Principles of ultrasound
Principles of Ultrasound -
Sounds are created by mechanical vibrations of molecules or particles through a medium. The movement of a sound wave through a medium occurs at a fixed speed, which is determined by the elasticity and density of the particular medium. The rate at which one particle vibrates is called the frequency or pitch of the sound and is measured in Hertz (Hz). The frequency of sound is the number of cycles per second.
Ultrasound is defined as, sound that has a frequency greater than the audible range of humans, ie greater than 20 Hz. Diagnostic medical ultrasound (imaging and Doppler) work at frequencies above 1MHz. Use of these high frequencies allows the ultrasound to be transmitted in well defined narrow beams, giving high resolution images. As ultrasound is poorly transmitted by air at these high frequencies acoustic ultrasound gel is used which acts as a coupling medium between the skin and transducer.
In medical ultrasound, the ultrasound wave originates from the transducer in the form of a small piezoelectric crystal driven by an oscillating electric voltage which causes it to vibrate. This transmits an ultrasound wave with the frequency of the electrical oscillation into any adjacent medium. For high resolution imaging, the transducer is usually caused to vibrate at its natural resonant frequency by exciting it with a very short electrical spike. The piezoelectric crystal is mechanically damped, to prevent ringing following excitation, and a short ultrasound pulse is transmitted into the adjacent medium. In a similar way, the same transducer can also work in reverse and detect ultrasound waves, by converting mechanical movement or vibrations from returning echoes, back into an electrical signal.
“When an observer is moving relative to a wave source, the frequency he measures is different from the emitted frequency. If the source and observer are moving toward each other, the observed frequency is higher than the emitted frequency, if they are moving apart the observed frequency is lower”.
In order for us to obtain a reading, blood flow must be changed to sound which can then be analysed by the spectral analyser. This is done by applying the Doppler principle and using a Doppler probe. The method for applying the Doppler principle in vascular ultrasound is somewhat different from Doppler's original theory, as blood cells are the ultrasound target of interest and they do not emit a radiating waveform. The transducer is both the source and the receiver, and directs pulses of ultrasound at the targets. The reflected or scattered waveform and the corresponding change in frequency from the transmitted frequency can then be seen. The difference between the transmitted frequency and received frequencies is called the Doppler shift frequency, (fd).
Figure ? shows how the frequency of the waveforms reflected (fr) by an approaching target is increased, while the waveforms frequency is decreased by a target moving away from the source. Mathematically it can be shown that a quantitative relationship exists between the Doppler shift frequency (fd) and blood cell velocity (v).
Fd = 2ft V Cos
Where, fd is the frequency emitted by the transducer, is the angle between the Doppler beam and c is the velocity of sound in the medium ie 1540ms-¹ approximately. It is extremely important in the clinical use of Doppler to understand the significance of the angle of insonation (Ɵ).
Generally the smallest Doppler angle consistent with keeping adequate signal strength should be used. This will give the greatest Doppler frequency and sensitivity to low flows. When taking flow velocities, the Doppler angle should be ≤ 60ᵒ.
(Insert picture here)
If = 0ᵒ, Cos = 1, and the maximum Doppler shift frequency is obtained for a given velocity. As increases, the Cos decreases and the Doppler shift frequency decreases until at = 90ᵒ and Cos = 0 there will be no Doppler shift and no signal can be heard.
In peripheral arteries not all the blood cells will be moving at the same speed. Blood closer to the vessel walls will be moving slower due to frictional forces than blood flowing in the middle of the centre of the vessel. This causes a range of velocities across the vessel called the velocity profile. At low velocities or in smaller vessels the velocity profile will be typically parabolic, but at higher velocities and in larger vessels the profile becomes flatter to produce plug flow.
Each of the velocities will produce a different Doppler shift frequency and the combination of these different frequencies reflected from across the lumen of an artery produce the Doppler spectrum. This is usually displayed as a function of time (sonogram). Sonogram is produced from the time varying echo signal received at the transducer by analysing the frequency components using a fast fourier transform (FFT) technique. This is repeated many times per second, usually 100x/s to produce a series of instantaneous Doppler spectra.
In each spectrum the power of the signal at each Doppler frequency is displayed on the y-axis using grey or colour scale. The higher the power the brighter or more intense the gray colour. Successive spectra are put beside one another along the x-axis to show the sonogram from which variation in frequency content or velocity with time can be seen.
