain
functional ambulation through the prevention and treatment of
neuropathy and infection. It is clear that development of peripheral
neuropathy in the diabetic is related to high blood sugar levels (23,33).
Frequent blood sugar tests for at-risk groups (e.g., overweight family
members) will aid in early diagnosis. Recently, the level of
hyperglycemia for the diagnosis of diabetes was lowered from 140 to 126
mg/dl (59), and at-risk group initial screening
may be lowered from 40 to 25 years of age. Aggressive management of
diabetes with patient education, diet, exercise, and medication yields
the best blood sugar control, resulting in decreased complications of
neuropathy and vasculopathy.

Many patients are unaware that they have diabetes, which
is demonstrated by the fact that almost half (43%) of all diabetics
have their first hospital admission or diagnosis of diabetes associated
with a foot infection (7,42).
Most patients, and many nurses and doctors, are unaware that neuropathy
is a main contributing cause of DFI. Ninety percent of these patients
have neuropathy that is associated with high blood sugar levels. Eye
problems in diabetics (retinopathy) and foot problems (peripheral
neuropathy) do not have the same etiology. Peripheral neuropathy is
mainly a chemical neuropathy, whereas retinopathy is due to ischemic
focal occlusion from plaques in athrosclerotic vessels. Although it was
previously believed that proper glucose control would not affect
diabetic retinopathy, it has been demonstrated that the diabetic
patient under “intensive control” can dramatically reduce the
progression of not only neuropathy and nephropathy but also retinopathy
(20,23,34).
Therefore, education of the patient, family, and health care team is
the key strategy in the prevention of these diabetic-associated
problems.

The American Orthopaedic Foot and Ankle Society has
published a brochure, “The Diabetic Foot,” to help the physician with
patient education.* One recommendation
presented in this publication is that diabetic patients should wear
shoes at all times, except in bed, to protect the feet from minor
injury. Because DFIs start as ulcers in the insensate skin, normal or
continual pressure on insensate skin causes the skin to break down.
Therefore, diabetics must frequently check their feet to remove
wrinkles in socks or foreign objects in shoes and vary pressure on the
feet. They must always be cautious to avoid injury and to look for and
immediately respond to any signs of infection in their feet. Insensate
skin will also break down due to new shoes or a change in the level of
use of the foot such as would occur in a new job requiring more
walking. One patient of ours, a school teacher, presented with a
cellulitic toe ulcer. When we showed him that his shoe had a roofing
nail in the sole, he said, “We are building a gazebo, but I visited the
building site 10 days ago.” He had acquired the nail in his shoe then
and had been walking on it since. The cellulitis was bad enough to
require admission, intravenous antibiotics, and debridement, followed
by a long course of oral antibiotics and wound care, with eventual
healing. He returned five years later with a small ulcer in the other
foot from another nail. He sheepishly took the nail out of his pocket
to show us and commented, “I found this in my shoe shortly after I had
been outside.” The second ulcer healed quickly with outpatient care and
oral antibiotics. At least he knew to check his shoes and feet, and he
knew the signs of infection. Even though his disease had progressed, he
had less of a problem with the second infection than with the first.

In the diabetic, nerves undergo metabolic changes due to a build-up of sorbitol and fructose, and a decrease of myo-inositol

and sodium-potassium-adenosine triphosphatase. These changes occur when
increased tissue glucose is metabolized by an alternate pathway as a
result of the lack of insulin, leading to decreased nerve cell function
and disruption of the membrane-associated sodium pump. This factor, in
turn, causes a reduction in the ability of the nerve cell to maintain a
normal polarized state, and leads to demyelination, nerve injury, and
eventually, nerve death (33).
Loss of large sensory fiber and motor nerves causes a decrease in light
touch sensation and proprioception, as well as ataxia and weakness.
Loss of small sensory fibers causes a decrease in pain and temperature
sensation. With decreased sensation, injuries may go unnoticed and
repeated insults to the soft tissue and bone can occur (9).
Also, loss of protective sensation in the joints often results in
excessive forces applied to ligaments, cartilage, and bone, leading to
joint erosions, dislocations, fractures, and Charcot’s joint (common
eponym for neuroarthropathy) development and necrosis (25,32). Neurovascular dysfunction and autonomic failure may also play roles in the development of the Charcot’s joint (9,31).

Multiple studies have shown a correlation between poor wound healing and poor nutrition.

