3. Definition
Infection, ulceration or destruction of deep
tissues associated with neurological
abnormalities & various degrees of peripheral
vascular diseases in the lower limb.
(based on WHO definition)
9. Sensory neuropathy
•Sensory neuropathy
•Appearing 1st distally then progressing proximally in stocking/glove pattern
•Large-fiber involvement : diminishes light touch sensation and proprioception,
resulting ataxic gait and intrinsic muscle weakness of hands and feet.
•Small fiber involvement: pain & temperature perception, making pt susceptible to
repetitive injury
10. Motor neuropathy
Damage to the
innervation of the
intrinsic foot muscles
Imbalance between
extension and
flexion of the
affected foot
Abnormal foot
deformities
Create abnormal
bony prominance
and pressure points
Skin breakdown and
ulcer
13. Autonomic neuropathy
Regulates sweating,
skin temperature
and arteriovenous
shunting cause it to
form thick, stiff
callus commonly in
areas of pressure
concentration
Loss of autonomic
control inhibits
thermoregulatory
function and
sweating
Result is dry, scaly
and stiff skin that is
prone to cracking
and allows a portal of
entry for bacteria
22. PRESENTING COMPLAINT
Pain due to
neuropathy
Pain due to ischemia
• Burning pain
Characteristic :
sharp shooting &
lightning pain Pain
relieve by cold
• Pain worse during
rest
• Persistent pain
• worse on elevation
• relieve by
dependency
• Claudication (pain
in calf on exercise
relieve by rest)
Skin Breakdown
Swelling
Discharge
Color Change
Pain
Pins and needles
Unpleasant tingling
Tightness
Cold
Heaviness
Numbness
23. PERIPHERAL NEUROPATHY OR PERIPHERAL
ARTERIAL INSUFFICIENCY
Neuropathy
Symptoms
•Sensory –glove
and stocking
distribution
•Motor – lack of
coordination and
falling
•Autonomic – heat
intolerance, lack
of sweat (dry and
cracked skin),
bowel and
bladder problems
Arterial Insufficiency
/ Ischemic Symptoms
•Most atherosclerotic
disease of the lower
extremities are
asymptomatic and
others develop
ischemic symptoms.
•Symptomatic
•Acute – pain, pallor,
pulselessness,
paresthesia, paralysis
•Chronic – intermittent
claudication, rest pain,
ulceration, gangrene.
•Rest pain is less
common in the diabetic
population. Fissure,
24. DIABETIC HISTORY
• General : Types of DM, duration, treatment (OHA or
Insulin)
• Complication of DM :
• Retinopathy : cataract, previous laser therapy
• Nephropathy : proteinuria, severe renal impairment,
renal replacement therapy (CAPD, haemodialysis,
renal transplant)
• Cardiovascular : Angina, heart failure, MI, coronary
artery angioplasty or bypass
• Cerebrovascular : transient ischemic attack, stroke
25. HISTORY OF FOOT ULCER
• Site, size, duration, odour and type of drainage
• Precipitating event or trauma
• Recurrences – number of times
• Associated infections
• Frequency of hospitalizations and treatment given
• Wound care / measures to reduce plantar pressure
• Patient compliance
• Previous foot trauma or surgery
• Features of Charcot’s joint
26. HISTORY OF FOOT PROBLEMS
• Daily activity and current diabetic foot status
• Footwear : shoes/ slippers/ sandals/ use different footwear/ Fit
• Foot-care : aware of foot problem / inspect foot / wash feet /
proper nail clipping
• Callus formation
• Deformities
• Previous ulcer treatment or foot surgery (amputation)
• Skin & nail problems – sweaty feet / fungal infections / skin
disease / blisters/ Ingrown toenails
27. PAST MEDICAL &
DRUGS HISTORY
Serious illness
(cancer, rheumatoid
arthritis)
•Accidents
•Known injuries
•Hospitals admission
•Operations
•Present medication
FAMILY
HISTORY
•presenting
illness
•Diabetes
•Cause of death
of near relatives
SOCIAL HISTORY
•Alcohol
•Tobacco
•Occupation
•Dietary habits
•Cultural habits (walk
barefoot, wets feet at work,
wear socks, walks a lot,
standing long hours)
•Financial income- afford
medications
•Perception on DM
29. INSPECTION
-
SKIN
SIGNS OF SKIN BREAKDOWN
➢ Dry skin, fissured (neuropathy)
➢ prominent dilated vein (autonomic neuropathy)
➢ Hair loss (neuropathy / ischemic)
➢ Atrophy of the subcut.layer, thin shiny & wrinkle skin (ischemia)
➢ Classical sign of skin breakdown is foot ulcer
➢ Abrasion, bullae, fissures
➢ Fungal skin infection (tinea pedis)
➢ Other skin lesions : Necrobiosis lipoidica diabeticorum (NLD)
➢Shin spots (diabetic dermopathy)
➢Corns : discrete area >1cm and extend depth of several mm.
