2 - Vascular Medicine & Surgery

CLINICAL PHASE

VASCULAR MEDICINE & SURGERY

DARWIN’S NOTEBOOK

TABLE OF CONTENTS

HYPERTENSION 1

HYPERLIPIDAEMIA 5

ATHEROMATOUS VASCULAR DISEASE 7

ANEURYSMS 8

CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE 12

ACUTE ARTERIAL OCCLUSIVE DISEASE 18

VASOSPASTIC DISORDERS 21

VENOUS DISEASE 24

VENOUS THROMBO-EMBOLIC DISEASE 27

LYMPHATIC DISEASE 31

VASCULAR MEDICINE & SURGERY – HYPERTENSION

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Outline the graded risk associated with increasing systemic blood pressure • Hypertension is a major risk factor for stroke, MI, heart failure, chronic kidney disease, cognitive decline

and premature death

• Each 2mmHg rise in systolic BP is associated with a 7% increase in risk of mortality from IHD and a

10% increase in risk of mortality from stroke

Outline the classification of blood pressure currently defined by the British Hypertension Society as optimal, normal, high normal or hypertension based on at least three measurements

• If the lowest blood pressure in the clinic is above 140/90mmHg ® offer ambulatory blood pressure

monitoring (ABPM) to confirm diagnosis:

1. ABPM ® two measurements per hour taken, average reading of at least 14values is used

2. Home blood pressure monitoring may be used if ABPM. Is not tolerated ® taking two

consecutive readings with own device, at least one minute apart, with the person seated ®

this needs to be done at least twice a day, ideally in the morning and evening, and thus must

continue for at least 4 days (ideally 7) ® discard measurements from the first day and average

the rest

• Stage 1 HTN ® clinic BP >140/90mmHg, and ABPM / HBPM >135/85mmHg

1. SBP is increased by 10mmHg for patients over 80

• Stage 2 HTN ® clinic BP > 160/100mmHg, and ABPM / HBPM >150/95mmHg

• Severe HTN ® clinic SBP >180mmHg or DBP >110mmHg

• If the hypertension is severe ® start antihypertensive medication straight away, without waiting for

ABPM / HBPM results

• At least three measurements are required to confirm hypertension

• Automated machines cannot be used to take BP measurements from patients with irregular pulses

• When considering diagnosis, take readings from both arms to see if they are within 20mmHg of each

other ® record values from arm with higher values

• If a patient has a clinic reading of 140/90mmHg ® take a second reading, and if this is substantially

different from the first, take another ® BP should be recorded as the lower of the last two readings

Describe the clinical and pathological features of ‘accelerated phase’ or ‘malignant’ hypertension

• Benign hypertension ® a gradual elevation of blood pressure over years, which leads to gradual

hypertrophy of the muscular media in artery walls, reducing their capacity to expand and increasing their

fragility

• Accelerated phase / malignant hypertension ® blood pressure higher than 180/20mmHg with signs of

papilloedema and/or retinal haemorrhage (or associated with grade III retinopathy and encephalopathy

• This occurs rapidly ® months to 1 or 2 years

• It more commonly affects people in their 3rd and 4th decades of life

• Such rapid increase in blood pressure, and strain upon vessels, causes fibrinoid necrosis of the vessel

wall in arterioles ® especially in the kidneys and abdominal viscera

• Due to major organ involvement, this causes LVH, acute heart failure, encephalopathy, severe renal

damage, and papilloedema may or may not be present


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• It is diagnosed if there is SBP >200mmHg or DBP >120mmHg and bilateral retinal haemorrhages /

exudates

• Carries an untreated 1-year mortality of 20%

Discuss the differential diagnosis of hypertension and the causes of secondary hypertension including renal disease, endocrine disease and coarctation of the aorta

• Hypertension is present in 20-30% of the adult population

• Isolated systolic hypertension affects >50% of over 60s, and doubles the risk of MI

• Renal diseases account for 80% of secondary causes

ESSENTIAL (PRIMARY) HYPERTENSION • Comprises 95% of cases

• The cause is not known but is likely to be multifactorial

SECONDARY HYPERTENSION • Adrenal cortical diseases:

1. Primary hyperaldosteronism (e.g. Conn’s) ® most common secondary cause

2. Cushing’s

3. Acromegaly

4. Adrenal hyperplasia

• Renal artery stenosis ® second most common cause, and bruits will be present

• Chronic kidney disease:

1. Diabetic nephropathy

2. Chronic glomerulonephritis

3. Polycystic kidney disease

4. Chronic tubule-interstitial disease

5. Renovascular disease

• Phaeochromocytoma (rare) ® HTN initially paroxysmal, presenting with sweating, pallor & palpitations

• Coarctation of the aorta ® congential narrowing of the aorta leads to increased peripheral vascular

resistance

• Neurogenic causes ® e.g. raised ICP

• Pregnancy ® occurs in 8-10% of pregnancies

Describe the pathological consequences of hypertension as they affect the cardiovascular, cerebrovascular and renal systems

• Essential hypertension accelerates arteriosclerosis and potentiates atheroma formation ® causes a

hyaline thickening of arteriole walls

• Heart ® left ventricular hypertrophy, with dilation and eventual failure

• Aorta ® predisposes to AAAs & aortic dissection

• Brain ® intracerebral haemorrhage due to vessel rupture, lacunar infarcts & microvascular aneurysms

(Charcot-Bouchard aneurysms)

• Kidney ® CKD due to progressive nephron ischaemia, nephrosclerosis & glomerular destruction

• Eyes ® hypertensive retinopathy


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Discuss the management of hypertension including side effects of common drugs APPROACH TO A HYPERTENSIVE PATIENT

• Confirm diagnosis ® ABPM / HBPM • Full history:

1. Any features of malignant HTN? ® headaches, epistaxis, fits, LOC

2. Any symptoms of secondary causes? ® signs of phaeochromocytoma / CKD / Conn’s / IHD /

renal artery stenosis • Full examination:

1. Assess for complications ® fundoscopy / CV examination: § Hypertensive retinopathy can show AV nipping, flame-shaped haemorrhages, cotton

wool spots § Malignant HTN will have bilateral papilloedema § Features of LVH / LVF

2. Assess for secondary causes: § Renal artery bruits ® RAS § Features of CKD § Radiofemoral delay ® coarctation of the aorta

• Further investigations: 1. Assess for complications:

§ Urine dip ® renal damage

§ ECG ® LVH

§ Echo ® LVF 2. Assess for secondary cause (if suspected):

§ RAS ® renal artery Doppler § CKD ® U&Es, eGFR

§ Phaeochromocytoma ® 3x 24hr urine collections. For free metadrenaline &

normetadrenaline 3. Assess overall CV risk:

§ HbA1c, lipids ® for QRISK2

HYPERTENSION TREATMENT • First-line is lifestyle interventions ® weight loss, increasing exercise, decreasing alcohol / caffeine /

sodium intake, and stopping smoking

• Drug treatment:

1. Start in ALL those with stage 2 HTN

2. Start in those under 80 with stage 1 HT ad one of the following:

§ A. 10-year CV risk >20%

§ Other comorbidities ® renal disease, known CV disease, end organ damage

3. Target clinic blood pressure ® <140/90mmHg (<150/90mmHg if aged over 80)

4. Target ABPM / HBPM blood pressure ® <135/85mmHg (<145/85mmHg if aged over 80)

• Follow the A/C rules to choose an appropriate pharmacological agent


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ACE INHIBITORS • E.g. ramipril or lisinopril ® act by RAAS antagonism

