DIABETIC FOOT ULCER (dfu)

1 in 6 malaysia have DM. (cpg Malaysia)

>60% LL amputation due to DFU (American diabetic association) .

Staphylococcus aureus (found in over 70% of cases), Streptococcus pyogenes,

S.epidemidis
sensory (reduced sensation to pain & temperature)
motor (causes muscle weakness and intrinsic muscle imbalance
leading to digital deformities such as hammered or clawed toes.)
autonomic (decreased sweating cause dry,cracked skin prone to
infection entry)

NEUROPATHY

Impaired host defenses secondary to hyperglycemia include defects

in leukocyte function and morphologic changes to macrophages
cause decrease blood supply to the foot and delayed the process of
healing

IMMUNOPATH
Y
VASCULOPATH
Y

PATHOGENESIS

Rise in blood glucose levels leads to increased enzyme production such as aldose reductase
and sorbitol dehydrogenase. These enzymes convert glucose into sorbitol and fructose. As
these sugar products accumulate, the synthesis of nerve cell myoinositol is decreased, causing
diabetic neuropathy.
Wagner classification
It grades diabetic foot ulcers based on depth of tissue penetration and necrosis. Low grades
are generally infected with gram-positive organisms and higher grades with polymicrobial
flora.

EXAMINATION
1) Monofilament test

2) Ankle-brachial index (ABI)

measuring the ratio of systolic blood pressures in the ankles (dorsalis pedis and
posterior tibial arteries) and arms (brachial artery). A normal ABI ranges from 0.9 to
1.2 mmHg. A lowed value indicates ischemia and a higher value indicates
atherosclerosis which lead to peripheral arterial dz.
3) General inspection; swelling, ulcer
Ulcer description; size, shape, site, the skin surrounding the ulcer was dry,
erythematous, sloughy with foul smelling pus discharge and necrotic patch.
Nails; fungal infection, CRT
Skin; shiny, hyper pigmented, loss of hair, pallor, cyanosis, temperature
Deformities; claw toes, hammer toes, mallet toe, Charcots joint, high arch foot,
Lower limb pulses includes posterior tibialis, popliteal and femoral were present.
Sensation to pain reduced up to below the knee level in stocking distribution.
Babinski sign, proprioception was intact, muscles power for dorsiflexion and
plantar flexion.
NNB; The advanced glycosylated end product also causes stiffness of the archilles tendon
which impair plantar flexion causing high arch foot and putting more pressure on the 1st
metartarsal. This will follow by formation of callus and ulcer.
Investigation;
1) Blood; FBC raised neutrophils, blood glucose profile, HbA1c, tissue culture and
sensitivity, gram stain, lipid profile, renal profile, CRP/ESR to TRO OM.
2) Imaging
Osteomyelitis changes, gas gangrene, and foreign body. Osteomyelitic changes includes
the presence of sequestrum, cloaca and involucrum.

MX
1) PHM; optimize hypoglycemic medication and compliances. Antibiotic; IV unasyn
(ampicillin + sulbactam)
2) Non phm; -wound dressing, -diabetic counselling, -diet control, -exercise to lose
weight, -foot care; daily inspection of their foot for wound, swelling, redness, ulcers,
blisters and nail problems, apply lotion on foot to prevent dry skin cracks and
decreases the risk of infection, avoiding walking barefoot to prevent injury, and wear
customized shoe wear to minimize the risk of pressure sore.
Types of ulcers
Site

Base
Pulse
Skin surrounding
Pain

VENOUS
Superior to medial

ARTERIAL
Anterior and outer

NEUROPATHIC
Heel and ball of the

maleolus

aspect of legs, toes,

foot

Red
Present
Hot

foot dorsum,
Pale
Absent
Cold with ischemic

Dry eschar
present
Normal

Painful

changes
Painful

painless