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DIABETIC FOOT
Jitesh Jain
MS, FNB(Sports medicine)
Consultant orthopedic and arthroscopic surgeon
Mahavir Jaipuriya Rajasthan Hopital
Jaipur.
Definition (WHO)
• In diabetic patients infection, ulceration or
destruction of deep tissues of lower limb
associated with neurological abnormalities
& various degrees of peripheral vascular
diseases
Disease burden
• Epidemiological studies have estimated
prevalence of foot ulcers in diabetic patients
ranging from 4% to 27%.
• One fifth of total hospital admissions and
20%-30% of total expenditure spent on
diabetes care is estimated due to foot ulcers
and leg problems .
Disease burden
• Lower limb
amputations are 15
times higher in
diabetic patients
compared to non
diabetic patients
DFU is analogous to cancer
• 5 year survival rate after appearance of a DFU
is around 50%-60%
• 40% of DFU patients develop a new ulcer after
healing of one foot ulcer within one year.
ETIOPATHOGENEIS: MULTIFACTORIAL
Causative factors Contributing factors
Peripheral neuropathy Peripheral vascular disease
Structural foot deformity leading to high foot plantar
pressure
Uncontrolled hyperglycemia
Trauma to foot
Etiopathogenesis: multifactorial
Sensory neuropathy
Motor neuropathy Autonomic neuropathy
sensation of pain,
pressure and
proprioception are
decreased or lost. This
results in loss of
protective sensation
and increases
vulnerability to
injuries to foot
leads to muscle imbalance in
the leg and foot muscles with
resultant plantar surface
pressure alteration and typical
foot deformities i.e. hammer
toe and hallux rigidus
contributes by causing dry
skin, fissures and crusting
Hyperglycemia Endothelial dysfunction and vasoconstriction in
peripheral blood vessels cause hypercoagulability
Risk factors for DFUs
History of prior ulceration
Poor control of blood sugar
Long duration of diabetes mellitus
Chronic renal disease
Risk factors for DFUs
Peripheral neuropathy
Foot deformity and decreased mobility of the
foot
Foot callosity
Improperly fitted shoes
Old age
Visual impairment
Classification of diabetic foot ulcer
Wagner stage 1
• Superficial diabetic ulcer- no exposed
bone/tendons
Wagner stage 2
• Exposed
tendons/ligament/
deep fascia/ joint
capsule/bone
• No
osteomyelitis/abscess
Wagner stage 3
• Osteomyelitis/abscess
• Bone exposed/involved- X ray changes are
seen
Wagner stage 4
• Localized/ partial foot gangrene
Wagner stage 5
Whole foot gangrene
PEDIS classification
• More relevant to the prognosis of the ulcer. Higher the grade of PEDIS (2 or >2)
poorer is the prognosis.
Stages of DFU development
Examination of DFU
 Size, depth, edge, floor,
base,location and numbers.
 Presence of sinus tract.
 Any exudate from the ulcer.
 Erythema, swelling,
discoloration and component of
cellulitis
Determining the etiopathogenesis
• Neuropathy assessment: Touch
To assess the neuropathy a 10 g monofilament test is currently
recommended. With both eyes closed, the monofilament is touched at 90° to
the skin and pressed till it buckles to 1 cm, patient is asked to say yes when a
touch is felt.
Vibration:128 Hz tuning fork
Screen the patient for peripheral
vascular disease.
• History of rest pain and intermittent
claudication
• pedal pulses and popliteal pulses.
• Ankle-brachial index
Values between 0.91 to1.3 is considered Normal and below 0.40 is suggestive of
critical ischemia
Culture from a DFU
• When infection is suspected (erythema,
purulent discharge) culture is best taken from
the purulent drainage or from the ulcer base.
Risk assessment in Diabetic foot:
• Low risk foot: only callus is present
• Medium risk foot: structural deformity/
peripheral neuropathy/peripheral arterial
disease
• High risk foot: previous ulceration or
amputation along with any of two: structural
deformity/ peripheral neuropathy/peripheral
arterial disease
Management: multidisciplinary approach
• vascular surgeon, orthopedician, podiatrist,
orthotist, endocrinologist, educator, specialist
nurse and dietician
Tips for foot care that should be
involved in patient education:
• Foot inspection
• Never walk bare feet.