• First-line in those <55yrs, and also in diabetics or those with CKD (renoprotective) • 10% of patients complain of a dry cough due to potentiation of bradykinin

1. Switch to AT1 receptor antagonists ® e.g. candesartan or losartan 2. These block the effects of ATII at the AT1 receptor 3. They are equally effective

• Other side effects: 1. Hyperkalaemia 2. First dose hypotension ® give at night

3. Worsened renal function in those with previously normal GFR ® monitor U&Es when initiating

• They are contraindicated in renal artery stenosis

CALCIUM CHANNEL BLOCKERS • E.g. amlodipine / nifedipine ® DIHYDROPYRIDINES ONLY

• They work by peripheral vasodilation • First-line in those >55yrs or of Afro-Caribbean descent • Side effects:

1. Peripheral oedema 2. Postural hypotension 3. Reflex tachycardia

• If the first-line monotherapy is ineffective ® combine ACEIs and CCBs

• If this is still not effective ® add thiazide-like diuretic therapy (e.g. bendroflumethiazide) • For resistant HTN ® combination diuretics may be used:

1. If potassium <4.5 ® spironolactone will be added

2. If potassium >4.5 ® a loop diuretic may be added

• a-blockers and b-blockers may also be introduced by specialists for resistant HTN

VASCULAR MEDICINE & SURGERY – HYPERLIPIDAEMIA

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Outline the epidemiological link between cholesterol and vascular risk • Hyperlipidaemia ® abnormally high levels of one or more lipoproteins in the plasma

• Primary hyperlipidaemia is due to a genetic predisposition to abnormal lipid metabolism ® e.g. familial

hypercholesterolaemia

• Secondary hyperlipidaemia is caused by a systemic metabolic disturbance ® e.g. obesity, alcoholism,

or diabetes

• Raised serum cholesterol is mainly a reflection of serum LDL ® which predisposes to atheroma if

serum cholesterol levels are >4mM

1. 4mM ® 2 deaths per 1000 men

2. 5mM ® 4.5 deaths per 1000 men



• The association is less strong with triglyceride and VLDL levels

• High HDL levels are protective against atheroma

• Raised cholesterol levels can lead to xanthelasmata / xanthomata ® lipid deposits on the eyelids /

cornea / tendons

• High LDL / low HDL is a modifiable risk ® targets are total cholesterol <5mM, LDL <3mM

Discuss the evidence and indications for using lipid lowering drugs in the prevention of CV disease, together with their side effects

• First-line treatment is with lifestyle changes

• Statins can be started if the lifestyle changes show no effect

• Fibrates are second-line ® mainly reserved for those with FH / comorbid hypertriglyceridaemia

• In all patients presenting with cardiovascular features ® the 10-year CV risk should be estimated using

the QRISK2 score

1. This takes into account age, sex, BMI, BP, lipid levels, smoking & diabetes, and a range of

other risk factors to give a 10-year risk of heart attack / stroke

2. Atorvastatin is indicated for any patient with a score of 10% ® as they have been shown to

reduce mortality regardless of serum cholesterol

STATINS • HMG-CoA reductase inhibitors ® thus stop the first step in the cholesterol synthesis pathway

1. This increases LDL receptor expression by hepatocytes ® leading to decreased LDL levels in

circulation

• They have been shown to reduce LDL, reduce mortality, reduce morbidity from strokes, and stabilise

atherosclerotic lesions

• They are generally well-tolerated and should be taken at night ® 40mg

• Common side effects are nausea, headache & muscle pains ® although these will generally decrease

over time

• There are a range of interactions ® as they are metabolised by CYP450 enzymes

• Muscle pain is a common side effect but should always be reported ® rhabdomyolysis can rarely occur

(dip urine)

VASCULAR MEDICINE & SURGERY – HYPERLIPIDAEMIA

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FIBRATES • Fibrates such has bezafibrate and gemofibrozil are PPAR-a activators, with the main effect of

reducing triglycerides ® also cause small increases in HDL & decreases in LDL

• In combination with statins ® they may cause rhabdomyolysis

OTHERS • Cholestyramine can also be used to decrease fat absorption

• Cholesterol absorption inhibitors such as ezetimibe also exist

VASCULAR MEDICINE & SURGERY – ATHEROMATOUS VASCULAR DISEASE

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Define atherosclerosis and list the risk factors associated with its development • Atherosclerosis is a complicated inflammatory process involving the intima of large and medium arteries

in the systemic circulation

• It involves accumulation of lipid, macrophages, smooth muscle cells, and collagen to form plaques

• NB: Arteriosclerosis is a general hardening and loss of elasticity in medium to large arteries

• Risk factors include:

1. Age

2. Gender

3. Obesity

4. Diabetes mellitus

5. Hypertension

6. Hyperlipidaemia

7. Low birth weight

8. Stress

9. Lack of exercise

10. Smoking

11. Alcohol

Distinguish between macro- and microvascular disease and briefly outline the differences in their clinical presentation

• Macrovascular disease may result in MI, stroke, or peripheral vascular disease, and would present as

such ® initially, ischaemia of the leg may provoke intermittent claudication

• Microvascular disease is unique to diabetes and includes nephropathy, neuropathy, and retinopathy,

presenting as a decline in organ function

List specific sites where atheroma may develop and describe the clinical consequences and complications

• Atheroma formation commonly occurs at:

1. The aortic bifurcation

2. Branch points

3. Around ostia ® funnel-shaped openings, especially in the abdominal aorta near the kidneys

• Clinical complications include:

1. Stenosis and resulting hypoperfusion of distal tissues

2. Thrombus on the plaque ® causing total occlusion

3. Bleeding into the plaque

4. Aneurysm formation

5. Cholesterol embolism to distal sites

Discuss ways to modify the atherosclerotic process including general lifestyle measure, pharmacological control of blood pressure, hyperlipidaemia and diabetes, and the use of anti-platelet agents

• Prothrombotic state is a risk factor for complications of atherosclerosis ® so antiplatelet agents reduce

the risk of complication

• Hypertension, hyperlipidaemia & diabetes are risk factors for progression of the disease state ® their

reduction via lifestyle, diet, and pharmacology will decrease the risk of complications

• General lifestyle measures may be the most important ® stop smoking, exercise more, and eat a

balanced diet with more fruit & vegetables and less fat

VASCULAR MEDICINE & SURGERY – ANEURYSMS

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Describe the common sites and relative incidence of atherosclerotic arterial aneurysms • Aneurysm ® a focal dilation of an artery to >150% of its normal diameter ® e.g. AAA >3cm

• They can present in different ways:

1. Mass effects ® pressuring adjacent structures

2. Embolic events ® due to development of mural thrombi

3. Haemorrhage ® due to rupture

• Causes include:

1. Atherosclerotic ® e.g. aortic, popliteal

2. Developmental ® e.g. berry aneurysm

3. Infective ® e.g. mycotic in endocarditis, syphilitic in tertiary syphilis

4. Genetic ® e.g. Marfan’s / Ehlers-Danlos syndromes

5. Trauma

• The more common sites are in descending, strong-flow vessels ® in descending order of incidence:

1. Abdominal aorta

2. Iliac artery

3. Popliteal artery

4. Femoral artery

5. Thoracic aorta

6. NB: Berry aneurysms typically occur in the Circle of Willis but are not atherosclerotic

• Abdominal aortic aneurysm is present in 5% of males >60yrs ® it is 5x more common in males, is

mainly asymptomatic, and develops in 1 in 4 children of affected individuals (i.e. some familial

component)

