A Practical Approach to Vascular & Endovascular Surgery Jaisom Chopra, VS Bedi
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History and Examination of the Arterial System1

JaisomChopra
History and examination in medical practice help us not only to reach at a provisional diagnosis but also to outline the appropriate investigations so that we can arrive at a final diagnosis. It is mandatory to first perform a general and systemic-orientated examination by combining history of present illness, past history, and personal history along with a thorough physical examination. In the arterial system, it is vital to reach at an early diagnosis and to start appropriate treatment so as to salvage the extremity or save a life. A casual approach wherein detail and accuracy are lacking may delay therapeutic decisions.
 
VASCULAR HISTORY
Those suffering from the arterial disease have characteristic clinical features helping us to arrive at a diagnosis even before conducting a physical examination.
 
Demographics
The patient's age gives us a strong indication on what could be the cause of peripheral arterial disease.
  • 20–40 years – Buerger's disease and large vessel vasculitis such as Takayasu's disease
  • After 40 years – atherosclerosis
  • After 65 years – Temporal arteritis and arterial aneurysmal disease.
Strong female predilection is seen in Raynaud's syndrome, lupus vasculitis, and Takayasu's arteritis.
 
PRESENTING COMPLAINTS
The nature of symptoms offers a clue to the diagnosis. There are three important questions we have to consider:
  1. Are we dealing with an acute arterial disease or a chronic arterial problem?
  2. Is it involving a larger artery or a small artery?
  3. Is it occlusive or aneurismal disease?
 
Acute Arterial Disease
This generally presents as an emergency where there is danger of not only loss of limb but also even loss of life (Fig. 1).
It is typically of sudden onset with the patient experiencing the classical 5 “Ps”:
  1. Pain is severe and of sudden onset
  2. Pallor—the limb goes pale and later with time cyanosed
  3. Pulseless—the pulses are absent distal to the site of blocked artery
  4. Paresis—the limb goes numb with loss of sensation
  5. Paralysis—there is reduced movement, which is a late sign.
Another finding is not a part of the classical 5 “Ps” but could be included as the sixth—Perishing with cold.
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Fig. 1: Cyanosed leg due to arterial blockage
2This condition is an emergency because we have only six golden hours to correct the outcome before irreversible changes occur. The patient and the doctor must act immediately and decisively.
 
Chronic Arterial Disease
There is decreased blood supply due to gradual narrowing progressing to blockage of the artery. The patients present with reproducible ischemic muscle pain known as claudication that occurs during exercise and is relieved by rest.
The most common cause is atherosclerosis. These patients are mostly smokers and present to the doctor years after the origin of the problem. If ignored and left untreated, they develop constant pain even at night while resting (rest pain), which is a precursor to ulcers and gangrene.
At this stage, there is a high risk of amputation. Abrupt deterioration of symptoms is generally due to superadded thrombosis or embolus.
 
Large Artery Occlusive Disease
It again can be acute or chronic. In the acute form, the extremity distal to the site of blockage becomes very painful, pale, and cold compared with the other side, numb with reduced power.
In the chronic form, there is pain on walking (claudication) distal to the site of blockage with absent pulses. If aorta is involved, then both extremities are affected, but beyond the aortic bifurcation, only one limb is involved.
 
Small Artery Occlusive Disease
Raynaud's syndrome is a vasospastic disease with sensitivity to cold and presents as a classic triphasic response—pale digits followed by cyanosis on exposure to cold, turning red on heating the part. Generally, wrist pulses are palpable. Raynaud's phenomenon is also seen in embolic occlusions from more proximal arteries such as subclavian and axillary. When tissue necrosis along with Raynaud's phenomenon occurs in the upper extremity, there generally is a proximal fixed obstructive lesion.
It is important to know whether the disease is intermittent or fixed. A good history tells us whether the disease is intermittent due to vasospasm or fixed due to a proximal occlusion.
Large artery (subclavian) involvement in the upper extremity is mostly asymptomatic. Chronic stenosis of the brachial artery presents as muscle fatigue or arm claudication.
In thoracic outlet syndrome, there are recurrent bouts of pain or numbness with activity involving a dermatological pattern.
 
