Diabetic Foot Kuliah Makbul 2016

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DIABETIC FOOT

A.MAKBUL AMAN
Sub Division of Endocrine and Metabolism, Department of Internal Medicine Hasanuddin
University / RSUP Dr. Wahidin Sudirohusodo/ RS. PENDIDIKAN UNHAS
Introduction
 1-4% of diabetics develop foot ulcer annually, 25% in
lifetime
 45-75% of all lower extremity amputations are in diabetics
 85% of these preceded by foot ulcer
 Two-thirds of elderly patients undergoing amputation do
not return to independent life
 Foot problems account for largest number of hospital bed
days used for diabetic patients
 25-50% of costs related to inpatient diabetes care
attributable to diabetic foot
Why worry about Diabetic
Feet?
Diabetic foot infections are common,
expensive and probably increasing in
frequency
The most frequent reason for
hospitalization in diabetic patients
The most common reason for amputations
Current treatment often fails to conform to
available evidence/ guidelines
optimal treatment requires a
multidisciplinary approach
85.000 lower extremity amputations
per year

1 leg is lost every 30 sec.


AMPUTATIONS IN DIABETES

Tragic: “Rule of 50”


 50% of amputations transfemoral/transtibial level
More than 80% are potentially
 50% of patients 2 amputation in  5y
nd
preventable
 50% of patients Die in  5y

 Clinical Care of the Diabetic Foot, 2005


Foot problems
The feet can be affected by:
Decreased blood supply poor healing

Nerve damage loss of feeling

High Blood Sugar levels decrease healing

DPMI Workforce Development – The Alfred Workforce Development Team June 2005
DIABETIC FOOT ULCERS
Chronic foot infections in patients with D.M are
common and difficult problems
“Rule of 15”
• 15% of diabetes patients Foot ulcer in lifetime

• 15% of foot ulcers Osteomyelitis

• 15% of foot ulcers Amputation

Clinical Care of the Diabetic Foot, 2005


PATHOPHYSIOLOGY
triangle of devil

infection

Neuropathy Vascular disease


Pathophysiology: diabetic foot
ulceration
Neuropathy

Motor Sensory Autonomic


Abnormal foot Loss of protective Reduced skin
biomechanics sensation compliance and
lubrication

Ulceration

Vascular
insufficiency
Infection
Diabetes Mellitus

Neuropathy Angiopathy

Motor Sensitive Autonomous

Limited Coordination and Peripheral Vascular


Decrease of
Articular Postural Desviation Microangiopathy Disease
painfeeling
Mobility

Regulation of
Decrease of the altered blood
sudation flow ?
Ischemia
Dry skin,
Foot deformity, fissures
pressure

Callus Traumatism Traumatism

Inappropiate footwear, Gangrene


non-fulfilment. Lack of
social and educational Ulcer
level
Infection

Amputation
“ How are blood vessels
affected?”
 High blood sugar expedites Peripheral arterial disease
artherosclerosis giving peripheral
vascular disease (reduction of blood Artherosclerosis
narrows or blocks
supply to the foot).
the arterial lumen
 The delivery of essential nutrients
and oxygen to the foot is Foot ischaemia
compromised leading to anaerobic
Foot ulcer Necrosis/ Gangrene
infections and tissue necrosis.

Infection

Artheroma plaque
narrowing the arterial
lumen
Ischaemic toes due
to artherosclerosis
Definition
Peripheral arterial disease (PAD)
encompasses a range of
noncoronary arterial syndromes that
Blood
are flowbyobstruction
caused in arteries
the altered structure
andexclusive
function of of
thethe coronary
arteries that &
supply thecerebral vessels
brain, visceral organs,
and theprimarily
limbs. caused by
atherosclerosis
Chronic : Atherosclerotic
Acute : Embolic, Thrombotic”
PAD Risk Factors
NON-MODIFIABLE RISKS:
 Age. The risk of limb loss due to PAD increases with age. People 65 or older are two to three times
more likely to have an amputation.
 Gender. Men with PAD are twice as likely to undergo an amputation as women.
 Race/ethnicity. Some racial and ethnic groups have a higher risk of amputation (i.e., African
Americans, Latino Americans, and Native Americans). This is because they are at increased risk for
diabetes and cardiovascular disease.
 Family history of heart disease. A family history of cardiovascular disease is an indicator for risk at
developing PAD.