Describe the pathophysiology of thoracic aortic dissection and outline its clinical presentation, complications and mortality risk

• The process begins with a tear of the tunica intima

• Blood penetrates into the media, and then tracks between the middle and outer 1/3 of media ®

producing a second ‘pocket’ of blood

• This may then:

1. Break back into the original lumen ® double-barrelled aorta

2. Rupture outwards through the adventitia ® haemorrhage

3. Spread in a retrograde fashion to involve the pericardial cavity ® haemopericardium

• Blood running in the tunica media cuts off the major branches of the arch of aorta as it passes

• They may be classified as:

1. Type A ® proximal to the left subclavian artery / involve the ascending aorta (70%)

2. Type B ® distal to the left subclavian artery / do not involve the ascending aorta (30%)

• Symptoms include tearing pain towards / radiating to the back of the chest and down the arms

• Patients may be shocked and have neurological symptoms secondary to loss of blood supply to the

CNS ® especially in type A dissection

• Peripheral pulses may be absent

• Renal failure, acute lower limb ischaemia, and visceral ischaemia may accompany other features


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• Investigations:

1. CXR ® mediastinum is classically widened

2. CT ® confirms diagnosis

3. ECG ® patterns similar to MI

• Complications occur as the dissection spreads:

1. Retrograde spread can lead to cardiac tamponade

2. If the dissection spreads distally, then the origins of the main arterial branches become

blocked, leading to symptoms depending on the arteries involved:

§ Coronary arteries ® MI

§ Brachiocephalic trunk ® unequal arm pulses and central neurological symptoms

(same if left common carotid and left subclavian occlusion)

§ Renal arteries ® haematuria, anuria, AKI

§ SMA / IMA ® acute mesenteric ischaemia

§ Iliac arteries ® acute lower limb ischaemia

• Management:

1. A-E resuscitation, with urgent cardiothoracic advice

2. Patients will be managed on ITU

§ BP controlled to keep SBP around 100 ® IVI esmolol (cardioselective b1 blocker)

3. Type A dissection:

§ Patients are considered for surgery if fit enough, due to risk of tamponade

§ Surgery is grafting of the aortic root ® carries high operative mortality

4. Type B dissection:

§ Patients are managed medically unless there are complications

List the symptoms and signs of a ruptured abdominal aortic aneurysm, discuss the differential diagnosis and outline an emergency management plan

• Presentation:

1. Until rupture, most AAAs are asymptomatic

2. Rupture may present as severe continuous / intermittent epigastric pain, radiating to the back /

groin

3. Pulsatile, expansile abdominal mass

4. Signs of shock ® tachycardia, hypotension, profound anaemia, and even sudden death

5. If the aneurysm is throwing off emboli, the patient may have ‘trash feet’ ® discoloured digits

secondary to arterial occlusion

6. NB: AAA should be suspected in any male >50yrs presenting with renal colic

• Differential diagnosis:

1. Renal colic

2. Diverticulitis

3. Pancreatitis

4. Gastric / duodenal ulcer perforation

5. MI

• Management:

1. Emergency A-E resuscitation


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2. Patient taken to theatre as soon as stabilised ® clamp the aorta above the leak, then insert a

graft

3. Only 50% of ruptured AAAs make it to hospital ® of these patients, 50% will not survive the

surgery

Describe the role of surveillance monitoring of abdominal aortic aneurysm • The UK Small Aneurysm Trial showed that patients with infrarenal AAA did best with an operation if the

aneurysm was >5.5cm, expanding >1cm/year, and symptomatic

• Patients with AAA <5.5cm should be followed up with regular ultrasound surveillance

• Prophylactic surgery is preferred to emergency surgery with rupture

Discuss the methods available for treating abdominal / thoracic aortic aneurysms, and discuss the indications, contraindications and risk factors for surgery in patients with unruptured AAA UNRUPTURED AORTIC ANEURYSM MANAGEMENT

• Abdominal aortic aneurysms that measure <5.5cm:

1. Monitored by regular USS / CT

2. Modification of risk factors ® e.g. control of HTN

3. 75% of monitored aneurysms will eventually require surgery

• Indications for surgery:

1. AAA >6cm ® risk of rupture increases from 1% to 25% at 6cm

2. AAA expanding at >1cm/year

3. Symptomatic aneurysms

• Rupture is more likely in patients with hypertension, family history of rupture, smokers, and females ®

so in these patients operation may be performed at an earlier stage

• Endovascular aneurysm repair (EVAR):

1. Most common surgery ® uses the femoral arteries to access and stent the aorta under

fluoroscopic guidance

2. Lower mortality rate than the conventional open operation

3. Lower postoperative morbidity and shorter hospital stay ® IT not required

4. Lifelong monitoring is required ® reintervention is not uncommon

5. Endoleaks are a common reason for reintervention

• Thorough preoperative assessment is important ® as these patients often have co-existing

cardiorespiratory / kidney disease that can affect the decision to operate

• CKD is a particular risk, as the contrast used in EVAR is nephrotoxic ® and in the open procedure,

there is prolonged ischaemia to the kidneys after the aorta is clamped

Describe the presentation, complications and treatment of popliteal aneurysms • Popliteal aneurysms are frequently associated with other aneurysms

• 10% of patients with a AAA will also have a popliteal aneurysm

• They are usually asymptomatic, or may present with complications:

1. Acute limb ischaemia ® due to rupture / thrombosis of the aneurysm or distal emboli

2. Chronic limb ischaemia ® gradual occlusion of the aneurysm

3. DVT ® if occluding popliteal veins


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• Investigations:

1. USS ® to determine the size of the aneurysm

2. Angiography ® prior to surgery to assess distal arterial tree

• Management:

1. Femoral to distal popliteal bypass grafts

2. Intravascular thrombolysis or embolectomy may occur at the time of surgery for distal emboli

Distinguish between a ‘true’ and ‘false’ aneurysm • True aneurysm ® all layers of the arterial wall are involved

• False aneurysm / pseudoaneurysm ® the surrounding soft tissues lined by thrombus form the wall of

the aneurysm, mainly following trauma

1. E.g. femoral artery puncture with inadequate compression

VASCULAR MEDICINE & SURGERY – CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

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List the clinical manifestations of chronic peripheral arterial occlusive disease • On exertion, patients report severe cramp, usually in the lower leg, which resolves on rest ®

intermittent claudication

• Patients may experience similar onset pain in the buttocks and thighs associated with male impotence

® due to ileal disease, known as Leriche syndrome

• It can occur in both legs but is often worse in one

• More severe disease is associated with rest pain ® defined as severe unremitting pain in the foot which

stops a patient from sleeping

• Even more severe disease may cause ulceration or gangrene

• Signs include cold, dry skin, with hair loss

• Pulses may be diminished, and peripheries may be discoloured

• Buerger’s test will be positive, and the angle of positivity should be established as <20o ® must look

for reactive hyperaemia to complete Buerger’s test

• Bruits may be heard over major arteries

• The Fontaine classification outlines the progression of chronic lower limb peripheral arterial disease:

1. Asymptomatic

2. Intermittent claudication

3. Ischaemic rest pain

4. Ulceration / gangrene

• Causes:

o Atherosclerosis ® by far the most common

o Fibromuscular dysplasia ® non-inflammatory artery wall thickening

o Buerger’s disease (thromboangiitis obliterans) ® acute inflammation and thrombosis of

lower limb arteries / veins, common in young heavy smokers

Differentiate symptoms of ischaemic rest pain and neuropathy as a cause of foot pain, and contrast gangrene in diabetic & non-diabetic patients

