Blood is transported to the tissues is via arteries. These branch into consecutively smaller vessels called arterioles which eventually supply the capillary beds. The walls of arteries consist of three layers, from inner to outer, the tunica intima, tunica media and tunica adventitia (Fig. 6.3A). The interface of the vessel with the streaming blood is lined with endothelial cells to form a smooth surface to prevent adhesion of blood components. These cells secrete a variety of substances essential for maintenance of the vessel wall and circulatory function. All the vessels have some smooth muscle in the tunica media to enable them to change diameter, but arterioles have the greater proportion (primarily under sympathetic control).

Figure 6.3 A Cross-section through an artery and vein showing tunica intima, media and adventitia B Cross-section through a capillary. Note the relative proportions of wall thickness in the artery and vein and the single cell thick capillary.

Figure 6.1 The major vessels of the cardiovascular system. In the body proper, the dorsal aorta and the vena cavae run in the central axis, but for purposes of clarity they are shown to the right and left of the body, respectively. RA = right atrium, RV = right ventricle, LA = left atrium, LV = left ventricle, GIT = gastrointestinal tract.

Venous tree

Blood is drained from the tissue beds by venules, which join to form the veins, a system with larger capacitance than the arteries. The three layers seen in the arterial wall are also present in veins but the proportions differ, as can be seen in Figure 6.3A. Veins are found either in the superficial fascia or deep to the muscle. Communicating veins allow drainage from the superficial to deep veins. The vascular endothelium is specialised to form semilunar valves. These prevent backflow of blood and are especially important in the perforating veins. The systemic veins of the lower limb drain into the inferior vena cava and return the deoxygenated blood back to the heart.

Networks of capillaries link the arterioles and venules. They are the smallest and most numerous vessel, having only a thin-walled endothelium (Fig. 6.3B). Capillaries facilitate delivery of oxygen and nutrients to local tissues and no cell is far from a capillary bed. Precapillary sphincters in short vessels called metarterioles control capillary bed perfusion. Capillaries can be bypassed by arteriovenous (AV) anastomoses or ‘shunts’ which are vessels forming a direct link between an arteriole and a venule (Fig. 6.4A). At cutaneous sites exposed to extremes of temperature, such as fingertips, apices of toes, nose and earlobes, the AV anastomoses are numerous and form specialised structures under the nail beds called glomus bodies or Sucquet–Hoyer canals (Fig. 6.4B). Shunting of blood from the superficial to deep, thus bypassing cutaneous regions, helps to preserve core body temperature.

Figure 6.4 A Diagram of the microcirculation showing an arteriole and a venule connected by an arteriovenous anastomosis (AVA) and a capillary network. The AVA is a shorter, tortuous, muscular vessel of a larger calibre. The capillary network comprises metarterioles, which have a muscular coat, and the distal portion of the capillary network, which consists solely of endothelial cells B The specialised AVA under the nail bed (glomus body).

Normal physiology of the cardiovascular system

The essential function of the CVS is to ensure that there is sufficient perfusion pressure to maintain, under all circumstances, an adequate flow of blood to the vital organs, especially the brain. This is achieved by alteration of the rate and force of contraction of the myocardium and by varying the diameter throughout the peripheral circulation.

The aorta and pulmonary arteries have a large proportion of elastic tissue in their walls. This distends as the bolus of blood is received from the ventricles and acts as a secondary pump during diastole when the elastic recoil propels the blood forwards. The rebound causes a shock wave to travel rapidly through the blood in the arterial tree, which can be felt as a pulse at certain anatomical points.

All vessels except capillaries are subject to some sympathetic influence or ‘tone’. The greater the sympathetic tone, the more vasoconstriction is achieved. Vasodilation occurs by a reduction in tone. This vasomotion produces changes in resistance to flow (peripheral resistance) and thus modifications in the work the heart has to do (afterload). The greatest effect is produced in the arterioles, which allow the CVS to control distribution of blood and, together with the heart, form the effector organs for blood pressure homeostasis.

The vascular assessment

The assessment of each part of the vascular tree includes the following:

• History, current medication and lifestyle factors

• Symptoms

• Signs

• Clinical tests

• Hospital/laboratory tests.

General overview of the cardiovascular system

Central problems such as congestive heart failure, ischaemic heart disease (angina and/or myocardial infarction), as well as systemic problems such as the anaemias may all influence the circulation to and from the lower limb (Box 6.1).