Therefore, it is imperative that the diabetic patient
learn to monitor blood sugars closely with visits to the
endocrinologist, diabetologist, internist, and nutritionist. When an
infection is present, blood sugar levels are more difficult to control,
and may require several days or weeks to stabilize after the infection
is controlled. A well-kept patient diary that records date, time, blood
sugar levels, food, and medication is a useful tool.

Limited joint mobility occurs in diabetics as the foot
loses its sensation, proprioception, and intrinsic muscle function.
Sensation and intrinsic muscle causes an “extrinsic plus” wide-based
gait for balance that progresses to claw toes, midfoot valgus, and
calcanealequinovalgus with decreased ankle and subtalar motion. Thus, a
flat, stiff, insensate foot is more prone to injury, further breakdown,
decreased mobility, and ulcer formation.

The family physician, internist, orthopedic surgeon,
vascular surgeon, plastic surgeon, nutritionist, diabetic nurse, and
social worker need to work with the patient and the patient’s family.
Regular, urgent, and emergent clinics that the diabetic patient can
easily access will prevent minimal

problems
from becoming major problems. The diabetic wound care nurse or
physician’s assistant plays a vital role as a part of the care team.
Special training, either with a skilled local foot care team or at
national courses, can give the nurse or physician’s assistant the
skills to organize a wound care clinic. This clinic should be open 5
days a week for dressing care, and a member of the foot care team must
be readily available to answer telephone inquires from patients and for
referrals. Education of local emergency rooms and primary care clinics
regarding preventive care and the decision of when to refer is
important. The most important members of this team are the patient and
family because they must become knowledgeable and involved. If they are
not or cannot be involved, then the prognosis of the patient is
typically poor and they will require more care by the doctors and
nurses in the clinic or hospital.

The treatment of DFIs is extremely important. Eighty
percent of amputations and 20% of hospital admissions each year are due
to DFIs (60). In a poorly treated foot ulcer, osteomyelitis increases the risk of amputation (3).
A good treatment plan must address the underlying cause of the skin
breakdown or infection and not just simply treat the ulcer itself.

We have found it helpful to teach the patient, family,
and health care team the most common causes of (and terms for)
infection and pathology in the diabetic foot. The team, which consists
of the patient, family, doctors, nurses, and assistants, must be able
to classify the infection and respond to it appropriately: “Is it more
red?” (i.e., cellulitis); “Is there a skin sore?” (i.e., ulcer); “Is
there a deep infection?” (i.e., abscess or bone infection); “Is there
dead tissue?” (i.e., gangrene); “Is it getting better or worse?” (i.e.,
do we continue with this treatment or go to the clinic for a check-up
or to the emergency room for admission?).

We have looked at diabetic infections in 1,752 cases
over a 20-year period and have concluded that a simple, common
classification system (Table 116.2) aids in consistent categorization and treatment for the best outcome (7,10,11).
The simplicity of the classification also facilitates as ease of
communication between the team and the patient. The best way to think
about the type of infection in order of increasing severity and stage
is cellulitis, ulcer, abscess, osteomyelitis, and gangrene. One or all
of these infection grades can be present, but typically one
predominates and the more severe type (i.e., the higher stages)
determines treatment. Furthermore, the presence of neuropathy and
ischemia make the treatment more involved.

Emphasize daily inspection of toes and feet. A mirror
can be used for self-examination of the bottoms of the feet. Patients
with impaired vision should have a family member inspect their feet
daily. It is important to stress daily foot washing, careful drying
between the toes, and daily application of a light water-based (not
alcohol-based) cream without moisturizing between the toes. Caution
patients

to
avoid exposure of feet to extremes of temperature. Have them test the
temperature of bath water with the elbow before immersion. Patients
also need to avoid using chemical agents or doing bathroom surgery to
remove corns or calluses, and application of adhesive tape to the feet
must be avoided. It is also important for the patient to inspect the
insides of their shoes daily for foreign objects, nail points, and torn
shoe linings. Wearing properly fitted stockings without seams or mended
areas may prevent unnecessary irritation. Caution patients against
wearing sandals or shoes without stockings. Patients should never walk
barefoot, especially on hot sandy beaches or around swimming pools.

Appropriate activity modifications should be suggested. Last, patients should avoid wearing garters or sitting cross-legged.