• Neuropathy is associated with tingling and numbness, and is not relieved by swinging a leg out of bed

• Neuropathy generally conforms to a glove and stocking distribution

• Ischaemic pain will get worse on raising the leg ® unlike neuropathic pain unless it is caused by nerve

entrapment (Buerger’s test can differentiate)

• Neuropathy may be accompanied by hyperalgesia and allodynia

IN DIABETIC PATIENTS • Diabetics are at greater risk of developing chronic peripheral arterial disease

• Presentation can be slightly different due to the presence of peripheral neuropathy, which has three

main effects:

o Sensory neuropathy ® reduces protective reactions to minor injury, and reduces awareness

of symptoms of infection / ischaemia

o Autonomic neuropathy ® a lack of sweating leads to development of dry, fissured skin,

allowing entry of bacteria

o Motor neuropathy ® wasting of the small muscles of the foot leads to loss of the arches and

the development of abnormal pressure areas in the feet


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• Peripheral neuropathy alone can lead to stabbing pains in the feet, which in the absence of any arterial

disease will be red and warm with strong pulses

• When arterial disease occurs in the presence of peripheral neuropathy ® the foot can be severely

ischaemic yet painless

o As such, diabetics with critically ischaemic limbs are more likely to present with ulceration ®

due to the combination of sensory, autonomic and motor neuropathy, combined with poor

arterial supply to heal ulcers

o This can rapidly progress to gangrene

GANGRENE • Dead tissue, normally colonised by bacteria:

o Wet gangrene ® infected with proliferating organisms

o Dry gangrene ® colonised, but organisms are not proliferating

• It presents in the toes first, progressing proximally to the line where there is adequate oxygenation

• Characteristically it is initially blue-purple in colour, with progressive blackening of tissues and

numbness

• In diabetics, gangrene generally presents earlier, affecting smaller areas ® e.g. a single toe, or

ischaemic areas of the foot

• This is due to the more extensive atherosclerotic changes of smaller vessels seen in diabetes

• Gangrene from pure arterial disease is likely to affect larger areas

Describe the pathophysiology of intermittent claudication and differentiate from other causes of leg pain PATHPHYSIOLOGY

• The calf is most often affected, as it is the femoral artery that most commonly becomes atheromatous

• At rest, the oxygen requirement of muscles is met by the collateral system of the profunda femoris:

o Deep femoral artery ® joins the popliteal artery just below the knee

• Exercise produces a demand that cannot be met ® the calf muscles become ischaemic

• By resting, the collateral system can once again supply enough blood for the pain to be relieved

DIFFERENTIAL DIAGNOSIS • Spinal stenosis:

o Most commonly due to spinal osteophyte formation

o Symptoms are due to lumbar nerve root / cauda equina compression

o Features are similar to intermittent claudication ® but pain is relieved by sitting down or flexing

the spine, rather than standing still

o Symptoms are variable day to day

o It is associated with numbness / tingling, and LMN signs

o Pulses will be present

o Diagnosis can be confirmed by MRI

• Venous claudication:

o Obstruction of the venous outflow of the leg ® iliofemoral occlusion

o Pain comes on gradually from the moment walking starts

o Pain affects the whole leg, and is ‘bursting’ in nature


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o Leg elevation can relieve the pain

o There are signs of venous disease, and often a history of DVT

• Other causes of leg pain are:

o Musculoskeletal (OA / RA) ® pain at rest

o Peripheral neuropathy (e.g. sciatica) ® pain is shooting in nature

o Popliteal artery entrapment ® young patients with normal pulses

Describe the non-invasive and invasive methods for investigation of arterial disease • Investigations:

o FBC (rule out anaemia), HbA1c, lipids

o ABPI is the most important initial investigation

o Doppler ultrasound scan / Duplex ultrasound scan

o Angiography ® MRI and CT angiography are not routinely performed

ANKLE-BRACHIAL PRESSURE INDEX • The ABPI is used to assess arterial disease:

o ABPI <0.8 ® arterial disease present

o ABPI <0.4 ® critical limb ischaemia

o NB: ABPI >1.2 may be a false negative due to calcification giving abnormally stiff vessels

• Management depends on ABPI result and level of symptoms

Outline the conservative management of arterial occlusive disease • If the ABPI >0.6 ® progression from intermittent claudication to critical limb ischaemia is unlikely, so

conservative measures are used

• Progression is more likely in diabetics, and those with a claudication distance <50m ® thus more

aggressive treatment may be considered in these patients

• Conservative measures:

o Lifestyle changes ® stop smoking, exercise to the point of claudication to improve collaterals,

weight loss

o Raising the heel of shoes ® decrease calf work

o Foot care ® to prevent minor trauma leading to ulceration etc.

o Optimisation of blood pressure (avoid b-blockers) and diabetes

o Start on antiplatelet (clopidogrel) and a statin (atorvastatin)

Describe the radiological and surgical treatment choices for patients with occlusive arterial disease

• If the ABPI <0.6, the disease is highly symptomatic leading to loss of function, or conservative

measures are ineffective, then more aggressive treatment is indicated:

o Percutaneous transluminal angioplasty (PTA): § Balloon inflated in narrowed segment ® good for short stenosis

§ Endoluminal stents may be used to keep the segment patent

o Surgical reconstruction: § Bypass grafting may be required in more extensive disease if distal arteries are not

diseased ® saphenous vein harvests are common


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o Sympathectomy ® may help relieve pain if surgery is contraindicated

o Amputation: § May relieve intractable pain, and prevent death from septicaemia

§ Level of amputation must be high enough to ensure healing ® but above-knee

amputation has worse rehabilitation that below-knee

§ Gabapentin started pre-op may help phantom limb pain

List criteria to help differentiate leg ulcers • Venous ulcers:

o 85% of leg ulcers are venous in origin

o Many will also have an arterial element

o Occur due to venous hypertension & oedema ® causing subcutaneous hypoxia

o An episode of minor trauma then precedes development of an ulcer ® as the skin is poorly

nourished and cannot heal

o Secondary infections by skin flora are common

• Arterial ulcers:

o 10% of ulcers are entirely the consequence of arterial disease

o They also commonly occur after an episode of minor trauma ® with inadequate healing due to

poor arterial supply

Clinical feature Venous ulcer Arterial ulcer History DVT, varicosities, obesity IC, IHD, HTN, DM

Pain Rare Exquisitely painful

Site Medial malleolus & ‘gaiter area’ Lateral malleolus & heel / toes

Progression Slowly increasing, but can

become very large

Rapidly increasing, but painful

so present small

Oedema Common Uncommon

Skin appearance Signs of venous insufficiency

Red & warm

Shiny, hairless, atrophic nails

Cool & pale

Ulcer appearance Shallow with a flat margin Small and ‘punched out’

• Diabetic ulcers:

o Can be considered somewhat separate to venous and arterial ulcers

o Occur due to the three neuropathy processes described above, which are compounded by

arterial disease & infection

o They usually occur on the foot ® with a classic unbalanced-looking foot with ulcers on the

pressure areas

MANAGEMENT OF ULCERS • Consider diabetes / vasculitis causes

• Perform ABPI / Duplex USS ® can show arterial and venous disease

• Conservative management:

o Lifestyle changes in suspected arterial disease

o Avoid prolonged standing in suspected venous disease

o Tightly control DM


DARWIN’S NOTEBOOK

16

• If ABPI >0.8 and signs of venous disease:

o 4-layer compression bandaging is the gold standard initial treatment

o Leg elevation is important to help decrease the venous hypertension

o Once healed ® long-term compression stockings are advised

• If the Duplex scan shows superficial disease only:

o Treatment of varicose veins may resolve the venous outflow issues, to allow ulcer healing

