Week 3 – Abdominal Aortic Aneurysm and Peripheral ......Week 3 – Abdominal Aortic Aneurysm and...

Week 3 – Abdominal Aortic Aneurysm and Peripheral Vascular Disease

1. Anatomy of Thorax, Abdomen, Upper and Lower Limbs 2. The Control of Blood Volume and Pressure

● Describe the control of blood volume and pressure and how it varies from the great vessels to the capillaries in the skin and end organs then back via the veins and lymphatics.

● Describe how this relates to the structure of the vessels walls. 3. Aortic Aneurysm

● Describe the physiological and cellular changes that occur during the formation of an Aortic Aneurysm. List the causes of Aortic Aneurysms and how they are classified.

● Describe the management of Aortic Aneurysm including thoracic for the pre rupture findings and also when they rupture. This will include the management of risk factors,

pharmacology and surgical intervention ● Discuss the screening for Aortic Aneurysm in the UK.

4. Limb Ischaemia ● Compare and contrast the pathophysiology of Acute and Chronic limb ischaemia.

Describe how this links to the history and examination. ● Describe the indications, options and complications of limb amputation, fitting and

rehabilitation. Discuss the variations in how individuals and families cope with major

circulatory life events 5. Peripheral Vascular Disease

● Describe the methods and findings for techniques used to investigate arterial disease, to include Doppler pressure measurements, Arteriograms and Duplex scanning. Describe the methods and findings for investigations used to investigate venous disease and lymphatic disease.

● Discuss the pharmacological management and surgical management of Peripheral vascular disease. Include the principles of revascularisation, endovascular

(angioplasty/stenting) and surgical bypass, include the complications.

M4, W3 – AAA and PVD Notes

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Anatomy of the Thorax, Abdomen, Upper and Lower Limbs

Arteries

There are two types of arteries:

● Elastic (conducting) arteries – arteries closest to the heart eg. The aorta. An artery with a large number of collagen and elastin filaments, giving it the ability to stretch in response to each pulse

● Muscular (Distributing) arteries and arterioles – medium sized arteries that draw blood from an elastic artery and branch into resistance vessels including small arteries and arterioles – contain

layers of smooth muscle

The Upper Limbs

Arterial Supply ● All arterial supply to the upper limb originates from subclavian arteries

o Right subclavian artery – comes from brachiocephalic trunk which is one of the three branches originating from the arch of aorta

o Left subclavian artery – branches directly from the arch of aorta

● From here, the right and left upper limb follow the same path ● The subclavian artery travels down the arm and crosses the lateral edge of the 1st rib when it is

then called the axillary artery ● This axillary artery passes through the axilla, just underneath the pectoralis minor muscle ● It then becomes the brachial artery at the level of the lower border of the teres major muscle –

the brachial artery is the main source of blood for the arm


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● The brachial artery then descends down the arm, immediately posterior to the median nerve, and bifurcates in the distal region of the cubital fossa into the radial (lateral) and ulnar (medial) arteries

● The radial artery supplies the posterior aspect of the forearm and the ulnar; the anterior ● The ulnar artery moves into the hand anteriorly to the flexor retinaculum (the fibrous band that

makes the carpal tunnel) and laterally to the ulnar nerve. It forms a deep and superficial branch and contributes mainly to the supply of the rest of the digits, and the medial side of the index

finger

● The radial artery enters the hand dorsally (at the back), crossing the floor of the anatomical snuffbox and moving in anteriorly and medially between the heads of the adductor pollicis (thumb adductor). It then joins the deep and superficial branches created by the ulnar artery

and contributes mainly to supply the thumb and lateral side of the index finger

● This anastomoses (joining) in the hand forms the two arches – the superficial and deep palmar arches, from which branches to the digits emerge


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Venous Drainage

● Can be divided into superficial and deep ● Superficial – major superficial veins are the cephalic and basilic veins.

They’re located in the subcutaneous tissue

o Basilic – arises from the dorsal venous network of the hand, ascends the medial aspect of the arm. At the border of teres major, the vein moves deep into the arm and joins the brachial veins to form the axillary vein

o Cephalic – again arises from the dorsal venous network of the hand, but then goes up anteriorly and laterally, passing anteriorly to the

elbow. At the shoulder, the cephalic vein travels between the deltoid

and pectoralis major muscles (deltopectoral grove) and enters the axilla, joining the axillary vein

o At the elbow, the basilic and cephalic veins are connected by the median cubital vein

● Deep – These are paired with the arteries mentioned above. The brachial veins are situated either side of the artery and the pulsation of the artery aids in venous return


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The Aorta and Abdomen ● The aorta is the largest artery in the body, initially being an inch wide ● Can be divided into four sections:

o Ascending aorta

o Aortic arch – begins at the level of the second sternocostal joint. Ends at level of T4 vertebra. The arch is still connected to the pulmonary trunk by the ligamentum arteriosum (remnant of the foetal ductus arteriosus)

o Thoracic (descending) aorta – goes from level T4 – T12. Begins to the left of the vertebral column but moves to the midline as it descends. It leaves

the thorax via the aortic hiatus in the diaphragm and becomes the abdominal aorta

o Abdominal aorta – Begins at T12 and ends at L4 by bifurcating into the common iliac arteries. Notably, gives rise to the renal arteries at L1-L2


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Venous Drainage ● All venous drainage from the structures below the diaphragm drain into the inferior vena cava ● Formed from the common iliac arteries at L5 ● Ascends up through the abdomen, located on the posterior abdominal wall and to the right of

the abdominal aorta

● It leaves the abdomen through the central tendon of the diaphragm at T8 (the caval hiatus) ● In the thorax, it drains into the right atrium ● However, the spleen, pancreas, gall bladder and the abdominal part of the GI tract drain into the

portal venous system first (the liver)