Factors that predispose diabetics for foot infections
include patient noncompliance and poor visual acuity, making daily foot
inspections unreliable. Patients with peripheral neuropathy often have
delays in diagnosis of infection owing to a failure to sense tissue
damage. Also, autonomic dysfunction leads to anhydrosis and a loss of
skin temperature regulation, which can result in dry, scaly,
easy-cracking skin contributing to ulcer formation. These cracks and
ulcers provide a portal for bacterial invasion that leads to infection.
Poorly controlled diabetics have these problems in greater frequency (27). When ischemia or malnutrition is present, infection is also more likely to develop.

The focused orthopaedic examination of a DFI should
begin with the evaluation of both lower extremities from the knee down.
Owing to peripheral neuropathy, diabetics with infection may not have
pain as a primary complaint. The patient and family will note fever,
chills, and recent hyperglycemia despite a normal dose of insulin. On
physical examination, look for erythema, swelling, induration, or
fluctuance, and probe ulcers for depth and the presence of an abscess
or exposed bone. Laboratory studies may show an elevated white blood
cell (WBC) count with an increase in polymorphonuclear cells and
elevated erythrocyte sedimentation rate, C-reactive protein, or
glycosylated hemoglobin.

Neuropathy assessment includes an evaluation of sensory,
autonomic, and motor functions. Although diabetics may have numbness,
they may still feel pain. The so-called “stocking-glove” description of
the sensory deficit distribution is not accurate. Although peripheral
neuropathy is usually more severe distally, the proximal border of the
neuropathic area is not, typically, a perfect cross section of the
affected limb. The border is typically more distal directly over the
major sensory nerves for evaluation of touch and more proximal farther
from the major nerves for evaluation of painful stimuli. Some patients
complain of severe paresthesia (spontaneous pain or burning) and
dysesthesia (contact pain), which is thought to be a result of
spontaneous depolarizations of injured or regenerating nerves (33).
Light touch, the pin-prick test, two-point discrimination, and the
Semmes-Weinstein monofilament can be used to document the sensory
deficit. About 10% of patients who have already had ulceration still
meet the supposed threshold criterion of feeling the 5.07%
Semmes-Weinstein monofilament (7). The pinwheel
test allows rapid cutaneous sensory mapping of fine point and pain
perception. Clean the pinwheel well with alcohol between patients or
use disposable pinwheels. Autonomic deficits present as dry, stiff skin
that easily cracks owing to a loss of skin temperature regulation,
abnormal sweating, and arteriovenous shunting (1,27).
Clawing, pes planus, and equinus contracture occur from motor
denervation of the intrinsics and compensation by the extrinsics. When
combined with decreased sensation, the likelihood of ulceration
increases dramatically.

Patients with good capillary refill do not require
additional diagnostic screening. Patients without pulses and good
capillary refill may benefit from vascular consultation and screening
with Doppler studies, transcutaneous

oxygen
measurements, or angiograms. Vasculopathy can be demonstrated by
blanching normal skin and releasing the pressure. Normal blood flow
results in capillary refill in less than 2 seconds. A mild decrease in
the blood flow requires 7 seconds, moderate flow takes up to 13
seconds, and severe impairment greater than 13 seconds. Assess the
temperature of the skin with the back of one’s fingers. Some other
signs of vascular insufficiency can be observed by skin changes that
include loss of hair and smooth or edematous skin.

Wagner has used ankle brachial Doppler pressure ratios of less than 0.45 to indicate the potential for poor wound healing (10,54,69).
For Doppler pressures, request toe pressures and pulse-volume
recordings (PVR) at different locations along the limb. The PVR is
normally triphasic, but when the vessel looses compliance, the waveform
becomes monophasic or biphasic (7). Toe
pressures less than 40 mm Hg are unlikely to result in healing of
ulcers and are at a higher risk for requiring reconstructive procedures
(2). We recommend the use of transcutaneous oxygen measurement (TcPO₂) for evaluating vascularity, healing potential, and soft-tissue viability (3,11,29). Values of TcPO₂ lower than 20 mm Hg often result in local surgical failure unless a vascular bypass is performed (13,14,70). Other useful studies are angiography or xenon clearance studies, but these procedures are more expensive and invasive.

