This document discusses diabetic foot disease, including its pathophysiology, clinical manifestations, management, and prevention. It notes that diabetic foot disease is caused by neuropathy, ischemia, and infection leading to tissue breakdown. The pathophysiology involves both metabolic neuropathy and neuroischemia. Clinical manifestations depend on whether the foot is primarily neuropathic or ischemic. Management involves debridement, wound dressing, antibiotic therapy, metabolic control, and potentially vascular interventions or amputation. Prevention emphasizes good foot care, inspection, and control of diabetes and related conditions.

1. DIABETIC FOOT
Dr. Muhammad Salman

2. INTRODUCTION
May be defined as a group of syndromes in
which neuropathy, ischemia and infection
leads to tissue breakdown resulting in
morbidity and possible amputation.

3. PATHOPHYSIOLOGY OF DIABETIC
FOOT DISEASE
Two overlapping processes
1. Metabolic Neuropathy
2. Neuroischemia

4. NEUROPATHY
 Loss of sensation
 Limited vasodilatory reserve
 Loss of mechanisms regulating capillary
and Av shunt flow and pre capilary
vasoconstriction
 Motor neuropathy that leads to clawing of
toes and arthropathy

5. ISCHEMIA
 Atheromas, involving the distal arteries
 Ulcers on the margins of foot
 No claudication b/c of neuropathy and
peripheral involvement

6. Neuropathy and ischemia ~local trauma of
Skin and soft tissue ~ infection~surrounding
bone involvement ~ osteomyelitis

7. SIMPLE STAGING SYSTEM: A TOOL FOR
DIAGNOSIS AND MANAGEMENT
 Stage 1:The foot is normal. No risk factors of
neuropathy and ischemia
 Stage 2:At risk foot. The patient has developed
risk factors, like ulceration, deformity, callus and
oedema.
 Stage 3:foot with ulcer. Two main types of
diabetic foot with characteristic ulceration.the
neuropathic foot and the ischemic foot.
 Stage 4:Foot with cellulitis
 Stage 5:Foot with necrosis, where infection is
the cause.

8. CLINICAL MANIFESTATIONS
 Both elements of neuropathy and ischemia co
exist
 NEUROPATHIC FOOT
 Warm/dry
 Palpable pulses
 Calluses, as penetrating ulcers at pressure
points or at sites of minor injury
 Painless necrosis of toes
 Ulcers on plantar surface, site of mechanical
pressure
 Neuropathic joint

9.  ISCHEMIC FOOT
 Cold
 Absent pulses
 Absent calluses
 Painful ulcers

10. MANAGEMENT
 Debridement
 Mechanical relief
 Wound dressing
 ANTIMICROBIAL THERAPY
 Metabolic management
 Amputation

11. DEBRIDEMENT
 With a scalpel is the central feature
 Causes
_conversion of chronic wounds into acute wounds
~removes callus
~decreases bacterial load
~decreases dead tissue
~releases growth factors for wound healing
~wound base swabs for culture

12. MECANICAL RELIEF
 Total contact casting for redistribution of
plantar pressure
 Use of boots that are removable
~made of fibre glass
~lined by inflatable air cells like a bivalved
cast

13. DRESSING
 Antiseptic dressing
 Easy to apply
 Non occlusive
 Reman intact while walking

14. ANTI MICROBIAL THERAPY
 Initial treatment of infected foot should be
with broad spectrum antibiotics followed
by swab results

15.  Local signs of infection/mild cellulits in a
neuropathic foot
 Patient treated as an outpatient
 Amoxicillin - clavunate/erythomycin if
allergic to pencillins
 Moderate cellulitis, inj. ceftrioxone 1 gm.
Daily
 Follow up

16.  Local signs of infection in ulcer with mild
cellulitisin neuroischemic foot
 Same treatment

17.  Neuropathic/neuroischemic foot with
severe cellulitis
 Surgical intervention to be sought
 I/V antibiotics,Ceftrioxone/metronidazole
 According to swab results
 Deep swabs to be taken after initial
debridement,positive culture antibiotic
according to sensitivity
 Weekly follow up

18. BACTERIA ASSOCIATED WITH DIABETIC
FOOT INFECTIONS
Gram positive Gram negative Anaerobes
Staphlococcus Proteus Clostrdium
Streptocoocus Klebsiella Bacteriodes
Enterocoocus Pseudomonas Pepto coccus
e. Coli
Acinobacter
Serratia

19. MICRO ORGANISM AND ANTIBIOTIC
ORGANISM ORAL I/V
Streptococcus Amoxacillin
Erythomycin
Clindamycin
ceftrioxone
staphlocoocus Amox-cavunate
clindamycin
Amox-clav
Gentamycin 5
mg/kg/day acc.
To levels
anaerobes Clindamycin
metronidazole
Clindamycin
metronidazole
Gram negative Ciprofloxacin
cefadroxil
Ceftrioxone
gentamycin

20.  Osteomyelitis
 Antibiotics with good bone penetration to
be given
 Ciprofloxacin /Clindamycin

21. METABOLIC MANAGEMENT
 Control hyperglycemia, hyperlipidemia and
hypertension
 Cessation of smoking to prevent
microvascular and macrovascular injury

22. VASCULAR INTERVENTIONS
 Done in patient with peripheral vascular
disease
 Antiplatelet tharapy with aspirin
 Plantar ulcers that fail to respond, in 6
weeks duplex imaging/transfemoral
angiography
 Angioplasty in short vessel occlusion less
than 10 cm.
 Widespread disease, arterial bypass

23. PREVENTION
 Amputation is preventable
 Good care saves legs
 Wash feet daily with warm water and dry them
especially between toes
 Not to walk bare feet
 Dia
 Betics tend to get dry feet esp. in winters apply
an emolient cream to prevent cracks esp.
around heels
 Toe nails to be cut straight across and filed
smooth
 Inspect their feet daily if cannot reach use a
hand mirror

24. RECENT ADVANCES
 Use of L arginine cream which improves blood
flow and temperature also wound healing of
ulcers
 Early aggressive debridement with exposed
bones down to bleeding vascular base and
grafting of epidermal sheet may improve healing
and dec. rate of amputation
 Home monitering of foot skin temp. with hand
held infra red thermometer.inc. temp.inc.risk of
ulceration

25. THANKS