Vascular Surgery

Question 1

Peripheral arterial disease

Answer 1

Peripheral arterial disease (PAD) refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication.

Question 2

Intermittent claudication

Answer 2

Intermittent claudication is a symptom of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity.

Question 3

Critical limb ischaemia

Answer 3

Critical limb ischaemia is the end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. There is a significant risk of losing the limb.. The features are pain at rest, non-healing ulcers and gangrene. Pain is worse at night when the leg is raised, as gravity no longer helps pull blood into the foot.

Question 4

Acute limb ischaemia

Answer 4

Acute limb ischaemia refers to a rapid onset of ischaemia in a limb. Typically, this is due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.

Question 5

Atherosclerosis

Answer 5

Athero- refers to soft or porridge-like and -sclerosis refers to hardening. Atherosclerosis is a combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls). Atherosclerosis affects the medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. Lipids are deposited in the artery wall, followed by the development of fibrous atheromatous plaques.

These plaques cause:

Stiffening of the artery walls, leading to hypertension (raised blood pressure) and strain on the heart (whilst trying to pump blood against increased resistance)
Stenosis, leading to reduced blood flow (e.g., in angina)
Plaque rupture, resulting in a thrombus that can block a distal vessel and cause ischaemia (e.g., in acute coronary syndrome)

Question 6

Atherosclerosis risk factors

Answer 6

It is important to break these down into modifiable and non-modifiable risk factors. We can do nothing about non-modifiable risk factors, but we can do something about modifiable ones.

Non-modifiable risk factors:

Older age
Family history
Male

Modifiable risk factors:

Smoking
Alcohol consumption
Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s)
Low exercise / sedentary lifestyle
Obesity
Poor sleep
Stress

Question 7

Medical co-morbidities and atherosclerosis

Answer 7

Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk:

Diabetes
Hypertension
Chronic kidney disease
Inflammatory conditions such as rheumatoid arthritis
Atypical antipsychotic medications

TOM TIP: Think about risk factors when taking a history from someone with suspected atherosclerotic disease (such as someone presenting with intermittent claudication). Ask about their exercise, diet, past medical history, family history, occupation, smoking, alcohol intake and medications. This will help you perform well in exams and when presenting to seniors.

Question 8

End results of atherosclerosis

Answer 8

Angina
Myocardial infarction
Transient ischaemic attack
Stroke
Peripheral arterial disease
Chronic mesenteric ischaemia

Question 9

Intermittent claudication

Answer 9

Peripheral arterial disease presents with intermittent claudication. Patients describe a crampy pain that predictably occurs after walking a certain distance. After stopping and resting, the pain will disappear. The most common location is the calf muscles, but it can also affect the thighs and buttocks.

Question 10

Acute limb ischaemia

Answer 10

The features of acute limb ischaemia can be remembered with the “6 P’s” mnemonic:

Pain
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or “pins and needles”)
Perishing cold

Question 11

Leriche syndrome

Answer 11

Leriche syndrome occurs with occlusion in the distal aorta or proximal common iliac artery. There is a clinical triad of:

Thigh/buttock claudication
Absent femoral pulses
Male impotence

Question 12

Examining peripheral arterial disease

Answer 12

Look for risk factors:

Tar staining on the fingers
Xanthomata (yellow cholesterol deposits on the skin)

Looks for signs of cardiovascular disease:

Missing limbs or digits after previous amputations
Midline sternotomy scar (previous CABG)
A scar on the inner calf for saphenous vein harvesting (previous CABG)
Focal weakness suggestive of a previous stroke

The peripheral pulses may be weak on palpation:

Radial
Brachial
Carotid
Abdominal aorta
Femoral
Popliteal
Posterior tibial
Dorsalis pedis

You can use a hand-held Doppler to accurately assess the pulses when they are difficult to palpate.

Signs of arterial disease on inspection are:

Skin pallor
Cyanosis
Dependent rubor (a deep red colour when the limb is lower than the rest of the body)
Muscle wasting
Hair loss
Ulcers
Poor wound healing
Gangrene (breakdown of skin and a dark red/black change in colouration)

On examination, there may be:

Reduced skin temperature
Reduce sensation
Prolonged capillary refill time (more than 2 seconds)
Changes during Buerger’s test

Question 13

Buerger’s test

Answer 13

Buerger’s test is used to assess for peripheral arterial disease in the leg. There are two parts to the test.

The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.

The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:

Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration

The dark red colour is referred to as rubor.

