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RLH MRCS > DrE: Vascular > Flashcards

DrE: Vascular Flashcards

1
Q

Peripheral arterial examination: inspection

A

Start: pt lying on bed, shirt unbuttoned/off & legs exposed

Inspection:

  • Hands - tar staning, muscle wasting (thoracic outlet syndrome)
  • Nail - tar staining onycholysis, thick and brittle
  • Face - xanthelasma, corneal arcus
  • Abdomen - pulsatile mass
  • Legs - discolouration - haemosiderin deposition, shiny skin
  • Ulcers - malleoli & pressure areas, ?between toes, lift lower limbs to check heals/beneath legs, describe BEDS
    • Base
    • Edges
    • Discharge
    • Structures visible
  • Guttering & gangrene - venous guttering, gangrenem tissue loss
  • Scars - amputation scars from previous op (cephalic & basillic vein harvesting scars from bypass procedures)
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2
Q

Peripheral arterial examination: Palpation

A
  • Pain
  • Pulses: Radial, brachial, carotid, AAA, Femoral, popliteal, DP, TP
  • CRT - upper and lower
  • Buerger’s angle: raise each leg, not angle of pallor, = to 20 - severe PAD, note venous guttering, test: swing leg down over side of bed, reactive hyperaemia = positive = PAD. Pole Test = level at which doppler signal is lost
  • Oedema = DVT, lymphoedema, post surgical
  • Allen’s test: occlude radial and ulnar artery, repeatedly open and clos till pale, release R/U, note time to reperfusion, repeat for other artery (ulnar normally dominant)
  • Temperature discrepency
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3
Q

Perirpheral arterial examination: auscultation

A

For bruits

  • Carotid
  • Aortic
  • Iliac
  • Femoral
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4
Q

Peripheral arterial examination: completion

A
  • ABPI: BP at brachial artery, hand held doppler, DP and TP, divide highest by brachial BP, If resting ABPI is normal -> 10 heel toe raises and recheck
  • VV examination - mixed arterial & venous disease
  • Cardiac examination - full cardiac exam & ECG
  • Neurological examination e.g. diabetic neuropathy
  • BP & HR - HTN and AF
  • Ix:
    • Duplex
    • MRA
    • CTA
    • IADSA
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5
Q

Varicose veins examination: Inspection

A

Start: Patient standing, exposed to underwear

  • 6Ss - site/size/shape/surface/symetry/scars
    • above SPJ = LSV
    • Below SPJ = SSV
  • Skin:
    • venous eczema, haemosidering deposition, lipodermatosclerosis
  • oedema: 2ndary to DVT/Lymphoedema
  • Ulcers:
    • LSV - medial malleolus
    • SSV - lateral malleolus
    • Bases/Edges/Discharge/Structures
  • Scars:
    • Groid crase - high tie and LSV stripping
    • Popliteal fossa scar - SPJ ligation op
    • Small scars - stab avulsions
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6
Q

Varicose veins examination: palpation

A

ask re pain

compare 1 limb to other

examine good leg first

  • SEC FFP TR - surface/edges/consistency/fluctuance/fixity/pulsatile and expansile/transiluminates/reducibility
  • saphena varix - palpate over SFJ for SV - 4cm below and lateral to PR, smooth/soft bluish swelling (disappears on lying down)
  • Cough/tap test : palpate VV distally, tap proximally/ask pt to cough, transmitted impulse through CC = incompetent proxima valves
  • Trengellenberg test: milk veins proximally, pressure over SFJ, ask pt to stand, if control is achieved ?incompetent SFJ
  • Tourniquet test - milk veins proximally, tourniquet proximally around thigh, pt stand, if control is achieved, level of incompetence is at/above tourniquet , if not, move down until control is achieved
  • Perthe’s test - once control is achieves by tourniquet, pt stand, move up and down on tip toes, if veins distend/pt experiences pain -> incompetent deep venous system, LSV strip may worsen symptoms
  • Hand held doppler - doppler over SPJ and SFJ squeeze calf, listen for doppler souns. 1x woosh with abrupt cut off - suggests competent valve, 2nd woosh = reflux
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7
Q

Varicose veins examination: auscultation

A

bruits: over femorals - AVF post femoral artery catheterisation/IVDUs

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8
Q

Varicose veins examination: completion

A
  • Abdo exam - incl PR - venous obstruction
  • ABPI: assessment required pre compression stockings
    • ​ABPI >1.3 - avoid stockings due to calcified vessels
    • ABPI 0.8-1.3 - safe to use compression stockings
    • ABPI 0.5-0.8 only light (class I) compression stockings
    • ABPI <0.5 - avoid conpression stocking - may compromise arterial blood supply
  • Investigations:
    • dupplex scan, MRV
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9
Q

What are the symptoms and signs of acute arterial insufficiency?