Box 6.1 Cardiac conditions which may affect lower limb perfusion

• Heart failure: left-sided and/or right-sided

• Ischaemic heart disease: angina or myocardial infarction

• Rheumatic fever (leading to valve disease)

• mitral regurgitation

• tricuspid regurgitation

• infective endocarditis

• Congenital heart disease:

• septal defects

• valve defects

• coarctation of the aorta

• Fallot’s tetralogy

History and medication

History taking is discussed in detail in Chapter 5. Any factors which compromise tissue perfusion will deprive the tissue of not only oxygen but also nutrients and prevent removal of waste products. This causes hypoxia to the associated tissues, referred to clinically as ischaemia. The most common cause of ischaemia is atherosclerosis and associated complications, which produce ischaemic heart disease (IHD) (coronary vessels), cerebrovascular accidents (cerebral vessels) and peripheral arterial disease (PAD). Atherosclerosis is predominantly a disease of large and medium-sized arterial vessels, although the distribution and progression of atherosclerotic disease is different in the diabetic population, with some small arteries affected (Aboyans et al 2006). Prognosis is thought to rely more on the predisposition of plaque erosion and/or rupture, than on the extent of atheromatous disease (Falk et al 1995, Libby 2001).

The presence of atheromatous disease anywhere in the body should alert the clinician to consider atherosclerosis in other areas, that is, the presence of angina may predict atherosclerosis in the vessels supplying the lower limb (Fisicaro 2003). The segments between the descending aorta and the popliteal artery are most likely to develop such disease. Below the level of the knee, the vessels are small arteries, which are generally not affected by clinically relevant atherosclerosis in the non-diabetic population. However, the majority of studies performed have been in the Caucasian population, and an extensive review of PAD and ethnicity indicated that prevalence of more distal disease may occur in black and Asian populations (Hobbs et al 2003).

The medical history enquiry should elicit information regarding IHD, as well as the presence of risk factors for atherosclerosis, such as smoking, hypertension or dyslipidaemia (Case history 6.1). Primary diabetes mellitus is strongly associated with earlier and more advanced atherosclerosis (Kallio et al 2003). The surgical history enquiry should include any intervention to cardiovascular structures, for example angioplasties (coronary, iliac, etc.), bypass surgeries and vein operations, for example sclerosis or stripping of veins.

6.1 Case history

A West Indian man aged 74 years presented with hard skin on the balls of his feet and a burning sensation. His medical and social history revealed that he had an aortic aneurysm resected at age 72, and he was a smoker. His brother has type 2 diabetes and he thinks he was last checked for diabetes about a year ago. He was taking bendroflumethiazide (bendrofluazide) 25 mg od to control hypertension, aspirin 75 mg od, atorvastatin 10 mg od and co-codamol 15/500 (osteoarthritis and back pain) as required.

Symptomatic history revealed the burning occurred mainly at rest and in bed and was similar in severity in both feet, but worse in the toes. There was no history of injury or previous ulceration. Mobility was poor due to osteoarthritis in both knees making a diagnosis of claudication difficult. A vascular assessment found telangiectases and haemosiderosis with normal skin texture and condition in both lower limbs, apart from dry skin. Varicose veins were present in the right leg, and hair was absent from legs and the feet, both of which felt cold. The fatty pad under the metatarsal heads was reduced and diffuse callus present with general plantar forefoot inflammation. All lower extremity pulses were palpable, regularly irregular with reduced PT pulses. His blood pressure (BP) was 145/96 mmHg. The ankle–brachial pressure index (ABPI) in the right leg was 0.9 and in the left leg was 0.75. Buerger’s test was positive for the left leg, with a flush occurring after 30 seconds.

Differential diagnoses for the pain are rest pain (although not present all the time and not ‘severe’), popliteal aneurysm (can occur bilaterally), pain from inflammation associated with the callosities or unprotected metatarsal heads (you would expect this to feel worse on walking), neuropathic pain from an undiagnosed cause, for example family history of diabetes, so he could have latent diabetes, or neuropathic symptoms as a side effect from the atorvastatin. Spinal stenoses can also cause burning feet as part of ‘root pain’. Combinations could include rest pain which is not felt as severe because of co-morbid sensory neuropathy. Venous disease can cause ‘restless legs’, which can be reported as ‘burning feet/legs’.

The findings imply there is an arterial deficit, with venous signs being relatively mild. The reduced PT pulses, left ABPI result and positive Buerger’s test all imply femoropopliteal (or distal) stenoses. No popliteal mass was found. His risk factors for atherosclerotic disease are hypertension, history of aortic aneurysm, smoking and raised lipids (as per the atorvastatin). An aortic aneurysm does increase the risk for popliteal aneurysm, hence its inclusion in the differential diagnosis. A West Indian background may predispose to more distal atherosclerosis, that is infragenicular.

The case warrants a referral to the general practitioner (GP) for modification of risk factors, namely blood pressure control (still higher than ideal despite the drug therapy, but only a one off reading) and help to stop smoking. A check-up for latent diabetes, a second opinion regarding suspicion of peripheral vascular disease and assistance with pain management are also required. In this scenario in the UK, it is not mandatory for a GP to refer on for a vascular opinion. Improved lifestyle and pain control should help mobility and encourage the development of a collateral circulation. If tissue viability becomes seriously threatened, angioplasty or bypass interventions may be considered.