Question 14

Arterial leg ulcers

Answer 14

Arterial ulcers are caused by ischaemia secondary to an inadequate blood supply. Typically, arterial ulcers:

Are smaller than venous ulcers
Are deeper than venous ulcers
Have well defined borders
Have a “punched-out” appearance
Occur peripherally (e.g., on the toes)
Have reduced bleeding
Are painful

Question 15

Venous leg ulcers

Answer 15

Venous ulcers are caused by impaired drainage and pooling of blood in the legs. Typically, venous ulcers:

Occur after a minor injury to the leg
Are larger than arterial ulcers
Are more superficial than arterial ulcers
Have irregular, gently sloping borders
Affect the gaiter area of the leg (from the mid-calf down to the ankle)
Are less painful than arterial ulcers
Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)

Question 16

Investigating peripheral arterial disease

Answer 16

Ankle-brachial pressure index (ABPI)
Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
Angiography (CT or MRI) – using contrast to highlight the arterial circulation

Question 17

Ankle-brachial pressure index

Answer 17

Ankle-brachial pressure index (ABPI) is the ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm. These readings are taken manually using a Doppler probe. For example, an ankle SBP of 80 and an arm SBP of 100 gives a ratio of 0.8 (80/100).

Results:

0.9 – 1.3 is normal
0.6 – 0.9 indicates mild peripheral arterial disease
0.3 – 0.6 indicates moderate to severe peripheral arterial disease
Less than 0.3 indicates severe disease to critical ischaemic

An ABPI above 1.3 can indicate calcification of the arteries, making them difficult to compress. This is more common in diabetic patients.

Question 18

Managing intermittent claudication

Answer 18

Lifestyle changes are required to manage modifiable risk factors (e.g., stop smoking). Optimise medical treatment of co-morbidities (such as hypertension and diabetes).

Exercise training, involving a structured and supervised program of regularly walking to the point of near-maximal claudication and pain, then resting and repeating.

Medical treatments:

Atorvastatin 80mg
Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)

Surgical options:

Endovascular angioplasty and stenting
Endarterectomy – cutting the vessel open and removing the atheromatous plaque
Bypass surgery – using a graft to bypass the blockage

Endovascular angioplasty and stenting involve inserting a catheter through the arterial system under x-ray guidance. At the site of the stenosis, a balloon is inflated to create space in the lumen. A stent is inserted to keep the artery open. Endovascular treatments have lower risks but might not be suitable for more extensive disease.

Question 19

Managing critical limb ischaemia

Answer 19

Patients with critical limb ischaemia require urgent referral to the vascular team. They require analgesia to manage the pain.

Urgent revascularisation can be achieved by:

Endovascular angioplasty and stenting
Endarterectomy
Bypass surgery
Amputation of the limb if it is not possible to restore the blood supply

Question 20

Managing acute limb ischaemia

Answer 20

Patients with acute limb ischaemia need an urgent referral to the on-call vascular team for assessment.

Management options include:

Endovascular thrombolysis – inserting a catheter through the arterial system to apply thrombolysis directly into the clot
Endovascular thrombectomy – inserting a catheter through the arterial system and removing the thrombus by aspiration or mechanical devices
Surgical thrombectomy – cutting open the vessel and removing the thrombus
Endarterectomy
Bypass surgery
Amputation of the limb if it is not possible to restore the blood supply

Question 21

Venous thromboembolism

Answer 21

Venous thromboembolism (VTE) is a common and potentially fatal condition. It involves blood clots (thrombi) developing in the circulation. This usually occurs secondary to stagnation of blood and hyper-coagulable states. When a thrombus develops in the venous circulation, it is called a deep vein thrombosis (DVT).

Once a thrombus has developed, it can travel (embolise) from the deep veins, through the right side of the heart and into the lungs, where it becomes lodged in the pulmonary arteries. This blocks blood flow to areas of the lungs and is called a pulmonary embolism (PE).

If the patient has a hole in their heart (for example, an atrial septal defect), the blood clot can pass through to the left side of the heart and into the systemic circulation. If it travels to the brain, it can cause a large stroke.

Question 22

Risk factors of VTE

Answer 22

There are several factors that can put patients at higher risk of developing a DVT or PE. In many of these situations (e.g., surgery), we give patients prophylactic treatment to prevent VTE.

Immobility
Recent surgery
Long haul travel
Pregnancy
Hormone therapy with oestrogen (combined oral contraceptive pill and hormone replacement therapy)
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia

TOM TIP: In your exams, when a patient presents with possible features of a DVT or PE, ask about risk factors such as periods of immobility, surgery and long haul flights to score extra points.

Question 23

Thrombophilias

Answer 23

Thrombophilias are conditions that predispose patients to develop blood clots. There are a large number of these:

Antiphospholipid syndrome
Factor V Leiden
Antithrombin deficiency
Protein C or S deficiency
Hyperhomocysteinaemia
Prothombin gene variant
Activated protein C resistance

TOM TIP: If you remember one cause of recurrent venous thromboembolism, remember antiphospholipid syndrome. The common association you may come across in exams is recurrent miscarriage. The diagnosis can be made with a blood test for antiphospholipid antibodies.

Question 24

VTE prophylaxis

Answer 24

Every patient admitted to hospital should be assessed for their risk of venous thromboembolism (VTE). If they are at increased risk of VTE, they should receive prophylaxis unless contraindicated. Prophylaxis is usually with low molecular weight heparin, such as enoxaparin. Contraindications include active bleeding or existing anticoagulation with warfarin or a DOAC.