• If ABPI <0.8:

o Refer to GP for CV risk modification

o Refer to vascular surgery for investigation of arterial disease

o In mixed arterial / venous ulcers ® the arterial problem should be surgically corrected, and

then compression can occur

o Arterial ulcers are a sign of critical limb ischaemia ® and thus are treated surgically if the

patient is fit

• Swab only if signs of infection ® ulcers are normally colonised, and this does not delay healing

• Biopsy if the ulcer looks atypical ® SCC can develop, known as Marjolin’s ulcer

Describe the signs, symptoms, investigations, differential diagnosis and treatment of chronic mesenteric vascular occlusive disease

• Chronic small bowel ischaemia:

o Severe post-prandial colic ® ‘gut claudication’

o PR bleeding

o Weight loss ® as eating is painful

o Malabsorption

§ This is difficult to diagnose, but can be visualised on angiography and treated with

angioplasty

• Large bowel ischaemia:

o Presents with ischaemic colitis:

§ Left-sided abdominal pain

§ Bloody diarrhoea

§ Pyrexia, tachycardia & leucocytosis

§ Can progress to gangrenous colitis ® with peritonitis and shock

o Investigations:

§ Barium enema / AXR ® ‘thumb printing’

§ MR angiography ® diagnostic

o Management:

§ Conservative ® most recover with fluids and antibiotics

§ Percutaneous transluminal angioplasty & stenting for severe cases

Describe the presentation, investigation and management of renal artery stenosis • Aetiology:

o 80% due to atherosclerosis

o 10% due to fibromuscular dysplasia ® young males


DARWIN’S NOTEBOOK

17

• Presentation:

o Resistant HTN

o Worsening renal function after ACEIs ® if bilateral

o Sudden onset pulmonary oedema ® with normal LV function

o Renal bruits on examination

• Diagnosis:

o Renal USS ® small affected kidney, Doppler showing disturbance in renal blood flow

o CT / MR angiography can then confirm diagnosis

o Renal angiography ® gold standard

• Treatment:

o Medical regimen ® ACEIs with statins & platelets

§ Contraindicated in bilateral disease

o Surgical management ® angioplasty & stenting

§ Thought to be equally effective as medical management

VASCULAR MEDICINE & SURGERY – ACUTE ARTERIAL OCCLUSIVE DISEASE

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18

List the causes of acute arterial occlusion • Causes:

o Embolus ® 40%

o Thrombus ® 40%

o Trauma ® including during angioplasty

o Popliteal aneurysm

o Aortic dissection

• Thrombosis is predisposed to by Virchow’s triad:

o Endothelial dysfunction ® trauma, inflammation or atheroma

o Changes in blood flow ® stasis or slow flow

o Changes in blood coagulability ® inflammatory response / congenital causes

• Thrombosis in situ may occur due to plaque rupture, hypovolaemia, or pump failure ® predisposing

factors include dehydration, hypotension, unusual posture, malignancy & hyperviscosity / thrombophilia

• Embolic occlusion is occlusion of a vessels by a mass of material transported in the bloodstream ®

most commonly fragments of a thrombus (thromboemboli) • Thromboemboli may arise from:

o The left atrium in AF

o The left ventricle post-MI

o Heart valves in endocarditis

o Mural thrombi from an AAA

Differentiate embolic and thrombotic occlusion EMBOLIC OCCLUSION

• Embolic occlusion will cause complete ischaemia ® characterised by paraesthesia & paralysis

• Onset will be within minutes and is more common in AF patients

• There will not have been a history of ischaemic symptoms previously

• The artery will feel soft, and a bruit will not be present as there has been no prior stimulus for developing

collaterals

• The contralateral area will be unaffected

THROMBOTIC OCCLUSION • Thrombotic occlusion will cause incomplete ischaemia ® collaterals will have developed

• Onset is within hours, and previous symptoms will have been present

• The artery will feel calcified, and a bruit from already developed collaterals will be present

• The contralateral area will have reduced pulses

Clinical feature Embolus Thrombus Onset Sudden onset ® very severe

symptoms due to lack of collaterals

Insidious onset ® less severe

symptoms due to advanced collaterals

Source Normally identifiable e.g. AF/ AAA No obvious source

Pulses Previously normal, normal

contralateral pulses

Long-standing decreased pulses

bilaterally

History No history of arterial disease Previous history of IC, stroke, MI etc.


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List the symptoms and signs of acute arterial occlusion • Clinical symptoms of the acutely ischaemic limb are the six Ps:

o Pulseless o Pain o Pallor

o Perishingly cold o Paralysis o Paraesthesia

• Paralysis & paraesthesia indicate a threatened limb ® as does pain on passive movement or squeezing

the calf (which indicates infarction has taken place)

• Fixed staining (colour changes that are non-blanching) of the limb, and rigid muscles indicate a non-

viable limb

Differentiate the symptoms and signs of acute arterial occlusion from acute venous occlusion • Acute arterial occlusion ® will cause the 6 Ps

• Venous occlusion ® will cause swelling, redness, warmth & pain

o Engorgement of superficial vessels, ankle oedema & Homan’s sign (pain on dorsiflexion of

the foot) may be present

Describe the natural history of treated and untreated acute arterial occlusion • Untreated ® the patient will lose the limb, and the degeneration process will cause life-threatening

illness

• Treatment hopes to save the limb ® acute limb ischaemia may lead to peripheral nerve damage and

chronic pain syndromes

• There is a maximum of 6 hours to re-establish flow in an acutely ischaemic limb:

o A-E resuscitation

o IV heparin as soon as the diagnosis is made ® to prevent propagation of the clot

o Assessment of the limb:

§ If the block seems to be resolving ® the collateral circulation may negate the need for

surgery, and thrombolysis may be used

§ If there is no apparent blood supply to the distal limb, and neurological changes are

present ® urgent surgery is indicated

o Urgent CT angiogram ® can help to differentiate between thrombotic / embolic causes

o Embolus management:

§ Open embolectomy ® performed using a Fogarty catheter

§ Local thrombolysis if the clot has propagated beyond the original embolus

§ Internal investigation into the underlying cause ® e.g. AF / AAA

o Thrombosis management:

§ Thrombolysis to restore patency

§ Interval angioplasty to treat the underlying disease

• If the condition of the patient precludes operative intervention, or the leg is not thought to be viable ®

amputation may be the only treatment option

• Post-operatively, it is important to observe for the potential complication of reperfusion injury leading

to compartment syndrome:

o Inflammation and oxidative damage when blood flow is restored to a tissue after a long period

of anoxia ® due to the reintroduction of nutrients and immune mediators

o In the limb ® this can lead to oedema and compartment syndrome in tight fascial planes


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Differentiate the pathophysiology, findings and treatment in common types of arterial injury • Useful investigations in suspected arterial bleeds include angiography or contrast CT

TRANSECTION • Haemorrhage can normally be arrested by applying pressure to gauze swabs

• If there is significant ischaemia ® vascular grafting / repair may be needed

• If the main artery and vein have been severed ® the vein will always be repaired first to allow venous

drainage before repairing the artery

ARTERIOVENOUS FISTULA (AVF) • An AVF is an acquired communication between an artery and a vein