The clinical presentation and findings on physical
examination determine the need for imaging studies. Imaging studies are
often overused. Plain radiographs suffice in the vast majority of DFI
cases. In all patients presenting with DFI, high-quality radiographs of
the feet include anteroposterior (AP), lateral, and oblique views. Look
for loss of soft-tissue planes, lucencies indicating gas, foreign
bodies that may have precipitated the infection, and bony changes such
as erosion and periosteal new bone formation that may indicate
osteomyelitis. The osseous radiographic changes of neuroarthropathy can
simulate osteomyelitis and the differential diagnosis can sometimes be
difficult. Lytic changes in bone without overlying skin ulceration is
usually not due to osteomyelitis but rather due to neuroarthropathy.
Radionuclide scans, computed tomographic (CT) imaging, and magnetic
resonance imaging (MRI) may be necessary to differentiate between
osteomyelitis and Charcot’s arthropathy, abscess, cellulitis, or early
osteomyelitis (19,30,50,55,68).
Although these studies are useful in certain instances, a sterile
aspiration or biopsy in clinic or on the hospital floor is an easy,
rapid, and painless procedure, because the patient has no sensation in
the involved area.

Cellulitis can range from mild redness around a callus
or ulcer to full foot or leg involvement, with swelling and lymphedema.
Underlying abscess, osteomyelitis, gas gangrene, or necrotizing
fasciitis that can cause sepsis and death should be ruled out by
examination and radiographs. Most mild cellulitis around a callus or
ulcer can be managed on an outpatient basis with local skin care and
oral antibiotics (Fig. 116.1). Mark the border
of the red cellulitic skin with a permanent pen to establish a baseline
before treatment is started. if the cellulitis worsens (extends 2 to 3
cm past the baseline) after 24 to 48 hours of oral antibiotics, the
patient should be re-evaluated and treated with different oral
antibiotics or hospital admission and intravenous antibiotics.

It is imperative to determine whether or not an ulcer is
infected before beginning wound care. Clinicians should diagnose ulcer
infection by looking for drainage, depth, erythema, and cellulitis
surrounding the wound; if infection is suspected, take wound cultures.
Swab cultures from the surface of an ulcer or from sinus drainage have
been shown to be poor indicators of the bacterial species below (64).
Therefore, clinicians should curet and culture an ulcer from the base
for aerobic and anaerobic organisms. Start with empirical antibiotics
if infection is suspected, and modify them, if necessary, when the
culture results and antibiotic sensitivities are available. The
bacterial species seen in DFIs are often multiple and range from
streptococcus or staphylococcus species (the two most common) to
gram-negative organisms and anaerobic organisms (Table 116.1).
Bacterial infections usually can be treated with empiric oral
antibiotics. We usually begin with first-generation cephalosporins and
modify treatment based on the response to treatment, antibiotic
sensitivities, and cultures. Quinolones may be added for gram-negative
coverage and penicillin-VK for clostridial infections (Table 116.3).
It the infection is arrested after 2 to 4 weeks of treatment, the
antibiotic may be stopped or the dose decreased. In patients with
advanced cellulitis, gas gangrene, or sepsis, treatment usually
requires hospital

admission, intravenous antibiotics, urgent surgical debridement, deep tissue cultures, and an infectious disease consultation.

In general, most ulcers can be treated on an outpatient
basis with local wound care in conjunction with redistribution of
pressure with total contact casts, orthotics, or diabetic shoes. The
evolution of wound management and wound care products has created the
need for standardized pathways for wound management. Accurately record
the size of the ulcer in centimeters with an anatomic sketch in the
patient’s chart. An alternative method is to trace the ulcer on a glove
or ziplock bag, then separate and dispose the side of the glove or bag
that touched the ulcer and tape the tracing in the chart. Digital
photographic prints of the wound are the easiest, most accurate means
of documentation. Make note of the size and color of the

wound
bed, and look closely at the wound margins to identify sinus tracts,
undermining or rimming. Describe the characteristics of the exudate by
including the type, amount, color, consistency, odor, and the adherence
to the wound base. These characteristics must receive ongoing
assessment so that an appropriate dressing can be used that is based on
the healing stage of the wound. The primary function of a wound
dressing is to promote the moist healing environment necessary for
tissue repair (72). The functions and indications of the most commonly
used dressing materials are listed in Table 116.4. Ulcers with significant drainage require gauze dressings with frequent changes.

After healing, further ulceration can be prevented by
using custom-molded, extra-depth, diabetic shoes. Deeper ulcers with
hyperkeratotic edges or necrosis can be debrided in the clinic and
successfully treated with the application of a total contact cast.
Treatment with intravenous antibiotics based on a swab culture, or
preferably, a deep culture, is helpful if significant cellulitis is
present.