Anti-embolic compression stockings are also used, unless contraindicated. The main contraindication for compression stockings is significant peripheral arterial disease.

Question 25

DVT presentation

Answer 25

DVTs are almost always unilateral. Bilateral DVT is rare and bilateral symptoms are more likely due to an alternative diagnosis such as chronic venous insufficiency or heart failure. DVTs can present with:

Calf or leg swelling
Dilated superficial veins
Tenderness to the calf (particularly over the site of the deep veins)
Oedema
Colour changes to the leg

To examine for leg swelling, measure the circumference of the calf 10cm below the tibial tuberosity. More than 3cm difference between calves is significant.

Always ask questions and examine with the suspicion of a potential pulmonary embolism as well.

Question 26

Wells score

Answer 26

The Wells score predicts the risk of a patient presenting with symptoms having a DVT or PE. It includes risk factors such as recent surgery and clinical findings such as unilateral calf swelling 3cm greater than the other leg.

Question 27

Diagnosing DVT

Answer 27

D-dimer is a sensitive (95%), but not specific, blood test for VTE. This makes it helpful in excluding VTE where there is a low suspicion. It is almost always raised if there is a DVT; however other conditions can also cause a raised d-dimer:

Pneumonia
Malignancy
Heart failure
Surgery
Pregnancy

Doppler ultrasound of the leg is required to diagnose deep vein thrombosis. NICE recommends repeating negative ultrasound scans after 6-8 days if a positive D-dimer and the Wells score suggest a DVT is likely.

Pulmonary embolism can be diagnosed with a CT pulmonary angiogram (CTPA) or ventilation-perfusion (VQ) scan. CTPA is usually preferred, unless the patient has significant kidney impairment or a contrast allergy.

Question 28

Initial management of DVT

Answer 28

The initial management for a suspected or confirmed DVT or PE is with anticoagulation. In most patients, NICE (2020) recommend treatment dose apixaban or rivaroxaban. It should be started immediately in patients where DVT or PE is suspected, and there is a delay in getting the scan.

The NICE guidelines (2020) recommend considering catheter-directed thrombolysis in patients with a symptomatic iliofemoral DVT and symptoms lasting less than 14 days. This involves inserting a catheter under x-ray guidance through the venous system to apply thrombolysis directly into the clot.

Question 29

Long term anticoagulation and VTE

Answer 29

The options for long term anticoagulation in VTE are a DOAC, warfarin, or LMWH.

DOACs are oral anticoagulants that do not require monitoring. They were called “novel oral anticoagulants” (NOACs), but this has been changed to “direct-acting oral anticoagulants” (DOACs). Options are apixaban, rivaroxaban, edoxaban and dabigatran. They are suitable for most patients, including patients with cancer.

Warfarin is a vitamin K antagonist. The target INR for warfarin is between 2 and 3 when treating DVTs and PEs. It is the first-line in patients with antiphospholipid syndrome (who also require initial concurrent treatment with LMWH).

Low molecular weight heparin (LMWH) is the first-line anticoagulant in pregnancy.

Continue anticoagulation for:

3 months if there is a reversible cause (then review)
Beyond 3 months if the cause is unclear, there is recurrent VTE, or there is an irreversible underlying cause such as thrombophilia (often 6 months in practice)
3-6 months in active cancer (then review)

Question 30

Inferior vena cava filter

Answer 30

Inferior vena cava filters are devices inserted into the inferior vena cava, designed to filter the blood and catch any blood clots travelling from the venous system, towards the heart and lungs. They act as a sieve, allowing blood to flow through whilst stopping larger blood clots. They are used in unusual cases of patients with recurrent PEs or those that are unsuitable for anticoagulation.

Question 31

Investigating unprovoked DVT

Answer 31

When patients have their first VTE without a clear cause, the NICE guidelines from 2020 recommend reviewing the medical history, baseline blood results and physical examination for evidence of cancer. The previous 2012 guidelines recommended routinely considering investigations such as a chest x-ray and CT abdomen-pelvis, although this is no longer recommended.

In patients with an unprovoked DVT or PE that are not going to continue anticoagulation (they have finished 3-6 months of treatment and are due to stop), NICE recommends considering testing for:

Antiphospholipid syndrome (check antiphospholipid antibodies)
Hereditary thrombophilias (only if they have a first-degree relative also affected by a DVT or PE)

Question 32

Varicose veins

Answer 32

Varicose veins are distended superficial veins measuring more than 3mm in diameter, usually affecting the legs.

Reticular veins are dilated blood vessels in the skin measuring less than 1-3mm in diameter.

Telangiectasia refers to dilated blood vessels in the skin measuring less than 1mm in diameter. They are also known as spider veins or thread veins.

Question 33

Developing varicose veins

Answer 33

Veins contain valves that only allow blood to flow in one direction, towards the heart. In the legs, as the muscles contract, they squeeze blood upwards against gravity. The valves prevent gravity from pulling the blood back into the feet. When the valves become incompetent, the blood is drawn downwards by gravity and pools in the veins and feet.