• Causes:

o Penetrating trauma ® most common

o Erosion of an aneurysm into a neighbouring vein

o Iatrogenic ® patients on haemodialysis

• There is shunting from the high-pressure arterial side to the low-pressure venous side

• Increased flow leads to dilation, thickening & tortuosity of the vein (‘arterialisation’), and the turbulent

flow gives a palpable thrill

• Peripheral venous pressures are increased ® leading to swelling, varicosities, and sometimes venous

ulceration in the limb

• Peripheral arterial resistance decreases ® thus the heart responds by increasing stroke volume,

eventually leading to left ventricular dilation and heart failure

• Patients with non-iatrogenic AVFs may complain of limb heaviness, aggravated with dependency and

relieved by elevation

• Pain is also a common symptom

• On examination ® there is oedema and prominent veins, with an audible murmur or palpable thrill (may

be pulsatile)

• Rarely, there can be signs of CCF if the communication is very large

• Blood gas will show higher oxygen saturations distal to the AVF ® there can also be consumptive

coagulopathies due to the changes in blood flow activating the clotting cascade

• Duplex USS or contrast CT can confirm diagnosis

• Most symptomatic AVFs are amenable to surgical or interventional treatment

VASCULAR MEDICINE & SURGERY – VASOSPASTIC DISORDERS

DARWIN’S NOTEBOOK

21

List the underlying diseases or disorders associated with vasospastic changes in the extremities

• Raynaud’s phenomenon ® general term describing episodic digital vasospasm in the absence of an

identifiable associated disorder

• Raynaud’s syndrome ® Raynaud’s phenomenon occurring secondary to another condition ®

secondary causes include:

o Connective tissue disorders:

§ Systemic sclerosis

§ Mixed connective tissue

disease

§ SLE

§ Sjögren’s syndrome

§ Polyarteritis nodosa

§ Rheumatoid arthritis

o Macrovascular disease:

§ Atherosclerosis

§ Thoracic outlet

obstruction

§ Buerger’s disease

o Occupational trauma:

§ Vibration white finger

§ Repeated extreme cold

or chemical exposure

o Drugs:

§ b-blockers

§ Cytotoxic drugs

§ Ergot-containing drugs

§ Smoking

o Haematological conditions:

§ Clotting factor mutations

§ Polycythaemia ruba vera

§ Leukaemia

§ Hepatitis B & C

o Nerve compression ® e.g. carpal

tunnel

o Others:

§ Malignancy ®

paraneoplastic

syndrome

§ AVF

• Acrocyanosis ® a disease characterised by oedema, cyanosis & cold peripheries

• Livedo reticularis ® a condition in which skin is mottled cyanotically

• Causalgia ® a severe burning pain, which may be due to vasospasm

Specify and explain the defining clinical characteristics of Raynaud’s disease (or phenomenon) including rapidity of onset, colour changes and sensory alteration

• Raynaud’s phenomenon can be brought on by cold exposure or emotional stress, and is usually

relieved by heat ® there are three phases:

1. Pallor ® due to digital artery spasm

2. Cyanosis ® due to accumulation of deoxygenated blood

3. Rubor ® erythema due to reactive hyperaemia

• It occurs in around 5% of the population ® mostly women

• Patients are generally affected bilaterally ® more commonly in the hands than the feet

• As the fingers return to normal ® there may be numbness, a burning sensation, and severe pain

• Attacks are usually <45min in duration but can last for hours ® with very severe cases involving tissue

infarction and loss of digits (<1%)


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List the features that may distinguish primary from secondary Raynaud’s disease • Primary Raynaud’s phenomenon does not require further investigation

• Features suggesting a secondary cause include:

o Dilated nail fold capillary loops ® seen with an ophthalmoscope

o Presentation in early childhood, or over the age of 30

o Asymmetrical distribution

o Male sex ® as primary Raynaud’s is far more common in females

List laboratory investigations used to assess vasospastic disorders and describe the medical and surgical approaches

• Baseline investigations:

o FBC ® polycythaemia, malignancy

o U&Es ® renal impairment / dysfunction

o Coagulation ® hepatic dysfunction

o Glucose ® DM

o TFTs

o ANA / RF / APA ® autoimmune screen if suspecting secondary cause

• Management:

o Keep extremities warm ® heated gloves etc.

o Stop smoking and stop exacerbating drugs ® b-blockers, OCP etc.

o Vasodilators may cause headaches due to action on cerebral vasculature ® however,

nifedipine (CCB) is licensed for first-line treatment

§ Losartan / prazosin / fluoxetine are second-line

o Sympathectomy or prostacyclin infusion may be helpful in severe disease ® but may be short-

lived

Describe anatomical mechanisms responsible for thoracic outlet obstruction and list appropriate investigations

• The thoracic outlet is the space between the first rib and clavicle, through which the subclavian artery,

subclavian vein & brachial plexus pass

• Thoracic outlet syndrome ® narrowing of the thoracic outlet, causing neurological or arterial

symptoms ® causes include:

o Cervical rib

o Healed clavicular fracture

o Excess muscle development

• Presentation:

o Neurological deficits in the T1 distribution ® wasting of the small muscles of the hand,

paraesthesia of the inner forearm and hand

o Arterial symptoms:

§ Upper limb claudication ® if working with their hands above their head

§ Post-stenotic dilatation (aneurysm) ® can thrombose to cause acute artery occlusion

o On examination ® the BP will be lower in the affected arm, and vary with posture


DARWIN’S NOTEBOOK

23

o Arteriography can confirm obstruction, and plain XR will show a cervical rib or healed clavicular

fracture

• Management is often surgical ® with excision of the cervical rib, and often the first rib with any

obstructing fibrous bands

• The post-stenotic subclavian aneurysm will also need grating

• Thoracic outlet obstruction forms a key differential of cervical myelopathy

VASCULAR MEDICINE & SURGERY – VENOUS DISEASE

DARWIN’S NOTEBOOK

24

Outline the normal venous physiology and describe the roles of superficial, deep and perforating veins and venous valves in the scheme of venous blood flow

• There are two venous systems taking blood from the

lower limb back to the trunk ® the superficial venous system and the deep venous system

• The deep venous system comprises a number of

veins that accompany the major arteries of the lower

limb, and drain the muscular compartment

• The superficial venous system comprises the medial

great saphenous vein which drains into the

saphenofemoral junction, and laterally-placed short saphenous vein which drains into the popliteal vein

• The superficial system drains the skin & superficial

tissues

• The two systems are joined at the saphenofemoral and saphenopopliteal junctions

• Perforating veins are additional communications

between the two systems:

o Hunterian perforators ® in proximal thigh

o Dodd’s perforators ® in distal thigh

o Boyd’s perforators ® below the knee

o Cockett’s perforators ® posterior arch vein in the distal lower leg

• All the leg veins have valves to prevent backflow

• There are no valves in the vena cava or common iliac veins ® creating a central pool of blood in the

trunk

• Venous return to the heart is driven by pressure from the muscular pumps below, and inspiration

decreasing intrathoracic pressure

• As the calf muscles contract ® the deep veins are squeezed and emptied, to force blood upwards

• As the muscle relaxes ® blood from the superficial system will flow into the deep veins via the

perforators, which will again be squeezed upwards as the calf muscles contract once more