MODIFIABLE RISKS:
 Cigarette smoking.  Smoking is a major risk factor for PAD. Smokers may have four times the risk of
PAD than nonsmokers. 
 Obesity. People with a Body Mass Index (BMI) of 25 or higher are more likely to develop heart disease
and stroke even if they have no other risk factors. 
 Diabetes mellitus.  Having diabetes puts individuals at greater risk of developing PAD as well as other
cardiovascular diseases. 
 Physical inactivity.  Physical activity increases the distance that people with PAD can walk without
pain and also helps decrease the risk of heart attack or stroke. Supervised exercise programs are one
of the treatments for PAD patients. 
 High blood cholesterol.  High cholesterol contributes to the build-up of plaque in the arteries, which
can significantly reduce the blood's flow. This condition is known as atherosclerosis. Managing
cholesterol levels is essential to prevent or treat PAD.
 High blood pressure. When blood pressure remains high, the lining of the artery walls becomes
damaged. Many PAD patients also have high blood pressure.
 High levels of Homocysteine. This is an amino acid found in plasma (blood). Some recent studies
show higher levels are associated with PAD.
Clinical Presentation of PAD

Initial PAD
Presentation

Asymptomatic PAD
Symptomatic PAD
20-50%

Intermittent Critical Limb


Atypical Leg Pain
Claudication Ischemia
40-50%
10-35% 1-2%

Hirsch AT, Haskal ZJ, Hertzer NR, et al. Available at http://www.acc.org/clinical/guidelines/pad/summary.pdf. Accessed
December 13, 2005.
Classification PAD
Fontaine Classification Rutherford Classification
Stage Clinical Grade Clinical
I Asymptomatic 0 Asymptomatic
IIa Mild Claudication 1 Mild
IIb Moderate to Severe 2 Moderate
Claudication
3 Severe
III Ischaemic rest pain 4 Ischaemic rest pain

IV Ulceration or gangrene 5 Minor tissue loss


6 Major tissue loss
Acute Limb Ischaemia Ischemia in Right Foot

15
Symptoms
Ranging from no symptoms,
intermittent claudication, rest
pain, tissue loss, and finally
non-healing wound / ulcer and
gangrene.
The most common symptoms of
PAD is claudicatio intermittent
 Cramping, or aching in the
calves, thighs, or buttocks that
appears reproducibly with
walking exercise and is
relieved by rest.
The 5 P’s

Peripheral signs of PAD are the classic 5 P’s


Pulselessness
Paralysis
Paraesthesia
Pain
Pallor
FOOT EXAM
Skin and Integument
A. Color
B. Temperature
C. Texture
D. Hair Growth
E. Moisture
F. Lesions-location, size, type
G. Condition of toenails
Vascular exam
A. Color
B. Varicosities/Edema
C. Pulses
Neurological
A. Light touch
B. Sharp-dull discrimination
C. Vibratory
D. Protective sensation
Clinical Examination
Assessment
– Temperature
– Colour
– Pulse pattern
» Common
femoral
» Popliteal
» Dorsalis pedis
» Post tibial
Auscultation
Diagnosis PAD

Figure 1: Monofilament testing

2006)4
(Edmonds & Foster
Figure 2: ABPI testing
Diagnosis :
Two reasons : Identify patient who has high risk of subsequent MI or
stroke and to elicit and treat symptoms of PAD
A variety of noninvasive examinations are available to assess the
presence and degree of peripheral arterial disease
 Ankle-brachial index (ABI)
 Exercise treadmill test
 Segmental limb pressures
 Segmental volume plethysmography
 Duplex ultrasonography
 An ABI of ≤0.90 has a high degree of sensitivity and
specificity for the diagnosis, using arteriography as
the gold standard

The history and physical examination (pulse evaluation and careful


examination of the leg) are usually sufficient to establish the
diagnosis
The Ankle-Brachial Index

Lower extremity systolic pressure


ABI =
Brachial artery systolic pressure

INTERPRETATION VALUE
Normal 0.91 - 1.30
Mild Obstruction 0.70 - 0.91
Moderate Obstruction 0.40 - 0.69
Severe Obstruction < 0.40
Poorly Compressible > 1.30
Algorithm for diagnosis of PAD TASC II ,2007

TBI :toe brachial index


VWF : velocity wave form
PVR : pulse volume recording
Management of PAD
1. Risk Factor modification
2. Medical Treatment
3. Intervention Procedures