Treat abscesses and osteomyelitis with thorough
debridement to remove all necrotic, infected tissue, followed by
reconstruction (Fig. 116.2C, Fig. 116.2D and Fig. 116.2E).
Surgery for diabetic abscess and osteomyelitis is more difficult than
that for a nondiabetic because of the poor blood supply and insensate
tissue. Toe amputations, ray resections, midfoot amputations, Syme’s
amputations, muscle flaps, or distal below-the-knee amputations (BKAs)
require good blood flow to heal and adequate protective sensation to
stay healed. If the area being treated is insensate, it allows more
aggressive debridement with less general anesthesia, which is safer
owing to the multiple system dysfunction (renal, cardiac, pulmonary) in
the diabetic. Some anesthesiologists may be unfamiliar with
diabetes-associated numbness and require guidance on the amount of
analgesia to use during procedures. We test for lack of sensation at
the incision site by squeezing with toothed tissue pick-ups before
administration of anesthesia. Most distal debridement and amputation
can be performed with a small amount of local or intravenous analgesia.
The anesthesiologist must be present to monitor cardiac, pulmonary, and
renal function. Amputation for the treatment of osteomyelitis is
commonly used to remove a chronic nidus of infection and to get to the
level of protective sensation for prosthetic wear. Antibiotic treatment
for deep abscesses and osteomyelitis are based on cultures and
antibiotic sensitivities. Only 2 weeks of antibiotics may be required
if the infected bone and soft tissue are removed and good bleeding soft
tissue is left. Up to 6 weeks may be required if there is
osteomyelitis. Hyperbaric oxygen helps the patient with marginal oxygen
levels to heal.

Gangrene or tissue necrosis can present as dry, wet, or
gas gangrene, or necrotizing fascitis. Although all gangrenous tissue
will eventually be removed, dry gangrene can be managed on an
outpatient basis with local wound care for long periods until the odor,
pain, or local infection requires surgical removal. Outpatient
management for dry gangrene requires that the patient, family, or local
care provider watch for signs of sepsis or gas gangrene. Although dry
gangrene usually is painless, some patients have good sensation, and in
this patient subset, the acid from the dead tissue can cause severe
pain that is relieved only with amputation (Fig. 116.3).
Outpatient management for forefoot gangrene can occasionally result in
“auto-amputation,” in which the necrotic tissue breaks off
spontaneously.

The need for and level of amputation is determined by tissue viability and protective sensation (Fig. 116.4). We use TcPO₂ greater than 40 mm Hg as an indication of good perfusion and potential for healing. A patient with a TcPO₂ of less than 40 mm Hg has an increased failure rate, and healing can be helped with hyperbaric oxygen (52).
If the patient refuses a higher amputation level or if the patient is
healthy, we use the lowest amputation level that will help with
ambulation and prescribe adjunctive hyperbaric oxygen therapy (Fig. 116.5). If the patient is ill or not able to use the lower amputation level for a prosthesis or ambulation and has a TcPO₂
of less than 40 mm Hg, we perform a higher amputation. To assess the
patient’s healing potential intraoperatively, we use William Wagner’s (69)
tourniquet technique. When a tourniquet above an amputation site is
deflated and poor bleeding results after as much as 5 minutes, wound
healing is unlikely. If bleeding begins 3 minutes after deflation,
there

is an 80% healing rate, and at 2 minutes or less, a 100% healing rate occurs (69) (Fig. 116.9D).

If the infection is not too severe and bleeding is
adequate, all lower extremity wounds should be closed. If the degree of
infection is too severe (i.e. purulence, cellulitis, or edema,), then
perform a staged debridment and closure, returning the patient to the
operating room in a few days for repeat debridement or wound closure,
or both. The surgeon must debride or amputate to a level on the limb
that produces sufficient bleeding indicative of adequate circulation
for healing.

Amputation can be lifesaving surgery if sepsis, gas gangrene, or necrotizing fasciitis is present (Fig. 116.6).
It can cause a great deal of stress for patients, so they may need time
and counseling before making a decision about an amputation. Of the
“stressful events of life” amputation is second only to loss of a loved
family member. Patients frequently go through the “stages of death and
dying” of denial, anger, negotiation, depression, and acceptance. Some
patients refuse to have an amputation for religious reasons or request
that the amputated part be stored for the time of burial. We describe
amputation to patients as a type of reconstructive surgery that is
necessary to remove infected or dead tissue so that the a patient’s
health and function may improve. Most patients understand this and work
very hard to rehabilitate. The design of prosthetic devices continues
to improve, thereby increasing the percentage of patients that have a
functional outcome. See Chapter 120 and Chapter 122 on amputation and prosthetics.