Plug flow is seen as an area of low Doppler power under the systolic peak ie acoustic window. To show flow both toward and away from the transducer, the zero frequency baseline can be moved above the bottom of the display.
Two types generally available - continuous wave and pulsed wave Doppler.
Continuous wave Doppler (CW)
This is a Doppler transducer which transmits and receives ultrasound continuously. It has separate transmit and receive crystals mounted on the end of a ‘pencil' type probe. The crystals are angled towards each other so as the beams converge and overlap forming a crossover section. Signals will be obtained from all moving targets passing through the crossover region. CW Doppler is generally used for peripheral vessels that are easy to locate. The disadvantage of CW Doppler is that it cannot distinguish between individual signals arising from different axial ranges within the crossover region. This can cause confusion in the presence of multiple vessels or collateral systems.
Pulsed wave Doppler (PW)
PW Doppler transmits short bursts of ultrasound and limits the time that echoes from a particular pulse are received to a particular axial range (depth) along the ultrasound beam. This is called range gating, and the area over which echoes are detected is called the sample volume (sv). Sample volume is determined by pulse shape, length of the range gate and the lateral beam width of the beam at that point. The sample volume is continuously interrogated by successive transmitted pulses fired at the pulse repetition frequency (PRF) and the detected Doppler signal is then built up over time from every transmitted pulse. Combining pulsed wave Doppler with grey-scale imaging will give a constant image update function. Grey-scale imaging means the sample volume can be placed precisely within the vessel lumen, and sounds from the blood vessels can be accurately obtained by pulsed wave Doppler.
This is the use of ultrasound to make a two-dimension grey scale image of structures within the range of the transmitted ultrasound beam. Short ultrasound pulses are transmitted from a transducer through the skin into the tissues. At every surface or boundary between tissues, some of the pulse energy will get reflected back to our transducer to be detected as an echo, and some of the pulse energy will keep going along the propagation of the ultrasound. The amplitude of ultrasound which is reflected back to the transducer depends on the difference in the acoustic impedance between near-by tissues. Acoustic impedance depends on the density and compressibility of tissue. A large difference will give us a high amplitude reflection, and a small difference will give us a low amplitude reflection. B-mode scanners allow every echo to be shown as a dot, which is plotted on the screen at the relative position of the range and direction of the target from the transducer. The brightness of each dot represents the echo amplitude. This is known as brightness modulation. Nowadays, most transducers consist of piezoelectric elements which pulse in sequence to produce image lines over a two-dimensional scan plane in real time. Echoes from every transmitted beam are received in sequence and this way a 2-D picture will be produced, which shows us the tissues and structures beneath the transducer. Grey scale imaging is used to observe blood vessels and structures surrounding them. It is also helpful in identifying plaque within the walls of the blood vessels.
These scanners use a combination of B-mode imaging and PW Doppler to display anatomy and blood flow velocity information at the same time. The size and position of the Doppler sample volume is shown on the image by a dedicated cursor. The Doppler angle (angle of interrogation) is entered manually by ensuring that the angle cursor lies parallel to the vessel walls. It is very important that the angle cursor line be aligned parallel to the vessel walls of the artery being examined every time before a measurement is taken from the Doppler spectrum. The angle information that is obtained allows the Doppler equation to be solved and the spectral display shows us the blood flow velocity rather than frequency. Imaging and Doppler modes perform best when the beams are steered in the perpendicular position. However, this causes conflict as the best image quality will be observed when the vessels lie parallel to the skin (and transducer surface), where the beam hits the vessel perpendicularly. Also, optimum Doppler signals will be obtained when vessels are not parallel to the skin, as there is a good angle of interrogation between the vessel and perpendicularly steered Doppler beam.
Where the vessels naturally lie parallel to the skin, we will get the best quality image, however the Doppler signal will be poor due to the angle of interrogation being 90ᵒ. In cases where the vessels lie at an angle to the skin, we will obtain images of poor quality, however the Doppler signals will be good as there is a small angle of interrogation.