The Lower Limbs Arterial Supply

● As we know, the abdominal aorta bifurcates into the common iliac artery at L4

● This then further bifurcates into the internal and external iliac arteries


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● Internal iliac artery – supplies the pelvic region ● External iliac artery – becomes the femoral artery when it goes under the inguinal ligament and

enters the femoral triangle

● The profunda femoris artery then branches from the femoral artery, it travels posteriorly and laterally and supplies most of the

posterior and lateral portion of the upper leg

● The femoral artery itself goes anteriorly down the leg in the anterior canal and supplies most of the anterior portion of the thigh

● It then moves through the adductor hiatus and enters the posterior part of the thigh, posterior to the knee, and is then

known as the popliteal artery ● This popliteal artery descends down the leg posteriorly and gives

off genicular branches to supply the knee

● At the lower border of the popliteus, the popliteal artery terminates by bifurcating into anterior and posterior tibial arteries

o The posterior tibial artery – this continues down posteriorly ad inferiorly, along the surface of the deep muscles. During

the descent, the fibula artery branches off, supplying the

lateral portion of the lower leg

o The anterior tibial artery – passes anteriorly between the tibia and fibula, runs down the leg, passes into the foot and

becomes the dorsalis pedis

● In the foot – blood is supplied by o Dorsalis pedis artery – when the anterior tibial artery enters the foot, passing anteriorly to

the tarsal bones and goes inferiorly, anastomosing with the lateral plantar artery to form the

deep palmar arch

o Posterior tibial artery – enters the sole of the foot through the tarsal tunnel. It then splits into lateral and medial plantar arteries. These supply the plantar region of the foot and

again, forms part of the deep palmar arch


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Venous Drainage ● Similarly to the upper limbs, the venous system can be split into deep

and superficial

o Deep – located under the deep fascia, accompanying the major

arteries

o Superficial – located in the subcutaneous tissue. Two main one:

▪ Great saphenous vein –formed by the dorsal arch of the foot. It ascends up the medial side of the leg, passing

anteriorly to the medial malleolus and posteriorly to the

medial epicondyle. It then drains into the femoral vein,

immediately inferior to the inguinal ligament

▪ Small Saphenous vein – also formed by the dorsal arch of the foot. It moves up the posterior side of the leg, passing

posteriorly to the medial malleolus and moves between the two

heads of the gastrocnemius to empty into the popliteal vein


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The Control of Blood Volume and Pressure

Why is it Important to Regulate the Blood Flow through an Organ? ● Match blood supply to tissue metabolism – active organs/tissues receive more blood ● Ensures sufficient supply of substrates and efficient removal waste products ● Increases or decreases heat loss from the body by redistributing blood ● Ensures blood flow to vital organs such as the brain and heart is maintained in the event of

severe challenges (e.g. haemorrhage) Mechanisms Involved in Blood Flow Regulation

● Altering cardiac output ● Changing the diameter (calibre) of the resistance vessels – the main resistance vessels are

arterioles ● Altering the amount of blood pooled in capacitance vessels (veins)

Mechanisms that Regulate the Calibre of Blood Vessels ● Smooth muscle around the blood vessel (the tunica media) exhibit resting tension, known as

vascular tone ● Changes in vascular tone alters the calibre of blood vessels and hence vascular resistance ● ↑ tone = vasoconstriction, ↓ tone = vasodilatation ● The factors that regulate vascular tone are divided into two broad categories – intrinsic (local –

within the organ or tissue) and extrinsic (systemic – outside the organ or tissue). Autoregulation

● Autoregulation is a manifestation of local flow regulation ● It is defined as the intrinsic ability of an organ to maintain a constant blood flow despite

changes in perfusion pressure ● So, looking at the graph on the right, in order for the organ to keep blood flow constant (see the

plateaux on the graph) despite an increase in perfusion pressure, it has to constrict. ● In order to keep blood flow constant when there is a decrease in perfusion pressure, it has to

dilate.

Myogenic Theory ● Thought to arise from the intrinsic contractile response

of the vascular smooth muscle to stretch ● It is independent of nerve supply and it depends on

perfusion pressure ● There are direct changes in vascular tone in response to

changes in perfusion pressure ● Myogenic theory is well developed in the kidneys, skin,

mesentery, skeletal muscle, liver, brain and myocardium

● Before getting into the myogenic theory it is important to know the structure of the vascular smooth muscle.


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Structure of Vascular Smooth Muscle (VSM)

● Cytoplasm of the VSM contains thin actin and thick myosin filaments ● Instead of being aligned into sarcomeres as in cardiac myocytes, groups of actin filaments

running roughly parallel to the long axis of the cell are anchored at one end into elongated dense bodies in the cytoplasm and dense bands along the inner face of the cell membrane

● Dense bodies and bands are linked by bundles of intermediate filaments composed of the proteins desmin and vimentin to form the cytoskeleton

The Mechanism ● Vascular smooth muscle in the vessel is stretched due to the increased perfusion pressure ● This stretch causes stretch sensitive ion channels to open, causing a Na+ and Ca2+ influx ● This leads to cell depolarisation, which is an additional stimulus for the opening of L-type Ca2+

ion channels, leading to an intracellular rise of the Ca2+ ion, causing vascular smooth muscular contraction (as it binds to calmodulin)