Claudication
Claudication means limping in Latin and is classically cramping pain or weakness on exercise and relieved by rest. It is restricted to the muscles groups such as buttock, thigh, or calf and is due to reduced blood supply. It is more prominent in the calf muscles because these muscles are metabolically more active. The amount of exercise needed to bring on the pain is inversely proportional to the degree of arterial narrowing brought about by the atherosclerotic disease. The pain presents one segment below the site of occlusion or stenosis. Thus, aortic disease presents with pain in both buttocks and legs. Iliac disease presents as pain in the same side thigh muscles and leg, while superficial femoral arterial occlusion presents as calf pain. As the disease is multifocal, symptoms are more prominent distal to the most significant arterial narrowing or area with poorest collateral support (Fig. 2).
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Fig. 2: Calf claudication due to reduced blood supply to the leg muscles
 
Upper Extremity Claudication
This is seen in subclavian artery stenosis. If stenosis is proximal to the vertebral artery origin, the subclavian steal may be seen.
 
Differential Diagnosis of Claudication
The conditions listed in Table 1 present as pseudoclaudication (false claudication) and may be mistaken for true claudication.
Night cramps are the most common nonvascular cause of leg pain due to exaggerated neuromuscular response to stretch.
The non-atherosclerotic causes of true claudication are listed in Table 2.
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Table 1   Differential diagnosis of pseudoclaudication at different sites in the leg
Condition
Description
Effects of exercise and stopping activity
Other specific features
Calf pseudoclaudication
Nocturnal cramps
Cramping calf pain at night relieved in few minutes
Occurs at rest
Relieved by postural change
Chronic compartment syndrome
Bursting pain in athletes or cyclists
Caused by strenuous exercise and subsides gradually
Elevation speeds recovery
Venous claudication
Bursting calf pain in extensive proximal deep venous thrombosis (DVT) (iliofemoral)
Walking increases and then pain gradually subsides on elevation
Elevation speeds recovery and signs of chronic venous insufficiency
Radiculopathy (herniated disc)
Sharp pain radiating down back of leg in a patient with back problems
Increased by postural change and not relieved by rest
May be relieved by postural change
Symptomatic Baker's cyst
Tenderness and swelling behind knee
Worse on activity and not relieved by rest
Signs of inflammation at back of knee
Hip/buttock pseudoclaudication
Hip arthritis
Ache related to the level of activity
Worse with activity and not relieved by rest
More relief by non-weight bearing. weather-sensitive symptoms
Neurogenic claudication (spinal cord compression)
Weakness more than pain
Symptoms on standing and relieved by rest
May have back problems
Foot pseudoclaudication
Arthritic/inflammatory processes
Continuous ache related to activity
Increased by weight bearing but may continue at rest
 
Rest Pain
As arterial insufficiency progresses, the blood supply becomes insufficient to supply the basal needs of the sensory nerves. There is severe continuous pain at night that begins over the metatarsal heads. It is relieved by dependency and worsened by elevation above the level of the heart. It is a sign of threat to the limb if no intervention is undertaken.
Metatarsalgia mimics rest pain, the difference being it is worsened by dependency and relieved on standing.
Table 2   Causes of true intermittent claudication other than arterial narrowing
Collagen vascular disease
Giant cell arteritis (Takayasu's and temporal)
Buerger's disease
Embolism (proximal sources)
  • Heart (Left ventricular [LV] thrombus, paradoxic embolus)
  • Aneurysms
Dissection
  • Traumatic
  • Inherited disorder of collagen metabolism
Adventitial cystic disease
Popliteal artery entrapment
Retroperitoneal fibrosis
Drugs
  • Ergot derivatives
  • 5HT1A/D agonists
 
Neuropathic Pain and Causalgia
This is a burning sensation in the extremity. Neuropathic pain is seen in diabetics whose nerves are involved in a glove and stocking distribution. In causalgia mostly upper extremities are involved and is triggered by some event which may be trivial or a major occurrence like myocardial infarction (MI), DVT of hip fracture.
 
Erythermalgia
Erythermalgia presents with redness and burning sensation in the extremity typically worsened by heat. It may be a primary condition or secondary to myeloproliferative disorders, diabetes, lymphoma, hypertension, and drugs such as calcium channel blockers and bromocriptine.
 