A

6x P’s of acute arterial insufficiency:

  • Pain - acute/sudden onset pain in affected limb
  • Paraesthesia - pins and needles sensation
  • Pallor - pale appearance
  • pulselessness - loss of distal pulses in comparison to opposite limb
  • paresis - motor weakness progressing to paralysis
  • perishingly cold - cold on palpation
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10
Q

What is the Fontaine classification?

A

I - asymptomatic

IIA - intermittent claudication walking >200m & no rest pain

IIB - intermittent claudication walking <200m & no rest pain

III - rest/nocturnal pain

IV - gangrene/necrosis

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11
Q

What is the significance of ABPI?

A

= 0.9 -> haemodunamic marker of PAD

ABPI:

  • >1.3 - abn vessel hardening e.g. arterial calcification due to diabetes
  • 0.9-1.3 - normal range
  • 0.5-0.9 - moderate arterial disease
  • <0.5 - severe arterial disease
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12
Q

What is critical limb ischaemia?

A

chronic ischaemic rest pain or the presence of ischaemic skin lesions (ulcers or gangene

Critical limb ischaemia only applies to chronic ischaemic disease; fontaine’s classification III/IV, lasting >2weeks

some papers further classify this into:

1) subcritical ischaemia: rest pain + ankle pressure >40 mmHg
2) Critical ischaemia: rest pain + tissue loss/ankle pressure <40

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13
Q

What is an abdominal aortic aneurysm?

A

Abnormal dilation of abdominal aorta by >50% of its normal diameter

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14
Q

What are the clinical features of AAA?

A
  • Asymptomatic; most asymptomatic, diagnosed insidentally on US
  • Mass - pulsatile abdo mass
  • Compression - early satiety, nausea, vomiting, UTI symptoms, venous thrombosis
  • Erosion - back pain due to erosion into adj vertebae
  • Embolisation - ischaemic toes
  • Rupture - hypovolaemia shock & sudden death
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15
Q

What is the risk of rupture of an AAA?

A
  • <5.5cm - <1% risk
  • 5-5.6cm - 10% risk
  • 6-6.5 - 20%
  • 6.5-7 - 25%
  • 7-8 - 30%
  • >8 - >50%
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16
Q

What is the elective management of a AAA?

A
  • <3cm - no aneurysm
  • 3-4.4cm - annual USS monitoring
  • 4.5-5.4cm - 3monthly monitoring offered
  • <5,5cn - referral to vascular surgeon, patient offered elective repair (open repair or EVAR) if possible
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17
Q

What are the indications for AAA repair?

A

Symptomatic

Diameter >5.5cm

Diameter increasing by 1cm per annum

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18
Q

What is thoracic outlet syndrome?

A

symptoms and signs caused by arterial venour or nerve compression as these structures pass between the clavicle and the 1st rib

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19
Q

What are the causes of thoracic outlet syndrome?

A
  • congenital: cervical rib
  • Acquired:
    • pathological enlargement of the 1st rib
    • Scalenus muscle hypertrophy
    • Fractured clavicle
20
Q

What are the clinical features of thoracic outlet syndrome?

A
  • artery:
    • arm/hand claudication (worse on rasing arm above head)
    • acutely ischaemic limb (secondary to emboli)
    • subclavian aneurysm
  • vein:
    • venous HTN
    • arm swelling
    • venous thrombosis
  • nerve:
    • motor or sensory deficit (commonly affects the lower 2 nerve roots, C8, T1)

Roo’s test

Adson’t test

21
Q

What are the differential diagnoses for thoracic outlet syndrome?