➢Callus : form diffuse plaques
➢They are thickened area of keratosis that which developed at sites of high
pressure and friction
30. Structure 1. Thickened nail : cause bleeding and lead to ulceration
2. Atrophic nail : neuropathy and ischemia patient
Colour 1. red, brown/ black : subungual hematoma due to trauma
2. Pale nail bed : acute ischemia
Abnormal
itiy under
the nail
1. Discharge of fluid from beneath or around the nail
2. Maceration and softness of nail plate : presence of ulcer
or infection
Signs of
nails
infection
1. Onycholysis : fungal infection of nail that invades the nail
plate dorsally (hallux)
2. Paronychia : nail with convex nail bed with tendency to
incurve in the corners cause repetitive microtrauma and
inflammation
INSPECTION
-
NAILS
31. • Swelling predispose to the ulcer and exacerbates a tight fit inside poorly fitting
shoes
INSPECTION
-
SWELLING
Bilateral foot swelling Unilateral foot swelling
✓ Cardiac failure
✓ Renal impairment 2ry to diabetic
nephropathy
✓ Chronic venous insufficiency
✓ Neuropathic oedema 2ry diabetic
neuropathy (rare)
✓ Primary lymphedema
✓ Severe ischemia a/w dependency
✓ Infection a/w erythema & skin
breaking
✓ Charcot foot a/w hot, red, swollen
foot
✓ Gout
✓ Trauma, fracture, muscle or tendon
rupture a/w bruising
✓ Deep vein thrombosis
✓ Venous insufficiency
✓ Secondary lymphedema due to
malignancy
✓ Common peroneal nerve palsy
✓ Fluctuant swelling may be due to
collection of pus or blood
32. Pes
cavus
Abnormal high of the medial long.arch lead to reduction of area of the foot in
contact with the ground during walking. A sign of motor neuropathy and a/w
clawing of lesser toes or trigger 1st toe
INSPECTION
-
DEFORMITY
33. Hammer
toes
A flexible or rigid deformity characterized by buckling of the toes commonly
caused by weakness of the small intrinsic muscle (interossei & lumbrical)
This deformity cause increase pressure over metatarsal head, IPJ and tip of the
toe
INSPECTION
-
DEFORMITY
34. INSPECTION
-
DEFORMITY
Charcot
foot
Bone and joint damage in tarsometatarsal joint and midtarsal joint lead to
deformity Rockerbottom deformity and medial convexity that a/w bony
prominence which prone to ulceration
FFPD Fibrofatty padding depletion : reduce thickness of fibrofatty over metatarsal
head due to previous ulceration that render metatarsophalangeal area prone to
ulceration
Hallux
valgus
Deformity of 1st metatarsophalangeal joint with lateral deviation of hallux and
medial prominence on margin of the foot. Frequent break down under pressure
of tight shoe
36. 1. Pulses : to detect ischemia (if absent check popliteal and femoral)
❑ dorsalis pedis = lateral to extensor hallucis longus
❑ Posterior tibial = below and behind medial malleolus
2. Temperature of foot warm or hot spots indicate inflammation
❑ Hot foot = cellulitis, Charcot foot, gout, venous insufficiency, DVT
❑ cold foot = chronic or acute ischemia, cardiac failure
3. Oedema
4. Crepitus = gas in tissues as a fine crackling sensation
PALPATION
37. ULCER
EXAMINATION
• Single / multiple
• Site
• weight bearing: heel/ plantar metatarsal head areas / tips of most
prominent toes (1st/2nd)
• subjected to trauma: malleoli
• subjected to stress: dorsal portion of hammer toes
• Shape
• Size