● This leads to contraction leads to vasoconstriction and a constant blood flow

Metabolic Theory ● Cellular metabolism leads to the accumulation of chemical by-products ● Some of these by-products cause relaxation of smooth muscles and hence vasodilatation,

therefore they are vasodilator substances/metabolites ● This leads to an increase in blood flow – this is known as functional hyperaemia ● The local changes during cellular metabolism include (bold, italicised ones are thought to be the

most important): o Hypercapnia (increased PCO2) o Increased K+ and lactate o Increased histamine and products of ATP breakdown (adenosine and inorganic

phosphate) o Decreased pO2 and pH o Rise in temperature o Increased osmolality (↑concentration of solutes in plasma)

● NB: In lungs, there is an opposite effect, this leads to vasoconstriction which directs blood from hypoxic regions


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Sympathetic Nervous System’s Role in the Regulation of Blood Flow

● Agonists in the sympathetic nervous system bind to the receptor causing voltage gated Ca2+ channels to open

● The rise intracellular Ca2+ promotes it binding to the cytoplasmic regulatory protein calmodulin (CaM)

● Once a calmodulin molecule has bound to 4 Ca2+ ions, it can activate the enzyme myosin light chain kinase (MLCK)

● MLCK in turn phosphorylates two 20-kDa subunits contained within each myosin molecule ● Phosphorylated myosin then forms a crossbridge with actin, using ATP hydrolysis as an energy

source to produce contraction and vasoconstriction

Local Mechanisms leading to Vasodilatation and Vasoconstriction ● There are a number of mechanisms acting locally in selected vascular beds under specific

circumstances.

Vasodilators ● For example, the inflammatory reaction, local infection or trauma causes the release of various

autocoids (local hormones), including arteriolar dilators: o Histamine o Prostaglandin E2 o Bradykinin o Platelet activating factor

● These increase blood flow and increase postcapillary venule permeability, thereby facilitating the access of leukocytes and antibodies to damaged and infected tissues.

● Prostaglandin I2 (prostacyclin) is synthesised and released in the renal cortex under conditions where renal blood flow is reduced by vasoconstrictors. Prostacyclin has a vasodilatory action that maintains renal blood flow. It also inhibits platelet aggregation.

● Nitric oxide (NO) is released by the endothelium under shear stress, having a vasodilatory effect


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Vasoconstrictors ● Inversely, the release of serotonin and thromboxane A2 (platelet aggregator) from platelets

during haemostasis causes vasospasm (sudden vasoconstriction), which helps to reduce bleeding

● Endothelins, which exist in three isoforms 1,2 and 3 are very powerful vasoconstrictors


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Aortic Aneurysm ● Definition - a bulging, weakened area in the wall of an artery, causing localised dilatation of an

artery, making the diameter at least 1.5 times larger than expected.

Any dilatation less than 1.5 times larger than the original diameter

is called 'ectasia'.

Classification

● Aneurysms can be categorised as 'true' or 'false' aneurysms.

True Aneurysms:

● Involve all three forms of the tunica, causing a bulging shape ● Produces a 'saccular' or 'fusiform' shape

o Saccular - these aneurysms bulge or balloon out at only one side

o Fusiform - these aneurysms bulge out on all sides of the artery, and are the

most common type of true aneurysm. ● Commonly found:

o Abdominal aorta

o Popliteal artery

o Femoral artery

o Thoracic aorta

o Thoracoabdominal aorta

False Aneurysms - AKA Pseudo-Aneurysms: ● Caused by a hole in the arterial wall ● Normally, there is a tear in the tunica intima - as a result, blood fills

in between the layers of the vessel wall ● Produces a haematoma which is pulsatile, surrounded by tissues ● Commonly found:

o Femoral

o Radial

o Anastomotic

Aortic Dissection

● A dissecting aneurysm is one that separates all three layers of the artery, rather than causing a bulge of the entire wall. However, this can eventually lead to a bulging sight, typical of an

aneurysm. Blood goes into the wall due to a tear ● Most cases begin suddenly with:

o Sharp, stabbing, tearing sensation

o Pain normally felt below the sternum

o Can move to the shoulders, neck, arms, jaw, abdomen and hips

o Pain can change position as the dissection progresses

● Also associated with: o Nausea


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o Anxiety o Heavy sweating o Rapid, weak pulse o Shortness of breath

● This is a life-threatening emergency and needs to be treated immediately! Contact the on-duty surgical registrars and anaesthetist as soon as possible

Epidemiology of AAA ● Responsible for 6,000 deaths per year in the UK ● Responsible for 2% of deaths in men over 65 years old ● 90% of patients with a ruptured AAA die before reaching the hospital ● 50% of the remaining 10% die after emergency surgery ● In comparison, only 2% of patients die after elective surgery if the AAA has not ruptured

Aetiology

● Can be caused by a congenital weakness of the artery wall ● Can be caused by damage to the artery wall e.g. trauma but is normally due to atheromatous

plaques

● Caused by high pressure within the circulation

Typical Symptoms of Aneurysms

● Expansion compresses on adjacent structures ● Rupture of the aneurysm ● Thrombosis ● Distal emboli can result from a break in a plaque

Risk Factors for AAA ● Male (over 65 years old) ● Smoking ● Hypertension ● 1st degree relative with AAA

Management ● In patients with small AAAs, expansion needs to be controlled as much as possible. Hypertension

is therefore aggressively controlled with beta-blockers to lower blood pressure and reduce

stress on the artery wall. ● Management plans for asymptomatic aneurysms depend on the diameter:

1. Normal (Aorta diameter 5.5cm)- Referred to a vascular surgeon and seen within 2 weeks – can have

open or endovascular repair


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Surgical Intervention

● Indications for surgical intervention depend on the type of aneurysm. ● If asymptomatic: surgery is indicated if the diameter is greater than 5.5cm OR there is a 1cm

increase in size per year

● If symptomatic: surgery is indicated if there is: o Pain/tenderness

o Rupture

o Distal embolization

Open Repair ● Open repair is a more approachable technique in aortic aneurysms than

thoracic aneurysms. Younger patients tend to do better – the lifelong benefits

are greater for this procedure however, and mortality matches that of the normal population if successful. The technique involves clamping the aneurysm proximally and distally to the diseased aorta. The aneurysm is then

removed and replaced with a synthetic graft. o For elective open repair, 30 day mortality is 5-8%

o For emergency repair of a symptomatic AAA, mortality is 10-20%

o For emergency repair of a ruptured AAA, mortality is 50%

● Complications of open repair includes: bleeding, ischemia (to limbs, colonic ischemia – checked post operatively), cardiac/respiratory/renal failure, infection, graft infection, aorto-enetric

fistula.

EVAR ● Endovascular aneurysm/aortic repair a minimally invasive used surgical procedure to repair

AAA’s. When treat thoracic aortic aneurysms, the procedure is called TEVAR (thoracic

endovascular aneurysm/aortic repair). ● The procedure involves placing vascular sheaths into either the

femoral or iliac arteries. Through this, guidewires, catheters and

the endograft are passed. An endovascular stent graft is inserted into the aorta under fluoroscopic x-ray guidance. This creates a lumen, reducing pressure on the aneurysm. Once inserted, the position of the graft is checked via angiography to

make sure it is in the correct location and that it has secured onto the artery walls. Over time the aneurysm begins to thrombose and shrink.

● There are some variants of the standard procedure, such as fenestrated EVAR, where the endograft is fenestrated (has holes). This is useful where a normal endograft cannot be fixed.

For example, if the aneurysm is located just over the renal arteries, inserting a standard graft would cover and cut off supply to the kidney. Blood is able to pass through the fenestrations in the endograft.


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● Another variant is branched EVAR, where graft branches can be inserted into

any major arteries branching from the aneurysm. This is still a rare procedure however.

● Potential complications arising from EVAR include: Damage to surrounding blood vessels, DVT, infections, groin hematoma, contrast/x-ray radiation, 5-10% re intervention, damage to access vessels, bleeding, spinal cord injury and endoleak – this is where leakage of blood out of the graft and into the

aneurysm sac can cause potential rupture. There are several types of endoleak:

o Type 1 endoleak – poor seal between the graft and aneurysm o Type 2 endoleak - back bleeding into the inferior mesenteric artery o Type 3 endoleak - poor seal between graft components (when more than one is used) o Type 4 endoleak - graft material porosity (begins to leak into area between the graft

and vessel)

Rupture Management ● Depends on the severity/suspicion of rupture ● If bleeding is suspected in conjunction with instability, rupture is suspected ● In emergency situations, consent/instigations are not required, and intervention is immediately

commenced. ● If the patient is stable and can manage some time, CT can be conducted to determine if there is

a rupture or not, and to guide subsequent surgical intervention. ● Ruptures are treated with open repair.

Screening ● Screening for an abdominal aortic aneurysm (AAA) is crucial. ● Around 80% of people with a ruptured AAA die during surgery or before they reach hospital. ● However screening along with education can significantly alter this negative outcome. ● The UK screening programme was set up in 2009 in England and since 2013 all of the UK health

services offer the same. ● Currently when a man turns 65 he will receive a letter from his GP recommending this screening

programme and contact details for it. If a man was over 65 during this time they are also able to request the scan- there are local AAA screening service which are very easy to contact.

● The risk for women and under 65 year old men of AAA rupture is so low that they do not undergo screening.

● The procedure itself is a quick, painless and easy ultrasound which takes roughly 10-15 minutes.

● The results are instant and will be sent to the patients GP in order to make a quick decision on treatment. Depending on these results depends on where the treatment direction goes: 1. Normal (Aorta diameter

2. Small (Aorta diameter 3cm-4.4cm) - Regular scans every year. Interestingly it is very unlikely

these will ever develop to a dangerous level but not worth the risk. 3. Medium (4.5cm-5.4cm) - Regular scans every 3 months. 4. Large (>5.5cm)- Referred to a vascular surgeon and seen within 2 weeks – can have open or

endovascular repair ● All these groups will be encouraged to assess how healthy their lifestyle and the technician may

recommend altering negative activities such as o Stopping smoking o Eating a balanced diet o Ensuring you maintain a healthy weight o Taking regular exercise o Compliance to important medication e.g. anti-hypertensives

Limb Ischaemia Acute Limb Ischaemia

● The sudden occlusion of an artery can cause tissue necrosis within 6 hours and is a vascular emergency. This depends on the collateral blood supply to the limb for example, the subclavian artery is one of a few arteries that supply the upper limb so the upper limb is less likely to suffer from ischaemia. The lower limb, however, has got an inadequate collateral supply so is much

more at risk of ischaemia. ● It may occur because of:

o Embolism

This is where something travels through the bloodstream and causes a blockage in a vessel (which is often narrowed). For example, they can be blood clots (often caused by atrial fibrillation), pieces broken of atherosclerotic plaques (fat embolus) or gas bubbles.