GOALS OF TREATMENT
To relieve exertional symptoms and improve
walking capacity  improve quality of life
To reduce total mortality as well as cardiac and
cerebrovascular morbidity and mortality
Risk Factors modification

Most people with PAD can be treated with


lifestyle changes :
Stop smoking, Avoid stress
Control diabetes.
Control blood pressure.
Be physically active (including a supervised
exercise program).
Eat a low-saturated-fat, low-cholesterol diet .
Two Major Goals in Treating Patients With PAD

Limb outcomes Cardiovascular morbidity and


mortality outcomes
Improved ability to walk
Decrease in morbidity from non-
– Increase in peak walking distance
– Improvement in quality-of-life (QoL) fatal MI and stroke

Prevention of progression to critical limb Decrease in cardiovascular


ischemia and amputation mortality from fatal MI and
stroke
Treatment of critical limb ischemia and
amputation
Treatment for chronic arterial occlusion
- Classification by the purpose of treatment -

Basic treatment Termination of smoking


Removal of
risk factors Antihyperlipidemic agents
Drug treatment Antihypertensive agents
Antidiabetic agents

Exercise treatment
Improvement of
peripheral circulation Anti-platelet agents
Drug treatment Vasodilators
Anticoagulants

Circulation
Surgical treatment
Removal of reconstructive surgery
thrombus and occlusion
Drug treatment Fibrinolytic agents,
Anticoagulants
Anti-platelet agents
Therapy of chronic arterial occlusion
Based on Fontaine’s classification
Physical treatment
Severity Symptoms
(warming/rest)

Feeling of coldness,
I
Numbness
conserva Drug treatment
tive
Intermittent claudication
II Mild case (<300m)
Severe case (<200m)
Exercise treatment

Circulation-
III Pain at rest reconstructive surgery
+ Drug treatment
surgical
Sympathectomy
IV Ulceration, Necrosis + Drug treatment
ACC/AHA guideline for the management
of PAD: Treatment of claudication
Drugs Available for PAD
ASPIRIN CILOSTAZOL
Inhibit cyclo-oxygenase & diminish Inhibition of Cyclic AMP
Phosfodiesterase ( primary &
formation of thromboxan A2
secondary platelet agregations )
TICLOPIDINE Have vasodilator effect
Inhibits ADP receptorP2Y1 &
Blocking ADP-dependent GP –IIb-IIIa
PENTOXIFYLLIN
fibrinogen complex on platelet Increas erytrhocyte deformability
surface.
NAFTIDROFURIL
CLOPIDOGREL Inhibition of Trhomboxan A2
Same with Ticlopidine but fewer side Anti vasoconstrictor
effect  Beware TTP.

PGI2 analog ( Beraprost ) Activating


adenylcyclase, cAMP  vasodilator
& inhibits platelet aggregation
Pharmacotherapy for PAD
Generic Name Mechanism of action Dose
Aspirin Cyclooxygnease pathway 1 x 75 – 325 mg/po
Clopidogrel ADP receptor antagonist, anti-platelet 1 x 75 mg / po
activity

Cilostazol Phosphodiesterase inhibitor  cAMP  2 x 100 mg/po


vasodilator & inhibits platelet aggregation

Pentoxifylline Decrease blood & plasma viscosity, 3 x 400 mg/po


RBC/WBC deformity, inhibit adhesion

PG-E1 Activating adenylcyclase, cAMP  1 x 40-60 µg /


vasodilator & inhibits platelet aggregation infusion 2 hrs

PG-I2 Activating adenylcyclase, cAMP  3 x 40 µg / po


(beraprost) vasodilator & inhibits platelet aggregation (3 x 20 µg / po)

ACE-I RAA pathway, increased NO, inhibits VSMC Depend on active


migration & proliferation, decreases substances
adhesion molecules

L-Arginine Restoring NO formation 2 x 8 g / infusion


PAD in Diabetic Patients
Risk factors:
– diabetic neuropathy
– structural foot deformity
– peripheral arterial disease

Platelets in DM Patients :
1. Ease to adhesion and agregations
2. Hypersensitive to agregator
3. Ease to interactions with plasma
4. Increase productions immunoreactive substrat
( PGG2, PGH2 )
PAD in diabetics has a poor prognosis
• PAD is 20 x more common in diabetics than non diabetics