Relevant social history includes smoking, alcohol, lifestyle, psychosocial stresses and socioeconomic circumstances. Smoking has numerous deleterious effects on blood vessels with the mechanism of action(s) not yet fully understood. Pathologies include increased platelet adhesion, endothelial lining damage, increased vasoconstriction and reduced antioxidant plasma levels and reduced fibrinolysis (Newby et al 2001, Tsuchiya et al 2002). Moreover, there may be damage to the endothelial lining by passive smoking as well (Barnoya & Glantz 2005, Otsuka et al 2001), therefore close contact with a smoker and occupation may be pertinent.

The effects of alcohol intake on circulation are less clear. Moderate drinking is associated with a lowered cardiovascular mortality (Mukamal et al 2005) for both genders, possibly linked to an anti-inflammatory effect (Albert et al 2003). However, a high intake has been linked to increased risk, associated with impaired fibrinolysis (Mukamal 2001). Lifestyle factors such as diet (e.g. salt, fat intake), exercise, occupation and stress levels should help form a picture of general mental and physical health, mobility and risk levels. Socioeconomic risk factors for cardiovascular disease include low socioeconomic status (Steptoe et al 2002) and low education levels (Grazuleviciene et al 2002).

Drugs may indicate cardiovascular disease is present (e.g. diuretic therapy), or influence circulation as a side effect. Many of the antihypertensive drug regimens such as diuretics, beta-blockers and calcium antagonists can affect the peripheral circulation. Diuretics act on various parts of the nephron in the kidney to reduce water and salt reabsorption, initially reducing preload and cardiac output and later affecting peripheral resistance, with both mechanisms reducing blood pressure. Beta-blockers prevent the stimulatory action of endogenous catecholamines on the heart, again reducing cardiac output and blood pressure. Even selective agents, such as atenolol, may cause some peripheral vasoconstriction. Calcium antagonists act by interfering with the process of vascular smooth muscle contraction, reducing peripheral resistance and so reducing blood pressure. Some act more peripherally than centrally, for example amlodipine and have some vasodilatory influence (currently not licensed for PAD).

Lipid-lowering drugs indicate risk factors for thrombotic disease, given the relationship between dyslipidaemia (high low-density lipoprotein (LDL), low high-density lipoprotein (HDL), high triglycerides, low apolipoproteins) formation of atheroma and cardiovascular disease (Hobbs 2003). The most common are the statin and fibrate drug groups. Anti-platelet drugs are most commonly taken for IHD (to prevent and/or to manage), and are also used for management of transient ischaemic attacks, stroke, PAD, and after some vascular surgeries e.g. angioplasty stunt. Taking an anti-platelet indicates risk of, or the presence of thrombotic disease and should alert the clinician to enquire about the nature of the problem. The most common drug is aspirin, but clopidogrel and dipyridamole are also used. Anticoagulation therapy, usually warfarin (non-acute), indicates cardiovascular disease such as atrial fibrillation, valve disease/replacement, history of deep vein thrombosis or pulmonary embolism, and it is sometimes used for the management of stroke.

Central symptoms

Angina and myocardial infarction (MI)

Pain in the chest on exercise or other stress indicates inadequate blood supply to the myocardium. The pain of angina can vary from a mild discomfort to an intense crushing sensation. It may radiate into the left arm or to the lower jaw. Unstable angina may be prodromal to an acute heart attack.

The chief distinguishing feature of an acute MI, as opposed to an angina pectoris attack is that the latter lasts only minutes and is usually relieved within 5 minutes of rest or by sublingual glyceryl trinitrate. There are many other causes of chest pain and while few closely mimic angina, indigestion and other gastrointestinal disorders may be confused with angina (Ch. 5). It is noteworthy that diabetic autonomic neuropathy, as well as age can mask symptoms of IHD, and silent heart attacks do occur (Fornengo et al 2006).

Breathlessness (dyspnoea)

Shortness of breath (SOB) is an important cardiac symptom/sign (it may be evident while in your surgery), as well as reflecting respiratory disease. It is a typical feature of angina and heart failure (left-sided or congestive).

Palpitations

The awareness (usually unpleasant) of one’s own heart beat can point to a cardiac arrhythmia. However, this is a common symptom, which often has no cause, or is associated with emotional stress or stimulatory substances, such as caffeine.

Fatigue

Significant cardiovascular disease, for example heart failure, or severe anaemia will cause fatigue, since muscle and brain tissue will be hypoxic.