• Trim nails
• Don’t try to remove callus at home
• Care of dry skin.
• Doctor’s Visit
Blood sugar control: most important
• Every 1% increase in HbA1C level increases the
relative risk of peripheral vascular disease by
more than 25% .
• Goal -keep the HbA1C below 7.0% to 7.5%
(150 to 170 mg/d).
Surgical management
• Sharp surgical debridement
• Regular weekly serial debridement should be
done if new necrotic tissues form
Surgical management
• In severe ischemia aggressive debridement
should be avoided and revascularization
procedure should be performed before serial
debridement if necessary.
Case 1: sharp serial debridement
Wound ready for skin grafting
Case 2 sharp surgical debridement
Wound ready for skin grafting
Other kinds of debridement
• Enzymatic debridement - papain,
streptokinase and streptodornase, are used to
remove necrotic tissues.
• Autolytic debridement - moist dressings such
as hydrocolloids, hydrogels
• Biologial debridement
Advance dressings for DFU
• Hydrogel and hydrocolloid dressings- have a
great absorbency and provide moistened
environment.
• Alginate and silver impregnated dressings
have antibacterial properties and commonly
used for infected wound.
Newer therapies for diabetic foot:
• Hyperbaric oxygen therapy (HBOT),
• Vacuum dressing (negative pressure wound
therapy, NPWT)
• Electric stimulation (ES) and
• Bioengineered skin (BES).
HBOT and ES: effective adjuvant to
surgical debridement
• HBOT therapy has been reported to decrease
tissue hypoxia and enhanced tissue perfusion
decreases sensitivity to inflammatory
cytokines and promotes collagen production
and angiogenesis thus improving healing
rates.
• ES improves blood flow, up-regulates cellular
responses and decreases infection.
HBOT: How its given?
– One treatment session takes approximately 120 min.
Patients are placed in a pressure chamber.
• First, the chamber is pressurised with
compressed air for 15 min. Patients are exposed
to 2.4 absolute atmosphere (ATA) pressure while
breathing 100% oxygen.
• Each therapy session consists of three
oxygenation periods. These periods last 25 min
each and are separated by 5-min air breaks. After
that, the chamber is decompressed for 15 min
and the therapy is finished.
HBOT chamber
Wagner type 5 DFU after serial
debridement and HBOT therapy
NPWT: Effective in chronic non healing
ulcers
• By continuously removing wound exudate it
reduces bacterial load and promotes cellular
proliferation, up-regulates cellular function
and enhances angiogenesis.
NPWT
• A sterile water tight
seal is created over
the wound with
polyurethane or
polyvinyl alcohol and
adhesive tape.
• A negative pressure
of 80-125 mmHg is
used in pulsed fashion
or continuously and
suctioned fluid is
collected in a
container at bed side.
Use NPWT cautiously
NPWT After debridement
2 VAC cycles of 6 days each
Bioengineered skin in DFUs
Bioengineered skin: RCTs have proved
efficacy of BES
• This method aims at changing the cellular environment to
more favorable milieu by replacing the diseased
extracellular matrix with a new ground substance matrix
with cellular components.
• Derma graft and Apligraf, are commercially available skin
equivalents for use in chronic non healing DFU.
• Oasis is an acellular biomaterial derived from porcine small
intestine submucosa. It contains many dermal components
including collagen, hyaluronic acid, proteoglycans,
fibronectin, and growth factors such as fibroblast growth
factor-2, transforming growth factor β1, and VEGF.
Offloading and pressure modulation
mainstays of management of neuropathic foot ulcers
Technique description advantage disadvantage
Total contact
cast (TCC)
POP cast is
molded to the
shape of the
foot with
minimal
padding. A
heel is given
for walking.
This cast so
designed that
it allows for
equal
distribution of
the pressure
on the sole
while
offloading the
ulcer area.
