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Diabetic Foot and Ulcer Dr. Sushil Vijay PG Student, D.Orth Santosh Medical college & Hospital 1

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Diabetic foot. Dr Sushil vijay D.orth

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Dr. Sushil Vijay PG Student, D.Orth Santosh Medical college & Hospital1

Why this topic is important??

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We

all want a fully functional, normal healthy pair of legs.

Also..

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The top 10 countries with Diabetes 2003 -2025

From Internations Diabetic Federation7

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Risk Level 3: Prior amputation Prior ulcer 2: Insensate and foot deformity or absent pedal pulses 1: Insensate 0: All normal

Foot Ulcer %/yr

28.1% 18.6%

6.3%

4.8% 1.7%10

Understand

pathogenesis of diabetic foot

ulcers Effectively

evaluate a diabetic ulcer for a treatment plan for diabetic

infection Formulate

ulcers11

Because!

It is haemodynamically poorly placed.

It is exposed to trauma by frequent contact with the ground. It is that part of the body farthest away from the CNS*12

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Definition Epidemiology Fate of diabetes Pathophysiology Etiopathogenesis Clinical features Stage of ulcer development Classification/grading of ulcer Evaluation of a patient Management Neuropathic joint- Charcot joint Patient Education Prevention/Treatment of metatarsal head ulcer Diabetic foot care for other ailments.

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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)14

Any

infection (as defined by International Consensus) involving the foot (below the malleoli) in a person with diabetes originating in a chronic or acute injury to the soft tissue envelope of the foot, with evidence of pre-existing neuropathy and ischaemia.

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Any

foot pathology that results directly from diabetes or its long term complications ( Boulton 2002).

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DM

is the largest cause of neuropathy. 50% patients dont know that they have diabetes. Foot ulcerations is most common cause of hospital admissions for Diabetics. Expensive to treat, may lead to amputation and need for chronic institutionalized care.

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Male

Sex DM > 10 years duration Abnormal foot structure Smoking Poor glycemic control

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Repeated Traumatized DFU

Greater & Persistent Inflammatory Response

More Neutrophils & Macrophages Migration

More Cytokine Release

More Inflammatory Cells & Fibroblasts recruited

More TNF-a & IL-1b release

More Macrophage Activation

Increased Release of SerineProteases MMP s TIMPs

Degradation of Matrix proteins, Growth Factors, & Receptors for GF

CHRONICITY OF DFU

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Diabetic Diabetic Charcot

foot ulcerfoot infections Joints

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Combination

of factors

Neuropathy Ischemic (Peripheral arterial disease) Abnormal foot biomechanics

Delayed wound healing

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NEUROPATHY

THE CRUCIAL TRIADREPETITIVE TRAUMA

DEFORMITY

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A.

Neuropathy

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Primary etiology: NEUROPATHY Sensory Motor

Autonomic

Associated etiology: Deformity Infection Peripheral Arterial Disease (PAD)

Associated Pathogenic Mechanisms: Ulceration Decrease in Neurokines including Substance P

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Truly

multi factorial but one may predominate others. Factors are 1. Neuropathy 2. Macrovascular disease 3. Microvascular disease 4. Connective tissue abnormalities 5. Infections 6. Hematological disturbances27

Glove & stocking type Can be

Sensory / motor/ autonomic Mono / poly radiculopathy

Most commonly neuropathy

distal

symmetric

sensory

Causes: 1]Metabolic factor(Due to hyper glycemia) 2]Microvascular disease Effects: 1]Extrinsic 2]Intrinsic28

Extrinsic:

Loss of somatic sensations of plantar aspect cause ulcer by: fitting shoe, toe nail, thermal injury, foreign body Pain is not perceived , So damage continues, & Established ulcer is the end point.

ill

Intrinsic:

Causes smooth motor neuropathy Weakness of intrinsic muscles . Abnormal movements of small bones &joint subluxation. Visceral neuropathy cause loss of proprioception . Patient keeps on walking on aching foot (which is not known to him). Stretching of joint capsules & bony changes take place. With continuous shear pressure cause callus & ulcer formation.29

MACROVASCULAR

MICROVASCULAR

Diabetics are 4 to 7 times more prone for atherosclerosis than normal.

Structural abnormalities in: 1]Basement membrane 2]Endothelial function Basement membrane: Leads to defect in movement of leucocytes & macromolecules. Endothelial Function :Defect leads to poor tissue perfusion & play important role in ulceration.30

Mostly affect tibial and peroneal arteries.Reduced oxygen partial pressure

Vascular calcification seen in xray & angiography.

Skin

cracks & fungal infection between toes are route of infection. Gram ve & +ve aerobes & anaerobes are noted. Causation of infections increased in diabetes due to:1.

2.3.

Deficiency of cell mediated immunity Impaired chemotaxis Impaired phagocytosis & opsonization.

