Diabetic foot infections and ulcers are common complications of diabetes that occur due to peripheral neuropathy, peripheral artery disease, and immune dysfunction caused by hyperglycemia. Risk factors include prior ulcers or amputations, foot deformities, and peripheral artery disease. Evaluation involves assessing infection severity, underlying bone involvement, and vascular status. Management requires wound debridement and dressings, antimicrobial therapy, glycemic control, and possible surgery. Close follow up is needed to monitor treatment response and detect any need for treatment modifications.

1. DIABETIC FOOT
Dr Ashish kharel (MS-JR1)
Bir Hospital

2. Background

3. Introduction: Diabetic Foot Ulcers
and Infections
• Most common problem in persons with
diabetes.
• Lifetime risk of a foot ulcer in Diabetes
patients: 25 %
• Account for approximately 25 percent of all
hospital stays for patients with diabetes

4. Risk factors
• Local trauma and/or pressure
• Prior ulcers or amputations
• Infection
• Effects of chronic ischemia, due to peripheral
artery disease
• Patients with diabetes also have an increased
risk for nonhealing related to mechanical and
cytogenic factors

5. Aetiopathogenesis
• Peripheral neuropathy and peripheral arterial
disease (PAD) (or both) play a central role
• Diabetic Foot Ulcers are classified as:
– Neuropathic
– Ischaemic
– Neuroischaemic

6. Peripheral Neuropathy
• Sensory Neuropathy
• Motor Neuropathy
• Autonomic Neuropathy

7. Sensory Neuropathy
• Loss of pain sensation
• Unnoticed and trivial trauma (thermal, chemical ,
mechanical )
• Progressive callous formation
• Tissue damage and necrosis
• Subcutaneous fluid collection and hemorrhage
• Tissue breakdown
• Ulceration

8. Motor Neuropathy
• Weakness of intrinsic foot muscles
• Progressive muscle wasting
• Foot deformities and joint subluxations
• Limited joint mobility
• Abnormal gait
• Chronic Internal pressure
• ulceration

9. Autonomic Neuropathy
• Decreased sweating
• Dry and brittle skin
• Fissures and cracks
• Secondary infections
• Ulceration

10. Peripheral Arterial Disease (PAD)
• People with diabetes are twice as likely to have PAD as
those without diabetes.
Macroangiopathy : atherosclerosis of arteries
Microangiopathy : increased and abnormal basement
membrane thickening and endothelial proliferation
Leads to capillary damage and release of ROS
Leading to decreased blood flow ---- poor antibiotic
penetration -- poor wound healing

11. Immune Dysfunction
Hyperglycemia impairs neutrophil function and
reduces host defenses.
• Persistently high pro-inflammatory cytokines
and proteases concentration
• Degrade growth factors, receptors and matrix
proteins
• Decreased PMNs migration and phagocytosis
• Decreased chemotaxis and intracellular killing

12. Typical features of DFUs according to aetiology.

13. Neuropathic DFU
Neuroischaemic DFU
Ischaemic DFU

14. Microbiology
• Most diabetic foot infections are polymicrobial
• Superficial diabetic foot infections :likely due
to aerobic gram-positive cocci.
• Ulcers that are deep, chronically infected
and/or previously treated with antibiotics are
more likely to be polymicrobial.

15. • Wounds with extensive local inflammation,
necrosis, malodorous drainage, or gangrene
with signs of systemic toxicity should be
presumed to have anaerobic organisms in
addition to the above pathogens.

16. Risk of specific organism
• MRSA: Prior antibiotic use, previous hospitalization,
and residence in a long-term care facility.
• Pseudomonas aeruginosa :Macerated ulcers, foot
soaking, and other exposure to water or moist
environments.
• Resistant enteric gram-negative rods: patients with
prolonged hospital stays, prolonged catheterization,
prior antibiotic use, or residence in a long-term care
facility.

17. Ulcer classification
University of Texas system
Grade 0: Pre- or postulcerative
Grade 1:Full-thickness ulcer not involving tendon, capsule, or bone
Grade 2: Tendon or capsular involvement without bone palpable
Grade 3: Probes to bone
• STAGE:
●A: Noninfected
●B: Infected
●C: Ischemic
●D: Infected and ischemic

18. Grade0: Pre- or postulcerative

19. Grade 1: Full-thickness ulcer not involving tendon, capsule, or bone

20. Grade 2: Tendon or capsular
involvement
without bone palpable

21. Grade 3: Probes
to bone

22. Wagner Classification:
• Grade 1: Skin and subcutaneous tissue
• Grade 2: To bone
• Grade 3: Abscess or osteitis
• Grade 4: Partial foot gangrene
• Grade 5: Whole foot gangrene