Triplex ultrasound is a combination of B-mode imaging, colour flow mapping and PW Doppler. In colour Doppler ultrasound, a colour display is superimposed onto the B-mode image to show areas in the image where echoes are Doppler shifted. The colour image is composed of many scan lines, every one is subdivided into many cells. The mean Doppler frequency in every cell along a scan line is determined and shown by an associated shade, which overwrites the B-mode image. Darker shades indicate low mean Doppler velocities, while lighter shades indicate high flow velocities. Generally, the display is arranged to show both flow away and towards the transducer, ie using red for one direction and blue for the opposite direction, with zero velocity in the middle. Colour flow Doppler is helpful as it, highlights areas of flow disturbance and indicates the direction of blood flow, which aids to define tortuosity or steal phenomena. It indicates absence of blood flow in occluded vessels and can show blood flow in vessels which may be too small to observe in B-mode.
Pitfalls encountered with Duplex and Triplex scanning
This is one of the most common problems for technicians while scanning. Calcification often occurs due to presence of atherosclerotic plaques. These plaques inhibit the transmission of ultrasound and causes acoustic shadowing. This can obscure the image of the underlying vessel and stop Doppler flow information being obtained, which makes it difficult to determine how severe or significant the plaque or atheroma is at a specific area of the vessel. We can sometimes overcome this situation by changing our scanning approach ie from anterior to posterior, if one of the walls only is affected. However, if the two walls are involved, the duplex will be limited to the amount of information provided. Great care needs to be taken when reporting on scans like these, emphasis needs to be made on the sub-optimal nature of the study due to calcific shadowing. In some cases alternative methods for diagnosing should be recommended for example, CT and MRA.
This occurs where there is a strong reflector or absorber of ultrasound in the scan field. The overall attenuation of the ultrasound beam cannot be compensated for by the time gain compensation. Therefore, this means the intensity of the ultrasound travelling to and from the reflectors lying behind the structure is greatly reduced. Severe shadowing happens behind bowel gas, bone and calcified plaques. We can try to overcome this problem and improve the image by moving the transducer on the skin, and observe the tissues from another plane.
Poor image quality
Some patients may produce poor quality imaged due to
- Tortuous vessel
- Deep vessels in obese or swollen limbs
- Extremely superficial vessels in very thin patients
This can occur in situations where, adjacent tissues have different compositions and attenuation characteristics. The dense structures for example bone or heavy calcification, acts as a mirror and vessels anterior to the demarcation are reflected as phantom vessels posterior to it, with phantom Doppler signals and colour filling.
Misinterpretation of lack of colour filling as a no-flow situation
Lack of colour filling can be caused by many situations, and not just no-flow.
- Inappropriate colour settings
- Highly calcified plaque on anterior wall
- Blood flow at 90ᵒ relative to ultrasound beam, giving us no Doppler signal and no colour filling
- Trickle flow ie very slow non-pulsatile flow, for example in arterial dissection
How to overcome these misinterpretations
- Optimise the Doppler angle by changing the colour box steering
- Reduce width of colour box
- Increase colour gain, colour sensitivity and colour v B-mode priority
- Use power Doppler mode
Atherosclerosis is a progressive disease which causes narrowing of blood vessels in the body. Although any artery can be affected, it is frequently observed in medium to large sized arteries for example, coronary, cerebral and peripheral vessel. Atherosclerosis will cause hardening of the arteries, due to the gradual build up of plaque within the vessel walls. Plaque is composed of cholesterol, calcium and fibrous tissue.
This disease begins at a very early age. The earliest pathologic lesions of atherosclerosis is the fatty streak and have been seen in the aorta and coronary arteries in most people by the age of 20. As atherosclerosis is asymptomatic, a plaque can quietly develop over many years. (ref)
Atherosclerosis is generally not diagnosed until the lesions damage to the vessels is severe enough to reduce blood flow, causing insufficient flow and blood clots.
Development of atherosclerosis
In order to properly understand the development of atherosclerosis, we need to look closely at the artery structure. The wall structure of arteries is made up of three layers, the intima, media and adventitia.
The intima is composed of an elastic lamina lined by a layer of endothelial cells one cell thick on the inner surface. The endothelium reacts to chemical agonists and to sheer stress produced by flow next to it, to produce nitric oxide. This leads to relaxation and vasodilatation.
The media is composed of mainly smooth muscle cells surrounded by fibrous tissue. This layer will vary in thickness depending on the function of the. The muscle fibres run circularly around the artery, which allows better control of the vessel diameter, therefore having control of flow of blood through the artery.