Signs

Oedema

Any factor which interferes with the normal process of tissue fluid formation and reabsorption may cause fluid to accumulate in the tissues. This is referred to as oedema, which will be observable in the peripheral tissues as swelling. It can be due to local factors, such as trauma or occluded drainage vessels, or to central factors such as right sided or congestive heart failure or renal disease. An important exacerbating factor is the renin–angiotensin–aldosterone system, which is triggered by a low cardiac output. This will cause renal retention of salt and water, thus imposing an even greater load on the failing heart.

Cyanosis

Central cyanosis is the bluish discoloration of lips, tongue and mucous membranes and indicates that arterial blood is inadequately oxygenated. It may be due either to defects in the pump such as a congenital hole in the heart, cardiac failure, or to deficiencies of ventilation such as chronic obstructive airways disease. Severe cardiac and respiratory failure will also cause peripheral cyanosis.

Pallor

A pale appearance, noticeable in the face, palmar or plantar areas, the conjunctiva or nail bed may indicate anaemia, but this is not a sensitive observation (Nardone et al 1990).

The tongue

Abnormalities associated with the anaemias include inflammation of the tongue (glossitis), which may appear smooth and either pale (pernicious anaemia) or bright red (vitamin B group deficiency).

The nails

Iron-deficiency anaemia may cause koilonychia (spoon-shaped nails), a sign also associated with connective tissue disease (Fawcett et al 2004). Clubbing of the finger nails may be due to subacute infective endocarditis or congenital cyanotic heart disease. It is also associated with a variety of other, primarily respiratory causes (Fawcett et al 2004). Splinter haemorrhages appear as subungual small brown/black splinters and can be associated with vasculitis (inflammation of a blood vessel(s)), although trauma is a common cause. If pathological, a local cause such as a digital septic thrombosis should be considered, as should widespread involvement of arteries of all organs, including coronary, splanchnic and cerebral, which can occur, for example in aggressive rheumatoid arthritis. Splinter haemorrhages may also indicate subacute bacterial endocarditis (Fawcett et al 2004).

Clinical tests

Heart rate and rhythm

Heart rate and rhythm are normally assessed by taking the pulse at the wrist (radial artery), with a normal adult resting rate at between 60 and 80 beats per minute. Arrhythmias are abnormal heart rates/rhythms and can be physiological or pathological, depending on the cause. A change in pace, but where sinus rhythm is sustained, may reflect a physiological response by the pacemaker for the heart, the sinoatrial node. Heart rates of less than 60 beats per minute are classified as bradycardia and those over 100 beats per minute as tachycardia. Athletes are an example of physiological bradycardia, whereas the bradycardia due to a complete heart block in the atrioventricular septum is pathological. Thyroid hormones, if present in excess, increase the affinity of beta₁-receptors to catecholamines and so induce tachycardia, as seen in hyperthyroidism. Rhythm is denoted as regularly regular (sinus rhythm), regularly irregular (a repeating irregularity, for example ectopic beats) or irregularly irregular, for example atrial fibrillation.

Pulse amplitude may be assessed centrally via the carotid artery. Small volume may reflect vessel stenosis, tachycardia and cardiac failure. A large amplitude or ‘bounding’ pulse is a pathological finding, with causes including a high output state, for example thyrotoxicosis or aortic valve regurgitation.

Blood pressure

Systemic hypertension has no known cause in 95% of cases (essential hypertension) and is usually asymptomatic unless very severe. Hypertension may be defined as persistent raised blood pressure above 140/90 mmHg (National Institute for Health and Clinical Excellence (NICE) 2006). High blood pressure can damage vital organs, such as the eye and kidney and, owing to blood vessel damage, MI, stroke and peripheral vascular disease may ensue.

Manual (see Box 6.2) or automated equipment may be used to obtain readings, with equally good repeatability, but with the precaution that differences in readings between devices may seem clinically relevant (Sims et al 2005). The British Hypertension Society recommend several readings are taken before ‘persistent’ high blood pressure is diagnosed. It is now commonplace for people to monitor their own blood pressure at home or have ambulatory blood pressure monitoring via a 24 hour tape, thus obtaining a more accurate mean value taken over 24 hours. The upper normal limit is lower in children and higher in elderly people. Assessment also includes determination of risk factors e.g. bodyweight, salt intake etc.

Box 6.2 Taking blood pressure – manual technique

The patient should be rested and seated comfortably with one arm flexed at the elbow and resting at heart level on a flat surface. It is conventional to use the right arm as the best representation of central blood pressure:

• The brachial pulse should be palpated.

• A sphygmomanometer cuff is wrapped around the arm, 2–3 cm above the elbow crease.

• The pressure cuff should be inflated until the brachial pulse can no longer be palpated. The value of this pressure should be noted and the pressure released rapidly.^*

• The diaphragm of the stethoscope is placed on the brachial artery in the antecubital fossa and the pressure cuff re-inflated to the same value as previously obtained. Nothing will be heard at this stage. All vessels will be occluded so that no blood can flow through the artery.