• 2D : length & width
• 3D : length, width & depth
38. ▪ Margin (line of demarcation between normal and abnormal)
• well-defined / irregular
▪ Edge (the part between the margin and the floor of an
ulcer):
• Punched-out (not healing) – arterial, neuropathic
• Sloping (healing) – venous
• Undermined (soft tissue affected more than the skin)
– tuberculous, pressure sores
• Irregular – melanoma
• Everted - squamous cell carcinoma
• Rolled – basal cell carcinoma
ULCER
EXAMINATION
39. ▪ Floor (the exposed surface of an ulcer-inspect):
• Describe anatomical structures involve - Bone, ligament, tendon
• Healthy (pink) – granulation tissue formation
• Slough
• Avascular (pale)
• Purulent
• Necrotic
▪ Base (on which the ulcer rests – better felt than see):
• Describe pathological state of the ulcer’s structure
• Induration
ULCER
EXAMINATION
▪ Discharge:
Serous – clear, straw colored
Purulent – yellow, grey, green with thick in consistency
Bloody (sanguinous) - red
Seropurulent
Serosanguinous
Hemoserous – clear, pink
▪Skin surrounding the ulcer:
Inflammatory changes – redness, swelling
Skin discoloration, dry or scaly
40. 1. MOTOR NEUROPATHY
❑ classical sign of MN is high medial longitudinal arch lead to prominent
metatarsal head and pressure point over plantar forefoot
❑ test the dorsiflexion of the foot to detect foot drop 2ry to common peroneal
nerve palsy (unilateral, affect gait)
2. AUTONOMIC NEUROPATHY
❑ dry skin 2ry to decrease sweating that occur in stoking distribution up to
knee
❑ distended vein over the dorsum of foot 2ry to arteriovenous shunting
3. SENSORY NEUROPATHY
❑ NO pain when significant foot lesion present
❑ Painless ulceration = evidence of peripheral neuropathy
NEUROLOGICAL
ASSESSMENT
42. A. Patient stands
feet together,
eyes open and
then closes both
eyes for 20-30 sec
without support
B. Positive test
with eyes open
– cerebellar
ataxia
C. Positive test
with eyes
closed –
impaired
proprioception
ROMBERG
TEST
45. • Type & condition of shoes / sandals
• Fit
• Shoe wear, pattern of wear, lining wear
• Foreign bodies
• Insoles, orthoses
FOOTWEAR
ASSESSMENT
Orthoses provide support for the foot by
redistributing ground reaction forces as well as
realigning foot joints while standing, walking or
running
49. ULCER EXAMINATION
No. Aspect Description
1 Site The location of the ulcer must be described in
exact anatomical terms
2 Size Use measuring tape to measure the length and
width of the ulcer
3 Shape
4 Base The base of an ulcer usually consists of slough or
granulation tissue (capillaries, collagen,
fibroblasts, bacteria and inflammatory cells).
Other recognizable structures such as tendon or
bone may be visible.
5 Edge Five types of edge:
- Sloping edge
- Punched-out edge
- Undermined edge
- Rolled edge
- Everted edge
50. No Aspect Description
6 Depth Record the depth of ulcer in millimeters, and
anatomically by describing the structures it has
penetrated or reached
7 Discharge The discharge of an ulcer may be serous,
sanguineous, serosanguinous or purulent
8 Relations Describe the relations of the ulcer to its
surrounding tissues
9 State of local
tissue
Pay attention to the local blood supply and
innervation of the adjacent skin. There may be
also evidence of previous ulcers that have
healed.