MODE OF ONSET OF ILLNESS
  • Acute arterial insufficiency typically presents as the 5 Ps— pain, pallor, poikilothermia, paresthesias, and paralysis.
  • Chronic arterial insufficiency shows progressive limitation of symptoms, which is very gradual.
  • Abrupt onset of pain with pallor is suggestive of embolic occlusion, though with arterial thrombosis, it is less dramatic. It is important to differentiate embolic from thrombotic arterial occlusion as responsible for limb ischemia (Table 3).
The symptoms becoming worse or better depend on collateral pathway. Thrombus superimposed on the previous arterial plaque leading to acute ischemia often occurs and is more common in the superficial femoral artery.
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Table 3   Differentiating between embolism and thrombosis
Embolism
Thrombosis in situ
History
Abrupt onset of pain
Previous cardiac event
Onset may or may not be abrupt. Symptoms acute but not abrupt
Physical examination
Cold mottled and paralyzed with clear demarcation
Normal contralateral limb
Cool bluish limb (slow progression) without clear demarcation
Abnormal contralateral pulse
Etiology
Cardiac thrombus (75–85%)
Aortic atheroma
Proximal aneurysm
Native artery plaque rupture
Graft occlusion
Prior vascular intervention
Usually none
Often yes
This thrombosis may be due to reduced blood flow as in reduced cardiac output seen in congestive heart failure (CHF) or MI.
The site of involvement often gives a clue to the diagnosis:
  • Bilateral claudication in lower limbs—atherosclerosis and Buerger's disease.
  • Foot claudication—small vessel disease—Buerger's or thromboembolism.
  • Bilateral upper limb involvement—vasculitic disorder.
  • Ulcer or gangrene in unilateral hand of acute onset— embolism from heart, proximal vessel, or aneurysm.
 
Past Medical History
Always ask the patient whether he has any other illness apart from pertaining to vascular disease. Make a note of the risk factors such as smoking, hypertension, diabetes, tobacco abuse, dyslipidemia, strokes, blood clot, or amputation.
Has the patient had any other vascular intervention in the past (percutaneous or surgical) that may have occluded?
 
Personal History
  • Occupation—usage of vibratory tools should raise the suspicion of Raynaud's syndrome, although work involving repeated trauma to the hand may cause hypothenar-hammer syndrome (Fig. 3).
  • Smoking has a strong association with Buerger's disease so much so that if one does not smoke, we may have to reconsider the diagnosis.
  • Sexual dysfunction is common in patient with PAD.
 
Drug History
This is very important. Migraine medication and ergot derivatives cause vasospasm.
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Fig. 3: Cyanotic fingers due to Raynaud's syndrome
 
β-blockers Worsen Raynaud's
Toxic vasculitis is associated with sulfonamide, allopurinol, phenytoin, carbamazepine, chlorthalidone, methylthiouracil, spironolactone, and tetracycline.
 
Family History
A family history of premature arterial disease suggests some inherent disorder in the mechanism of thrombosis, lipoprotein metabolism, and hyperhomocysteinemia.
A family history of sudden death from aneurysmal rupture or of joint or skin laxity would suggest collagen disorder. This could occur in Marfan's syndrome or Ehlers–Danlos syndrome.
 
PHYSICAL EXAMINATION OF THE ARTERIAL SYSTEM
Examine the patient region-wise from head to toe (Fig. 4).
 
General Examination
This can lead to the diagnosis.
  • Arm span greater than height as seen in patients with longer pubis to head distance than pubis to foot. These are present in arachnodactyly and chest deformities— Marfan's syndrome.
  • Yellowish orange papules over neck and flexure areas with angioid streaks in the retina—pseudoxanthoma elasticum.
  • Coarctation of the pararenal aorta with proximal stenosis of the renal arteries—neurofibromatosis and cafe-au-lait spots.
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    Fig. 4: The arterial tree
  • Tendinous xanthomas—seen subcutaneously or over the extensor tendons in patients with type II hyperlipoproteinemia.
  • Tuberoeruptive xanthomas—on extremities and palms and associated with systemic atherosclerosis.
  • Cutaneous telangiectasias are often associated with arteriovenous (AV) malformations.
  • Nevus vinosus (port-wine stain) that does not regress is associated with three syndromes:
    • Sturge–Weber syndrome: Port-wine stain in trigeminal distribution and associated with seizures and vascular malformation of the retina and leptomeninges.
    • Klippel–Trenaunay syndrome: Port-wine stain involving an extremity with associated venous varicosities and absent deep venous system.
    • Parke–Weber syndrome: A subset of Klippel-Trenaunay syndrome with arteriovenous malformation and a tendency for congestive heart failure.
 
