Peripheral Arterial Disease (Chronic Limb Ischemia)

Dr. Hesham Aboloyoun

Lecturer of Vascular & Endovascular Surgery Assiut University
Introduction & Epidemiology
• Gradual decrease of blood supply to the limb.
• Wide spectrum of symptoms from asymptomatic to frank gangrene.
• Disease of older age with higher male to female ratio.
• Mainly caused by atheroslerosis and usually associated with other occlusive diseases like
ischemic heart disease and/or cerebrovascular disease etc….
Risk factors
✓ Smoking (Most important) ✓ Dyslipidemia
✓ Older man ✓ Hypertension
✓ DM ✓ Obesity
Etiology
 Atherosclerosis: Most common over 90%: Fat deposit below the intima (subintimal)
 Less common causes: Burger’s disease, Vasculitis, popliteal entrapment and aortic
coarctation.

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Clinical presentation:
 Asymptomatic pulseless limb: (20-50%)
Although distal pulsation is absent, patients have no complaint regarding walking and
everyday activity.
 Intermittent claudication: (10-35%)
- Cramping or dull compressing pain in big muscle groups like the calf muscles (most
common), gluteal muscles or thigh muscles due to→ increased oxygen demand of
muscles during activity with limited blood supply → leading to shifting to anerobic
oxidation with lactic acid accumulation. Pain is usually severe and forces the patient
to stop→. After few minutes, lactic acid is washed out, and the patient can resume
his activity.
- The maximum distance the patient can walk before pain is severe is called
claudication distance.
 Rest pain:
- Continuous burning pain of the foot.
- It happens when blood flow is insufficient to meet the metabolic demand of the
tissues even during rest.
- Pain increases with limb elevation, and decreases with dependency (standing or
sitting)
- Pain usually interferes with sleeping.
 Tissue loss:
- This happens when blood supply is not even enough to
keep the vitality of tissues
- Begins with trophic changes (hair loss, brittle nails), and
ends with ischemic ulcers(very painful) and/or frank
gangrene.
- Usually affects the most distal areas like the tip of toes, or
pressure points like the heel or bases of toes.
✪ The natural history of the disease is slowly progressive and
usually takes years to reach gangrene. This is due to the ability of the body to use collateral
circulation to compensate for blood shortage.

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✪ Levels of ischemia according to absent pulsations: Aortoiliac, SFA, Infrapopliteal levels.
✪ Fontaine classification of PAD:
GI: Asymptomatic disease
GII: Intermittent claudication pain
GIII: Rest pain
GIV: Tissue loss
Differential diagnosis
✓ Neurogenic claudication: Spinal canal stenosis (improved by leaning forward).
✓ Venous claudication: develops with post- thrombotic syndrome (after DVT). This pain is
relieved with leg elevation.
✓ Diabetic neuropathy: causes severe pain with preserved pulse.
✓ Severe arthritis (Preserved pulse).
Investigations
➢ Ankle brachial index measurement:
- First line diagnostic test for PAD.
- Normally between 1 and 1.4
- If more than 1.4→indication of heavy
calcification.
- Between (0.9-1)→borderline ischemia
- Less than 0.9→Ischemic limb (PAD)
➢ Tissue perfusion measurement: with
transcutaneous oximetry

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 ➢ Color Duplex:
- identifies the length of lesion, proximal and distal
patency, and provides wave form (hemodynamic)
analysis.
- Can be solely used if there is a contraindication to MR or
CT scan
- Important for postoperative surveillance.
➢ C.T and M.R angiography:
o done when vascular intervention is planned.
o They show a detailed map of the arterial system
provided that the patient’s kidney functions are
compensated, as the contrast used may cause
nephropathy.
➢ Direct angiography:
o reserved for intended intervention. Direct angiography
o It is an invasive procedure, that provides a
perfect, real time, hemodynamic picture of the
arteries with the facility of angioplasty at the
same setting.

