Why Diabetic Foot Ulcer Should Not Be Ignored but Managed Diligently?

CME INDIA Presentation by Prof (Dr.) L. Sreenivasamurth, MD, FRCP (Edinburgh), FRCP (Glasgow) FRCP (London), FACP (USA), FICP, FRSSDI, PDCR, ACCR, Senior Consultant Physician & Diabetologist, Life Care Hospital and Research Centre, Sahakaranagara, Bangalore. Former consultant at Fortis hospitals, Gleneagles Global & Apollo hospitals.

Diabetic Foot Ulcer

Shocking facts

75% of amputations are preventable.
The estimated annual cost to treat diabetes related chronic complications such as DPN is $58 Billion (US).
DPN is the most common type of neuropathy.
It is estimated that someone loses a leg every 18 minutes as an ultimate
complication from neuropathy.
Average cost for a below-knee amputation (BKA) is $45,000. There are 80,000 BKA performed/year.
Usually, the opposite limb develops an ulcer within 18 months 58% go on to have a BKA of the residual limb within 3-5 years.

Why Diabetic foot to be treated?

Diabetic foot is a disease complex that can develop in the skin, muscles, or bones of the foot as a result of the nerve damage, poor circulation and/or infection that is associated with diabetes.
The Diabetic Foot may be defined as a syndrome in which neuropathy, angiopathy, and infection will lead to tissue breakdown resulting in morbidity and possible amputation (WHO 1995).
Any foot pathology that results from diabetes or its long – term results (Boulton 2002).
It’s unwise to consider that major diabetic foot problem occurs all of sudden.

Know 3-pointed Agenda

Predisposing factors (Neuro- and angiopathy)
Precipitating factors (Trauma and tinea)
Perpetuating factors (Pt’s factors & delay healing

CPR of Diabetic Foot

Why We Need to Treat This?

Peripheral neuropathies are reported to be the most common complication of diabetes mellitus (DM).

Statistics of DPN:

Half of all limb amputations are caused by diabetes.
Risk of limb amputations is increased 40 times in diabetes.
70% of people die five years following an amputation.
All amputations begin with an ulcer.
49-85% of amputations can be prevented.

Anything and everything need to be done to combat this progressive nerve disorder

Neuropathic pain of PDN (Painful diabetic neuropathy) negatively affects quality of life

Pain may significantly interfere with a patient’s ability to exercise or walk. Walking has been shown to improve HbA 1C in patients with diabetes regardless of change in body mass.
Pain often intensifies at night and may significantly interfere with sleep. Sleep debt has been shown to have a negative impact on metabolic and endocrine control.
Pain is significantly correlated with depression in diabetic patients.

PDN is a complication of diabetes that often is undertreated.

83% of people with diabetic neuropathy report experiencing pain, but HCPs estimate that fewer than half (41%) of their diabetic neuropathy patients experience pain.
Fewer than half of those with PDN say they speak about it with their HCP.
More than half of patients (56%) report that PDN symptoms can be difficult to describe.

High risk for diabetic foot

Long duration and uncontrolled Diabetes Plus
One or more:
• Peripheral neuropathy
• Peripheral vascular disease
• Trauma
• Previous ulcers
• Diabetic nephropathy or retinopathy
• Obesity
• Lack of education
• Male gender

Other risks for ulcer/amputation

Failure to adequately care for the feet:
• Inadequate patient education
• Inadequate patient motivation
• Depression, anxiety, anger more common in diabetes
• Physical disability
• Cannot see feet 2° to retinopathy
• Cannot reach feet 2° to obesity, age (50% of patients)
• Limited access to podiatry services

Precipitate 85% of amputations: “Rule of 15”

Tragic: “Rule of 50”

Autonomic Neuropathy
- Regulates sweating and perfusion to the limb
- 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

Motor Neuropathy
- Mostly affects forefoot ulceration
- Intrinsic muscle wasting – claw toes
- Equinous contracture

Sensory Neuropathy
- Loss of protective sensation
- Starts distally and migrates proximally in “stocking” distribution
- Large fibre loss – light touch and proprioception
- Small fibre loss – pain and temperature
- Usually a combination of the two

Two mechanisms of Ulceration
- Unacceptable stress few times
- Rock in shoe, glass, burn
- Acceptable or moderate stress repeatedly
- Improper shoe ware
- Deformity

Detecting Feet-at-Risk

History:
• Prior amputation
• Prior foot ulcer
• PAD: known or claudication at < 1 block
Exam:
• Insensitive to 5.07/10g monofilament
• Major foot deformities
• PAD
• Absent DP and PT pulses
• Prolonged venous filling time
• Reduced Ankle-Brachial Index (ABI)
• pre-ulcerative cutaneous pathology

Patient Evaluation

Medical

Optimized glucose control
Decreases by 50% chance of foot problems

Vascular

Assessment of peripheral pulses of paramount importance
If any concern, vascular assessment
Sclerotic vessels
Toe pressures (n>40-50mmHg)
pO 2 >30 mmHg
Expensive but helpful in amputation level

Orthopaedic

Ulceration
Deformity and prominences
X-ray
- Lead pipe arteries
- Bony destruction (Charcot or osteomyelitis)
- Gas, Foreign bodies Contractures
CT can be helpful in visualizing bony anatomy for abscess, extent of disease.
MRI has a role instead of nuclear medicine scans in uncertain cases of osteomyelitis.