The adventitia is the outer most layer of an artery and is made up mainly of connective tissue, which gives structural support and great elasticity to the artery.
(Insert picture) - query reference?
Progression of atherosclerosis
No single theory of the development of atherosclerosis has been formulated; however the most widely accepted theory is the reaction to injury hypothesis. This theorises that the lesions of atherosclerosis are started as a response to injury to the cells lining the inside of the artery, the arterial endothelium.
→ The first step in atherosclerotic development is the endothelium becoming damaged. Immune, physical, mechanical, viral, chemical and drug factors have all shown to cause damage to the endothelium, which can bring about atherosclerosis.
→ When the endothelium becomes damaged, sites of injury becomes more vulnerable to plasma constituents especially lipoproteins. The binding of lipoproteins to glycosaminoglycans causes weakening of the connective tissue matrix and causes an increased affinity for cholesterol. When there is significant damage, monocytes and platelets stick to the damaged area where growth factors are released. This stimulates smooth muscle cells to move from the media into the intima and multiply.
→ The smooth muscle cells dump cellular debris into the intima, which leads to a further progression of the atheroma.
→ A fibrous cap is formed over the intimal surface. Fat and cholesterol deposits accumulate. The atheroma will keep growing until the vessel eventually becomes blocked. Symptoms of atherosclerosis usually are not apparent until the lesion is severe enough to restrict blood flow.
→ On the other hand, the endothelium can remain undamaged. However, growth factors secreted by smooth muscle and endothelial cells continue to enlarge the plaque.
(Reference and picture)
Homocysteine theory and pyridoxine deficiency
The homocysteine theory of atherosclerosis theorises that a chemical form of endothelial damage due to a deficiency in pyridoxine (B6). Homocysteine is derived from methionine during protein breakdown and converted to a non-toxic derivative with the aid of pyridoxine. Pyridoxine deficiency can lead to increased levels of homocysteine, damaging the endothelial cells and leading to atherosclerosis.
Pyridoxine may also be of interest in other aspects of atherosclerosis. Lysyl oxidase, is a copper dependant enzyme responsible for normal cross linking of both collagen and elastin and is also pyridoxine dependant. It has been said that because the first visible lesion of atherosclerosis is a focal splitting of the internal elastic intima, that this lesion could be the result of imperfect cross-linking of the arterial elastin and collagen. This defect could be caused from impaired lysyl oxidase activity, secondary to a copper or pyridoxine deficiency. Pyridoxine also inhibits platelet aggregation.
This is a theory which states that plaques form as the result of benign cancerous growths initiated by mutations. Mutagens could be chemicals from the environment, body metabolites or viruses. The aryl hydrocarbons (including benzypyrene and methylcholanthrene) which are found in cigarette smoke are extremely potent mutagens which directly damage arteries, as well as evoke cancerous growth of vascular cells.
Anatomy of the lower limb arterial system -
The abdominal aorta is the largest artery in the abdomen, which takes blood from the heart to viscera and lower limbs. The abdominal aorta extends from the T12 to L4 vertebrae and has many branches, which supply the major intra-abdominal arteries and the gut.
At the level of the umbilicus the aorta bifurcates into the right and left common iliac arteries (CIA). Each of these bifurcates further into the internal iliac artery (IIA), which supplies the pelvis and the buttocks and the external iliac artery (EIA), which continues down to become the common femoral artery (CFA) at the groin crease.
At the level of the groin the common femoral artery arises and lies in the femoral triangle in a sheath of connective tissue with the femoral vein and nerve. The smaller common femoral artery branches are the lateral and medial circumflex arteries and the articular branches, these vessels supply blood flow to the hip joint.
Approximately 1-2 cm beneath the groin crease the common femoral artery divides into two main branches. The deep femoral artery which is more commonly known as the profunda femoral artery (PFA), lies deep in the within the muscle and supplies the thigh muscle. The other branch is the superficial femoral artery (SFA), as it does not lie as deep as the profunda. The superficial femoral artery is the longest artery in the lower limbs and there are no named branches in the thigh. It mainly acts as a conduit to supply the distal areas of the legs. The superficial femoral artery enters the adductor hiatus, the origin of the adductor canal, in the lower thigh just above the level of the knee (8cm approx), where it becomes the popliteal artery (PA).