Treatment
 Risk modification:
- Indicated in all stages of the disease. CT angiography
- Includes smoking cessation, control of diabetes and
hypertension, and lipid lowering drugs.
 Structured exercise:
- recommended first line therapy for claudication.
- It promotes collateral circulation and increases walking distance.

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 Vasodilators:
indicated in disabling claudication despite exercise and risk modification.
✓ Cilostazol: A phosphodiesterase III inhibitor with vasodilator and antiplatelet effect.
✓ Naftidrofuril : A serotonin antagonist.
✓ Prostaglandins: relax vessels smooth muscles causing vasodilation.
 Revascularization:
Indicated in critical limb ischemia (G III, GIV) and disabling claudication.
✓ Endovascular therapy using balloon dilatation and stenting.
✓ Surgical Endarterectomy.
✓ Surgical treatment with Bypass

Balloon mounted stent

Femoral endarterectomy

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Types of bypass

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 Revascularization procedures for PAD

Endovascular therapy Surgical revascularization

(Percutaneous transluminal
angioplasty)
Procedures • Balloon dilatation • Bypass surgery (using vein graft
• Stenting or PTFE grafts)
• Endarterectomy
Indications • Short segment disease • Average risk patients
• High risk patients • Extensive and complex disease
• Stents are used in • Unsuccessful endovascular
residual lesions or in case therapy
of dissection or restenosis. • Endarterectomy indicated in
localised common femoral
disease.
Complications • Access site complications: • Infection
hge, pseudoaneurysm, or • Thrombosis
AVF • Bleeding
• Procedure complications:
dissection, thrombosis,
perforation
• Stent dislodgement or
migration
 Amputation:
- Minor amputations for gangrenous parts after successful revascularization.
- Major amputation(BKA or AKA) in cases of unsalvageable limb.
 Supportive care:
- Foot care and wound management.
- Analgesia for severe pain.

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 Carotid Artery Stenosis
BY
Dr. Mahmoud Ismael
Carotid artery stenosis
✪ Extracranial cerebrovascular disease consisting of atherosclerotic occlusive disease of the
carotid artery is considered to be one of the key preventable causes of ischemic stroke.
✪ Symptomatic; symptoms in the past six months or Asymptomatic
Definitions
 Stroke is a sudden onset focal neurological dysfunction, with symptoms lasting > 24 hrs ,
which is of non-traumatic, vascular origin.
 Transient ischemic attack (TIA) is an episode of focal brain, retinal or spinal cord
dysfunction lasting < 24 hrs which is of a non-traumatic, vascular origin
Classification of stroke
 20% are hemorrhagic (intracranial, subarachnoid)
 80% are ischemic:
(1) large artery atherosclerosis (LAA): defined as ≥ 50% stenosis or occlusion of an extra- or
intracranial artery);
(2) cardioembolic;
(3) small vessel occlusion.
(4) other aetiologies (arteritis, dissection)
(5) undetermined aetiology (two potential causes, no cause identified, incomplete
investigations)

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Risk factors of Ischemic stroke
• Sex • COVID-19 pandemic
• Age • Obesity
• HTN • Physical activity
• Smoking • Alcohol
• Diabetes • Hypercholestremia
• Family history • AF
Pathophysiology
Carotid artery plaque can cause TIA or stroke by two mechanisms:
✓ Embolization.
✓ hypoperfusion.

Anatomy of Internal carotid artery

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Clinical picture of Carotid artery stenosis
 Symptoms of TIA or stroke resulting from carotid disease are related to the cerebral
vascular territory affected.
 The carotid artery supplies the anterior circulation; thus, carotid disease can result in
symptoms associated with injury to brain parenchyma of the anterior cerebral artery or
middle cerebral artery distribution.
 Ischemic stroke related to the carotid artery can present with sudden contralateral
sensorimotor loss, speech deficit, and ipsilateral monocular blindness
 Motor symptoms (contralateral mild hemiparesis to complete hemiparalysis).
 Sensory deficits (contralateral mild numbness or comp lete paresthesia).
 Language loss (dysarthria, dysphasia, or aphasia) when the dominant hemisphere is
affected.
 Amaurosis fugax (transient monocular blindness or field cuts) resulting from emboli to the
retinal artery via the ophthalmic artery, is considered to be the classic symptom of TIA
related to carotid artery lesions
Imaging strategies in Carotid artery stenosis
 Color Duplex ultrasound.