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Hyperglycemia

affect structure and function of proteins like keratin, collagen. Changes in them and structures become weak & inelastic affect bone structure leading to foot ulcers. `

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They1. 2. 3. 4.

cause:

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Ischemia Ulceration Spread of infections Red cell deformities ---Hypercoagulability & increased plasma viscocity. All these increase chances of infections.

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Sensory NeuropathyLoss of Protective Sensation Unrecognized Foot Trauma Ulceration Infection & Impaired Healing

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Motor Neuropathy

Muscle Atrophy

Foot Deformity

Altered Biomechanics

Areas of High Pressure Unrecognized Foot Trauma

Ulceration

Infection & Impaired Healing

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Autonomic NeuropathyDry Skin due to Hypohidrosis Altered Cutaneous Blood Supply

Cracks & Fissures

Ulceration

Infection & Impaired Healing

PAD 36

Sensory Neuropathy

Motor Neuropathy

Autonomic Neuropathy

Unrecognized Foot Trauma

PAD

Ulceration

Infection & Impaired Healing

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B.

DEFORMITY38

Abnormal

weight bearing Fixed foot deformities Hammer toe Claw toe

Prominent metatarsal heads Charcots joints

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Hammer Toes

Claw Toes40

Hallux Valgus

Hallux valgus deformities are more common in persons with diabetes and result in high pressure points from shoe gear at the distal end of the proximal phalanx.

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A marked Hallux valgus deformity and early hammer-toe deformities from diabetic motor neuropathy. Note the areas of persistent erythema over pressure points on the first MTP joint and on the dorsum of the proximal phalanges. This patient requires a modification of shoe gear to relieve pressure and prevent callus and ulcer formation. 42

Severe hammer and claw-toe deformities.

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This patient has a pes cavus or high plantar arch deformity that has resulted in pressure points and callus formation over the heels, metatarsal heads, and along the medial aspect of the great toe. Extensive callus increases the subcutaneous pressure immediately beneath the callus and can result in a subcutaneous hemorrhage, the so-called pre-ulcer.

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Impaired

wound healing

Does not allow resolution of fissures and

minor injuries Increased chances of infection

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To Summarize all the factors we studied till now

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Causal Pathways for Foot UlcersNeuropathy

Deformity

% Causal Pathways Neuropathy: Minor trauma: Deformity: 78% 79% 63%

Minor Trauma- Mechanical (shoes) - Thermal - Chemical

Behavioral

?

Poor self-foot care

ULCER47

Neuropathic

Vascular

disease Small muscle wasting-claw foot Loss of architecture of the foot Pressure points and ulcers

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Shape: change in shape lead to areas

of pressure on prominent metatarsal heads,hammertoes,collapsed mid foot.Callus: Callus is seen with excessive

wear &tear of tissue.

Skin: Skin is dry and without sweatingdue to autonomic neuropathy. Crack easily & a route infection. of

Sensations: Loss of sensations

which are assessed by traditional modalities like ankle jerks, tendon reflex . Pain sensation :reduced & is assessed by biosthesiometer& nylon monofilament.49

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NUMEROUS GRADING SYSTEMS

UT: University of Texas SINBAD: Site, Ischemia, infection, Ulcer Area, Depth Neuropathy, Bacterial

S(AD)SAD: Size (Area, Depth), Sepsis, Arthropathy, Denervation

PEDIS: Perfusion, Extent, Depth, Infection, SensationWagner Duss53

GRADE 0 1 2 3 Foot At Risk

DESCRIPTION

INFECTION None None Superficial Infection Deep Infection

Superficial Ulceration Ulcer penetrating to tendon or capsule Ulcer penetrating to bone or joint

ISCHEMIC GRADES:

A = No ischemia; B = Ischemia w/o gangrene; C = partial gangrene; D = complete gangreneBeckart S, Witte M, Wicke C, et al. Diabetes Care 29: 988-92, 2006

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Palpable Pedal Pulses: Yes = 0, Probing-to-Bone: Site of Location: No. of Ulcers: No = 0, Toe = 0, Single = 0,

No = 1 Yes = 1 Foot = 1 Multiple = 1

Maximum score of 4 possible High score correlate with healing, hospitalization, amputation.

Beckart S, Witte M, Wicke C, et al. Diabetes Care 29: 988-92, 2006

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Site, Ischemia, Neuropathy, Bacterial infection, Ulcer Area, Depth

SITE: ISCHEMIA:

0 = Forefoot

1 = Midfoot, Hindfoot

0 = Pedal Flow Intact; at least one pedal pulse palpable, 1 = Clinical evidence of reduced pedal blood flow

NEUROPATHY: 0 = Protective sensation intact 1 = Protective sensation lostBA. INFECTION: 0 = None 1 = Present 1 = Ulcer