The popliteal artery extends from the adductor hiatus and lies within the adductor canal and the popliteal fossa behind the knee. The smaller branches of the popliteal artery are the muscular and articular (genicular) arteries which supply the knee joint. The popliteal artery gives rise to three major branches, the anterior tibial artery (ATA) and the tibioperoneal trunk (TPT) which divides into the posterior tibial artery (PTA) and the peroneal artery (PERA).
The anterior tibial artery lies anteriorly in the calf between the tibia and fibula. It supplies the extensor muscles of the ankle. The anterior tibial artery crosses the ankle on the anterior aspect, nearly on the mid-line and continues into the foot where it is known as the dordalis pedis artery (DPA).
The tibioperoneal trunk is a short vessel (4-6cm approx)and smaller in calibre than the popliteal artery. The tibioperoneal trunk bifurcates into the posterior tibial artery which takes a medial course in the leg. It supplies the flexor muscles on the medial aspect of the calf. The posterior tibial artery lies behind the medial malleolus and divided into various small branches.
The peroneal artery is the deepest of the calf arteries, it too arises from the tibioperoneal trunk, approximately 1 cm below the lower border of the popliteus muscle. Initially, it lies in the mid-line, then on the posterolateral aspect of the calf and finally behind the lateral malleolus.
Altogether the anterior, posterior and peroneal arteries are known as the crural or tibial vessels. They all supply the ankle and communicate freely with one another.
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Pathogenesis of Peripheral arterial disease
Peripheral arterial disease (PAD) is a manifestation of systemic atherosclerosis that is common and is associated with an increased risk of death and ischaemic events.(ref)
The worldwide prevalence of PAD is estimated to be in the range of 3-10%. The main complaint of PAD is intermittent claudication (ie pain/discomfort felt in legs on exertion and relieved by rest) which can range from mild to severe. The prevalence of intermittent claudication is approximately 3% in patients aged 40 and increases to 6% in patients ages 60.
A number of modifiable risk factors have been identified. These include smoking, diabetes and hypertension.
Only 1-3.3% of people suffering with intermittent claudication will require amputation over a five year period. Amputation is used as the primary treatment of approximately 25% of patients with critical limb ischaemia.
PAD, coronary artery disease and cerebrovascular disease are commonly seen together. 40-60% of patients with PAD have concurrent coronary and cerebrovascular disease.
The 15 year mortality rate for patients with intermittent claudication is approximately 70%, with most of these deaths attributable to coronary artery disease. (ref)
While atherosclerosis is the initial process of PAD leading to intermittent claudication and other symptoms of PAD such as critical limb ischaemia, ulceration, rest pain and gangrene. There are other factors which may be attributable to PAD.
→ Blood flow is altered in PAD. Quantification of blood flow properties can be made by measuring blood plasma viscosity, whole blood viscosity haemocrit and haemoglobin. “Whole blood viscosity is independently related to PVD (peripheral vascular disease), and plasma viscosity related to the degree of arterial narrowing for claudication. Increased levels of haemoglobin and plasma viscosity were found in people with PAD”. (Edinburgh Artery Study). The increased plasma viscosity has been shown to be linked with increased symptoms of PAD. Although, factors such as whole blood viscosity are also found to be abnormal in the risk factors for PAD such as, diabetes and hypertension. However, an independent relationship of whole blood viscosity and PAD has been seen.
→ Abnormal blood constituents in PAD have been noted, but most are related to the coagulation and fibrinolytic systems. For example, plasma fibrinogen is essential in the blood coagulation system. However, at the ‘usual' plasma levels of 1.5-4.5g/l it far exceeds the minimum concentration of 0.5 g/l necessary for haemostasis (this is a process whereby the blood is kept within a damaged blood vessel, ie opposite of haemorrhage). So in theory elevated levels of plasma fibrinogen could indicate a hypercoaguable or prothrombotic state. Other indices of interest are fibrin degradation products for example fibrin D-dimer, which reflect intravascular fibrin turnover and intravascular thrombogenesis. The fibrinolytic system is represented by measurement of plasminogen activator inhibitor (PAI-1) and tissue plasminogen activator (tPA) activities. As tPA antigen is also produced by the endothelium, as is von Willebrand factor (vWF), elevated levels of these indices have been used to represent generalised endothelial damage. Fibrinogen is the plasma precursor to fibrin, the base matrix of a clot. It has been shown that increased fibrinogen is associated with the presence of PAD. Increased levels can be linked increased severity of disease at angiography as well as ABI (ankle brachial index). Homocystein - Elevated levels of homocysteine have been implicated as a risk factor for PAD and the progression of the disease. It's also seen as a risk factor for failure of vascular intervention. Raised levels of homocysteine could damage the endothelium, it also promotes auto-oxidation of low density lipoprotein cholesterol and thrombosis. There is increased prevalence of hyperhomocystinaemia in people with premature arterial occlusive disease, and homocysteine is increased among older people with known PAD. As well as progression of atherosclerotic vascular disease, increased homocysteine is significantly associated with death from cardiovascular disease in people who are already symptomatic.