The deep and superficial veins are connected by vessels called the perforating veins (or perforators), which allow blood to flow from the superficial veins to the deep veins. When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them. This leads to dilatation and engorgement of the superficial veins, forming varicose veins.

Question 34

Chronic venous insufficiency

Answer 34

When blood pools in the distal veins, the pressure causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs. This gives a brown discolouration to the lower legs.

Pooling of blood in the distal tissues results in inflammation. The skin becomes dry and inflamed, referred to as venous eczema.

The skin and soft tissues become fibrotic and tight, causing the lower legs to become narrow and hard, referred to as lipodermatosclerosis.

Question 35

Risk factors for varicose veins

Answer 35

Increasing age
Family history
Female
Pregnancy
Obesity
Prolonged standing (e.g., occupations involving standing for long periods)
Deep vein thrombosis (causing damage to the valves)

Question 36

Presentation of varicose veins

Answer 36

Varicose veins present with engorged and dilated superficial leg veins. They may be asymptomatic or have symptoms of:

Heavy or dragging sensation in the legs
Aching
Itching
Burning
Oedema
Muscle cramps
Restless legs

Patients may also have signs and symptoms of chronic venous insufficiency (e.g., skin changes and ulcers).

Question 37

Special tests for varicose veins

Answer 37

Tap test – apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests incompetent valves between the varicose vein and the SFJ.

Cough test – apply pressure to the SFJ and ask the patient to cough, feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ (called saphenous varix).

Trendelenburg’s test – with the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.

Perthes test – apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis.

Duplex ultrasound can be used to assess the extent of varicose veins. It is an ultrasound that shows the speed and volume of blood flow.

Question 38

Managing varicose veins

Answer 38

Varicose veins in pregnancy often improve after delivery.

Simple treatment measures include:

Weight loss if appropriate
Staying physically active
Keeping the leg elevated when possible to help drainage
Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)

Surgical options:

Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation
Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein
Stripping – the veins are ligated and pulled out of the leg

Question 39

Complications of varicose veins

Answer 39

Prolonged and heavy bleeding after trauma
Superficial thrombophlebitis (thrombosis and inflammation in the superficial veins)
Deep vein thrombosis
All the issues of chronic venous insufficiency (e.g., skin changes and ulcers)

Question 40

Chronic venous insufficiency

Answer 40

Chronic venous insufficiency occurs when blood does not efficiently drain from the legs back to the heart. Usually, this is the result of damage to the valves inside the veins. This damage may occur with age, immobility, obesity, prolonged standing or after a deep vein thrombosis. It is often associated with varicose veins.

The valves are responsible for ensuring blood flows in one direction as the leg muscles contract and squeeze the veins. When the valves are damaged, the pumping effect of the leg muscles becomes less effective in draining blood towards the heart. Blood pools in the veins of the legs, causing venous hypertension.

Chronic pooling of blood in the legs leads to skin changes. The area between the top of the foot and the bottom of the calf muscle is the area most affected by these changes. This is known as the gaiter area.

Haemosiderin staining is a red/brown discolouration caused by haemoglobin leaking into the skin.

Venous eczema (or varicose eczema) is dry, itchy, flaky, scaly, red, cracked skin. These eczema-like changes are caused by a chronic inflammatory response in the skin.

Lipodermatosclerosis is hardening and tightening of the skin and tissue beneath the skin. Chronic inflammation causes the subcutaneous tissue to become fibrotic (turning to scar tissue). Inflammation of the subcutaneous fat is called panniculitis. The narrowing of the lower legs causes the typical “inverted champagne bottle” appearance.

Atrophie blanche refers to patches of smooth, porcelain-white scar tissue on the skin, often surrounded by hyperpigmentation.

As well as the skin changes above, chronic venous insufficiency can lead to:

Cellulitis
Poor healing after injury
Skin ulcers
Pain

TOM TIP: Chronic venous changes are very common in older patients. It is very easy to find patients with these skin changes to use in OSCE examinations, so it is worth getting familiar with their appearance and confidently presenting your examination findings. These changes are often misdiagnosed as cellulitis, and patients are given a course of antibiotics. The broken skin does leave patients prone to skin infections, so this does need to be considered, although keep in mind that “bilateral cellulitis” is quite unusual, and chronic skin changes related to venous insufficiency will not resolve with antibiotics.

Question 41

Managing chronic venous insufficiency

Answer 41

Management involves:

Keeping the skin healthy
Improving venous drainage to the legs
Managing complications

The skin is kept healthy by:

Monitoring skin health and avoiding skin damage
Regular use of emollients (e.g., diprobase, oilatum, cetraben and doublebase)
Topical steroids to treat flares of venous eczema
Very potent topical steroids to treat flares of lipodermatosclerosis

Improving venous drainage to the legs involves:

Weight loss if obese
Keeping active
Keeping the legs elevated when resting
Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)

Management of complications involves:

Antibiotics for infection
Analgesia for pain
Wound care for ulceration

Question 42

Leg ulcers

Answer 42

Leg ulcers are wounds or breaks in the skin that do not heal or heal slowly due to underlying pathology. They have the potential to get progressively larger and become more difficult to heal over time. There are four common types of skin ulcers:

Venous ulcers
Arterial ulcers
Diabetic foot ulcers
Pressure ulcers

This section mainly covers arterial and venous ulcers.