1. Most
studied and
effective for
neuropathic
ulcer.
2. Faster
healing rate
compared to
other
techniques
3. Gold
standard for
neuropathic
ulcers.
1. It needs weekly change and
expert cast technician
2. It can’t be applied in case of
infection as it does not allow for
inspection of the ulcer
3. If not properly applied, rigid
cast can cause irritation or even
ulceration to insensate
neuropathic foot
4. It need to be covered during
shower
5. poor compliance
Total Contact Cast
Steps of TCC application
• Stockinette is applied to eliminate wrinkles
• Verticle felt strips are placed down the medial
and lateral sides of leg and malleoli
• Cast padding is applied over them
• Felt pad for plantar surface is applied
• Self adhesive foam is placed over toes and
trimmed. Cat is applied over all layers.
• Plantar plywood platform is incorporated in the
cast
• Cast shoe is applied.
Application of TCC
Removable cast walker (RCW)
Removable
cast walker
(RCW)
It is a shoe
shaped cast-
like device
that is easily
removable.
1. It allows
for self-
inspection
and topical
application of
dressing on
the ulcer.
2. More
compliant for
the patient as
it can be
removed
during sleep
and shower.
3. It can be
used for
infected ulcer
1. Healing rate is slower than
TCC
Removable cast walker
Instant TCC
Instant TCC It is a
combinatio
n of TCC and
RCW. In this
method
RCW is
worn and
elastotape
or adhesive
bandages
are
wrapped
around it
for tight
fitting.
1.Healing
rates are
comparable
to TCC
2. It can be
removed by
the patient
as and
when
required.
1. A few studies have shown
healing rates comparable to
TCC but more RCTs are
required to establish it as
gold standard for
neuropathic ulcer.
Instant TCC
Foot wears for diabetic patients
Charcot arthropathy
Neuropathic (charcot) osteoarthropathy is a non infective destructive ,
lesion of a bone and joint resulting from a fracture or dislocation in a patient
who has peripheral neuropathy
Charcot foot: Epidemiology
Pathophysiology
Classification
Classification
Classification
classification
Clinical presentations
Warmth and erythema may
be present
Management : nonoperative
• In stage I and stage II- well-padded total-
contact cast and protected weight bearing
• In stage III, continued bracing may be
necessary to accommodate deformity and to
prevent ulceration over bony prominences.
Management: operative
• Exostectomy
• If deformity correction is required,
arthrodesis of the involved joints may be
performed
Diabetic foot  Dr Jitesh Jain

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Diabetic foot Dr Jitesh Jain

  • 1. DIABETIC FOOT Jitesh Jain MS, FNB(Sports medicine) Consultant orthopedic and arthroscopic surgeon Mahavir Jaipuriya Rajasthan Hopital Jaipur.
  • 2. Definition (WHO) • In diabetic patients infection, ulceration or destruction of deep tissues of lower limb associated with neurological abnormalities & various degrees of peripheral vascular diseases
  • 3. Disease burden • Epidemiological studies have estimated prevalence of foot ulcers in diabetic patients ranging from 4% to 27%. • One fifth of total hospital admissions and 20%-30% of total expenditure spent on diabetes care is estimated due to foot ulcers and leg problems .
  • 4. Disease burden • Lower limb amputations are 15 times higher in diabetic patients compared to non diabetic patients
  • 5. DFU is analogous to cancer • 5 year survival rate after appearance of a DFU is around 50%-60% • 40% of DFU patients develop a new ulcer after healing of one foot ulcer within one year.