64. 1. Full blood count
– Elevated white cell count indicative of acute inflammation
2. Erythrocyte sedimentation rate
– Marker for underlying inflammatory process
3. Blood culture & sensitivity
– To detect causative organism and direct antibiotic treament
4. Renal profile
– Renal function & preoperative assessment
65. IMAGING OF FOOT
1) Plain radiograph of the foot.
– Osteomyelitis
– Other possible findings: osteolytic, fractures,
dislocations, medial arterial calcification, soft-tissue
gas and Charcot's joint.
66.
67. 2) CT Scan
– Look for suspected bone or joint pathology not evident
on plain radiograph
3) Radioisotope Technetium bone scans.
• Technetium-99 methylene diphosphonate (Tc-99 MDP)
bone scans are often used in diabetic foot infection
• Detect early pathology such as osteomyelitis, fractures, and
Charcot’s arthropathy.
68. 4) Magnetic Resonance Imaging (MRI)
■ Evaluate both soft tissues and bone pathologies.
■ Aid in diagnosis of osteomyelitis, deep abscess, septic
join, tendon rupture and is superior to the other
imaging modalities.
■ Helps in surgical planning
69. VASCULAR INVESTIGATION
Aim:
■ Evaluate the extent of occlusive vascular disease.
■ Assess the healing potential especially when clinical examination
suggesting ischaemia.
■ The tests:
I. Ankle-Brachial Systolic Index (ABSI), with Doppler Segmental
Artery Pressures.
II. Toe pressure measurements.
III. Transcutaneous oxygen tension (TcPO2)
IV. Doppler segmental artery pressure
70. = Ankle systolic blood pressure
Brachial systolic blood pressure
I) Ankle Brachial Systolic Index (ABI)
• Can be misleading due to arterial calcification, hence
giving rise to higher pressure of ankle.
• Normal value = 0.91-1.3
Abnormal <0.9
74. II) Toe pressure measurements.
■ Reliable in assessing healing
potential.
■ 85-100% will heal if
pressure>40mmHg
■ less than 10% will heal if
pressure<20mmHg
77. III) Transcutaneous oxygen tension
(TcPO2)
■ <10mmHg correlates with
non-healing
■ >30mmHg correlates with
healing
78. NEUROLOGICAL
INVESTIGATION
I. 2 point discrimination
II. Monofilament test (10gm)
III.Vibration perception
To assess peripheral
sensory neuropathy,
which is a major
independent risk factor for
DFU
84. II. MONOFILAMENT TEST
1. Show the 10-g Semmes-Weinstein monofilament to the patient.
2. Touch it first to the patient’s forehead or sternum so that the sensation is
understood.
3. Instruct the patient to say “yes” every time the monofilament stimulus is
perceived.
4. With the patient’s eyes closed, apply the monofilament to the dorsum of
the great toe proximal to the nail bed. Use a smooth motion-touch the skin,
bend the filament for a full second, then lift from the skin.
85.
86. ■ Avoid areas with callus, ulcer.
■ Positive when have at least 4 insensate area.
87. III. VIBRATION PERCEPTION
■ 1. Strike the tuning fork against the palm of your hand hard enough
that it will vibrate for approximately 40 seconds.
■ 2. Apply the base of the tuning fork to the patient’s forehead or
sternum and ensure that the vibration sensation (not just the touch
sensation) is understood.
■ 3. With the patient’s eyes closed, apply the tuning fork to the bony
prominence situated at the dorsum of the first toe just proximal to
the nail bed. Ask if the vibration sensation is perceived.
88. III. VIBRATION PERCEPTION
■ 4. Ask the patient to tell you when the vibration stimulus is
stopped, and then dampen the tuning fork with your other hand.