Arterial ulcers result from insufficient blood supply to the skin due to peripheral arterial disease.

Venous ulcers occur due to the pooling of blood and waste products in the skin secondary to venous insufficiency.

Mixed ulcers are a combination of arterial and venous disease causing the ulcer.

Question 43

Diabetic foot ulcers

Answer 43

Diabetic foot ulcers are more common in patients with diabetic neuropathy. Patients who have lost the sensation in their feet are less likely to realise they have injured their feet or have poorly fitting shoes. Additionally, damage to both the small and large blood vessels impairs the blood supply and wound healing. Raised blood sugar, immune system changes and autonomic neuropathy also contribute to ulceration and poor healing. Osteomyelitis (infection in the bone) is an important complication.

Question 45

Arterial ulcers

Answer 45

Occur distally, affecting the toes or dorsum of the foot
Are associated with peripheral arterial disease, with absent pulses, pallor and intermittent claudication
Are smaller than venous ulcers
Are deeper than venous ulcers
Have well defined borders
Have a “punched-out” appearance
Are pale colour due to poor blood supply
Are less likely to bleed
Are painful
Have pain worse at night (when lying horizontally)
Have pain is worse on elevating and improved by lowering the leg (gravity helps the circulation)

Question 46

Venous ulcers

Answer 46

Occur in the gaiter area (between the top of the foot and bottom of the calf muscle)
Are associated with chronic venous changes, such as hyperpigmentation, venous eczema and lipodermatosclerosis
Occur after a minor injury to the leg
Are larger than arterial ulcers
Are more superficial than arterial ulcers
Have irregular, gently sloping border
Are more likely to bleed
Are less painful than arterial ulcers
Have pain relieved by elevation and worse on lowering the leg

Question 47

Investigating leg ulcers

Answer 47

Ankle-brachial pressure index (ABPI) is used to assess for arterial disease. This is required in both arterial and venous ulcers.

Blood tests may help assess for infection (FBC and CRP) and co-morbidities (HbA1c for diabetes, FBC for anaemia and albumin for malnutrition).

Charcoal swabs may be helpful where infection is suspected, to determine the causative organism.

Skin biopsy may be required in patients where skin cancer (e.g., squamous cell carcinoma) is suspected as a differential diagnosis. This will require a two week wait referral to dermatology.

Question 48

Managing arterial ulcers

Answer 48

The management of arterial ulcers is the same as peripheral arterial disease, with an urgent referral to vascular to consider surgical revascularisation. If the underlying arterial disease is effectively treated, the ulcer should heal rapidly. Debridement and compression are not used in arterial ulcers.

Question 49

Managing venous ulcers

Answer 49

The management here is based on the NICE CKS (last updated January 2021). Patients may require referral to:

Vascular surgery where mixed or arterial ulcers are suspected
Tissue viability / specialist leg ulcer clinics in complex or non-healing ulcers
Dermatology where an alternative diagnosis is suspected, such as skin cancer
Pain clinics if the pain is difficult to manage
Diabetic ulcer services (for patients with diabetic ulcers)

Patients require input from experienced nurses, such as the district nurses or tissue viability nurses. Good wound care involves:

Cleaning the wound
Debridement (removing dead tissue)
Dressing the wound

Compression therapy is used to treat venous ulcers (after arterial disease is excluded with an ABPI).

Pentoxifylline (taken orally) can improve healing in venous ulcers (but is not licensed).

Antibiotics are used to treat infection.

Analgesia is used to manage pain (avoid NSAIDs as they can worsen the condition).

Question 50

Lymphoedema

Answer 50

Lymphoedema is a chronic condition caused by impaired lymphatic drainage of an area.

The lymphatic system is responsible for draining excess fluid from the tissues. The tissues in areas affected by an impaired lymphatic system become swollen with excess, protein-rich fluid (lymphoedema).

The lymphatic system also plays an important role in the immune system. Areas of lymphoedema are prone to infection.

Primary lymphoedema is a rare, genetic condition, which usually presents before aged 30. It is a result of faulty development of the lymphatic system.

Secondary lymphoedema is due to a separate condition that affects the lymphatic system. The most common example is when patients develop lymphoedema after breast cancer surgery, due to the removal of axillary lymph nodes in the armpit.

Lipoedema is an important differential diagnosis, where there is an abnormal build-up of fat tissue in the limbs, often the legs. The feet are spared in lipoedema, unlike lymphoedema. This affects women more often than men. It can cause pain, psychological distress and significantly affect the patient’s quality of life.