A
  • Arterial:
    • raynaud’s disease/syndrome
    • Thomboangitis obliterans
    • takayasu’s arteritis
  • venous:
    • axillary vein thrombosis
    • damage to axillary drainage e.g. post mastectomy
  • neurological
    • cervical spondylosis
    • pancoast tumour
    • cervical intervertebral disc protrusion
    • ulnar nerve neuropathy
22
Q

What is raynaud’s syndrome?

A

syndrome characterised by digital vasospasm resulting in 3 distinct phases with visible colour changes:

  • White - arterial spasm causing blanching of the digits (may lead to gangrene)
  • Blue - cyanosis & pain caused by insufficient oxygenation
  • Red - reactive hyperaemia once blood flow is restored
23
Q

How do you classify the cause of Raynaud’s syndrome?

A
  • Primary; idiopathic i.e. Raynaud’s Disease
  • Secondary:
    • arterial - atherosclerosis
    • blood disorders e.g. polycythaemia
    • connective tissue disorders e.g. RA, scleroderma
    • drugs e.g. BBlockers, caffeine, OCP, Smoking
    • Trauma e.g. vibrating tools (chronic usage)
24
Q

What is the management of raynaud’s syndrome?

A
  • Conservative:
    • heated gloves
    • avoid precipitants e.g. BBlockers, caffeine, cold weather, OCP, smoking
  • Medical:
    • nifedipine, alpha blockers, iloprost infusion
  • Surgical:
    • sympathectomy (T1-3, thorascopic)
    • digital sympathectomy
    • amputation - if gangrene present
25
Q

How do you classify carotid artery stenosis?

A

carotid artery stenosis is classified as either symptomatic or assymptomatic

symptomatic senosis is assoc with amaurosis fugax, TIA, CVA

26
Q

What is the management of carotid artery stenosis?

A
  • Conservative:
    • smoking cessation
    • exercise
    • healthy diet
  • medical:
    • statins
    • antihypertensives
    • aspirin
    • DM control
  • Surgical:
    • carotid stenting
    • carotid endartectomy
27
Q

what are the indications for carotid endartectomy?

A
  • Controlled trials have shown that surgery reduces the risk of strok in symptomatic patients with 50-99% carotid stenosis, more effectively than best medical therapy, if performed within 2 weeks of an event
  • In asymptomatic patients, <75yrs, with significant stenosis, surgery reduces the 5-year risk of stroke by 50%

Ops:

Symptomatic with >70% stenosis - clear benefit from surgery

Symptomatic with 50-69% stenosis - less benefit from surgery

Asymptomatic with >60^ stenosis - some benefit from surgery, especially if male

28
Q

How can a risk of a stroke be estimated following a TIA?

A

ABCD2 scoring system

  • A - Age - >60 = 1
  • B - BP - >140/90 = 1
  • C - Clinical features
    • Unilateral weakness = 2
    • Speach impairment, no weakness = 1
  • D - Duration of symptoms
    • >/= 60 mins = 2
    • 10-59mins = 1
  • D - Diabetes mellitus = 1

0-3 = low risk

4-5 = moderate risk

6-7 = high risk

29
Q

What is a deep vein thrombosis? (DVT)

A

Phlebothrombosis of deep veins

30
Q

What are the causes of DVT?

A

Related to virchow’s triad…

  • Endothelial damage:
    • atheroma, radiotherapy, trauma e.g. cannulation
  • Stasis/turbulent blood flow:
    • immobility, obesity, pelvic surgery, lower limb surgery, aneurysm, cardiac/vascular stents, cardiac valve replacements, DVT history
  • Hypercoagulable states:
    • dehydration, malignancy, OCP/HRT/smoking, protein C/S deficiency, factor V leidin, antithrombin deficiency
31
Q

What are the clinical features of DVT?

A
  • 75% clinically silent
  • painful calf/leg swelling that is hot and erythematous
  • Homan’s sign = pain on foot dorsiflexion
  • Distended superficial veins due to blockage within deep venous system
  • Phlegmasia alba dolens = painful white leg swelling (iliofemoral vein partial occlusion )
  • Phlegmasia caerulea dolens = painful blue leg swelling resulting in gangrene (iliofemoral vein complete occlusion)
32
Q

What investigations might you consider?