• Venous disease in the deep veins leads to deep venous insufficiency

• Venous disease in the superficial veins leads to simple varicose veins

o These both result from valvular incompetence

Recognise varicose veins and describe their anatomical distribution • Varicose veins ® abnormally dilated, tortuous and lengthened superficial veins, commonly in the lower

limbs ® they are more common in the great saphenous vein

• They are extremely common in Western countries

• They can be primary (idiopathic) or secondary

• Primary:

o Represent the most common cause of varicose veins

o Twice as common in women, with pregnancy accentuating symptoms


DARWIN’S NOTEBOOK

25

o Likely to be due to an underlying primary superficial valve defect, with familial elements

o There is no deep venous incompetence

• Secondary ® superficial varicosities occur due to deep venous incompetence:

o Previous DVT ® although occluded veins recanalise, their valves remain incompetent

o Raised systemic venous pressure ® due to compression occluding venous return (e.g. pelvic

tumour, pregnancy), arteriovenous fistula, or severe tricuspid incompetence

o Congenital ® e.g. Klippel-Trénaunay syndrome (disorder involving abnormal development of

blood vessels, patients are commonly born with a port-wine stain)

• Saphena varix ® dilation of the saphenofemoral junction, which has a blueish tint and may disappear

on lying down

o Not to be mistaken for a femoral hernia ® both show positive cough impulse

List the complications of varicose veins • The immediate cosmetic implication is of varicosities, and this may be the only symptoms ® most

patients are most affected by the unsightly appearance

• Patients may describe a feeling of heaviness, tension, tiredness, aching, or throbbing of the legs

• Pain is not usually present unless thrombophlebitis is present ® this is an inflammation of the superficial

vein due to venous stasis

• Itching and nocturnal cramps are reported

• Oedema of the ankles ® particularly on standing for long periods

• Minor haemorrhage may occur into subcutaneous tissue, or major haemorrhage at a higher-pressure

venous junction

• Lipodermatosclerosis, haemosiderosis, and varicose eczema

• Chronic venous insufficiency may occur as combinations of any symptoms

DEEP VENOUS INSUFFICIENCY (AKA POSTPHLEBITIC LIMB) • Occurs when the valves of the deep venous system are incompetent

• The calf pump can no longer efficiently return blood to the thoracic cavity

• Again, it can be primary (congenital absence of valves) or secondary (DVT causing valvular damage or

AVF raising venous pressure)

• Features:

o Lower limb aching pain / discomfort

o Oedema of the lower leg

o Superficial varicose veins ® raised central pressure causes perforator incompetence

o Haemosiderosis in the gaiter area (area extending from just above the malleolus to below the

knee, on both lateral and medial aspects)

o Eczema ® particularly over the pigmented area and around the ankles, causing pruritus

o Atrophie blanche ® abnormality of skin scar formation

o Lipodermatosclerosis ® subcutaneous tissue replaced by thick fibrous tissue, giving an

inverted champagne bottle appearance of the calf

o Ulceration

• Duplex sonography or venography can be used to confirm diagnosis of deep venous insufficiency

• There is no successful way to repair / replace the deep valves of the venous system


DARWIN’S NOTEBOOK

26

Describe the use of the hand held Doppler and Duplex scanning test in diagnosing venous disease, and be aware that the Trendelenburg test is no longer a recognised method

• Hand held Doppler ® can identify backwards reflux of blood at saphenofemoral / saphenopopliteal

junctions

• Colour duplex scanning ® can diagnose valvular and perforating vein incompetence, as well as large

vein occlusion

• Venography:

o Tourniquet placed around the ankle to occlude superficial veins, and contrast then injected into

the foot

o Fluoroscopy then used to see the progress through the deep system, with deep vein occlusion

and perforating vein reflux readily detected

• The Trendelenburg test is no longer a recognised method of diagnosis:

o Elevate the leg to 45 degrees to empty the superficial veins (assist manually)

o Tourniquet applied distal to saphenofemoral junction

o Patient asked to stand ® if there is isolated saphenofemoral reflux then the varicosities will

take >15 seconds to refill from the arterial circulation

o The test is then repeated with the tourniquet taken off immediately on standing ® if the

varicosities fill immediately, this suggests there is reflux at this level

o This test is repeated, moving to tourniquet further down the leg to find the lowest point of deep

to superficial incompetence

Outline the management of varicose veins including indications for surgery TREATMENT INDICATIONS

• Grossly dilated / symptomatic varicosities

• Haemorrhage

• Concomitant deep venous insufficiency ® e.g. skin changes

• Incompetent perforator veins ® can be treated minimally invasively

TREATMENT • Lifestyle advice ® avoid prolonged standing, exercise regularly & lose weight

• Graded compression stockings ® for minor varicosities, the elderly / unfit, and for pregnancy

• Endothermal ablation ® often the treatment of choice, with a laser fibre passed along the vein (USS-

guided) and then fired to cause heat and endothelial ablation, causing the vein to thrombose

• Sclerotherapy:

o For cosmetically undesirable superficial varicosities

o Chemical sclerosant is injected into an empty vein, and the vein is kept compressed with

bandaging for two weeks to allow fibrosis to take place

o USS-guided foam sclerotherapy is becoming more commonly used

• Surgery:

o Remains the gold standard treatment ® but recently indications are under scrutiny

o Procedure involves disconnecting the great saphenous vein from the femoral vein (± ‘stripping’

/ removal of the vein)

o Any incompetent perforators are individually ligated

VASCULAR MEDICINE & SURGERY – VENOUS THROMBO-EMBOLIC DISEASE

DARWIN’S NOTEBOOK

27

Identify the common anatomic locations of deep vein thrombosis • DVT occurs in the deep veins of the pelvis and legs, particularly the calf ® originating around the valves

• The most common veins to thrombose are the anterior tibial, posterior tibial, perineal, superficial

femoral, or popliteal veins

• Superficial thrombophlebitis commonly affects the saphenous veins

• Axillary vein thrombosis is uncommon but occurs

Describe the risk factors for venous thrombosis and the use of the Wells score in assessing the probability of DVT and risk of pulmonary thrombo-embolism

• Risk factors:

o Venous thrombosis often occurs in normal vessels ® thus stasis and hypercoagulability factors

are the main risk factors:

§ Age / immobility

§ Pregnancy / OCP

§ Malignancy

§ Obesity

§ Surgery ® typically

occur in week 2 post-

surgery

§ Previous DVT

• Wells score:

o Used to estimate the pre-test probability of a DVT

o 1 point for each risk factor, with -2 points for an alternative diagnosis

o Scoring:

§ £0 ® low pre-test probability

§ 1 or 2 ® moderate pre-test probability

§ ≥3 ® high pre-test probability

o If pre-test probability is low ® perform d-dimer test ® if this is negative, then DVT can be

excluded

o If pre-test probability is moderate or high, or if d-dimer test is positive ® perform compression

USS to confirm DVT


DARWIN’S NOTEBOOK

28

Describe the clinical features of a deep vein thrombosis and the use of a d-dimer test to triage patients with suspected DVT

• Most DVTs are silent ® classical clinical features include:

o Calf tenderness & firmness

o Oedema

o Erythema & calor

o Distension of superficial veins

o Superficial thrombophlebitis ® tender, erythematous, palpable superficial vein

o Homan’s sign ® pain on dorsiflexion of the ankle, however this is unreliable (as it occurs in all

lesions of the calf) and should not be tested for as it may dislodge the thrombus

• There are some atypical presentations:

o Iliofemoral thrombosis can present with severe pain but few physical signs

o Complete occlusion of a large vein can lead to cyanotic discolouration and severe oedema