6Examination of the Head, Neck and Chest
 
Inspection
The oral mucous membrane and conjunctiva of the eyes are examined for clues of systemic vascular disease.
  • Subconjunctival hemorrhage and petechiae suggest infective endocarditis.
  • Blue sclerae are seen in osteogenesis imperfecta and aneurysmal disease.
  • Hollenhorst's plaques are seen in the retina of those with monocular symptoms and transient ischemic attacks (TIAs).
 
Neck and Chest
  • Pulsatile neck masses suggest aneurysms or kinking of arteries at the root of the neck. This is more common on the right side and is seen in elderly hypertensive or with carotid body tumor.
  • Carotid artery aneurysm is the most common in the common carotid artery and seen below the angle of the mandible.
  • Aneurysms of the internal carotid artery are not visible, as they lie below the fascia.
  • Supraclavicular pulsations are from subclavian artery or its thyrocervical branch.
 
Palpation
Palpating the pulses is the most important part of any arterial examination and the following points are to be stressed:
  • Pulse volume—if expansile indicates aneurysmal dilatation, although if diminished it may show proximal occlusion or stenosis.
  • Condition of the arterial wall—if hard is atheromatous.
  • Record the pulse volume on a scale: 0 – absent; 1 – trace; 2 – moderately reduced; 3 – mildly reduced; 4 – bounding.
The common carotid artery is felt in the carotid triangle lying anterior to the sternomastoid muscle against the carotid tubercle of the sixth cervical vertebra. The carotid pulses are felt strongly in occlusion of the internal carotid artery.
The superficial temporal artery is felt in front of the tragus of the ear, and if prominent, it excludes significant stenosis of the common or external carotid artery of that side.
An expansile lesion in the neck is certainly aneurysmal and must be distinguished from kinking of the carotid. Here, the pulsations are along the axis of the artery, although they are at right angle to the artery in an aneurysm.
Carotid body tumor is at the angle of the mandible and is mobile laterally but fixed along the vertical axis of the artery as it is fixed by the carotid sheath. It is a painless mass.
Vertebral artery cannot be palpated.
 
Auscultation
Auscultation should be performed over all superficial arteries and swellings. Carotid bruits in the neck may originate in the chest along the aorta. Noninvasive vascular studies are a must to assess the lesion. Bruits over the subclavian suggest stenosis.
 
Examination of the Lower Extremity
 
Inspection
Always place the contralateral limb alongside to assess changes by comparison. These changes are seen distal to the site of occlusion.
In the initial stages of acute ischemia, there is paresthesia with reduced sensation to light touch and position that progress to complete anesthesia. With further ischemia, paralysis and cyanosis followed by gangrene occur (Fig. 5).
In chronic ischemia, there is reduced subcutaneous fat, shininess, hair loss, and nail changes, which are brittle with transverse ridges and ulcerations (Fig. 6 and Table 4).
The dependent foot may turn purple—dependent rubor is due to filling of dilated capillaries with deoxygenated blood.
In microembolization, there are palpable pulses with cyanotic toes known as the blue toe syndrome.
Capillary filling time—the limb is pale on elevation and takes time to become pink on dependency (20–30 s). It may progress to dependent rubor.
Vascular (Buerger's) angle—it is the angle at which the limb turns pale on elevation, usually 30° in critical ischemia.
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Fig. 5: Gangrene foot
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Fig. 6: Chronically ischemic lower limb
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Table 4   Urgency of treatment in various grades of limb ischemia
Category
Description
Motor/sensory findings
Arterial Doppler signals
I – Viable
Not immediately threatened
None
Audible
IIa – Marginally threatened
Salvageable if promptly treated
Minimal sensory deficit or none
Often audible
IIb – Immediately threatened
Salvageable with immediate revascularization
Mild to moderate weakness Sensory deficit extends beyond toes and is associated with rest pain
Usually inaudible
III
Major tissue loss or permanent nerve damage inevitable
Profound motor paralysis with extensive sensory deficit
Inaudible and venous sounds also absent
Venous filling time—the limb is elevated for a while and laid flat. The veins should fill within 5 s, but in ischemic limb, they take considerably longer.
Examination of gangrenous area—the extent is according to the level of occlusion and it may be wet (diabetics) or dry. The line of demarcation must be noted.
Livedo reticularis – mottled discoloration (fishnet) of the skin as seen in atheroembolism. It may be seen in young females (20–40 years) with Raynaud's and hypertension. It is also noticed in vascular collagen disease—systemic lupus erythematosus (SLE), polyarteritis nodosum (PAN), hyperviscosity syndrome, and drugs such as amentidine.
Pernio—seen in females with bluish red lesions on the toes and shin. There is burning and severe itching. The lesions last less than 10 days. Chronic pernio is called chilblains and seen on toes on exposure to cold (Figs 7 and 8).
 