Question 51

Assessing lymphoedema

Answer 51

Stemmer’s sign can be used to assess for lymphoedema. The skin at the bottom of the second toe or middle finger is gently pinched together using two fingers. If it is possible to lift and “tent” the skin, Stemmer’s sign is negative. If it is not possible to pinch the skin together, lift and “tent” it, Stemmer’s sign is positive, suggesting lymphoedema.

Limb volume can be calculated using:

Circumferential measurements at various points along the limb
Water displacement (putting the limb into water and measuring the volume of water displaced)
Perometry (a square frame with perpendicular light beams is moved along the limb, measuring the outline and volume)

Bioelectric impedance spectrometry can be used to measure the volume of fluid collected in the limb. Electrodes are placed on the limb, and an electrical current is passed through the limb, between the electrodes. The resistance to electrical flow through the tissues estimates the volume of lymph fluid in the tissues.

Lymphoscintigraphy is a type of nuclear medicine scan. A radioactive tracer is injected into the skin, and gamma cameras (scintigraphy) are used to assess the structure of the lymphatic system.

Question 52

Managing lymphoedema

Answer 52

A specialist lymphoedema service manages patients with lymphoedema.

Non-surgical treatment options include:

Massage techniques to manually drain the lymphatic system (manual lymphatic drainage)
Compression bandages
Specific lymphoedema exercises to improve lymph drainage
Weight loss if overweight
Good skin care

Lymphaticovenular anastomosis is a surgical procedure that involves attaching lymphatic vessels to nearby veins, allowing the lymphatic vessel to drain directly into the venous system. This and other surgical procedures are occasionally used where other treatments fail.

Antibiotics are required if cellulitis (infection in the skin) develops.

Cognitive behavioural therapy and antidepressants can be used to manage any psychological impact of having lymphoedema.

TOM TIP: Avoid taking blood, inserting a cannula, giving injections or performing a blood pressure reading in a limb with lymphoedema.

Question 53

Lymphatic Filariasis

Answer 53

Lymphatic filariasis is an infectious disease caused by parasitic worms spread by mosquitos. The worms live in the lymphatic system where they can cause damage, leading to severe lymphoedema. This severe lymphoedema is associated with thickening and fibrosis of the skin and tissues, and is referred to as elephantiasis. It is most common in the tropics of Africa and Asia.

Question 54

Abdominal aortic aneurysm

Answer 54

Abdominal aortic aneurysm (AAA) refers to dilation of the abdominal aorta, with a diameter of more than 3cm. Often the first time patients become aware of an aneurysm is when it ruptures, causing life-threatening bleeding into the abdominal cavity. The mortality of a ruptured AAA is around 80%.

Question 55

Risk factors of abdominal aortic aneurysm

Answer 55

Men are affected significantly more often and at a younger age than women
Increased age
Smoking
Hypertension
Family history
Existing cardiovascular disease

Question 56

Screening for AAA

Answer 56

All men in England are offered a screening ultrasound scan at age 65 to detect asymptomatic AAA. Early detection of an AAA means preventative measures can stop it from expanding further or rupturing.

Women are not routinely offered screening, as they are at much lower risk. The NICE guidelines (2020) say a routine ultrasound can be considered in women aged over 70 with risk factors such as existing cardiovascular disease, COPD, family history, hypertension, hyperlipidaemia or smoking.

Patients with an aorta diameter above 3cm are referred to a vascular team (urgently if more than 5.5cm).

Question 57

Presentation of AAA

Answer 57

Most patients with an AAA are asymptomatic. It may be discovered on routine screening or when it ruptures.

Other ways it can present include:

Non-specific abdominal pain
Pulsatile and expansile mass in the abdomen when palpated with both hands
As an incidental finding on an abdominal x-ray, ultrasound or CT scan

Question 58

Diagnosing AAA

Answer 58

Ultrasound is the usual initial investigation for establishing the diagnosis.

CT angiogram gives a more detailed picture of the aneurysm and helps guide elective surgery to repair the aneurysm.

Question 59

Classifying AAA

Answer 59

The severity of the aortic aneurysm depends on the size:

Normal: less than 3cm
Small aneurysm: 3 – 4.4cm
Medium aneurysm: 4.5 – 5.4cm
Large aneurysm: above 5.5cm

Question 60

Managing AAA

Answer 60

The risk of progression of an AAA can be reduced by treating reversible risk factors:

Stop smoking
Healthy diet and exercise
Optimising the management of hypertension, diabetes and hyperlipidaemia

The Public Health England (updated 2017) screening and surveillance programme recommends follow up scans:

Yearly for patients with aneurysms 3-4.4cm
3 monthly for patients with aneurysms 4.5-5.4cm

The NICE guidelines (2020) recommend elective repair for patients with any of:

Symptomatic aneurysm
Diameter growing more than 1cm per year
Diameter above 5.5cm

Elective surgical repair involves inserting an artificial “graft” into the section of the aorta affected by the aneurysm. There are two methods for inserting the graft:

Open repair via a laparotomy
Endovascular aneurysm repair (EVAR) using a stent inserted via the femoral arteries

Gov.uk (April 2021) advise that patients must:

Inform the DVLA if they have an aneurysm above 6cm
Stop driving if it is above 6.5cm
Stricter rules apply to drivers of heavy vehicles (e.g., bus or lorry drivers)

Question 61

Ruptured AAA

Answer 61

The risk of rupture increases with the diameter of the aneurysm (roughly 5% for 5cm and 40% for 8 cm aneurysm). Ruptured AAA has an extremely high mortality (around 80%).