• Pulmonary embolism is more common with iliofemoral thrombosis, and is rare with thrombosis below

the knee ® presenting with sudden onset unexplained dyspnoea, pleuritic chest pain & haemoptysis

• In 20-30% of patients, spread of thrombosis can occur proximally without clinical evidence

D-DIMER TEST • D-dimers are breakdown products of fibrin ® and therefore formed by the process of fibrinolysis

• Highly sensitive, but not specific for DVT ® increased inn infection, pregnancy, malignancy, and post-op

• Used to rule out DVT if negative combined with a low pre-test probability

• If positive or high / intermediate pre-test probability ® do compression USS

• Clinical diagnosis combined with raised d-dimer testing has a sensitivity of 80%

Describe the role and range of imaging modalities used when investigating suspected DVT • Confirmation of an iliofemoral DVT can usually be made with B mode venous compression

ultrasonography or Doppler ultrasound (with a sensitivity & specificity >90%) ® non-collapsing veins

indicate the presence of DVTs

• Venography, via injection of contrast into the foot, is a definitive test ® detects virtually all thrombi that

are present ® MRI may be used but is expensive

• Thrombophilia screen is done prior to commencing anticoagulant therapy if there are no predisposing

factors

Describe a differential diagnosis in patients who present with pain or swelling in the lower limb distinguishing between deep vein thrombosis, superficial thrombo-phlebitis, chronic venous insufficiency, acute arterial ischaemia and hypoproteinaemia

• Superficial thrombophlebitis ® tender, erythematous, palpable superficial vein

• Chronic venous insufficiency ® will show VVV LAPS (varicose veins, venous ulcers, venous stars,

lipodermatosclerosis, atrophie blanche, pitting oedema, scars)

• Cellulitis ® presents with the four cardinal signs of inflammation (pain, heat, swelling, redness)

• Acute arterial ischaemia ® identified by the 6 Ps (pain, pallor, pulseless, cold, paralysis, paraesthesia)

• However, all should be considered in the patient presenting with an acute limb


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Discuss the treatment of a proven DVT, methods of administering the appropriate anticoagulants and how anticoagulation is monitored, and outline the indications for primary thrombo-prophylaxis

• Preventing post-surgical DVT:

o Stop the COCP 4 weeks pre-operatively

o Mobilise as early as possible

o Immobile patients should be heparinised

o At risk patients should have support hosiery, or intermittent pneumatic pressure (until 16 hours

post-op)

• Treating a proven DVT:

o LMWH to prevent propagation of the clot ® with warfarin started simultaneously

o The LMWH can be stopped when INR = 2-3

o Length of warfarin treatment:

§ 3 months if post-operative DVT

§ 6 months if there was no precipitating cause

§ Lifelong if known thrombophilia or recurrent DVT

o If anticoagulation fails to prevent PE, or causes active bleeding ® an inferior vena cava filter

may be used to minimise the risk of PE

Describe the range of clinical presentation and associated pathology of pulmonary embolic disease depending on the clot size and cardiopulmonary haemodynamics

• Pulmonary emboli are generally caused by DVTs in the legs

• They classically present with sudden onset dyspnoea, pleuritic pain & haemoptysis ® however, PE

should be included in almost any respiratory differential as they are so common and variable in

presentation

• They lead to increased pulmonary artery pressure (right heart strain) and ischaemia of the lung, with a

ventilation / perfusion mismatch

• They often occur around day 10 post-surgically

• PE status can be grouped as massive, major, or minor ® prognosis is dependent on the size of

thrombus and previous cardiorespiratory status

• Minor PE ® 85%:

o Small peripheral vessels are blocked, and patients may be asymptomatic (haemoptysis is rare)

o Tachycardia, tachypnoea, crackles in the region of the embolus, may be some pleuritic pain

o Massive PE may ensue following a minor PE ® known as the ‘premonitory embolus’

• Major PE ® 10%:

o Middle-sized pulmonary arteries are blocked ® leading to dyspnoea, pleuritic chest pain &

haemoptysis

• Massive PE ® 5%:

o >60% of the pulmonary circulation is blocked ® leading to rapid cardiovascular collapse

• Signs:

o Evidence of a DVT

o Raised JVP

o Cyanosis if the embolus is large

• Risk factors are as for a DVT


DARWIN’S NOTEBOOK

30

• Investigations:

o FBC, U&Es, clotting, d-dimer

o ABG ® type 1 respiratory failure

o CXR ® often normal, or dilated pulmonary artery, wedge-shaped opacities

o ECG ® tachycardia, RBBB, RV strain (classical S1Q3T3 pattern is rare)

§ Large S-wave in lead I

§ Q-wave in lead III

§ T-wave inversion in lead III

o Echocardiography ® can confirm right heart strain

o CT pulmonary angiography (CTPA) ® this is the gold standard

§ V/Q if this is unavailable, but less accurate if there is pre-existing lung disease

• Treatment:

o Major / minor PE should be managed as per DVT above

o Massive PE:

§ Emergency A-E resuscitation

§ IV morphine + antiemetic § Heparin therapy ® LMWH / unfractionated

§ If SBP >90mmHg ® commence anticoagulant therapy (LMWH + warfarin)

§ If SBP <90mmHg ® start vasopressors (e.g. noradrenalin) before commencing

thrombolytic therapy

VASCULAR MEDICINE & SURGERY – LYMPHATIC DISEASE

DARWIN’S NOTEBOOK

31

Define lymphoedema and outline common causes • Lymphoedema ® swelling which results from abnormal accumulation of fluid in the interstitial space of

soft tissues, due to failure of lymphatic drainage

• It causes chronic non-pitting oedema ® most commonly affecting the legs and progressing with age

• Chronic disease may cause a secondary cobblestone thickening of the skin

• The best place to establish the presence of lymphoedema is the second toe ® Stemmer’s sign

• It may be due to primary or secondary disease

• Primary lymphoedema ® presents early in life, and is a result of a congenital deficiency / abnormality

of lymphatic vessels (e.g. Milroy’s disease)

• Secondary lymphoedema ® due to obstruction of more proximal lymph vessels

o May be caused by parasites (e.g. filariasis), inflammation (e.g. recurrent cellulitis), malignancy,

or injury (e.g. post-operatively)

o Lymph node extraction (as in suspected breast cancer) may cause lymphoedema

o Radiotherapy can cause fibrotic disruption to lymphatics

• Lymphoscintography ® can be used to confirm diagnosis, after other causes of oedema have been

excluded (e.g. CCF, renal disease, deep venous insufficiency)

• Management involves elation, compression stockings, and physical massage ® with long-term

antibiotics for recurrent cellulitis (each episode further damages lymphatic drainage)

• Surgery should be avoided

Describe the indications for magnetic resonance angiography, duplex ultrasound, CT angiography and invasive investigations

• Duplex USS ® gives anatomical and physiological (flow) information non-invasively, but requires an

experienced operator

• Angiography ® used when invasive procedures are planned, with contrast injected by a series of

catheters most commonly introduced at the femoral artery ® fluoroscopy is then used to visualise the

arterial system

o Risks include contrast reaction, haematoma / pseudoaneurysm / AVF formation, or arterial

occlusion

• CTA / MRA ® now more commonly being used for the evaluation of the arterial system

o CTA ® used more for carotid / cerebral disease

o MRA ® used to assess thoracic, abdominal or limb disease

Documents

2 - Vascular Medicine & Surgery