• The pressure should be released slowly and steadily (2 mm/s), watching the needle on the manometer face. As the pressure falls to the level of the patient’s systolic blood pressure a knocking sound will be heard in the stethoscope. At this stage the pressure in the cuff is sufficient to prevent flow of blood during diastole, but not during systole, so that systolic flow can be heard. The value when the first sound returns is recorded as the systolic blood pressure.

• The pressure should continue to be released. The sounds will first increase then decrease in intensity and finally disappear. At this stage the pressure in the cuff is insufficient to occlude the artery at any stage in the cardiac cycle and this point is taken as the value for the diastolic blood pressure.

• The practitioner should ensure that the cuff is deflated completely.

• The mean of three recordings should be taken.

Pitfalls

• The rubber tubing may wear out.

• The valve may be faulty.

• The cuff may be the wrong size for the diameter of the limb.

• The arm may not be at heart level.

^* With experience many clinicians will guess the point of cut-off for inflation and if when the cuff is released, no sound is still heard, the cuff is inflated further.

Clinical examination of the heart

Useful information is gleaned from examining the precordium. Techniques of palpation and listening with a stethoscope are used to detect abnormalities such as flow disturbances, for example valve regurgitation and murmurs.

Blood tests

Assessment of cardiovascular problems may be assisted by lipid profiles and a full blood count (indicating anaemias, platelet disorders, infection). Following an MI, necrotic myocardial cells produce markers of cardiac damage such as troponin and creative kinase (peaks 24 hr post infection).

Hospital tests

These are performed to confirm diagnosis, establish extent of disease and to identify the exact site(s) of a problem as a prerequisite to medical and/or surgical management.

Non-invasive imaging

• Chest X-ray

A plain radiograph of the chest may show enlargement of the heart, pericardial effusion and calcification of heart structures and vessels.

• Electrocardiogram (ECG)

The electrical activity of the heart is recorded using limb and chest leads attached to the skin. Many pathologies of the heart, such as MI or ventricular enlargement in a failing heart, will alter the normal PQRS waveform. Exercise may be used to highlight problems not apparent at rest.

• Echocardiography

This uses reflected ultrasound waves to construct an image of the heart, which can inform about some structural, for example valve disease, and functional abnormalities, for example cardiomyopathies. Anatomical barriers restrict full access to the heart. Haemodynamics can be observed by Doppler imaging, which may be enhanced by ‘stress’ via exercise or cardiac stimulants, or by introducing contrast agents.

• Cardiac magnetic resonance imaging (MRI)

Magnetic fields and radiowaves (non-ionising radiation) in conjunction with an ECG are used to obtain cardiac images (chambers and flow dynamics) which can help diagnose congenital heart disease, valve pathologies, abnormal masses and pericardial disease. This may be performed with or without contrast material. Intravenous gadolinium can be used to highlight blood vessels. MRI cannot visualise vessel calcification.

• Cardiovascular computed tomography (CT)

Ultrafast slices are taken to overcome the movement of the beating heart. It is helpful to assess coronary calcification and thus the risk level for coronary artery disease.

Invasive imaging techniques

• Coronary angiography

A radiopaque catheter is introduced into a vein in the groin or arm and threaded through to the heart under real time X-ray images. Contrast material can then be injected, allowing visualisation of the coronary vessels by X-ray fluoroscopy, illustrating regions of stenosis. Chamber pressures may be measured and blood samples taken for information on oxygen saturation and metabolite levels, for example lactate. People can react to the contrast material and there is a small risk of other serious complications, for example MI or cerebrovascular accident (CVA). Image enhancement by ‘subtracting’ a series of images taken before contrast injection, removes the non-iodinated background structures and improves image quality (digital subtraction angiography).

• Intravascular ultrasound

Specially designed long, thin catheters attached to ultrasound equipment allows visualisation of the lumen and subluminal surfaces. This can help assess the stage and vulnerability of plaques, as well as check on stents after surgery.

• Nuclear scans

The volume of blood available for the myocardium and myocardial function may be assessed by nuclear imaging. Injected radiopharmaceutical agents, such as thallium-201 or technetium-99m, are taken up by the myocardial tissue, and images are taken using gamma cameras or positron emission tomography techniques.

Peripheral vascular system

Peripheral vascular disease (PVD) in the singular is often taken to mean the manifestations of atherosclerosis distal to the aortic arch. PAD or peripheral arterial occlusive disease (PAOD) are more accurate terms. The plural term peripheral vascular diseases refers to all anatomically relevant vascular pathologies. It is important to distinguish between an impoverished arterial supply, reduced venous drainage and impaired lymphatic drainage, although more than one pathology may be present.

