Vascular Flashcards

1
Q

Peripheral arterial disease

A

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.

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2
Q

What are the stages of peripheral vascular disease?

A

Intermittent claudication

Acute limb ischaemia

Critical limb ischaemia

Necrosis and gangrene

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3
Q

Intermittent claudication

A

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.

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4
Q

Critical limb ischaemia

A

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. The features are pain at rest, non-healing ulcers and gangrene. There is a significant risk of losing the limb.

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5
Q

Acute limb ischaemia

A

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.

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6
Q

What is meant by gangrene compared to necrosis?

A

Necrosis refers to the death of tissue.

Gangrene refers to the death of the tissue, specifically due to an inadequate blood supply.

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7
Q

What are the features of critical limb ischemia?

A

The 6 P’s

  • Pain
  • Pallor
  • Pulseless
  • Paralysis
  • Paraesthesia (abnormal sensation or “pins and needles”)
  • Perishing cold
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8
Q

Signs on examination of PAD:

A

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
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9
Q

Description of arterial ulcers

A

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

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10
Q

Venous ulcers

A

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)

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11
Q

Investigations of PAD

A

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

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12
Q

Management of PAD:

A

Lifestyle and exercise training to push through claudication.

Medication: Atorvastatin, clopidogrel

Surgery:

  • Endovascular angioplasty and stenting
  • Endarterectomy – cutting the vessel open and removing the atheromatous plaque
  • Bypass surgery – using a graft to bypass the blockage
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13
Q

Management of critical limb ischemia

A

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

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14
Q

Management options for acute limb ischemia:

A
  • 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
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15
Q

Common DVT risk factors:

A
  • 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
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16
Q

Top tip:

A

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.

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17
Q

Thrombophilias are what?

  • examples of thrombophilias
A

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
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18
Q

TOP TIP:

What condition can cause recurrent thromboembolism and lead to recurrent miscarriage?

  • How do you test to this condition?
A

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.

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19
Q

VTE prophylaxis - read summary

A

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.

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20
Q

How do you examine for calf swelling?

A

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

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21
Q

What is Wells score?

A

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.

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22
Q

How is DVT diagnosed and what other investigations should be done?

A

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.

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23
Q

Management of DVT/PE

A

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.

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24
Q

Long term anticoagulation for VTE:

A

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.

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25
Q

How long should a patient stay on anti-coagulation for following VTE?

A
  • 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)
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26
Q

When are Inferior vena cava filters indicated?

A

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.

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27
Q

What sould be investigated in patients with an unprovoked DVT?

A

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.

28
Q

Read varicose vein definitions and categorisation:

A

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.

29
Q

Why haemosiderin deposits, venous eczema and lipodermatosclerosis occur - skim!!

A

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.

30
Q

Management of varicose veins

A
  • 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
31
Q

Complications of varicose veins:

A

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)

32
Q

What is the cause of chronic venous insufficiency?

A

Valvular incompetence

33
Q

How does chronic venous insufficiency present?

A
  • 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
34
Q

How is chronic venous insufficiency managed?

A

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)
35
Q

How are the complications of chronic venous insufficiency managed?

A
  • Antibiotics for infection
  • Analgesia for pain
  • Wound care for ulceration
36
Q

What are leg ulcers?

A

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.

37
Q

What are the four common types of leg ulcer?

A

Venous ulcers

Arterial ulcers

Diabetic foot ulcers

Pressure ulcers

38
Q

Summary of diabetic foot ulcers:

  • what is the most important complication?
A

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.

39
Q

Pressure ulcers: - read out loud

A

Pressure ulcers typically occur in patients with reduced mobility, where prolonged pressure on particular areas (e.g., the sacrum whilst sitting) lead to the skin breaking down. This happens due to a combination of reduced blood supply and localised ischaemia, reduced lymph drainage and an abnormal change in shape (deformation) of the tissues under pressure. Extensive effort should be taken to prevent pressure ulcers, including individual risk assessments, regular repositioning, special inflating mattresses, regular skin checks and protective dressings and creams. The Waterlow Score is a commonly used risk assessment tool for estimating an individual patient’s risk of developing a pressure ulcer.