■ 5. One point is assigned for each vibration sensation perceived
(vibration “on”). Another point is assigned if the correct timing of
dampening of the vibration is perceived (vibration “off ”).
■ 6. Repeat this procedure again on the same foot, then twice on
the other foot in an arrhythmic manner so the patient does not
anticipate when the stimulus is to be applied.
■ 7. Though this test can be used to rule out the presence of
neuropathy, unlike for the monofilament described above,
threshold scores do not exist to indicate the risk of future onset of
neuropathy.
91. ■ High plantar foot pressures have been identified as a
significant risk factor for ulceration.
■ Measurements are to be done regularly as important changes
in the distribution and level of pressures under diabetic
neuropathic feet occur during a relatively short period.
■ Harris mat and computer techniques allow qualitative and
quantitative measurements of plantar foot pressures
respectively.
■ They are able to identify potential areas of ulceration.
97. •PRINCIPLES OF TREATMENT
• Debridement of necrotic tissue
• Wound care
• Reduction of plantar pressure
• Treatment of infection
• Management of ischaemia
• Management of co morbidities
• Surgical management
• Reduce risk of recurrence
98. ● Debridement is the removal of all non-viable tissues and slough
from the ulcer
A. DEBRIDEMENT OF NECROTIC TISSUE
TYPES EXPLAINATION ADVANTAGES DISADVANTAGES
1) Surgical
❑ Abscess → Incision and drainage (immediate)
❑ Osteomyelitic bones, joint infection or
gangrenous digits → Resection or partial
amputation
❑ Efficient
❑ Effective
❑ Pain
❑ Bleeding
❑ May need
anesthesia
2) Mechanical
❑ Surgical debridement + wet-to-dry dressings +
high pressure irrigation
❑ Inexpensive
❑ Efficient
❑ Slow
❑ May lead to
infection
3) Enzymatic
❑ Topical proteolytic enzymes as adjuvant in
managing chronic wounds. Their efficacy is
however controversial.
❑ Does not
require
physician
❑ Low risk of
bleeding
❑ May be painful
❑ May damage
surrounding tissue
❑ Slow
❑ Prone for infection
4) Autolytic
❑ Occurs naturally in healthy, moist wound
environment with adequate circulation ❑Painless
❑ Slow
❑ Inefficient
❑ May lead to
infection
100. ● To promote wound healing & to cover the ulcer to protect it
from trauma and contaminants
✓ Dressing (wound size, depth, location, surface, discharge)
>Normal saline dressing
✓ Adjunctive local therapies
> Growth factors
~Becaplemin gel,
~Autologous platelets
> Dermal/skin substitutes
✓ Hyperbaric oxygen therapy
-for hypoxic diabetic foot ulcers
B. WOUND CARE
101. CATEGORY INDICATIONS CONTRAINDICATION
Dressings
•Transparent films –
polyurethane film with
adhesive layer, semi
permeable
•Hydrogels – gel, sheet,
gauze, 95% water or glycerin
•Foam – polyurethane foam,
open cell absorbent.
•Hydrocolloids – wafer with
adhesion,carboxymethylcellul
ose; pectin gelatin;
impermeable to oxygen.
•Calcium Alginates – pad
made of fibre from seaweed.
•Gauze pads - sterile cotton
•Collagen dressing –
composite pads with
collagen component.
Dry to minimal draining
Dry to minimal draining
Moderate, large exudates clean
wound surface
Low to moderate drainage
Heavy exudates wounds
Low to heavy draining, surgical
wounds
Low to heavy draining wounds.
Infected or clean wound to
Infection; significant
drainage.
Moderate to heavy
drainage
Dry wounds
Heavy drainage
Dry wounds
Undefined
Dry wounds
Allergies to
components
102. CATEGORY INDICATIONS CONTRAINDICATIONS
Topical therapies
•Saline- amorphous
hydrogels, skin cleansers
• Detergents/ antiseptics
– povidone-iodine, etc ·
•Topical antibiotics –
Silver sulfadiazine,
Bacitracin, Mupirin, etc.