Many authors have emphasised the central role of the clinical examination, which when performed competently, can provide information both sensitive and specific for PAD diagnoses (Boyko et al 1997, Criqui et al 1992). Of the non-invasive tests, the ABPI remains the global gold standard (Collins et al 2006, Hiatt et al 1995, Hirsch et al 2001, McDermott et al 2000, Newman et al 1993). Invasive tests are usually reserved for presurgical evaluation. The non-invasive assessment yields information to help confirm the presence of PAD, determine the extent and distribution of stenoses, monitor changes following interventions and/or over time, and make clinical judgements regarding healing potential. Despite the poor prognostic outlook and the plethora of clinical methods applied to PAD assessment, it remains under-diagnosed (Hirsch et al 2001).

One of the most important indicators for undertaking an assessment of lower limb circulation is the condition of diabetes mellitus. While the approach is broadly the same, it has been demonstrated that the reliability of key tests such as the ABPI, the toe brachial index and pulse waveform analysis may be compromised, particularly in the presence of diabetic neuropathy (Williams et al 2005). This will influence the interpretation of the test results.

Arterial insufficiency

Medical history

Conditions which can affect the arterial supply to the lower limb can be viewed as acute, chronic or transient (Table 6.2). Most arterial problems affecting the lower limb are chronic and involve the progressive narrowing of peripheral arteries, most commonly the aortoiliac bifurcation and the iliac segments. While this can result in claudication pain and to varying degrees poor tissue viability, only a small percentage of people (1–6% in 5 years, rising to 18% in 10 years) require surgery (Andreozzi & Martini 2004). Up to 5% develop critical ischaemia requiring amputation (Dormandy et al 1989, McDaniel & Cronenwett 1989), although this figure may double over 10 years (Andreozzi & Martini 2004). Age-related and generalised vessel disease is referred to as arteriosclerosis, involving thickening and hardening of the vessel wall.

Table 6.2 Causes of arterial insufficiency in the foot

Acute	Extrinsic: tight clothing tourniquet plaster cast trauma frostbite immersion foot Intrinsic: thrombosis embolus ruptured aneurysm oedema
Transient (usually lead to acute problems but may progress to chronic)	Raynaud’s phenomenon Chilblains Hereditary cold fingers
Chronic	Atherosclerosis Vasculitis Thromboangiitis obliterans (Buerger’s disease) Arteriolosclerosis?

The most common cause of PAD is atherosclerosis. This is a pathological process involving formation of a fatty plaque (atheroma) in the subintimal space of large and medium-sized arteries (Murphie 2001a). The atheroma itself may protrude into the lumen and reduce or obstruct flow. However, the greatest risk arises from predisposition of the overlying fibrous cap to ulcerate, promoting thrombus formation. This may cause further narrowing (stenosis) or even complete blockage of the vessel. In addition, fragments of the thrombus can embolise and be swept away, causing obstruction further down the arterial tree. Global risk factors for systemic atherosclerosis are similar and recognised in descending order as hypertension, hypercholesterolaemia and diabetes, with obesity and tobacco usage being other key factors (Bhatt et al 2006). A clinical history that indicates atherosclerotic complications assists in the assessment of vascular health. Angina, MI and coronary or peripheral bypass surgery all indicate the extent and stage of atherosclerotic disease. Aneurysm must also be taken into consideration, as the most frequent underlying pathology is atherosclerosis (Fig. 6.6). Furthermore, an association exists between aortic and popliteal aneurysms, so this must always be checked.

Figure 6.6 CT anteriogram showing a large abdominal aortic aneurysm.

The clinician should be aware of pathological vascular calcification, as high levels in coronary vessels are linked to an increased risk of sudden death and MI (Greenland et al 2004, O’Rourke et al 2000). The clinical relevance in the lower limbs is poorly understood, but there are implications for test selection (see the sections on ABPI and toe pressures) and management of vasculopathies. Vessel wall calcification (Fig. 6.7) is most commonly seen in advanced atherosclerotic plaques, giving the ‘sclerotic’ or hardening component of the plaque in the subintimal space. The resulting rigidity will alter vascular resistance and elasticity. Normally mechanisms are in place to prevent abnormal calcium deposition in non-osseous tissues, for example via protective matrix proteins such as osteopontin. More research is needed to discover the pathogenesis of calcific damage.

Figure 6.7 Vessel calcification (posterior tibial).

A distinct process of dystrophic calcification can affect the smooth muscle layer of the vessel wall, often referred to as medial arterial calcification or Mönckeberg’s sclerosis. The condition is associated with atrophy of the smooth muscle arising from autonomic neuropathy (Forst et al 1995, Gilbey et al 1989) and it follows that this is seen with age (Elliott & McGrath 1994) and diabetes (Chantelau et al 1997, Edmonds 2000, Watkins & Edmonds 1983). It generally affects arteries not associated with atherosclerosis, for example distal small arteries (Figs 6.7, 6.8) and breast and thyroid vessels, although it is found in the aorta. One study on a population of people with type 2 diabetes found medial sclerosis in 17% and intimal-type calcifications in 23% (Niskanen et al 1994). The calcium deposits are laid down upon the circumferential smooth muscle and it is this process which is attributed to non-compressible vessels in the diabetic population (Edmonds et al 1982). Atherosclerotic and medial wall calcification may coexist and both contribute to rigid and inelastic vessel walls.