A ruptured aortic aneurysm presents with:

Severe abdominal pain that may radiate to the back or groin
Haemodynamic instability (hypotension and tachycardia)
Pulsatile and expansile mass in the abdomen
Collapse
Loss of consciousness

An abdominal aortic aneurysm is a surgical emergency requiring immediate involvement of experienced seniors, vascular surgeons, anaesthetists and theatre teams.

Permissive hypotension refers to the strategy of aiming for a lower than normal blood pressure when performing fluid resuscitation. The theory is that increasing the blood pressure may increase blood loss.

Haemodynamically unstable patients with a suspected AAA should be transferred directly to theatre. Surgical repair should not be delayed by getting imaging to confirm the diagnosis.

CT angiogram can be used to diagnose or exclude ruptured AAA in haemodynamically stable patients.

In patients with co-morbidities that make the prognosis with surgery very poor, a discussion needs to be had with senior doctors, the patient and their family about palliative care.

Question 62

Aortic dissection

Answer 62

Aortic dissection refers to when a break or tear forms in the inner layer of the aorta, allowing blood to flow between the layers of the wall of the aorta. There are three layers to the aorta, the intima, media and adventitia. With aortic dissection, blood enters between the intima and media layers of the aorta. A false lumen full of blood is formed within the wall of the aorta. Intramural refers to within the walls of the blood vessel.

Question 63

Classifying aortic dissection

Answer 63

Aortic dissection most commonly affects the ascending aorta and aortic arch but can affect any part of the aorta. The right lateral area of the ascending aorta is the most common site of a tear of the intima layer, as this is under the most stress from blood exiting the heart. There are two classification systems.

The Stanford system:

Type A – affects the ascending aorta, before the brachiocephalic artery
Type B – affects the descending aorta, after the left subclavian artery

The DeBakey system:

Type I – begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta
Type II – isolated to the ascending aorta
Type IIIa – begins in the descending aorta and involves only the section above the diaphragm
Type IIIb – begins in the descending aorta and involves the aorta below the diaphragm

Question 64

Risk factors for aortic dissection

Answer 64

Aortic dissection shares the same risk factors as peripheral arterial disease, such as age, male sex, smoking, hypertension, poor diet, reduced physical activity and raised cholesterol.

Hypertension is a big risk factor. Dissection can be triggered by events that temporarily cause a dramatic increase in blood pressure, such as heavy weightlifting or the use of cocaine.

Conditions or procedures that affect the aorta increase the risk of a dissection, such as:

Bicuspid aortic valve
Coarctation of the aorta
Aortic valve replacement
Coronary artery bypass graft (CABG)

Conditions that affect the connective tissues can also increase the risk of a dissection, notably:

Ehlers-Danlos Syndrome
Marfan’s Syndrome

TOM TIP: For your exams, a man aged around 60 with a background of hypertension, presenting with a sudden onset tearing chest pain, has aortic dissection. Marfan’s and Ehlers-Danlos syndrome are worth remembering as risk factors, as these may be options on an MCQ exam.

Question 65

Presentation of aortic dissection

Answer 65

Aortic dissection can be difficult to spot. The diagnosis is often missed.

The typical presentation is a sudden onset, severe, “ripping” or “tearing” chest pain. The pain may be in the anterior chest when the ascending aorta is affected, or the back if the descending aorta is affected. The pain may change location (migrate) over time. Some patients with aortic dissection do not have chest pain.

Other features that may suggest aortic dissection are:

Hypertension
Differences in blood pressure between the arms (more than a 20mmHg difference is significant)
Radial pulse deficit (the radial pulse in one arm is decreased or absent and does not match the apex beat)
Diastolic murmur
Focal neurological deficit (e.g., limb weakness or paraesthesia)
Chest and abdominal pain
Collapse (syncope)
Hypotension as the dissection progresses

Question 66

Diagnosing aortic dissection

Answer 66

An ECG and chest x-ray are often used to exclude other causes (such as myocardial infarction), although they may be normal and falsely reassuring. Myocardial infarction can occur in combination with aortic dissection, and treatment of the myocardial infarction (e.g., thrombolysis) can cause fatal progression of the aortic dissection.

CT angiogram is usually the initial investigation to confirm the diagnosis and can generally be performed very quickly.

MRI angiogram provides greater detail and can help plan management but often takes longer to get.

Question 67

Managing aortic dissection

Answer 67

Aortic dissection is a surgical emergency and needs immediate involvement of experienced seniors, vascular surgeons, anaesthetists and intensive care teams. There is a very high mortality.

Analgesia (e.g., morphine) is required to manage the pain.