• Enzymes – collagenase,
papain-urea, etc.
Clean or infected wounds
Contaminated or infected
wounds
Contaminated or infected
wounds
Necrotic or escharotic
wounds
Undefined
Healthy granulating
wound
Healthy granulating
wound
Healthy or infected
wounds
103. ● To reduce the pressure of the diabetic foot > reduce the trauma to the
ulcer > faster healing process (P=F/A)
C. REDUCTION OF PLANTAR
PRESSURE (OFF-LOADING)
➢ Total non-weight bearing
➢ Total contact cast
➢ Foot cast or boots
➢ Removable walking braces with rocker
bottom soles
➢ Total contact orthoses – custom
walking braces
➢ Patellar tendon bearing braces
➢ Half shoe or wedge shoes
➢ Healing sandal : surgical shoe with
molded plastazote insole
➢ Accommodative dressing: felt, foam,
felted-foam
➢ Shoe cutouts (toe box, medial, lateral
or dorsal pressure points).
➢ Assistive devices: crutches, walker
cane, etc.
104. Total contact cast
Removable walking braces with
rocker bottom soles
Plastazote insole
Patellar tendon
bearing braces
105. ● Infection is usually secondary to ulceration
● Local/systemic
➢Early incision and Drainage
➢Debridement
➢Antibiotic therapy
➢Early amputation – if there is co-existing gangrene or extensive tissue lost
D. TREATMENT OF INFECTION
106. Non-limb Threatening Limb Threatening
The ulcer is superficial A deep ulcer
Mild to moderate infection Severe gangrene, necrotising
fasciitis and abscess
Usually monomicrobial
(Staph. Aureus, Staph. Epidermidis
and Streptococci)
Polymicrobial organism
(gram-positive and negative
organisms, anaerobic organismsand
enterococci )
No symptoms of systemic
involvement
Ill patient, with septic features
107. ● Start with empiric regime first!
● Non-limb threatening infections→ Gram positive coverage
● Limb threatening infection → Empirical IV broad spectrum antibiotic
ANTIBIOTIC THERAPY
Mild to moderate (1-2 weeks) Severe (>2 weeks)
✓ Oral Cloxacillin
500mg QID
Or
✓ Oral Amoxicillin/ Clavulanate
625mg BD
✓ IV Unasyn (Ampicillin/
Salbactam 1.5-3g QID
Or
✓ IV Zinacef (Cefuroxime) 750mg-
1.5g TDS
Or
✓ Ceftriaxone 1-2g OD+/- IV
Metronidazole 500mg TDS
108. ● Early assessment of vascular supply to
the affected limb should be done
● Non-invasive vascular studies (ankle-
brachial index) to confirm diagnosis
● Revascularization or vascular
reconstruction surgery prior to
definitive surgical management
E. VASCULAR MANAGEMENT OF
ISCHAEMIA
109. ● Co-morbidities must be assessed & managed via
multidisciplinary team approach
● Patient compliance
F. MANAGEMENT OF CO-
MORBIDITIES
110. ➢ Chronic foot ulcers are usually associated with areas of increased peak pressure
where off loading and wound care techniques are not effective.
➢ These ulcers are best treated surgically which includes removal of infected bone or
joints.