Palpation
Skin temperature—Use the back of the hand to assess the degree of warmth and coolness that will help us to differentiate between healthy tissue and ischemic one.
Capillary filling time—press finger pulp firmly on hard surface and note the time for pallor to disappear. Elevate the leg to empty the capillaries. Now make it dependent. Normally, capillaries fill in less than 5 s, but in ischemia, they would take less than 20 s.
Pulses—those below the occlusion will be absent unless there are excellent collaterals in which case it may be diminished but does not disappear. The dorsalis pedis is felt lateral to the tendon of extensor hallucis longus but is absent in 10%. The posterior tibial artery lies behind the medial malleolus midway between the malleolus and the tendon Achilles. The anterior tibial artery lies midway between the two malleoli against the lower end of the tibia, above the ankle joint, and lateral to the extensor hallucis tendon. The popliteal artery is palpated behind the knee by making the patient prone and flexing the knee. It may also be felt with the patient lying supine with the knee flexed to 40° and the artery felt against the upper end of the tibia by rolling the fingers from side to side. The femoral artery is felt just below the inguinal ligament midway between the pubis and the anterior superior iliac spine.
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Fig. 7: Livedo reticularis hands and knees
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Fig. 8: Pernio or chilblains involving toes
 
Neurological Evaluation
In advanced limb ischemia, light touch, two-point discrimination, vibratory perception, and proprioception are lost well before deep pain and pressure. Motor involvement is a sign of advanced limb threatening ischemia. Diabetic individuals have pre-existing sensory deficits that add to the confusion (Table 4).
 
8Evaluation of the Upper Extremity
 
Inspection
Severe pallor is seen in severe ischemia or during attack of Raynaud's syndrome. Note nail bed changes such as hemorrhages, cyanosis, ulceration, and gangrene. Abnormally dilated capillaries, as seen by the capillary microscope, are seen in progressive systemic sclerosis (PSS)/calcinosis, Raynaud, esophagus, sclerosis telangiectasiae (CREST), while abnormal capillary rarefaction may suggest collagen vascular disease such as SLE or rheumatoid arthritis in patients presenting with secondary Raynaud's syndrome.
 
Palpation
Temperature—use the back of the hand to determine the warmth or coolness that points to the viability and ischemia.
Capillary filling time—press the finger pulp against a hard surface and note the time for pallor to disappear. Subclavian aneurysms are palpated in the supraclavicular fossa.
Pulses—subclavian artery is felt above the middle of the clavicle. Brachial artery is felt in the medial upper arm between the bellies of the biceps and the triceps and at the elbow medial to the biceps tendon. Radial and ulnar arteries are felt at the lateral and medial volar aspects. Ulnar artery may be absent in 3% from birth. Absent radial and ulnar pulses in young adults suggest Takayasu's arteritis.
 
Auscultation
Blood pressure is recorded in both upper extremities, and if a difference of over 10 mm Hg is noted, it is considered abnormal. Low blood pressure in both upper extremities is an indication to see blood pressure in lower extremities.
Thoracic outlet syndrome maneuvers—the radial artery pulse is felt digitally or with Doppler at rest and after the provocative maneuver. A positive test is diminution of the pulse after the maneuver. Adson's test—patient sitting upright is asked to take a deep breath and look upwards while turning the head to the affected side. Hyperabduction maneuver—the symptomatic extremity is hyperabducted to 180°. The pulse disappears to reappear when normal position is restored. Costoclavicular maneuver—patient thrusts both shoulders backwards and downwards maximally. EAST maneuver (external rotation-abduction stress test) may be the most reliable test. The patient is in a “stick up posture”, with arms extended, externally rotated, and behind the head. He then makes fists repeatedly for 3 minutes after which the pulse is felt. Branham's sign— done for AV fistula. Pressure of the artery proximal to the fistula will reduce the swelling, disappearance of bruit, and reduction in pulse rate.
 