Figure 6.8 Vessel calcification (dorsalis pedis).

Primary diabetes mellitus has deleterious effects on arteries, accelerating the atherosclerotic process and worsening the prognosis for cardiovascular morbidity and mortality (Kallio et al 2003). PAD is twice as likely to occur in the diabetic population (Wattanakit et al 2005). Amputation rates (Aksoy et al 2004, McAlpine et al 2005) and mortality associated with PAD are also increased (Leibson et al 2004). The pattern of diabetic atherosclerotic lesions varies from the non-diabetic population, in that extensive involvement of vessel segments is seen, as well as more distal occlusions, for example the posterior tibial artery (van der Feen et al 2002). Such multilevel disease not only has implications for tissue viability but also presents major problems for management (Faries et al 2001).

Renal disease has a number of effects on blood vessels and as a frequent complication of diabetes mellitus, kidney disease poses an additional threat to peripheral perfusion and tissue viability when these coexist. Medial arterial calcification is accelerated with significant renal disease (Leskinen et al 2002) and this is likely to be related to failure of calcium and phosphate regulation. Impaired vitamin D conversion and hyperparathyroidism will also contribute to disturbed mineral metabolism.

There appears to be little evidence for atherosclerosis in the microcirculation (Murphie 2001b). Although hyalinisation (arteriolosclerosis), thickening of basement membranes and functional abnormalities of small vessels have been observed, these changes occur mainly in renal and retinal vessels, and are not considered to have major effects on the vascular status of the foot. However, in the diabetic population, there has been considerable focus on abnormalities of the microcirculation, since this is suspected to contribute to the non-healing wound.

Less common causes of PAD include thromboangiitis obliterans, vasculitis, vasospastic disorders and embolic disease. Thromboangiitis obliterans is characterised by inflammatory changes in small and medium-sized arteries and veins. It mainly affects young men and there is a very strong association with smoking. All signs and symptoms of arterial ischaemia and superficial phlebitis of the hands and feet may be present. Eventually, distal necrosis occurs.

Vasculitis is inflammation of blood vessels seen in a large number of rheumatic and connective tissue diseases. Any vessel can be affected, with the most serious consequences being in the arterial tree, resulting in partial or total occlusion. Some of the conditions associated with vasculitis are:

• rheumatoid arthritis

• systemic lupus erythematosus (SLE)

• polymyositis

• dermatomyositis

• systemic sclerosis

• polyarteritis nodosa

• giant-cell arteritis

• erythema nodosum

• Henoch–Schönlein purpura.

Raynaud’s disease and phenomenon (when linked to another disease) affects approximately 5% of the population and, in severe cases, may produce digital atrophy, necrosis and ulceration (Case history 6.2). Chilblains are also thought to rise from increased vasoreactivity to non-freezing cold. Arterial emboli can be composed of any obstructive body that lodges in the smaller vessels of the arterial tree, causing ischaemia distally. The most common embolus is formed by a thrombus fragment, for example from the heart during atrial fibrillation, from an aortic aneurysm or following an MI. Where smaller arteries branch or narrow, impaction occurs and in the lower limb, vulnerable sites include the common femoral bifurcation and the popliteal trifurcation.

6.2 Case history

A 35-year-old Caucasian woman presented in winter complaining of numbness and pain in her fingers and toes. Her general health is good, she gave up smoking 3 years ago (20/day for 12 years) and she drinks 30–40 units/week, believing this to assist her circulation. She denies taking recreational drugs. She takes the contraceptive pill and relates a long history of poor circulation from her teenage years. Her father has very poor circulation and a variety of health problems, but she does not know the cause. Occupation is in administration. She presently lives alone, having recently separated from her partner. Her footwear is inadequate for winter, and general hygiene is poor.

Symptomatic history revealed long-standing problems with fingers that turn white and numb in the cold and small wounds on the tips of fingers and toes which follow episodes of cold exposure. Recently one of the toes became infected, prompting her to seek help. She has joint pain in the hands and feet.

Generally she is thin and pale. Examination of the lower limbs revealed pale skin and cold toes. The lesser toes were held in flexion deformities. No hairs were present. The skin was tight, shiny and smooth. There were small, painful ulcers on the apices of the third and fourth toes bilaterally. One ulcer showed signs of infection. Pedal pulses were palpable but feeble. Popliteal pulses were within normal limits. ABPI at the dorsalis pedis artery for right and left foot was 1.0 and 0.97, respectively. Leg elevation tests were negative. No joint changes in the hands were evident. The nails were thin and broken, with pale nail beds and small erythematous patches on the finger tips, but no ulceration.