A

high index of suspicion is requiref

diagnosis involves eliciting risk factors from history e.g. recent long haul travel/surgery through examination and confirmation by duplex scan

33
Q

What are the management options for a DVT?

A

Primarily preventative

when indicated, Rx dose LMWH may be commenced followed by conversion to DOAC/Warfarin

3months in first instance

if recurrence/unprovoked may be extended/lifelong

  • Conservative:
    • maintain good hydration
    • leg exercises
    • thromboembolic deterrent stockings
  • mechanical:
    • intermittent pneumatic compression devices
  • Medical:
    • OCP - stop 4 weeks prior to elective op
    • LMWH prophylaxic
    • IV fluids
  • Surgical:
    • avoid general where possible
    • early mobilisation post op
    • Vena cava filters - prevent PE
34
Q

What are the complications of DVT?

A

PE and sudden death

+ damage to venous valves -> venous insufficiency & venous HTN disease

35
Q

What is deef venous insufficiency?

A

AKA post thrombotic/post phlebitic limb

disruption of venous return of deep venous system with assoc valvular incompetence, results in high pressure reflux into superficial veins

36
Q

What are the causes of deep venous infufficiency?

A

congenital absence of deep vein valves

DVT resulting in deep vein valve damage

arterio-venous malformations

37
Q

What are the clinical features of deep venous insufficiency?

A
  • Varicose veins: tortuous dilated veins often affecting the lower limbs
  • varicose eczema: variose pruritic rash results in scratching, potential skin abrasion increases the risk of venous ulceration and infection
  • haemosiderin pigmentation - venous leak into soft tissues
  • lipodermatosclerosis - silvery-grey patches of skin where fibrous tissue has replaced normal cutaneous tissue
  • peripheral oedema - may be inflammatory or directly related to venous HTN & increased intraluminal hydrostatic pressure
  • venous ulceration - due to venous HTN, scratching -> repeat excoriations. skin affected by lipodermatosclerosis = less robust, nutrient exchange decreased, prone to delayed healing. Precipitate vicious cycle -> delays healing
  • Infection - cellulitis
38
Q

What specific investigations would you consider for deep venous insufficiency?

A

Dupplex scan

Venography

39
Q

What are the treatment options for deep venous insufficiency?

A
  • Conservative:
    • Rx underlying cause and complications
    • avoid long periods of standing, leg elevation, compression stockings
      *
40
Q

What are varicose veins?

A

Tortuous dilated viens

most often affecting long (greater) & short (lesser) saphenous veins of lower limbs

41
Q

What are the causes of varicose veins?

A
  • Primary:
    • idiopathic
    • Familial
  • Secondary:
    • DVT
    • pregancy
    • Tumour
    • Klippel-Trenaunay syndrome (varicose veins, port-wine stains, soft tissue limb hypertrophy)
    • Parkes Weber syndrome (AVF, limb hypertrophy)
42
Q

What investigations would you consider for varicose veins?

A
  • History and examination
  • Venous duplex scan:
    • site of incompetence
    • assess deep venous system
43
Q

What is the management of varicose veins?

A
  • Conservative:
    • Support stockings
    • weight loss & exercise
  • Surgical:
    • injection foam sclerotherapy
    • Ligation SFJ/SPJ, vein stripping (LSV/SSV), stab avulsions
    • Endovenous laser therapy (EVLT)
    • Radiofrequency ablations

CLaSS trial: slightly worse disease specific quality of life in foam group compared to surgical group)

44
Q

What is gangrene?

A

abnormal irreversible tissue necrosis due to decreased vascular nutrient supply

45
Q

How would you classify gangrene?

A
  1. Dry - mummification of tissue without infection e.g. PAD
  2. Wet - superadded infection, often anaerobic e.g. clostridium perfringes/bacteroides
  3. Gas - clostridium perfringes (gas forming, gram positive anaerobe -> exotoxin -> tissue necrosis, disease spread, local crepitus)
46
Q

What are the treatment options for gangrene?

A
  • Conservative: treatment strategies - preventatic/Rx underlying cause
  • Medical: Infection -> ABx
  • Surgical: debridement/amputation

RLH MRCS (22 decks)

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