 CTA or MRA
aortic arch, supraaortic trunks, carotid bifurcation, distal ICA and intracranial circulation, which
is important before CAS.

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 Treatment of carotid artery disease
Optimal Medical Therapy
✓ Lifestyle measures (diet, exercise, smoking cessation, and weight loss)
✓ Antiplatelet therapy
✓ Lipid lowering therapy
✓ Management of hypertension
✓ Management of Diabetes Mellitus (DM
Indications of intervention
Asymptomatic Stenosis > 60 % (+ clinical/imaging criteria)
Symptomatic Stenosis > 50 %
Lines of treatment
➢ Carotid endarterectomy (CEA)
➢ Carotid stenting (CAS)
Clinical/imaging criteria for identifying a higher risk of stroke on BMT (>50%
asymptomatic)
✓ Silent infarction on CT/MRI,
✓ > 20% stenosis progression,
✓ Large plaque area >80 mm2
✓ large juxtaluminal black area >8 mm2 on computerised ultrasound plaque analysis,
✓ plaque echolucency (DUS)
✓ IPH on MRI.
✓ Impaired CVR (cerebral vascular reserve )
✓ > 1 spontaneous micro embolic signals (MES ) during > 1 hour of transcranial Doppler
monitoring.
✓ Contralateral TIA/stroke

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Treatment of asymptomatic carotid stenosis

Treatment of Symptomatic Carotid Artery Disease

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 Carotid endarterectomy (CEA)

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Carotid endarterectomy (CEA) Complications:
✓ Stroke, death
✓ Post-endarterectomy hypotension, hypertension
✓ Hyper-perfusion syndrome
✓ Neck hematoma
✓ Cranial nerve injury (CNI) hypoglossal (3.8%), mandibular branch of facial nerve (1.6%),
glossopharyngeal (0.2%) and the spinal accessory (0.2%)
✓ Prosthetic patch infection
✓ Re-stenosis
 Carotid stenting (CAS)

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Advantages
✓ Minimal invasive
✓ Short recovery
✓ Suitable for high risk patients
✓ No surgical incision
✓ No cranial nerve injury.
✓ No carotid clamping
Complications
✓ Stroke
✓ haemodynamic instability (hypotension, bradycardia)
✓ Thrombosis
✓ Dissection, spsasm
✓ Restenosis
✓ stent infection

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 Varicose Veins & Venous Leg Ulcer
By
Dr. Ahmed Hassan Bakr

Anatomy of lower extremity veins

Deep veins

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Hemodynamics
 The ability to decrease foot venous
pressure on walking — is the most
important function of calf muscle pump
+ normal venous valves
 Inability to decrease pressure on
walking results in Ambulatory Venous
Hypertension Chronic Venous
Insufficiency

Epidemiology of chronic venous insufficiency:

 Telangiectasiae (also known as spider veins) (C1) have been reported to affect up to 80% of
the population.
 Varicose veins (C2) are also extremely common, with a variable reported incidence ranging
from 20% to 64%.
 The more advanced stages of venous disease, CVI (C3-C6), appear to affect about 5% of the
population, with the prevalence of the end stages of CVI (active and healed venous ulcers,
C5-C6) estimated at 1-2%.
 In the large scale Bonn Vein study, the progression rate from varicose veins to CVI was 4%
per year.

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The CEAP classification was published in 1994 by an international ad hoc committee of the
American Venous Forum and endorsed by the Society for Vascular Surgery, and as widely
accepted as the best available (and most widely used) classification system.

