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Introduction
PAD is a group of disorders characterized by
narrowing or occlusion of the arteries resulting in
gradual reduction of blood supply to the limbs.
PAD in DM may be asymptomatic until it reaches
an advanced stage.
Prevalence
The Hoorn study
Welborn, et al
Walters, et al
Incidence
Risk Factors
Age
Gender
DM Duration and
degree of
hyperglycaemia
Pathogenesis1
The most important metabolic aberrations are chronic
hyperglycaemia, insulin resistance and dyslipidaemia
susceptible to atherosclerosis.
Starts with microangiopathy : involvement of blood vessels at
the level of the arterioles and capillaries, causing thickening of
the basement membrane and making it more permeable to
plasma solutes.
DM impairs endothelial function, through hyperglycaemia, excess
circulating free fatty acids, oxidative stress and inhibition
endothelial nitric oxide(NO) NO, prostacyclin, and
endothelin-I, angiotensin-II
Pathogenesis2
DM augments the process of atheroma formation plasma
and cellular concentration of histamine endothelial
permeability in diabetic patients with PAD
T lymphocytes migrate to intima become monocyte ingest
oxLDL foam cells (fattty streak formation)
DM inhibit collagen production by smooth muscle, secrete
MMP plak rupture and thrombus formation.
Hyperglycaemia in platelets glucose production of
platelet-derived NO and excess production of oxygen free
radicals
Pathogenesis3
DM disturb calcium haemostasis.
DM production of fibrinogen and platelet activator (thrombin
and vWF), levels of procoagulants (tissue factor, factor VII),
decreased levels of anticoagulants (antithrombin-III, protein C)
Impaired glucose tolerance patient CRP inhibits
endothelial NO synthase and stimulates production of
procoagulant tissue factor, leucocyte adhesion molecules,
chemotactic substances and (PAI)-1
Clinical presentation1
Diabetic patients with PAD commonly show involvement of the
arteries below the knee and involvement of the profunda femoris.
more commonly symmetrical and multi-segmental, and stenoses
can be seen even in the collateral vessels
The majority of diabetic patients with PAD are asymptomatic (up
to75%)
Clinical presentation2
Patient with DM develop more symptomatic forms of PAD such
as intermittent claudication, foot ulcers and critical limb
ischaemia symptoms
Diabetic patients with PAD have poorer lower extremity function
compared with non-diabetic subjects with PAD they have
shorter mean walking distance and slower fast pace velocities
than non-diabetic patients with PAD.
Diagnosis1
A history of claudication, findings of chronic ischaemia in the
peripheries such as cold feet, pallor on limb elevation and
dependent rubor, trophic skin changes and distal gangrene are
all diagnostic of PAD.
Non-invasive tests currently available : Peripheral Doppler
ultrasonography, colour duplex scanning, ABI measurement,
plethysmography, transcutaneous oximetry [transcutaneous
partial pressure of oxygen (TcPO2)] and magnetic resonance
angiography
Diagnosis2
The sensitivity and
specificity of ABI
were 70.6% and
88.5%.
Pre and post
exercise ABI :
measured with ankle
SBP just before and
after 5 min of
exercise.
Treatment
Treatment
Outcomes
Re-stenosis rates are higher in diabetic compared with nondiabetic patients after femoropopliteal PCTA.
Graft occlusion after peripheral revascularization procedures is
higher and limb salvage rates are lower in patients with DM.
Limb salvage rates were similar in diabetic and nondiabetic
patients after distal revascularization in some studies
Summary
PAD begins earlier, progresses more rapidly and is more
commonly asymptomatic in DM.
Drug therapy is advised in patients who do not respond to
lifestyle modification
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