Blood pressure and heart rate need to be well controlled to reduce the stress on the aortic walls. This usually involves beta-blockers.

Surgical intervention from the vascular team will depend on the type of aortic dissection.

Type A may be treated with open surgery (midline sternotomy) to remove the section of the aorta with the defect in the wall and replace it with a synthetic graft. The aortic valve may need to be replaced during the procedure.

Type B may be treated with thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the descending aorta. Complicated cases may require open surgery.

Question 68

Complications of aortic dissection

Answer 68

Myocardial infarction
Stroke
Paraplegia (motor or sensory impairment in the legs)
Cardiac tamponade
Aortic valve regurgitation
Death

Question 69

Carotid artery stenosis

Answer 69

Carotid artery stenosis refers to narrowing of the carotid arteries in the neck, usually secondary to atherosclerosis. Plaques build up in the carotid arteries, reducing the diameter of the lumen. There is a risk of parts of the plaque breaking away and becoming an embolus, travelling to the brain and causing an embolic stroke.

The risk factors for developing carotid artery stenosis are the same as for atherosclerosis and arterial disease in other areas, such as age, male sex, smoking, hypertension, poor diet, reduced physical activity and raised cholesterol.

Patients with a transient ischaemic attack (TIA) or stroke are investigated for carotid artery stenosis, usually with a carotid ultrasound.

Patients with carotid artery stenosis are very likely to have arterial disease and atherosclerosis elsewhere. They are at high risk of coronary artery disease and myocardial infarction (heart attacks).

Question 70

Classifying carotid artery stenosis

Answer 70

The severity of carotid artery stenosis is categorised as:

Mild – less than 50% reduction in diameter
Moderate – 50 to 69% reduction in diameter
Severe – 70% or more reduction in diameter

Question 71

Presentation of carotid artery stenosis

Answer 71

Carotid artery stenosis is usually asymptomatic. Usually, it is diagnosed after a TIA or stroke.

A carotid bruit may be heard on examination. This is a whooshing sound heard with a stethoscope over the affected carotid artery, caused by turbulent flow around the stenotic area during systole (contraction of the heart).

Question 72

Diagnosing carotid artery stenosis

Answer 72

Carotid ultrasound is usually the initial investigation to diagnose and assess carotid artery stenosis.

CT or MRI angiogram may be used to assess the stenosis in more detail before surgical interventions.

Question 73

Managing carotid artery stenosis

Answer 73

Conservative management involves addressing modifiable risk factors and medical therapy:

Healthy diet and exercise
Stop smoking
Management of co-morbidities (e.g., hypertension and diabetes)
Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
Lipid-lowering medications (e.g., atorvastatin)

Surgical interventions are considered where there is significant stenosis. The options are:

Carotid endarterectomy
Angioplasty and stenting

Endarterectomy involves an incision in the neck, opening the carotid artery and scraping out the plaque. This is the first-line treatment for most patients requiring surgical intervention. A key complication of the procedure is stroke (around 2%).

During endarterectomy, nearby nerves can be injured. This may be temporary or permanent. Symptoms depend on the nerve:

Facial nerve injury causes facial weakness (often the marginal mandibular branch causing drooping of the lower lip)
Glossopharyngeal nerve injury causes swallowing difficulties
Recurrent laryngeal nerve (a branch of the vagus nerve) injury causes a hoarse voice
Hypoglossal nerve injury causes unilateral tongue paralysis

Angioplasty and stenting is an alternative to endarterectomy. This is an endovascular procedure. A catheter is inserted into the femoral artery in the groin, passed through the aorta under x-ray guidance, up to the affected carotid artery. A balloon is inflated in the narrowed area to widen the lumen (angioplasty), and a stent is left in place to keep it open (stenting).

Question 74

Buerger disease

Answer 74

Buerger disease is also known as thromboangiitis obliterans. It is an inflammatory condition that causes thrombus formation in the small and medium-sized blood vessels in the distal arterial system (affecting the hands and feet).

Buerger disease typically affects men aged 25 – 35 and has a very strong association with smoking.

Notable features (included in the diagnostic criteria) are:

Younger than 50 years
Not having risk factors for atherosclerosis, other than smoking

Question 75

Presentation of Buerger disease

Answer 75

The typical presenting feature is painful, blue discolouration to the fingertips or tips of the toes. The pain is often worse at night. This may progress to ulcers, gangrene and amputation.

Corkscrew collaterals are a typical finding on angiograms, where new collateral vessels form to bypass the affected arteries.

Question 76

Managing Buerger disease

Answer 76

Completely stopping smoking is the main component of treatment. This usually results in a significant improvement. Cutting down or using nicotine replacement products does not seem to be adequate to improve the condition.

Other specialist treatments may be considered, including intravenous iloprost (a prostacyclin analogue that dilates blood vessels).

TOM TIP: The key presentation to remember for your exams is a young male smoker with painful blue fingertips. The exam question may ask the diagnosis (Buerger disease or thromboangiitis obliterans) or ask the most important aspect of management (completely stopping smoking).