o metatarsal head resections
o exostectomy
o sesamoidectomy
o digital arthroplasty
G. SURGICAL MANAGEMENT
111. AMPUTATION
• MAJOR AMPUTATION
• Ray amputation
• Transmetatarsal amputation
• Syme’s or Boyd’s amputation
• MINOR AMPUTATION
• Amputation below knee
• Amputation above knee
Indications :
● Removal of gangrenous or
infected tissue
● Removal of portions of the
foot that is frequently
ulcerated
● To accommodate either
normal or modified shoe
gear
112. Factors determining level of amputation :
● Level of disease
● Blood flow
● Psychological state
● Cosmetic requirements
113. ● Ischemia / gangrene of one or
more toes
● Infection of one or more toes
● Presence of at least one
palpable foot pulse ( dorsalis
pedis / posterial tibial)
1. Ray Amputation
114. ● Ischemic/ gangrene
● Infection of forefoot only
● Palpable PT or DP pulses
2. Transmetatarsal amputation
115. ● Infection of foot up to mid-foot
only
● Gangrene of fore/mid-foot
● Strong PT pulse palpable
3. Syme’s Amputation
116. ● Infection up to ankle
● Ischemia / gangrene of whole
foot:
- ABSI <0.5
- Rest pain
4. Amputation Below Knee
117. ● Failed below knee amputation
● Infection up to middle leg
● Ischemia up to middle leg
5. Amputation Above Knee
118. ● Require multidisciplinary approach
+Podiatrist
+Orthopaedic surgeon
+Vascular surgeon
+Physician
+Infection control nurse
+Others (cardiologist, nephrologist, neurologist)
● Patient education (foot hygiene, daily inspection,
proper footwear, identification and early treatment of
new lesions)
H. REDUCE RISK OF RECURRENCE
119. ● Ministry of Health Malaysia, Management of Diabetic Foot, Clinical
Practice Guidelines 2004
● DIABETIC FOOT Lower Extremity, Arterial Disease and Limb Salvage,
1st edition, Anton N. S; Lippincott Williams & Wilkins; 2006.
● http://www.orthobullets.com/foot-and-ankle/7046/diabetic-foot-ulcers
● https://www.uptodate.com/contents/management-of-diabetic-foot-
ulcers
REFERENCES
124. TYPE ORGANISM CHARACTERISTICS
Type 1 Polymicrobial
(Typical 4-5 aerobic & anerobic species )
• combination of Gram-positive cocci,
Gram-negative rods, and anaerobes
• Most common (70-80%)
• Seen in immunosuppressed
• Post-op abdominal & perineal
infections (Fournier's gangrene)
Type 2 Monomicrobial
• Group A β-hemolytic Streptococci (most
common), MRSA
• 20-30% of cases
• Seen in healthy patients
• Extremities, associated with toxic
shock syndrome
Type 3 Gram negative monomicrobial
• Vibrio spp.
• Marine exposure
•Uncommon but high mortality
(30-40%)
Type 4 Fungal infection:
• Candida
• Very rare
• Traumatic wounds and burns
and in those who are severely
immunocompromised.
ETIOLOGY ( necrotizing
fasciitis)
129. INVESTIGATION
FULL BLOOD COUNT
•Anemia
•Leukocytosis
Renal profile
•Malnourish
•Dehydrated
CRP and ESR
•Detect inflammation
Skin swab for culture
• cause of infection
Fluid culture
•Cause of infection
Blood culture and
sensitivity
•Cause of infection
MRI
•To distinguish bone and
tissue infection
132. Preferred Alternative
Type 1 Cloxacillin 2g IV q4-6h
PLUS
Metronidazole 500mg IV q8h
PLUS
Gentamicin
5mg/kg IV q24h
3rd gen. Cephalosporins
PLUS
Metronidazole 500mg IV q8h
OR
β-lactam/β-lactamase inhibitors, e.g.