• lower limb amputation is 15 x more common in diabetics

• ten year cumulative incidence of lower limb amputation is 5.4% in


type I diabetes and 7.3% in type II

• 10% of diabetics get an ulcer (10% are purely ischaemic, 45% are
ischaemic with associated neuropathy, infection, biomechanical
abnormalities and Charcot deformity)

Increased risk of CVD, CAD, nephropathy,


retinopathy and death
DM and PAD
 Increased by age, duration of diabetes and presence of
neuropathy
 Strongly associated with femoral-popliteal and tibial PAD (
below the knee), rarely proximal limb
 Difficult to determine the prevalence :
a. Most patient asymptomatic
b. Pain  blunted by neuropathy
Attend doctor with ischemic ulcer or gangrene
The American Diabetes Association recommends
screening for PAD in patients with diabetes

A screening ABI should be performed in patients with diabetes

Those >50 years of age Those <50 years of age who have
other risk factors associated with
• If normal an exercise PAD
test should be • Smoking
carried out • Hypertension
• The ABI test • Hyperlipidaemia
should be repeated • Duration of diabetes
every 5 years >10 years

• Foot care is also important in diabetic patients as PAD is a


major contributor to diabetic foot problems2

1. American Diabetes Association. Diabetes Care 2003; 26: 3333-3341.


2. Estes JM, Pomposelli FB Jr. Diabet Med 1996: 13: S43- S57.
DIABETIC FOOT
INFECTION:

 A serious complication of diabetes that may lead to amputation


 Cellulitis occurs 9 times more frequently in diabetics than non-diabetics
 Osteomyelitis of the foot 12 times more frequently in diabetics than non-diabetics
 Foot ulcerations and infections are the most common reason for a diabetic to be
admitted to the hospital
 40-80% of these ulcers will become infected
 25 % of these will become deep
 50 % of patients with cellulitis will have another episode within 2 years
 25-50 % of diabetic foot infections lead to minor amputations
 10-40 % require major amputations
 Treatment: surgical debridement plus broad-spectrum antibiotics
DM and Infections
Many infections are more common in diabetic patients
Increased severity
Increased risk of complications

Suppressed Immunity in DM Patients


PMN functions  (particular when acidosis is present):
Lecukocyte adherence 
Chemotaxis 
Phagocytosis 
Antioxidant activities 

Improving glycemic control might improve immune function


DM and Foot Infections
 Foot infections are a major cause of hospitalization
in diabetics
 Factors of high risk for foot infections:
 Sensory neuropathy
 Motor neuropathy
 Autonomic neuropathy
 Peripheral arterial disease
 Hyperglycemia
 PAOD also predisposes to ischemic ulcers and foot
infections in patients without diabetes
Immune defects in diabetes
 Neutrophil function is depressed affecting adherence to
endothelium, chemotaxis and phagocytosis
 Cell mediated immunity is probably depressed
 Antioxidant systems involved in bactericidal activity may
be compromised
 These impairments are exacerbated by hyperglycemia
and acidemia but also reversed by normalization of
glucose and pH levels
Definition of a Diabetic Foot Infection
 No generally-accepted definition
 Foot infections in diabetics can be ulcer- or non-
ulcer related
 ~15% of diabetics develop chronic non-healing foot ulcers
 Not all chronic foot ulcers are infected
 Infection- mostly secondary to ulcer
Overview of Diabetic Foot Infections
7 % o f P o p u la tio n
D ia b e tic

1 5 -2 5% D e ve lo p F o o t U lc er

4 0 -80 % In fec ted


(o r su sp e cte d )

4 0 % M ild 3 0 -40 % M o d e ra te 2 0 -3 0 % S e ve re

Slide courtesy of Ben Lipsky, Puget Sound VA, Seattle


Infection and Healing in Diabetic foot
Healing

Infection
ReplaceLose
footwear
footwear
Off-
loading

Amputation
Wound
Classification Systems for Diabetic Foot Infections

Classification systems
Severity of Infection
Foot Ulcer (Wound)

•No generally-accepted classification


•Differ in criteria & complexity
•Require validation for clinical trials
Wagner Classification
0- Intact skin. No ulcer in a high risk foot.

1- Localized superficial ulcer.

2- Deep ulcer to tendon, bone, ligament or joint.


No abscess formation
3- Deep abscess or osteomyelitis.