Realignment and restoration of normal foot mechanics
with attention to nerve and vascular function are the main principles
of foot reconstruction. After the infected, dead tissue is removed,
wound closure with a good weight-bearing stump is essential. Do not
leave bony prominences or less than five toes or metatarsals because
this produces an unbalanced foot that almost guarantees further surgery
in the next year. It is also of no value to perform inadequate
debridement or close ischemic skin or muscle.

Good glucose control and attempting to maintain HbA1c levels at less than 8% help prevent progression of neuropathy (20).
Analgesics and other pharmaceuticals [e.g., amitriptyline (Elavil) 25
to 100 mg at bedtime for sleep, or fluphenazine (Prolixin)] can be
helpful in controlling the paresthesias and dysesthesia (1,42,65).

Orthotics should be accommodating but not rigid, with
adequate padding to relieve overloaded bones and tissue. Soft
Plastazote is better than Pelite to avoid shear stress and give a firm
underlayer of support. A wide toe box with extra-depth shoes is
necessary to provide room for toe deformities. Shoes should fit well
when purchased and should not be expected to stretch out with wear.

Surgical treatment of the underlying deformity is often
necessary to heal the ulcers or prevent recurrence. With good blood
supply, an ostectomy may relieve the pressure of a bony prominence.
Balancing of muscle forces such as percutaneous tendoachilles
lengthening for tight heel cords, as well as procedures for intrinsic
minus clawing can relieve excessive pressure on the metatarsal heads.

Plastic surgery consultation may be needed when soft-tissue coverage is needed (46). See Chapter 112, Chapter 113, Chapter 114, Chapter 115 and Chapter 118 for details on foot reconstruction.

Studies have shown that pentoxifylline is effective in
diabetic patients with chronic ulcerations that do not heal despite
other treatment options. Pentoxifylline and its metabolites decrease
the viscosity of blood, therefore improving its flow properties. It
improves tissue oxygenation. In addition, pentoxifylline 800 mg/day was
shown to improve walking distance, paresthesia, skin temperature, and
subjective overall response (12).

For vascular insufficiency, consider vascular surgery
for possible reconstruction. This procedure may range from a single
vessel angioplasty to multiple by-pass arterial procedures. In the
diabetic vessel, bypass operations are more distal owing to the higher
number of diseased arteries below the trifurcation of the popliteal
artery (58). Revascularization can heal ulcerations and allow more distal foot reconstructions or amputation (29).

Diabetes is the most common cause of neuropathic
arthropathy. It is believed to be caused by a loss of protective
sensation about joints, allowing repetitive microtrauma to have
additive effects on bone and joint destruction (21).
The inflammatory changes of erythema and increased blood flow seen in
Charcot’s arthropathy may be due to autonomic neuropathy and can
contribute to the bone and joint destruction that sometimes occurs
despite adequate immobilization and rest (43).
Neuropathic arthropathy is accelerated osteoarthritis that causes
hypermobility of the joint. Typically, joint fragmentation and
fractures occur with destruction of the articular cartilage and bone,
with accompanying synovitis and pannus formation (9).

Other diseases that can cause neuropathic arthropathy
are syphilis, syringomyelia, alcoholism, stroke, congenital
insensitivity to pain, spinal cord or peripheral nerve injury, and
spina bifida (35). Patients with these
diseases, however, usually do not have the severe vascular and
immunologic changes that diabetics experience. Other severe problems
might also be present (e.g., alcoholism, malnutrition, cord injury, and
total paralysis), but the neuropathic arthropathy can be managed much
like that for diabetics.

Patients frequently complain of foot swelling, redness,
and numbness. A recent increase in shoe size may also be reported. Pain
is not typically a chief complaint, and when it is present, it is
usually less than expected. Neuroarthropathy is commonly found in
middle-aged diabetics with a history of poor glucose control. Fever,
chills, nausea, and malaise are generally absent, but may be present
with an infected Charcot joint. Capillary refill can be assessed with a
blanch test or foot elevation, or both, and is typically normal in the
Charcot foot. If the foot remains red and warm with elevation,
infection may be present.