They often lodge at points of bifurcation where the vessel gets narrower. o Thrombotic disease

A thrombus forms and blocks the vessel. Quite often it is associated with

atherosclerosis. Also, patients with thrombophilia (e.g. due to malignancy). o Cervical rib/band syndrome/thoracic outlet syndrome

A piece of fibrous tissue (like a rib) comes from C7 vertebra which can compress the

subclavian artery causing upper limb ischaemia. (This is rare). o Graft occlusion

This is where a bypass graft (either from the saphenous vein or prosthetic) somehow

blocks the artery. For example, there may be hyperplasia at the sites where the graft is attached or, if a graft made from a vein, a valve may be retained.

o Trauma


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If an artery is cut, there is a haematoma, fractured or dislocated bone compressing an

artery this can cause ischaemia. This can be iatrogenic e.g. during a hip replacement, the

ileac artery may become compressed.

Presentation ● Handily all the symptoms and signs for acute limb ischaemia begin with P


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History

Pain This is often very severe requiring opioids. Depending on the degree nerves are affected, the pain may be predominantly neuropathic or absent.

Paraesthesia Thin nerve fibres are affected by a lack of perfusion first and these respond to light touch. Therefore, numbness starts first. The nerve fibres that conduct pain are less ‘ischaemia-sensitive’ so numbness to the point where pain cannot be felt is a late symptom of ischaemia.

Paralysis Ischaemia can damage motor neurones and it can also damage the muscle both causing paralysis. After a while of limb ischaemia the opposite limb may spasm indicating muscle necrosis of the ischaemic limb. At this point, it is too late to re-vascularise the limb.

Examination

Pallor Initially arterial spasm and constriction causes whiteness (see picture) and then cyanotic blue blotches appear. When these don’t blanch, the capillary bed is affected and the ischaemia is irreversible.

Pulselessness Useful to compare to opposite limb. If the toe is affected, the blockage may be distal to dorsalis pedis and tibialis anterior so these pulses may be palpable.

Perishing cold/poikilothermia

The limb will feel cold approximately one joint below the blockage.

(Poikilothermia = the limb takes on the temperature of the environment)

Chronic Limb Ischaemia ● Chronic limb ischaemia covers a spectrum of severities from asymptomatic peripheral arterial

disease and intermittent claudication to critical limb ischaemia. The phrase ‘critical limb ischaemia’ implies a chronic ischaemia and is not interchangeable with acute limb ischaemia. Chronicity here is > 2 weeks.

● Atherosclerosis is nearly always the underlying pathophysiology causing narrowing of the vessels and a restriction of blood flow. Atherosclerosis is likely to affect multiple vessels and 40-60% of patients with atherosclerotic changes in their legs will also have narrowed coronary vessels.

● As there is such a spectrum, the Fontaine classification is used:

● When blood supply is not adequate, the muscle cells are not able to respire aerobically so anaerobic respiration takes place and lactic acid builds up. The time before pain on activity sets in will decrease as the disease progresses until the pain is present at rest. The pain is typically

worse at night because, with the limb elevated, gravity is not helping tissue perfusion. If this

persists for > 2 weeks, the ischaemia is classified as critical limb ischaemia

Presentation

History ● As mentioned, patients can be asymptomatic. This can be due to mild disease but more severe

disease may be asymptomatic if patients do not exercise for other reasons. As a disease of the elderly, respiratory disease, musculoskeletal disease etc. will be common and may limit activity so symptoms are not noticed.

● Intermittent claudication is the initial presenting complaint in 30% of symptomatic patients – as previously described, it is pain in the calf, thigh and buttocks, unilateral or bilateral, when walking which is relieved within 5 minutes of stopping the activity.

● More advanced disease may present with a similar pain to claudication but present at rest and worse at night.

● Critical limb ischaemia is the presence of pain at rest for > 2 weeks.

Examination

● Increased capillary refill time ● Absent peripheral pulses ● Cold limb (but this is often not the case in chronic ischaemia)


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Stage Symptoms Description

1 Asymptomatic

2 Intermittent claudication When active patient gets calf muscle, thigh or buttock cramps which are relieved within 5 minutes of rest

3 Rest pain Pain continues at rest, often in feet and worse at night.

4 Tissue loss Ulcers, gangrene

● A critically ischaemic foot may appear red, even redder than the unaffected foot. This is called

‘sunset foot’ (shown on right) and is due to the foot being ‘dependent’ (low so gravity is aiding perfusion). It looks red rather than the normal pink because arterioles dilate to try to help remove lactic acid. It is easily mistaken for cellulitis. Use Buerger’s test – at what angle does the

limb need to be at to go white and then how quickly does it take for it to return to a normal colour when down. Elevation of

o Impairment: the physical effects caused by the disease or previous trauma causing

problems with physiology. This leads to an amputation. o Disability: the limitations in their activity, skills and learning caused by the amputation.

Rehabilitation involves teaching the patient how to walk again. It is important to make SMART goals to maximise improvement.

o Handicap: the reduced independence and restricted participation caused by the amputation. Rehabilitation helps the patient to find an adaptable job that allows them more independence. For example, providing a prosthesis to put on their stump (the distal end of the limb that is left after the amputation) and training them to use it to

gain the most efficient gait. ● There are many factors that would influence unemployment, and therefore many factors to

consider when helping an amputee to get back into work. These include the individual (their physical state and psychological trauma due to limb loss), social factors (such as family support and organisational support), legislations (including the social security system and welfare right), the employer (including the size of the firm and the flexibility of the work force) and the work environment.

● When monitoring the stump, observation of tissue healing, optimal muscle control and normal sensation is required.

● If without prosthesis, patients would require teaching on wheelchair skills, transfer skills (from bed to chair and toilet), activities of daily life and personal care.