→ Abnormal vessel wall - Wall damage can be divided into many categories when discussing PAD. Where there is plaque occupying part of the wall, which in itself could be seen as damage, but tends to be covered in endothelium. There is also plaque rupture, which reveals the thrombogenic lipid core. Rupture is often caused due to haemorrhage into the vessel lumen, exposing the core which causes fibrinogen activation and platelet aggregation which can result in vessel occlusion. Even without an atheromatous lesion, some properties of the blood vessel may be abnormal in PAD. For example, the elastic properties of SFA, CFA and PA are reduced in patients with proven PAD. Arterial waveforms are altered in patients with PAD, which suggests the presence of abnormal structure or tone in the peripheral arteries. However, in (insert word), peripheral artery compliance is significantly reduced in patients with no clinical evidence of PAD. Also, arterial compliance by analysis of the waveform is reduced in sedentary smokers with no evidence of PAD. Therefore, it could be possible that part of the mechanism of development of PAD in these people are still connected to abnormalities in arterial compliance. Further enhancing the potential for wall asymmetry is the effect of sheer stress, promoting even greater abnormalities of “vessel wall” and perhaps blood flow. Atherosclerosis is known to be a geometrically focal disease that has the propensity to invade the outer edges of blood vessel bifurcations. In these particular places the blood flow is slow and often changes direction with the cardiac cycle. Places with low sheer stress have a much higher disease susceptibility than the faster flowing inner edges.(ref)
These abnormalities may be related to the severity of the disease as well as the prognosis. Revascularisation and some interventions could potentially alter these abnormalities. Attention to the prothrombolic or hypercoaguable state in PAD may possibly provide answers to the management and development of new prevention strategies. (ref)
Lower Limb Revascularisation
PAD is a serious cause of morbidity. As we have seen the disease itself can have many symptoms that include, claudication which can be mild - severe, ulceration, rest pain and in the worst case scenario ischaemia which may require amputation. The primary reason for intervention in people suffering with PAD is to prevent further progression of the disease which will ultimately improve patient comfort and quality of life.
Today there are two main treatments in the management of PAD, they are angioplasty and bypass surgery.
Angioplasty which is also known as PTA (Percutaneous Transluminal Angioplasty) is a minimally invasive procedure, where a catheter is inserted into the artery, usually through a groin incision, and guided to the diseased segment of the vessel.
Once here a small balloon is inflated and deflated for a few minutes (depending on the severity of the disease). While the balloon is inflated, the pressure causes the plaque/atheroma to be forced onto the vessel walls, which will open up the artery and improve the blood flow.
In some cases of angioplasty a stent may also be used. To place the stent, the angioplasty catheter is removed and a new one placed in. On this catheter a closed stent surrounds a deflated balloon. The stent is then guided to the segment where the angioplasty balloon inflated initially. The balloon is then inflated within the stent causing it to expand. The balloon is then deflated and removed. The stent will remain in place, and gives support to the artery. The artery wall will grow over the stent, which helps prevent it from moving.
There are new stents being developed which are coated in drugs. These drugs may help prevent scar tissue from forming inside the stents, thus reducing the risk of restenosis. Patients where drug eluting stents were used are shown to have higher patency rates, reduced restenosis rates and less clinical recurrence requiring repeat angioplasty. (ref)
Risks involved with lower limb angioplasty
As angioplasty is a minimally invasive procedure, there are few risks involved compared with lower limb surgery (Bypass). The most common risk of angioplasty/stenting is a restenosis, which may require a repeat prodcedure if severe enough.