40
Q

An ulcer where pain is relieved by elevation and worse on lowering the leg is likely what type?

A

Venous ulcer

41
Q

What investigations are carried out in cases of ulceration?

A
  • 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.
42
Q

What is the managment of arterial ulcers?

  • must know!
A

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.

43
Q

What is the management of venous ulcers?

A
  • Vascular surgery where mixed or arterial ulcers are suspected
  • 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).
44
Q

Abdominal aortic aneurysm dilation greater than what…?

A

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%.

45
Q

What is the screening programme in the UK for AAA?

A

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.

46
Q

How do AAA present?

A

When they rupture.

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

47
Q

How is AAA severity categorised?

A
  • Normal: less than 3cm
  • Small aneurysm: 3 – 4.4cm
  • Medium aneurysm: 4.5 – 5.4cm
  • Large aneurysm: above 5.5cm
48
Q

The NICE guidelines (2020) recommend elective repair for patients with any of what criteria?

A

Symptomatic aneurysm

Diameter growing more than 1cm per year

Diameter above 5.5cm

49
Q

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

A

Open repair via a laparotomy

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

50
Q

How do ruptured triple A’s present?

A

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

51
Q

Management of a ruptured triple A:

A

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.

52
Q

Aortic dissection:

A

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.

53
Q

Aortic dissection most commonly affects what region of the aorta?

A

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.

54
Q

Risk factors of aortic dissection:

A

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

55
Q

Buerger disease

A

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.

56
Q

How does Buerger disease present?

A

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.

The key presentation to remember for your exams is a young male smoker with painful blue fingertips.

57
Q

How is Buerger disease managed?

A

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.

58
Q

Midline sternotomy scar indicates what previous procedure?

A

Coronary artery bypass graft

Aortic valve replacement

Mitral valve replacement

59
Q

Describe the murmur aortic stenosis causes.

A

Aortic stenosis causes an ejection-systolic, high-pitched murmur (high velocity of systole). This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole.

60
Q

What are the most common organisms that cause infective endocarditis?

A

Staphylococcus

Streptococcus

Enterococcus

61
Q

Skim classic history of a pneumothorax patient:

A

Pneumothorax occurs when air gets into the pleural space, separating the lung from the chest wall. It can occur spontaneously, or secondary to trauma, medical interventions (“iatrogenic”) or lung pathology. The typical patient in exams is a tall, thin young man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports.

62
Q

Management of a tension pneumothorax:

A

“Insert a large bore cannula into the second intercostal space in the midclavicular line.”

63
Q

Managment of a 3cm pneumothorax:

A

Aspiration followed by reassessment

When aspiration fails twice, a chest drain is required

64
Q

Where should a chest drain be inserted?

A
  • The 5th intercostal space (or the inferior nipple line)
  • The midaxillary line (or the lateral edge of the latissimus dorsi)
  • The anterior axillary line (or the lateral edge of the pectoralis major)

The needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. Once the chest drain is inserted, obtain a chest x-ray to check the positioning.

65
Q

Treatment of ulcers:

A

Treatment is to reverse the aetiology:

  • Arterial- identify lesion and treat it.
  • Neuropathic- offload the ulcer.
  • Venous leg ulcer- compression ( exclude arterial) treat venous lesion.
66
Q

What does a positive carotid sinus massage used to assess syncope show?

A

Carotid sinus hypersensitivity may be cardioinhibitory (ventricular pause of >3 seconds) or vasodepressive (a fall in the SBP by >50mmHg)

67
Q

How are pressure ulcers managed?

A

In the management of pressure ulcers, all patients require wound dressings, appropriate analgesia, and a nutritional assessment.

Antibiotics only indicated if there are signs of infection?