● Challenges amputees experience with a prosthesis with their gait include: o Ground clearance in swing

o Loss of ability to absorb energy

o Maintaining mid-stance on the prosthetic limb

o Loss of foot eversion/inversion

o Transmission of centre of gravity

o Loss of push off in terminal stance

● Rehabilitation for using a prosthesis includes improving standing balance and gait training. Gaiting training involves practice with parallel bars and early walking aids. Early walking aids include a P-PAM (Pneumatic post amputation mobility) aid, used for trans-tibial and trans-femoral amputations, and femurett, used for trans-femoral amputations (these consist of an adjustable socket and a thigh tube).

● To use a femurett walking aid, a patient has to be able to weight-bear and balance on one leg, and have good leg, hip and arm-strength. These are used as early as 5 days post-amputation and

are a temporary measure useful to assess suitability for an artificial limb.

Complications of Amputations ● Local stump complications include skin breakdown and ulcers in pressure areas. This could be

due to a number of reasons, including poor socket fitting, associated neuropathy, change in

stump volume, changing in gait pattern and infection. This is managed by establishing the cause, minimising use of the prosthesis, adjusting fitting and managing the ulcer (antibiotics if infected, regular dressings with reviews)


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● The stumps of dialysis patients’ increase and decrease in size pre- and post- dialysis respectively.

This means they require different sizes of prostheses for different points in their dialysis regime. ● Phantom pain is a severe and traumatic complication of an amputation.

o Phantom pain is feeling pain in the missing limb

o Phantom sensation is feeling the missing limb o Superadded phantom is a sensation of something being over the missing part (for

example a tight wristwatch, or tight shoe)

o Different types of phantom pain include kinaethetic sensation, kinetic sensation and exteroceptive sensation

o Kinaethetic sensation is to do with the awareness of body position, proprioception and equilibrium.

o Kinetic sensation involves spontaneous and twitching movements. o Exteroceptive sensation involves feeling touch, temperature, pressure, itching and

tingling. o The mechanism of phantom pain is unknown, however, it has never occurred after

congenital amputations suggesting it is to do with the learned experience.

o The first line of management is prevention - giving analgesia pre-operatively (using the analgesic ladder). Treatment of clinical depression may also be necessary.

o Physical symptoms have the following management options, working for everyone in different ways: physiotherapy, massage, heat, desensitisation, acupuncture, electromagnetic, TENS, electro-acupuncture.

o There are psychotherapy methods that are commonly used, including: distraction, relaxation, autogenic hypnosis and biofeedback (Ramachandran's mirror box).

o Ramachandran's mirror box works best with kinetic sensation phantom pain. The patient receives artificial visual feedback of the "resurrected" limb moving. This helps some patients,

o Both physical methods and psychotherapy methods seem to use the gate control theory of pain (module 1), which hypothesizes that the spinal cord contains a neurological gate which either blocks or allows pain signals to pass on to the brain. Factors that open the gate (allowing pain to be more severely felt) include stress, tension, boredom and being sedentary. Factors that close the gate (thus reducing amount of pain felt) include happiness, hobbies, being active, as well as massage, electrical stimulation and

acupuncture.

Coping Mechanisms ● Coping mechanism definition: "constantly changing cognitive and behavioural efforts to

manage specific external and/or internal demands that are appraised as taxing or exceeding

resources"


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Why is Coping Important? ● It allows for an adaptation to be achieved via physiological, behavioural, cognitive, emotional

response ● The patient can be the active agent in managing stressors by reducing perceiving discrepancy

between demands and resources ● Coping is a complex organisational construct covering a multitude of specific actions.

Classifying Coping ● In terms of function served, methods and type of action. ● Types include:

o Emotion-focussed coping: to regulate emotional distress caused by the potential stressor ▪ This is used when the person has little or no control ▪ For example delegation, social withdrawal and opposition

o Problem-focussed coping: the attempt to alleviate or eliminate stressful situations through trying to take control

▪ This is more construction and is used in controllable situations

▪ For example, problem solving, support seeking and cognitive restructuring

● The type of coping best to use depends on an individual’s personality and the stressful situation - we all have the potential to use both. Coping is a process that changes over time.

Coping in the Acute Phase ● Emotion-focused coping is often unavoidable/the only option and is helpful in the short term.

Hospitalisation limits opportunities for problem-focused coping due to the lack of control patients have on the situation.

● Effective use of emotion-focused coping may make later problem-focused coping possible allowing more control and management

Coping in the Chronic Phase ● Long term emotion-focussed coping can be problematic ● Problem-focused coping is important in the ongoing management of the condition and self-care

What Influences coping? ● Illness-related factors (e.g. level of threat to life/functioning, treatment regimens, side effects

of treatments) ● Background/personal factors (e.g. personality, socio-demographics, timing in life, knowledge,

beliefs, motivation, emotions, experience, education) ● Physical/environmental factors (e.g. hospital/home environment, social support, finance,

resource availability, educational opportunities) ● For a child with chronic illness, their outcome will be affected by how flexible, cohesive and

supportive the family are, how open and clear their communication is, how supportive their other support system are, their previous understanding of disease and their pre-illness personality and functioning.

What does Social Support Do? ● Provides emotional and practical assistance to enhance effective coping and adjustment ● Presence of support alone is not enough - carers may not be coping themselves, there are

burdens associated with relationships (protection, guilt, expectations)


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● The clinician plays a key role in forming supportive relationship by providing opportunities for

disclosure, effective listening, ensuring continuity and follow up

Peripheral Vascular Disease Investigating Arterial Disease

● ABPI: Ankle Branchial Pressure Index. This is when blood pressure is taken in the arm and in the lower leg (near the ankle) and a ratio is formed between the two. The arm is used as a reference because arteries in the upper limb are less susceptible to PAD (peripheral arterial disease) than

the lower limb. If the blood pressure is lower in the ankle peripheral vascular disease is indicated.