Ulcer Classification

University of Texas Wound Classification System of Diabetic Foot Ulcers

Grade I-A: non-infected, non-ischemic superficial ulceration
Grade I-B: infected, non-ischemic superficial ulceration
Grade I-C: ischemic, non-infected superficial ulceration
Grade I-D: ischemic and infected superficial ulceration
Grade II-A: non-infected, non-ischemic ulcer that penetrates to capsule or bone
Grade II-B: infected, non-ischemic ulcer that penetrates to capsule or bone
Grade II-C: ischemic, non-infected ulcer that penetrates to capsule or bone
Grade II-D: ischemic and infected ulcer that penetrates to capsule or bone
Grade III-A: non-infected, non-ischemic ulcer that penetrates to bone or a deep abscess
Grade III-B: infected, non-ischemic ulcer that penetrates to bone or a deep abscess
Grade III-C: ischemic, non-infected ulcer that penetrates to bone or a deep abscess
Grade III-D: ischemic and infected ulcer that penetrates to bone or a deep abscess

Wagner’s Classification

Grade-0 High risk foot and no ulceration.
Grade-1 Superficial Ulcer
Grade-2 Deep Ulcer (cellulitis)
Grade-3 Osteomyelitis with Ulceration or abscess.
Grade-4 Gangrenous Patches. Partial foot gangrene.
Grade-5 Gangrene of entire foot

Patient education

Ambulation
Shoe ware
Skin and nail care
Avoiding injury
Hot water
F. B’s

Manage Intelligently

Wagner 0: Prevention

1: Antibiotics and good glycaemic control

2: Needs hospital admission, as they need

Total contact cast (Distributes pressure and allows patients to continue ambulation)

Principles of application (Changes, Padding, removal)

Antibiotics if infected:

Aminoglycosides, Clindamycin, new Penicillin derivatives and Cephalosporins are commonly used.

Wagner 0-2

Surgical if deformity present that will re-ulcerate
Correct deformity
Exostectomy

Wagner 3

Excision of infected bone
Wound allowed to granulate
Grafting (skin or bone) not generally effective

Wagner 4:

Wide debridement and
Amputation

Wagner 5:

Preferred treatment is below knee amputation

Treatment-Bilayered Cellular Matrix (BCM)

Diabetic neuropathic foot ulcers treated with BCM showed a faster rate of wound healing than those treated with standard care alone (moist saline gauze).
Is made of human dermal cells cultured in bovine collagen sponge.
The absorbable matrix is used as a wound dressing.
The collagen framework provide strength to the skin and contains no cells that can cause rejection or irritation

Basic Foot Care Concepts

Daily foot inspection

May require mirror, magnification, or caregiver
Educate patient to recognize/report ASAP:
Persistent erythema
Enlarging callus
Pre-ulcer (callus with haemorrhage)

Commitment to self-care:

Wash/dry daily
Avoid hot water; dry thoroughly between toes
Lubricate daily (not between toes)
Debride callus/corn to reduce plantar pressure 25%
Avoid sharp instruments, corn plasters
No self-cutting of nails if:
Neuropathy, PAD, poor vision

Protective behaviours:
- Avoid temperature extremes
- No walking barefoot/stocking-footed
- Appropriate exercise if sensory neuropathy
- Bicycle/swim > walking/treadmill
- Inspect shoes for foreign objects
- Optimal footwear at all times

Quick Take Aways

Multi-disciplinary approach needed
Going to be an increasing problem
High morbidity and cost
Solution is probably in prevention
Most feet can be spared, at least for a while

CME INDIA Tail Piece

Diabetic foot pneumonic shared by Dr. A.K. Virmani, Jamshedpur:

IDIOOT

I – Immediate treatment

D- Debridement

I- Ischemia Treatment

O- Off Loading

T- Treat Infection

Dr. A. K. Tiwary, Lucknow

Add Glycaemic control

Dr. N. K. Singh:

Then it becomes IDIOT G😊

References:

Novak P, et al. J Rehabil Med 2004; 36:249–252. 5. Zelman DC, et al. Clin J Pain 2006;22:681–685.
Boule NG, et al. JAMA 2001;286:1218–1227. 6. Spiegel K, et al. Lancet 1999;354:1435–1339.
American Diabetes Association. Diabetes Care 2011;34(Suppl1):S11–S61. 7. Åkerstedt T, Nilsson PM. J Intern Med 2003;254
Spiegel K, et al. Lancet 1999;354:1435–1339.
Quattrini C, et al. Diabetes Metab Res Rev 2003;19:S2–S8.
Åkerstedt T, Nilsson PM. J Intern Med 2003;254:6–12.
Age Ageing 1992; 21:333 Diabetes Care 2003; 29:495 Diab Metab Res Rev 2004; 20(Suppl 1):S13