24. WIFI Classification
• Measures 3 factors:
– Wound
– Ischemia
– Foot Infection

26. Clinical manifestation
Diabetic foot infections typically take one of
the following forms:
• Localized superficial skin involvement at the
site of a preexisting lesion
• Deep-skin and soft-tissue infections
• Acute osteomyelitis
• Chronic osteomyelitis

27. History
• Duration of diabetes
• Glycemic control
• Presence of micro- or macrovascular disease
• History of prior foot ulcers, lower limb
bypasses or amputation
• Presence of claudication
• History of cigarette smoking

28. Physical examination
Assessment for the presence of
• existing ulcers
• peripheral neuropathy
• loss of protective sensation
• peripheral artery disease, and
• foot deformities
– claw toes and
– Charcot arthropathy

30. Examination of Ulcer
• Predominantly neuropathic, ischaemic or
neuroischaemic?
• Is there critical limb ischaemia?
• Any musculoskeletal deformities?
• Ulcer Characteristics:
size/depth/location/wound bed
• wound infection
• status of the wound edge

31. Screening tests for peripheral neuropathy
• Vibration sensation
• Pressure sensation
• Superficial pain (pinprick) or temperature
sensation
• Scoring Systems

32. The Tuning Fork Test
• 128Hz tuning Fork used
• Placed on the interphalangeal joint of the
right hallux and compared with dorsal wrist.
– Severe Deficit: no senation in hallux
– Mild/Moderate: vibration feels stronger at the
wrist
– Normal: vibration feels no different at the wrist.

33. Semmes-Weinstein Monofilament Test

34. • Procedure:
– Quiet Surrounding
– Eyes Closed for the test
– Supine position
– Testing in inner aspect of arm/hand
– Apply the monofilament perpendicular to the skin
surface with sufficient force to bend it
– Ask: whether they felt it?/Where they felt it?
– Duration: 2 secs
– 3 applications in each site with at least 1 mock

35. • Inference:
– Protective sensation is present at each site if the
patient correctly answers two out of three
applications
– Protective sensation is absent with two out of
three incorrect answers

36. Scoring Systems for Peripheral
Neuropathy
• The San Antonio Consensus
• The Mayo Clinic criteria
• The Toronto criteria
• United Kingdom screening test
• Michigan Neuropathy Screening Instrument

37. Feldman EL, Stevens MJ, Thomas PK, et al. A practical two-step quantitative clinical and
electrophysiological assessment for the diagnosis and staging of diabetic neuropathy. Diabetes
Care 1994; 17:1281.

38. Physical signs of peripheral artery disease
• diminished foot pulses,
• decrease in skin temperature,
• thin skin,
• lack of skin hair, and
• bluish skin color

39. Quantitative clinical tests:
• measurement of venous filling time
• Doppler examination of lower limb pulses
• leg blood pressure measurements (eg, ankle-
brachial pressure index [ABI])

40. Diagnosis of Diabetic Foot Infection
• Primarily based on suggestive clinical manifestations
• The presence of two or more features of inflammation
(erythema, warmth, tenderness, swelling, induration
and purulent secretions) can establish the diagnosis
• Presence of microbial growth from a wound culture in
the absence of supportive clinical findings is not
sufficient to make the diagnosis of infection

41. Diagnosis of underlying osteomyelitis
• Grossly visible bone or ability to probe to bone
• Ulcer size larger than 2 cm2
• Ulcer duration longer than one to two weeks
• Erythrocyte sedimentation rate (ESR) >70 mm/h
• A conventional radiograph with consistent
changes can be helpful in making the
diagnosis ((MRI), which is highly sensitive and
specific for osteomyelitis )
• Culture of bone biopsy specimens is also
important for identifying the causative organisms

42. Differential diagnosis
• trauma
• crystal-associated arthritis
• acute Charcot arthropathy
• fracture
• thrombosis
• venous stasis

43. Determination of severity
• Assessment of the severity of diabetic foot
infections is important for prognosis and to
assist with management decisions (eg, need
for hospitalization, surgical evaluation, or
parenteral versus oral antibiotic therapy)

44. Infectious Diseases Society of America and International Working Group on the Diabetic Foot
Classifications of Diabetic Foot Infection

45. Management
Management of diabetic foot infections
requires:
• Attentive wound management
• Good nutrition
• Appropriate antimicrobial therapy
• Glycemic control, and
• fluid and electrolyte balance.