Ampicillin/Sulbactam 1.5g IV q8h
OR
Amoxycillin/Clavulanate 1.2g IV q8h
PLUS/MINUS
Gentamicin
5mg/kg IV q24h
NECROTIZING FASCITIS
Preferred
Type 2
Group A streptococcus
Benzylpenicillin 2-4 mega units IV q4h
PLUS
Clindamycin 600mg IV q8h
133. Cellulitis Necrotizing fasciitis
Site of infection Dermis and subcutaneous tissues Deep subcutaneous tissues
and superficial fascia
Clinical presentation No necrosis and gangrene of skin Extensive necrosis and
gangrene of the skin and
underlying structures
Blisters are rare Blisters are common late
presentation
Lymphatic involvement (lymphangitis,
lymphadenitis, lymphadenopathy) may
present
Lymphatic involvement is rare
Subcutaneous tissues can be palpated
and are yielding/pitting
Wooden-hard feel of the
subcutaneous tissues fascial
planes and muscle
groups (cannot be discerned
by palpation)
No gas in soft tissues (except in
infection by anaerobes)
Gas in the soft tissues,
detected by palpation or
imaging
No cutaneous anesthesia Cutaneous anesthesia (may
preceed skin necrosis)
Treatment Respond to antimicrobial treatment
alone
Requires operative
intervention
135. INTRODUCTION
• progressive condition
affecting the bones and
joints of the foot
• is characterised by joint
dislocation, subluxtion and
pathologic fracture of the
foot of neuropathic patients
• often resulting in
debilitating deformity
(The Foot in Diabetes, 4th Ed)
136. EPIDEMIOLOGY
• The reported prevalence of Charcot arthropathy is low
it affects only 0.1-0.5% of all patients
with diabetes.
• Bilateral involvement : 30% of patients with charcot feet
• commonly seen in fourth or fifth decades of life and in patients with long duration
of diabetes
• majority of lesion occur in the midfoot (tarso-metatarsal region)
137. French Theory
Charcot 1868 neurovascular theory
• arthritic changes were the result of damage to the CNS within the centres that
control bone and joint nutrition.
PATHOGENESIS
138. German theory
Volkman and Virchow neurotraumatic theory
✓ “ peripheral neuropathy leading to loss of protective sensation may render the foot
susceptible to injury from either repeated or acute trauma “
✓ Insensitive joint
✓ Allow mechanical trauma normaly prevented by pain
✓ Spontaneous fracture, subluxation and dislocation
140. CLINICAL FEATURES
• Earlist manifestation (acute charcot foot):
1. Swelling/edema over the foot or ankle
2. Pain or discomfort
3. Redness
4. Unilateral warmth ( >2 celcius compared with contralateral
foot)
• May be slowly progressive into a chronic stage
chronic stage : painless, without temperature differential
in deformed foot
• “rocker-bottom” foot
• Collapse of the arch of the midfoot
141.
142. INVESTIGATIONS
• Lab (when indicated)
❖Full blood count and inflammatory markers (ESR and WBC) should be normal if
uncomplicated with infection
❖Bone biopsy to distinguish between osteomyelitis and osteoarthropathy
❖Synovial fluid no crystal or organism
• Imaging
✓ Plain radiograph
reveal bone and joint destruction, fragmentation and
remodeling in advanced cases, but in early changes may
be subtle or undetectable
✓ MRI may be useful
144. MANAGEMENT
• Goal: providing the patient with a
stable, well aligned plantigrade
foot that is free infection and is
shoeable or braceable
Conservative
Long term immobilization
– Total Contact Cast (TTC)
– Charcot restraint orthotic walker
(CROW)
– Scotchcast Boot (SCB)
145. SURGICAL MANAGEMENT
➢ Acute Charcot Foot Contraindicated
➢ Chronic Ulcerated and fixed deformity indication of surgery
remove bony prominent and correct the deformity
– Exostectomy
– Arthrodesis
– Tendon Lengthening
Midfoot charcot deformity
• Exostectomy of a bony plantar prominance that has created
an area of increased pressure on the underlying skin
146. Hindfoot
• case with minimal deformity and clear bony fracture:
managed with total contact casing or bracing untill full
consolidation
• case with greater deformity : realignment/ arthrodesis
• Amputations
– Failed previous surgery (unstable arthrodesis)
– recurrent infection
147. REFERENCES
1. Louis Solomon, Apley’s System of Orthopaedics and Fractures,9th Ed,2010
2. Andrew J.M.Boulton, The Foot in Diabetes, 4th Edition,2006
3. http://emedicine.medscape.com/article/1234293-overview
4. http://www.uptodate.com/contents/diabetic-neuropathic-arthropathy