● BLOOD PRESSURE IN ARM/ BLOOD PRESSURE IN LEG

● You use a Doppler (ultrasound) to assess the blood pressure. You inflate the cuff until the sound from

the artery is abolished. Then you deflate the cuff noting the pressure at which the sound returns. You repeat this on both arms and use the higher of the

two values in your calculation. The procedure is repeated for the legs. Note that it is the systolic blood pressures that are used. ABPI has a high

sensitivity and specificity for detecting PAD but it may not be accurate for patients with calcified arteries. The table below shows what different ABPI values indicate and how to treat a leg ulcer

with each result.


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ABPI value Interpretation Action Ulcer, if any

Above 1.2 Abnormal. Vessel has been hardened by calcification via PVD.

Refer Venous, so use compression bandages

0.9-1.2 Normal None None.

0.8-0.89 Some arterial disease Manage risk factors Venous, so use compression bandages

0.5-0.79 Moderate arterial disease

Routine specialist referral

Mixed ulcers, so use Stage 1 compression bandaging

Under 0.5 Severe arterial disease Urgent specialist referral

Arterial, so don’t use compression bandaging

● A toe brachial index (TBI) should be used to establish the diagnosis of PAD in patients where there is clinical suspicion of lower-extremity PAD but the ABPI test is unreliable. This may be due to non-compressible vessels in those with diabetes, renal problems or the very elderly. For this test a result of

Arteriograms ● These use x-rays and contrast dye to look at the lumen of blood vessels.

Digital subtraction techniques eliminate bony and dense body tissue artefacts so we can view arteries. Percutaneous catheter insertion is necessary, making it an invasive procedure, and usually the femoral artery is

used but the brachial artery may be used. ● In the picture to the right you can see superficial femoral artery stenosis. ● CT scans may be performed to get a better picture of the internal anatomy

and are now used as one of the gold standard tests for diagnosis. However, it still requires IV contrast.

● MR angiography (MRA) is also a gold standard test using MRI. It is very sensitive to stenosis. However, those with pacemaker, defibrillators and

some cerebral aneurysm clips cannot be scanned safely.

Investigations for Abdominal Aortic Aneurysms ● The 1st test to order would be an abdominal ultrasound which would show aortic dilation of

>1.5 times the expected anterior-posterior diameter of that segment for the patient’s sex and body size (usually 3cm)

● ESR/CRP would be elevated ● FBC could show leucocytosis/anaemia ● CT and MRA scans can also show abnormal aortic dilation. ● Aortography may be necessary if the patient cannot undergo a CT scan. This is when a catheter

is placed in the aorta and contrast dye is injected whilst x-rays are taken.

Investigating Venous Disease ● Duplex scanning can be used as described above as a first line test however the results are

different. For veins we are looking for reversed flow and a valve closure time of >0.5 seconds. ● Venography (shown on the right) may need to be used in complex cases. This is also known as

ascending phlebography. An x-ray is taken of the veins after contrast has been injected into the veins or bone marrow. This is a very expensive and invasive test.

● CT venography and Magnetic resonance venography can be used to reveal detailed venous anatomy. A general CT of the abdomen and pelvis may reveal any masses that could cause venous obstruction.

● Intravenous ultrasound is only used in specialist centres. This involves inserting a catheter with the proximal end of the catheter

attached to computerised ultrasound equipment.

How to investigate Peripheral Oedema ● Tests to investigate:

o Blood tests: FBC, renal and liver function tests, plasma albumin concentration, thyroid function, thyroid function tests.

o Urine tests: 24 hour urine excretion tests.


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o ABG

o ECG o Chest radiography o Echocardiography

o Ultrasound ● These tests are to look for symptoms of heart and renal failure. Oedema in heart failure is due

to generalized salt and water retention due to neurohumoral stimulation.

● A lymphoscintigram may also be used. Radiographic images are taken after Tc99-m labelled protein has been injected into the dorsal web space of affected extremity. A normal examination shows visualisation of the proximal lymph nodes, normal proximal migration of the

radiolabelled contrast and the absence of dermal backflow after injection.

Management of Peripheral Vascular Disease Pharmacological Management

● Most therapy to actually treat peripheral vascular disease is surgical, however drugs can be very useful in a preventative role but also if surgery is off the cards.

● Drugs to modify risk factors: o Anti-hypertensives are indicated in all patients with a BP of 140/90, diuretics such as

bendroflumethiazide, Ace inhibitors like ramipril or beta blockers such as atenolol. (The criteria changes when the patient is either diabetic or older than 60 or both.)

o Lipid Lowering agents are recommended in all patients with a low density lipoprotein

greater than 2.59 mmol/L, such as atorvastatin or simvastatin.

o Effort has to be made to lower cardiovascular risk factors in a patient with a history of

things like CAD, previous MI, or angina as well as lots of other things. ACE inhibitors and Beta Blockers are really useful here and often patients will already be on them or at least something similar.

o One of the most important things to control is clotting, and either clopidigrel or aspirin

can be used, as they are both antiplatelets medications. There is the fear that platelet aggregation will worsen existing clots

o Not a drug but stopping smoking is always an incredibly important alteration in a

patients behaviour, as is taking on more exercise and diet alteration to reduce

cholesterol and fat intake.

Drugs to Reduce Claudication: ● Intermittent Claudication is described by patients as a gripping pain in the calf often triggered by

exercise and relived through brief rest. It is caused by poor circulation of blood to muscles. ● Though all the above medications and lifestyle factors help to reduce claudication; none of them

actually remove the blockage; only increase blood flow to muscles. If the claudication is classed as ‘lifestyle restricting’- i.e. it stops people from doing the normal activities that they do on a daily basis, then other options are available.