Examination of the Abdomen
This is a must in any vascular examination.
 
Inspection
Pulsations are normally not seen, but in aortic dilatation, they may visible in a thin subject.
 
Palpation
Normal aorta is the size of the width of the patient's thumb. In aneurysm, the pulse is expansile and larger than a full centimeter. If one cannot feel the upper end of the aneurysm due to the costal margin or xiphoid, then we are dealing with a suprarenal aneurysm or a thoracoabdominal aneurysm. Tenderness over the aneurysm is a bad sign and implies impending rupture.
 
Auscultation
Bruits present should raise the doubts of atherosclerotic aneurysmal disease or a stenosis in the aorta or renals. Renal arteries bruits are normally systolic-diastolic in nature. A diastolic bruit indicates severe stenosis, as there is continued flow during diastole. These bruits are in the lower abdomen and femoral areas.
 
ASSESSING THE OUTCOMES AND IMPROVEMENTS IN ARTERIAL DISEASE
The clinical categories of limb ischemia are summarized in Table 5.
Patients with irreversible ischemia are treated with urgent amputation rather than with attempted revascularization, as large quantities of muscle metabolites released into the circulation cause sepsis, multiple organ failure, and ultimate death. Patients presenting with severe limb ischemia (class IIb) progress to class III in 6 hours when irreversible changes are seen leading to amputation. The time frame may not allow diagnostic investigations and angiography. The clinical categories of chronic limb ischemia are outlined in Table 6.
Table 5   The clinical categories of acute limb ischemia
Categories
Description
Neuromuscular findings
Doppler study
I
Viable
No sensory or muscle weakness
Audible arterial and venous signals
IIa
Threatened marginally
Minimal
Often inaudible arterial and audible venous signals
IIb
Threatened immediately
Mild to moderate associated with pain
Usually inaudible arterial and audible venous signals
III
Irreversible
Profound deficit
No arterial or venous signals
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Table 6   The clinical categories of chronic limb ischemia
Grade
Category
Clinical description
Objective criteria
0
0
Asymptomatic; no significant disease
Normal treadmill or stress tests
I
1
Mild claudication
Completes treadmill exercise Airway pressure (AP) >50 mm Hg but 25 mm Hg <BP
I
2
Moderate claudication
Between category 1 and 3
I
3
Severe claudication
Cannot complete treadmill exercise AP after exercise <50 mm Hg
II
4
Ischemic rest pain
Resting AP <40 mm Hg. Flat or barely pulsatile ankle wave form. Toe pressure (TP) <30 mm Hg
III
5
Minor tissue loss. Focal gangrene or non-healing ulcer
Resting AP <60 mm Hg ankle wave forms flat. TP <40 mm Hg
III
6
Major tissue loss extending to the ankle. Foot no longer salvageable
Same as category 5
Table 7 gives the follow-up parameters to assess the improvement in peripheral artery disease (PAD) patients.
 
CONCLUSION
  • A detailed history and thorough examination of arterial system is needed for accurate diagnosis, diagnostic planning, and therapy.
  • Differential diagnosis of upper extremity lesions is more in number than lower extremity lesions.
  • Atherosclerosis is the most common form of disease in lower extremity and presents as intermittent claudication.
Table 7   Follow-up parameters to assess the improvement of peripheral vascular disease
Clinical parameters
Patient-based parameters
  • Mortality
  • Limb salvage
  • Ankle brachial indices
  • Absolute and initial claudication distance.
Procedure-based parameters
  • Technical success
  • Primary and secondary patency rates (percutaneous and graft)
  • Procedural morbidity and mortality
Surrogate markers
  • Perfusion-related end points
  • Doppler blood flow
  • TcPO2
  • Skin perfusion by laser Doppler perfusion
  • Reactive hyperemia perfusion by various modalities
  • Vessel-related end points
  • Contrast angiography
  • Intravascular ultrasound
Biomarkers
  • C-reactive protein (CRP)
  • CD40 ligand
  • Asymmetric dimethylarginine (ADMA)
Quality of life instruments
General health (SF-36v2)
PAD-specific questionnaire
  • Walking impairment questionnaire
  • PAD-physical activity recall (PAD-PAR)