  • 6. ETIOPATHOGENEIS: MULTIFACTORIAL Causative factors Contributing factors Peripheral neuropathy Peripheral vascular disease Structural foot deformity leading to high foot plantar pressure Uncontrolled hyperglycemia Trauma to foot
  • 7. Etiopathogenesis: multifactorial Sensory neuropathy Motor neuropathy Autonomic neuropathy sensation of pain, pressure and proprioception are decreased or lost. This results in loss of protective sensation and increases vulnerability to injuries to foot leads to muscle imbalance in the leg and foot muscles with resultant plantar surface pressure alteration and typical foot deformities i.e. hammer toe and hallux rigidus contributes by causing dry skin, fissures and crusting Hyperglycemia Endothelial dysfunction and vasoconstriction in peripheral blood vessels cause hypercoagulability
  • 8. Risk factors for DFUs History of prior ulceration Poor control of blood sugar Long duration of diabetes mellitus Chronic renal disease
  • 9. Risk factors for DFUs Peripheral neuropathy Foot deformity and decreased mobility of the foot Foot callosity Improperly fitted shoes Old age Visual impairment
  • 11. Wagner stage 1 • Superficial diabetic ulcer- no exposed bone/tendons
  • 12. Wagner stage 2 • Exposed tendons/ligament/ deep fascia/ joint capsule/bone • No osteomyelitis/abscess
  • 13. Wagner stage 3 • Osteomyelitis/abscess • Bone exposed/involved- X ray changes are seen
  • 14. Wagner stage 4 • Localized/ partial foot gangrene
  • 15. Wagner stage 5 Whole foot gangrene
  • 16. PEDIS classification • More relevant to the prognosis of the ulcer. Higher the grade of PEDIS (2 or >2) poorer is the prognosis.
  • 17. Stages of DFU development
  • 18.
  • 19. Examination of DFU  Size, depth, edge, floor, base,location and numbers.  Presence of sinus tract.  Any exudate from the ulcer.  Erythema, swelling, discoloration and component of cellulitis
  • 20. Determining the etiopathogenesis • Neuropathy assessment: Touch To assess the neuropathy a 10 g monofilament test is currently recommended. With both eyes closed, the monofilament is touched at 90° to the skin and pressed till it buckles to 1 cm, patient is asked to say yes when a touch is felt. Vibration:128 Hz tuning fork
  • 21. Screen the patient for peripheral vascular disease. • History of rest pain and intermittent claudication • pedal pulses and popliteal pulses. • Ankle-brachial index Values between 0.91 to1.3 is considered Normal and below 0.40 is suggestive of critical ischemia
  • 22. Culture from a DFU • When infection is suspected (erythema, purulent discharge) culture is best taken from the purulent drainage or from the ulcer base.
  • 23. Risk assessment in Diabetic foot: • Low risk foot: only callus is present • Medium risk foot: structural deformity/ peripheral neuropathy/peripheral arterial disease • High risk foot: previous ulceration or amputation along with any of two: structural deformity/ peripheral neuropathy/peripheral arterial disease
  • 24. Management: multidisciplinary approach • vascular surgeon, orthopedician, podiatrist, orthotist, endocrinologist, educator, specialist nurse and dietician
  • 25. Tips for foot care that should be involved in patient education: • Foot inspection • Never walk bare feet. • Trim nails • Don’t try to remove callus at home • Care of dry skin. • Doctor’s Visit
  • 26. Blood sugar control: most important • Every 1% increase in HbA1C level increases the relative risk of peripheral vascular disease by more than 25% . • Goal -keep the HbA1C below 7.0% to 7.5% (150 to 170 mg/d).
  • 27. Surgical management • Sharp surgical debridement • Regular weekly serial debridement should be done if new necrotic tissues form
  • 28. Surgical management • In severe ischemia aggressive debridement should be avoided and revascularization procedure should be performed before serial debridement if necessary.
  • 29. Case 1: sharp serial debridement
  • 30.
  • 31. Wound ready for skin grafting
  • 32.
  • 33.
  • 34. Case 2 sharp surgical debridement
  • 35.
  • 36.
  • 37. Wound ready for skin grafting
  • 38.
  • 39. Other kinds of debridement • Enzymatic debridement - papain, streptokinase and streptodornase, are used to remove necrotic tissues. • Autolytic debridement - moist dressings such as hydrocolloids, hydrogels • Biologial debridement
  • 40. Advance dressings for DFU • Hydrogel and hydrocolloid dressings- have a great absorbency and provide moistened environment. • Alginate and silver impregnated dressings have antibacterial properties and commonly used for infected wound.