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● Pentoxifylline is a phosphodiesterase inhibitor, which through the increase of cAMP causes the

erythrocytes of the body to stop deforming in the blood stream and clumping up (known as red blood cell deformability), it also decreases plasma concentrations of fibrinogen and accentuates fibrinolytic effects. Overall it decreases blood viscosity and increases the flow of blood within vessels.

● Cilostazol is another phosphodiesterase inhibitor, works very similarly to the above, although cilostazol should not be used in patients with heart failure due to a risk of exacerbating that condition.

● Naftidrofuryl is a 5 hydroxytryptamine type 2 antagonist that reduces platelet and erythrocyte aggregation. It can be associated with some GI problems and discomfort.

Drugs for Treatment of Acute Limb Ischemia: ● When the perfusion to a limb plummets and it looks likely that the tissues are in grave danger

of death it is vitally important to address this as quickly as possible. Normally this will be via revascularization/ amputation but if the limb is deemed ‘viable’ i.e. there is no significant, permanent damage then ‘clot busting drugs’ may be used to buy some time so that the limb may be assessed longer.

● Urokinase is the most widely used drug for acute limb thrombolysis. N.B. it should not be given as a systemic infusion, as the risk of bleeding is too great, instead it should be administered locally into the artery of occlusion.

Surgical Management ● The problems caused by peripheral vascular disease (PVD) often can’t be completely solved by

medications alone, sure patients can manage okay but the inherent problems with their blood vessels aren’t actually being corrected by the drugs, hence sometimes surgery is required fix things.

Revascularization ● If a patient continues to suffer from the symptoms of PVD (such as

calf pain) then revascularization is recommended. ● In the most basic terms revascularization means restoring blood flow

to parts of the body that have suffered from ischemia due to the occlusion of an artery, this happens for example in a coronary artery bypass graft in coronary heart disease.

o It can be performed either via open surgery or using endovascular techniques; it depends on the size and location of the blockage. The picture above shows a femoral artery bypass and would be performed as open surgery.

o Bypasses aren’t the only type of revascularization technique however and stents, balloons and even lasers can be used to open up an artery

Endovascular ● Often described as key-hole surgery, a small incision is made into

the patient and the required apparatus is inserted and threaded through whatever blood vessel the blockage has happened in.

● An example to the right is a Fogarty Catheter that is used in a procedure known as an arterial embolectomy. The device is inserted into the artery and the attached balloon is inflated,


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allowing the blockage to be dragged backwards towards the insertion site and removed

Angioplasty: ● A stent is a thin metal tube that can be expanded once inside the body in

order to widen an artery and treat stenosis. Often used in operations known as angioplasties, where a guide wire with a mounted stent and inflatable balloon are passed into an artery, the balloon is then inflated and removed, leaving only the stent.

Artherectomy ● Another type of endovascular procedure, here a catheter capable of cutting

into a blockage is used to remove the plaque from the arterial wall. ● It may do this via a laser or simple sharp edge. ● Though effective, it does not seem to offer any advantage over an angioplasty.

Surgery ● Often surgery can be preceded by an attempt at an endovascular technique if suitable apart

however from in a blockage that is infrapopliteal, as here a failed attempt at endovascular surgery will normally preclude surgical revascularization, presumably due to the small size of the blood vessels and damage may be done to them.

● The two broad types of surgical revascularization are either bypass or endarterectomy ● In a bypass, a graft is sewn onto the artery above and below the blockage in order to create an

anastomosis, allowing blood to flow. The graft may be synthetic, as pictured or from a donor/ the patients themselves. Veins can sometimes be repurposed for use in bypass surgery, the great saphenous is an example.

● Examples of lower limb bypasses include aorto-bifemoral as pictured to the right, femoral femoral (from one side to the other) and femoral- tibial.

● Another option for surgery is to simply cut the plaque out and then sew either a graft, or tissue over the site of the removed plaque.

Endovascular vs Surgery ● According to one of the vascular surgeons who lectured us, if you are not fit for surgery then you

are not fit for endovascular procedures. This is based on the rationale that if something goes

wrong during the endovascular op, surgery will be needed to correct this and potentially save a life.

● There is a counter argument however in the sense that often people who are too frail or old etc. to undergo surgery can cope just fine with endovascular techniques, due to the minimally invasive nature of it. Choosing the right type of op can be difficult and it is paramount to include the patient in decision-making, especially with the knowledge of recovery times (drastically

shorter in endovascular ops) and also possible complications

Complications ● As with all operations, even the simplest procedure carries a degree of risk. ● Pretty irrespective of the surgery, there will nearly always be a risk of bleeding, infection or

nerve damage. I’ve taken to using the pneumonic BIN, as an aid.


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● More specifically the side effects associated with the endovascular procedures include the

bursting of the inflated balloon (which may then cause infarction itself) and neuropathy caused by the use of contrast (often this is injected to help with radiographic imaging)

● Vascular surgery carries with it far more inherent risks. The risk of bleeding is exponentially bigger than that of endovascular techniques, as is the risk of infection and nerve damage. It requires in general a younger, fitter patient who can cope with any potential complications.

● Specific complications include the graft material leaking/ not being firmly sewed on, clotting due to immobility or even DVT. A final complication may be the excessive scarring that can occur from the surgery, as often large amounts of skin have to be cut through for access. The endovascular scar is about the size of a small coin

● Endovascular surgery is unlikely to kill anyone and one study of 51 patients did not find that any had died due to complications from their operation after 5 years.


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