Clinical presentation:
 heaviness, tiredness, itching of the skin, nocturnal cramps, and aching of the legs, which is
exacerbated by prolonged standing, and symptomatic relief may be achieved by leg
elevation, and exercise.
 In patients with chronic outflow obstruction, venous claudication may typically occur
during walking or climbing stairs.
 Uncommonly, bleeding can be a presentation of CVD. This is commonly associated with a
traumatized superficial varicosity.
 Clinical recurrence of varicose veins. +/- superficial/ deep vein thrombosis (pain)
 Venous Ulcer:
The most striking feature of
venous microangiopathy is the
contrast between an
abnormally increased skin
bloodbflow, and a &creased
oxygen delivery to the tissue.

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Assessment

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Investigations
 Hand held Doppler:
- non-invasive procedure using ultrasound information to determine venous flow, With
no information on venous morphology,
- therefore it is unsuitable for the determination of any anatomical component of any
venous disease.
 Duplex ultrasound examination (DUS):
- based on a combination of ultrasound imaging and pulsed wave Doppler with which
information can be obtained on both the anatomy and the hemodynamic features of
the venous system.
- DUS is also used in the pre-operative assessment of patients undergoing surgery and is
an ideal tool for follow up.
 Other imaging:
- Phlebography:
▪ The indication for using phlebography in CVD patients with varicose veins has
decreased significantly with the advent of DUS,
▪ however, in the diagnosis of pelvic vein obstruction or incompetence (gonadal
veins, iliac veins) and of vascular malformations, when alternative imaging
techniques are inconclusive, phlebography can represent a necessary
investigation.
- Both CTV and MRV
▪ have evolved significantly in recent years and it is now possible to obtain detailed
three dimensional reconstructions of the venous system. Ilio-caval and pelvic
venous pathology (post-thrombotic obstruction, venous compression/ stenosis
like Nutcracker syndrome or May-Thurner syn- drome and pelvic varicocele) can
be reliably identified. in varicose vein disease the use of CTV and MRV should be
limited to the specific indications mentioned above.

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Treatment
 Compression Therapy:
- remains the cornerstone of conservative treatment.
- It includes: Stockings/ Bandages.
- They compress varicose veins, reduce venous reflux, and improve calf muscle pump
function.
- Compression therapy is recommended as the initial treatment modality to promote
healing in patients with venous leg ulcers, however, another invasive intervention is
mostly needed to maintain healing.
- Compression is recommended after superficial venous surgery, endogenous truncal
ablation, and sclerotherapy.
- Leg elevation may be considered when compression cannot be tolerated because of
acute inflammation.
 Medical treatment
- has been used for decades, but its place as a treatment modality for CVD is a topic of
continuing debate.
- They include venactive drugs (eg. MPFF), and they are effective only to ameliorate pain
and edema.
 Sclerotherapy:
- involves injection of dilated veins, including major refluxing trunks or tributary
varicosities, venules, or telangiectasias, with liquid or foam chemical agents to damage
the endothelium and eventually ablate the veins.
- Best indications are:
• atypical varicose veins less than 5-7 mm in diameter,
• telangiectasia and reticular veins,
• recurrent varicose veins,
• elderly and frail patients with venous ulcer.
- Transcutaneous LASER may be indicated for treatment of telangiectasia only when
sclerotherapy is not applicable.

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 Endovenous treatment of refluxing truncal veins (GSV/ SSV):
- Thermal with tumescence: LASER / Radiofrequency
- Non- thermal/ non-Tumescence: USGF (+/- tumescence)/ Glue/ Mechanocemical
(Clariven)
 Surgical treatment of refluxing truncal veins (GSV/ SSV):
- High ligation of (SFj/ SPJ)+ stripping +/- phlebectomy of varicosities.
 Percutaneous transluminal dilatation + stenting
- for chronic iliocaval or iliofemoral vein symptomatic vein occlusion.
- -Stenting should be deployed in all interventions
- -Surgery is not recommended as a primary line of treatment.
- -Treating the obstruction has the priority of treating the reflux
- -Treating deep vein reflux is only considered after treatment of deep vein obstruction
if any, and/or ablation of superficial vein reflux.
- -Treatment of deep vein reflux is done with either: to replace the affected valve by
transposition or transplantation of a vein segment containing a valve; the second is
to create a neovalve from the thickened vein wall.

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