Restenosis is a major problem after initially successful angioplasty occurring in 35-50% of lower limb arteries within one year after the initial angioplasty procedure. Therefore, by requiring further interventions restenosis has not only clinical but also economical implications. The causes of restenosis are complex and not fully understood. It is thought that restenosis is most commonly secondary to myointimal proliferation, arterial re-modelling and or platelet deposition with subsequent release of platelet derived growth factor. Many mediators are related to these patho-physiological mechanisims and contribute to the development of restenosis post angioplasty of the peripheral arteries. (ref)
Other complications include bleeding or bruising at the site of entry of the catheter (groin). A pseudo-aneurysm (false aneurysm), can occur in the groin where the catheter was inserted into the vessel. After removing the catheter bleeding can occur. A clot is produced and forms a small sac with blood in the middle. The blood pulses as it is joined to the artery via the hole made by the catheter. However, this complication is easily treated by injecting thrombin into the sac which causes the blood to thrombose and block the hole in the vessel.
Commonly patients will feel tender and sore around the groin area, due to incision site, however, this usually resolves within a few days and the discomfort abates allowing the patient to become more mobile/active.
While angioplasty is a minimally invasive procedure, bypass for the lower limbs is an invasive surgical procedure with greater risks, longer hospital stay and higher levels of morbidity. Surgical bypass actually creates a detour around the stenosed or occluded segment of the artery. A new pathway for blood flow is created by using a graft. Grafts can be either a vein (taken from another site of the body) or a synthetic tube.
Firstly, if a vein is being used for the procedure, this will be removed (The GSV ie great saphenous vein, is very commonly used if seen as a suitable conduit). If there are no suitable veins available a synthetic graft will be used.
An incision is made over the artery which is to be bypassed. Below the stenosis or occluded segment the artery is opened, this is where the one end of the graft will be connected. The graft is held in place with permanent stitches. The other end of the graft is then routed through muscles and tendons to a normal segment of the vessel above the stenosis/occlusion. Again the artery is opened here and connected to the graft with permanent stitches.
Risks involved with lower limb bypass surgery
The graft may become occluded and the blood flow to the leg will be reduced to the levels they were pre-operatively. In some cases if the graft occludes, especially if this happens in the first hours or weeks post op, the blood flow may be even worse than it was before surgery. If this happens an amputation may be required, unless the graft can be salvaged and the flow of blood restored.
Infections are not uncommon in bypass surgery. This is due to the length of the incision (which can often begin in the groin and continue to the level of the ankle), the operations are prolonged and the tissues of the leg are often already damaged and can be swollen. However, these infections are generally easily treatable with a combination of dressings, antibiotics and sometimes drainage of the infection.
If the infection involves the graft, especially if the graft is synthetic eg, PTFE or Dacron, it is much more serious. It is impossible to remove infections from artificial materials, therefore the entire graft would have to be removed. If this occurs the blood flow through the graft is also removed. If another route for bypass cannot be established this could result in amputation. Fortunately, this situation is very uncommon and affects only 5% of prosthetic grafts. Infection around a vein graft is much more controllable. Vein grafts are preferred due to their lack of complications. 5 year assisted patency rates in grafts constructed with vein approach is 60%, and those constructed with prosthetic material are usually less than 35%. (ref). One type of graft infection could be critical for any type of graft. This is when the anastamosis of the graft is involved. If this happens there is a serious risk of bleeding from the anastamosis as it becomes weakened by the infection.
This is a common complaint post bypass procedure. For the most part it will resolve, however in some cases a small amount of swelling may persist, this is not dangerous but may cause the patient ongoing discomfort.
To date there is no evidence to favour bypass surgery over angioplasty in terms of the effect on walking distance, complications and disease progression, amputations or death.
There is evidence in patients with critical limb ischaemia (CLI), that surgery may be associated with increased surgical complications and longer hospital stay, when compared with those who has angioplasty.(ref). Also, there is evidence to suggest that bypass surgery is more expensive than angioplasty. In the first year hospital costs are approximately 1/3 higher, when compared to angioplasty. (ref)
In a situation where endovascular revascularisation and open repair/bypass of a specific lesion causing symptoms of PAD give equivalent short and long term symptomatic improvement, endovascular techniques should be used first.(ref)