4- Gangrene of toes or forefoot /Localized gangrene.

5- Gangrene of whole foot.

Wagner FW: The diabetic foot and amputations of the foot. In Surgery of the Foot. 5th ed.
Mann, R editor. St Louis, Mo. The C.V. Mosby Company.
Clinical Classification of Diabetic Foot Infection
Clinical Manifestations of Infection ( PEDIS )
Wound without purulence or other evidence of inflammation
More than 2 of purulence, erythema, pain, tenderness, 1 Uninfected

Mild infection
warmth or induration. Any cellulitis/erythema extends ≤2
cm around ulcer and infection is limited to skin/superficial
subcut tissues. No local complications or systemic illness Mild 2
Infection in patient who is systemically well & metabolically

Moderate infection
stable but has any of: cellulitis extending >2 cm;
lymphangitis; spread beneath fascia; deep tissue
abscess; gangrene; muscle, tendon, joint or bone involved Moderate 3
Infection in a patient with systemic toxicity or metabolic
instability Severe infection

International Severe 4
Working Group
on the Diabetic
Foot, 2003
MANAGEMENT 
Management of diabetic foot infections requires
1. Attentive wound management
2. Good nutrition
3. Antimicrobial therapy
4. Glycemic control

5. Fluid and electrolyte balance.


6. Serum albumin level >3.5 g/dl
DIABETIC FOOT INFECTION
Treatment
Management of infection:
1- antibiotics.
2-Incision and drainage.
3-soft tissue, joint and bone resection
4-amputation
Most diabetic foot infections are
polymicrobial, with up to five or seven
different specific organisms involved.
Principles of treatment
 Recognition and correction of underlying cause
 Wound care
 Evidence-based regimes
empirical therapy vs specific therapy
 Optimal dosage
 Optimal duration
 Identification and removal of infective focus
 Recognition of adverse effects
 Prevention of recurrence
Principles of management-1
A multidisciplany Approach
I. Resuscitation first, diagnosis later
(biochemistry/haematology/radiology/microbiology)
II. General supportive measures
-Correction of Anaemia/ hypoproteinemia/renal failure/dehydration
-switching over to IV Insulin therapy
-high calorie/protein diet
-IV broadspectrum poly antimicrobial therapy( covering aerobes and
anaerobes)
-monitoring of polymicrobial infections by frequent microbial studies
Principles of management-2
III. Local care
Guiding principle: Limb saving attitude
• Assesment of vascularity:
Clinical: skin colour, temperature, hairs, nail
colour and circulation, pulses.
Poor pulse: best assessed by doppler
A/B Index: N=0.8, if <0.5 chances of tissue
survival is poor
What are 3 basic ways antimicroial
therapy is used?

 Empiric therapy
Initiation of treatment prior to determination of a
firm diagnosis
 Definitive therapy
Organism and susceptibilities are known
 Prophylaxis
Prevent initial or recurrent infection
Duration of therapy
1. Patients with infection also requiring surgical debridement
should receive intravenous antibiotic therapy perioperatively.
2. In the absence of osteomyelitis, antibiotic therapy should be
administered in conjunction with attentive wound care until
signs of infection appear to have resolved (2 to 4 weeks of
therapy is usually sufficient).
3. If there is a good response to parenteral therapy, oral agents
can be used to complete the course of treatment.
4. If clinical evidence of infection persists beyond the expected
duration, consider issues of patient adherence to therapy,
development of antibiotic resistance, an undiagnosed deep
abscess, or ischemia

58
Duration of therapy
 Mild infection : 1-2 weeks
 Moderate infection : 2 to 4 weeks, unless
osteomyelitis
 Severe infection : soft tissue up to 4 weeks
unless osteomyelitis
 Osteomyelitis: depends on degree of resection
( 4 weeks – 6 month of antibiotic therapy )

59
PREVENTION DIABETIC FOOT INFECTIONS
Do’s and Don'ts of foot care
Patient should
– check feet daily
– Wash feet daily
– Keep toenails short
– Protect feet
– Always wear shoes
– Look inside shoes before putting
them on
– Always wear socks
– Break in new shoes gradually
Six Principles of Prevention of Foot Ulcers

1. Podiatric care
2. Pulse examination
3. Protective shoes
4. Pressure reduction
5. Prophylactic
surgery
6. Patient Education
Diabetic foot successfully treated !!

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