Differential diagnoses include autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus or systemic sclerosis, all of which may cause joint pain and deformities of the hands and feet and are linked to Raynaud’s phenomenon and vasculitis. The third decade is associated with the onset of such autoimmune conditions. The flexion position of the toes and skin changes can arise from systemic sclerosis (scleroderma). Raynaud’s disease can occur in isolation as well. Rarely female carriers of Fabry’s disease can present with arteriopathies and there are also rare cases of Buerger’s disease among female smokers. The family history can be helpful with regard to such conditions, although the history provided here was insufficient.

Some features of an anaemia were present, which could be relevant to an autoimmune diagnosis, or in isolation could contribute to poor healing and immunity. Alcoholic disease must be deliberated, since typically the units confessed to are at least half of what the real intake is. This may link into an anaemia from malabsorption and also the apparent self-neglect. Thromboses in the microvasculature could cause peripheral ulceration and risk factors for thrombophilia should be taken into account, in this case the use of the contraceptive pill. If drugs were being injected into the dorsal venous arch (used when proximal veins have been destroyed by chronic drug misuse), local vasculitis can also result.

The findings of this vascular examination are helpful to exclude macrovascular disease and certainly this would be unusual in this age group. There are features consistent with microvascular disease, suggestive of Raynaud’s disease/phenomenon and/or vasculitis. Blood tests, including full blood count, liver function tests, autoantibodies and rheumatoid factor, are required to establish a diagnosis, with consideration for other thrombophilia markers, for example homocysteine levels.

Symptoms

An acute occlusion, for example femoral embolism, produces signs and symptoms known as the six Ps:

If the occlusion is prolonged (more than 6–8 hours), the tissues eventually suffer irreversible damage and this stage can be recognised by mottling, muscle tenderness, motor or sensory deficit and necrosis. Prompt embolectomy is required for limb salvage. Amputation may be required (Campbell et al 1998). Rarely, fat emboli may lodge in small/microvascular peripheral vessels causing vasculitis and necrosis, for example following vascular surgery. This can be seen in the foot.

Chronic PAD may share some of these signs and symptoms and certainly pain on walking (see intermittent claudication), at rest (see rest pain) and in the extremities, can arise from chronic ischaemia. However, PAD is asymptomatic in 80–93% of cases (Fowkes et al 1991, Newman et al 1993), with smoking and diabetes mellitus associated with a higher probability of symptom absence (Eason et al 2005). Pain may develop suddenly following thrombosis overlying a plaque, but if atherosclerosis has been present long-term, symptoms may be less severe than for an acute embolism, since collateral vessels will have formed. The following types of ischaemic pain can occur (also see Fontaine’s classification (Table 6.3)).

Table 6.3 Fontaine’s classification of peripheral vascular disease

Stage	Symptoms
1	Occlusive arterial disease but no symptoms (due to collaterals)
2	Intermittent claudication
3	Ischaemic rest pain (usually worse at night, relieved by dependency)
4	Severe rest pain with ulceration/necrosis (gangrene)

Intermittent claudication

Just as angina pectoris indicates insufficient blood supply to the myocardium, so intermittent claudication indicates inadequate blood supply to the periphery. The deficiency will be accentuated on exercise, occurring at a reproducible distance (the claudication distance) with a characteristic cramping or aching pain. Sometimes the complaint will be tightness, fatigue or burning in the affected muscle group. The exercising muscles have to respire anaerobically and produce metabolites which are not cleared by the blood. These cause ischaemic pain, which forces the patient to stop the activity. Resting for a few minutes reduces the amount of metabolites produced and allows the patient to continue walking for a further period. It is typical of claudication pain to subside within 10 minutes of rest. The distance walked before onset of the pain is a good indication of the severity of the condition, which may affect mobility and quality of life (Dumville et al 2004). Accurate assessment and diagnosis of claudication may be achieved using the Edinburgh claudication questionnaire (Leng & Fowkes 1992), which has a high sensitivity and specificity of 91% and 99%, respectively.

The region of the ischaemic muscle pain can indicate the site of the occlusion (see Box 6.3), with symptoms typically one level below the constriction. Calf pain is common (Buckenham 2003), with thigh, hip, and buttocks affected when more extensive proximal lesions are involved. Non-arterial sources of pain should be considered, for example arthritis, degenerative spinal disease, not only as part of the differential diagnoses but also because such conditions may mask the presence of symptomatic PAD (Newman et al 2001). It should be borne in mind that patients with neuropathy may not complain of intermittent claudication.

Box 6.3 PAD distribution according to claudication symptoms