46. Wound management
• Local wound care for diabetic foot infections typically
includes debridement of callus and necrotic tissue, wound
cleansing, and relief of pressure on the ulcer
DEBRIDMENT:
• Debridement is essential for ulcer
healing
• choice of debridement
– sharp,
– enzymatic,
– autolytic,
– mechanical, and
– biological)
Fig: Neuropathic ulcer
Top: Pre debridement
Bottom: Post debridement

47. DRESSINGS
• After debridement, ulcers should be kept clean
and moist but free of excess fluids
• Dressings should be selected based upon ulcer
characteristics, such as the extent of exudate,
desiccation, or necrotic tissue
Adjunctive local therapies :
• negative pressure wound therapy (NPWT)
• use of custom-fit semipermeable polymeric
membrane dressings
• cultured human dermal grafts
• application of growth factors

48. • Wound Management Dressing Guide
International Best Practice Guidelines: Wound Management in Diabetic Foot Ulcers.

49. • Wound Management Dressing Guide Continued...

50. Surgery
Required for cure of infections complicated by
• abscess,
• extensive bone or joint involvement,
• crepitus, necrosis, gangrene or necrotizing fasciitis
• And for source control in patients with severe sepsis
In addition to surgical debridement, revascularization (via
angioplasty or bypass grafting) and/or amputation may
be necessary.

51. Antimicrobial therapy
EMPERIC THERAPY:
Mild infection: Outpatient oral antimicrobial
therapy.
Should include activity against skin flora
including streptococci and S. aureus
Agents with activity against methicillin-resistant S.
aureus (MRSA) should be used in patients with
purulent infections and those at risk for MRSA
infection

52. • Moderate infection: Deep ulcers with extension to
fascia. Should include activity against
streptococci, S. aureus (and MRSA if risk factors
are present), aerobic gram-negative bacilli and
anaerobes
– can be administered orally
• Empiric coverage for P. aeruginosa may not
always be necessary unless the patient has
particular risk for involvement with this organism,
such as a macerated wound or one with
significant water exposure

53. Severe infection: Limb-threatening diabetic foot
infections and those that are associated with
systemic toxicity should be treated with
broad-spectrum parenteral antibiotic therapy
In most cases, surgical debridement is also
necessary.

55. Duration of therapy
• Mild infection should receive oral antibiotic
therapy in conjunction with attentive wound
care until there is evidence that the infection
has resolved (usually about one to two weeks)
• Patients with infection also requiring surgical
debridement or amputation should receive
intravenous antibiotic therapy perioperatively

56. • In case of osteomyelitis:
• No data support the superiority of specific
antimicrobial agents for osteomyelitis
• Appropriate regimens for empiric therapy are
similar to that for moderate to severe diabetic
foot infections
• Therapy should be tailored to culture and
sensitivity results, ideally from bone biopsy.
• Patients who were initiated on parenteral
therapy, a switch to an oral regimen is
reasonable following clinical improvement

57. Extensive surgical debridement or resection is
preferable in the following clinical circumstances
• Persistent sepsis without an alternate source
• Inability to receive or tolerate appropriate
antibiotic therapy
• Progressive bone deterioration despite
appropriate antibiotic therapy
• Mechanics of the foot are compromised by
extensive bony destruction requiring correction
• Surgery is needed to achieve soft tissue wound or
primary closure

58. Adjunctive therapies
• vacuum-assisted wound closure,
• hyperbaric oxygen and
• granulocyte colony-stimulating factor (G-CSF)

59. Follow-up
• Close follow-up is important to ensure
continued improvement and to evaluate the
need for modification of antimicrobial
therapy, further imaging, or additional surgical
intervention

60. Summary
• Hyperglycemia, sensory and autonomic
neuropathy, and peripheral arterial disease all
contribute to the pathogenesis of lower
extremity infections in diabetic patients
• Evaluation of a patient with a diabetic foot
infection involves determining the extent and
severity of infection through clinical and
radiographic assessment

61. • The presence of two or more features of inflammation
(erythema, warmth, tenderness, swelling, induration,
or purulent secretions) can establish the diagnosis of a
diabetic foot infection. The definitive diagnosis of
osteomyelitis is made through histologic and
microbiologic evaluation of a bone biopsy sample
• Management of diabetic foot infections requires
attentive wound management, good nutrition,
antimicrobial therapy, glycemic control, and fluid and
electrolyte balance

62. References::
• Lipsky BA, et al. 2012 Infectious Diseases Society of
America clinical practice guideline for the diagnosis and
treatment of diabetic foot infections. Clin Infect Dis
2012; 54:e132.
• International Best Practice Guidelines: Wound
Management in Diabetic Foot Ulcers. Wounds
International, 2013.
• Gulf Diabetic Foot Working Group. Identification and
management of infection in diabetic foot ulcers:
International consensus. Wounds International 2017.
• www.uptodate.com
• Internet

63. THANK YOU!!!!