  • 41. Newer therapies for diabetic foot: • Hyperbaric oxygen therapy (HBOT), • Vacuum dressing (negative pressure wound therapy, NPWT) • Electric stimulation (ES) and • Bioengineered skin (BES).
  • 42. HBOT and ES: effective adjuvant to surgical debridement • HBOT therapy has been reported to decrease tissue hypoxia and enhanced tissue perfusion decreases sensitivity to inflammatory cytokines and promotes collagen production and angiogenesis thus improving healing rates. • ES improves blood flow, up-regulates cellular responses and decreases infection.
  • 43. HBOT: How its given? – One treatment session takes approximately 120 min. Patients are placed in a pressure chamber. • First, the chamber is pressurised with compressed air for 15 min. Patients are exposed to 2.4 absolute atmosphere (ATA) pressure while breathing 100% oxygen. • Each therapy session consists of three oxygenation periods. These periods last 25 min each and are separated by 5-min air breaks. After that, the chamber is decompressed for 15 min and the therapy is finished.
  • 45. Wagner type 5 DFU after serial debridement and HBOT therapy
  • 46. NPWT: Effective in chronic non healing ulcers • By continuously removing wound exudate it reduces bacterial load and promotes cellular proliferation, up-regulates cellular function and enhances angiogenesis.
  • 47. NPWT • A sterile water tight seal is created over the wound with polyurethane or polyvinyl alcohol and adhesive tape. • A negative pressure of 80-125 mmHg is used in pulsed fashion or continuously and suctioned fluid is collected in a container at bed side.
  • 49. NPWT After debridement 2 VAC cycles of 6 days each
  • 51. Bioengineered skin: RCTs have proved efficacy of BES • This method aims at changing the cellular environment to more favorable milieu by replacing the diseased extracellular matrix with a new ground substance matrix with cellular components. • Derma graft and Apligraf, are commercially available skin equivalents for use in chronic non healing DFU. • Oasis is an acellular biomaterial derived from porcine small intestine submucosa. It contains many dermal components including collagen, hyaluronic acid, proteoglycans, fibronectin, and growth factors such as fibroblast growth factor-2, transforming growth factor β1, and VEGF.
  • 52. Offloading and pressure modulation mainstays of management of neuropathic foot ulcers Technique description advantage disadvantage Total contact cast (TCC) POP cast is molded to the shape of the foot with minimal padding. A heel is given for walking. This cast so designed that it allows for equal distribution of the pressure on the sole while offloading the ulcer area. 1. Most studied and effective for neuropathic ulcer. 2. Faster healing rate compared to other techniques 3. Gold standard for neuropathic ulcers. 1. It needs weekly change and expert cast technician 2. It can’t be applied in case of infection as it does not allow for inspection of the ulcer 3. If not properly applied, rigid cast can cause irritation or even ulceration to insensate neuropathic foot 4. It need to be covered during shower 5. poor compliance
  • 54. Steps of TCC application • Stockinette is applied to eliminate wrinkles • Verticle felt strips are placed down the medial and lateral sides of leg and malleoli • Cast padding is applied over them • Felt pad for plantar surface is applied • Self adhesive foam is placed over toes and trimmed. Cat is applied over all layers. • Plantar plywood platform is incorporated in the cast • Cast shoe is applied.
  • 56. Removable cast walker (RCW) Removable cast walker (RCW) It is a shoe shaped cast- like device that is easily removable. 1. It allows for self- inspection and topical application of dressing on the ulcer. 2. More compliant for the patient as it can be removed during sleep and shower. 3. It can be used for infected ulcer 1. Healing rate is slower than TCC
  • 58. Instant TCC Instant TCC It is a combinatio n of TCC and RCW. In this method RCW is worn and elastotape or adhesive bandages are wrapped around it for tight fitting. 1.Healing rates are comparable to TCC 2. It can be removed by the patient as and when required. 1. A few studies have shown healing rates comparable to TCC but more RCTs are required to establish it as gold standard for neuropathic ulcer.
  • 60. Foot wears for diabetic patients
  • 61. Charcot arthropathy Neuropathic (charcot) osteoarthropathy is a non infective destructive , lesion of a bone and joint resulting from a fracture or dislocation in a patient who has peripheral neuropathy
  • 65.
  • 69. Clinical presentations Warmth and erythema may be present
  • 70. Management : nonoperative • In stage I and stage II- well-padded total- contact cast and protected weight bearing • In stage III, continued bracing may be necessary to accommodate deformity and to prevent ulceration over bony prominences.
  • 71. Management: operative • Exostectomy • If deformity correction is required, arthrodesis of the involved joints may be performed

Notes de l'éditeur

  1. Burden of diabetes has increased in the world considerably in recent decades and so as the morbidity and mortality from diabetic foot ulcers
  2. Diabetes related lower limb complications  are a large and growing contributor to the disability burden worldwide. We can prevent such extreme disability by combined efforts of skilled clinical team and patient education.
  3. Many studies have shown a temporal relationship between simultaneous occurrence of onset of dialysis and foot ulceration in diabetics (16-18). Probably inflammation associated with DFU diminishes the renal function.
  4. The presence of peripheral neuropathy seems to contribute to the development of ulceration and those with pre-ulceration, callosities and deformity seem to be at increased risk.
  5. Diabetic ulcers are most common in the forefoot beneath one of the metatarsal heads (Fig. 82-2) or the interphalangeal joint of the hallux
  6. A classification of diabetic ulcers by Brodsky does not include gangrene. In this scheme, grade 0 is intact skin, but represents a preulcerative lesion, with erythema, callus formation, and possible intradermal sheer hemorrhage over a bony prominence. Grade I is a superficial but full-thickness skin ulcer down but not through the subcutaneous tissue. Grade II ulceration is down to the tendon and joint capsule, but neither the joint nor the bone is visible. Grade III ulceration implies exposed bone or joint and osteomyelitis or pyarthrosis
  7. Most common location of DFU
  8. A graduated tuning fork (128 Hz) is used to screen the vibration perception threshold.
  9. Ankle-brachial index is the ratio of the highest systolic blood pressure at the ankle to the systolic blood pressure at the arm, and is measured using a Doppler device
  10. In diabetics polymicrobial infection predominates and both aerobic and anaerobic cultures should be asked for
  11. Timely management, systemic disease Patients should be taught their responsibility for their own health. Health care givers should teach the patient about importance of controlling blood sugar and regular monitoring of blood glucose level. Written information should be given by educator nurse regarding modifiable cardiovascular risk factor such as diet, BMI, alcohol, smoking and exercise
  12. Inspect your foot daily and wash them with water at room temperature. Especial attention should be given to area between the toes. Never walk bare feet. Always wear socks and shoes. Trim nails timely and don’t try to remove callus at home with knife or chemical agent. For dry skin use oil or creams but it should not be applied in between toes. Visit your health care giver at earliest whenever you notice a cut, scratch, and changes in the colour or texture of the foot or sore/ulcer.  
  13. Hyperglycemia is the main cause of the development of DFU. It delays wound healing by hampering phagocytosis and chemotaxis thus compromising cellular immunity. Early control of blood sugar delays the development of neuropathy in diabetic patients but it has not been shown by any study that glycemic control can reverse the established neuropathy
  14. Sharp surgical debridement is the gold standard for the management of diabetic foot ulcers. Surgical debridement involves removal of all necrotic tissues, debris and infected tissues and disruption of surface bio films with scalpel, scissors and curettes.
  15. Enzymatic debridement is useful for ischemic ulcer where aggressive sharp surgical debridement is very painful
  16. It is mainly used as an adjuvant therapy to debridement and antibiotics
  17. Studies have shown a faster healing rate, faster time for wound closure and less time for healthy granulation tissue in non-healing ulcers with use of NPWT.
  18. The pathogenesis of neuropathic diabetic foot ulcers involves mechanical trauma due to focal pressure and repetitive moderate stress. Offloading the affected foot has been used as a useful management strategy as it allows for the pressure to be spread over a wider area away from the affected part. A variety of offloading techniques are in use including surgical offloading.