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)
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
3
Q
Perirpheral arterial examination: auscultation
A
For bruits
- Carotid
- Aortic
- Iliac
- Femoral
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
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
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
7
Q
Varicose veins examination: auscultation
A
bruits: over femorals - AVF post femoral artery catheterisation/IVDUs
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
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
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
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
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
13
Q
What is an abdominal aortic aneurysm?
A
Abnormal dilation of abdominal aorta by >50% of its normal diameter
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
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%
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
17
Q
What are the indications for AAA repair?
A
Symptomatic
Diameter >5.5cm
Diameter increasing by 1cm per annum
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
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
How do you classify carotid artery stenosis?
carotid artery stenosis is classified as either symptomatic or assymptomatic
symptomatic senosis is assoc with amaurosis fugax, TIA, CVA
26
What is the management of carotid artery stenosis?
* Conservative:
* smoking cessation
* exercise
* healthy diet
* medical:
* statins
* antihypertensives
* aspirin
* DM control
* Surgical:
* carotid stenting
* carotid endartectomy
27
what are the indications for carotid endartectomy?
* 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
How can a risk of a stroke be estimated following a TIA?
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
What is a deep vein thrombosis? (DVT)
Phlebothrombosis of deep veins
30
What are the causes of DVT?
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
What are the clinical features of DVT?
* 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
What investigations might you consider?
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
What are the management options for a DVT?
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
What are the complications of DVT?
PE and sudden death
+ damage to venous valves -\> venous insufficiency & venous HTN disease
35
What is deef venous insufficiency?
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
What are the causes of deep venous infufficiency?
congenital absence of deep vein valves
DVT resulting in deep vein valve damage
arterio-venous malformations
37
What are the clinical features of deep venous insufficiency?
* 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
What specific investigations would you consider for deep venous insufficiency?
Dupplex scan
Venography
39
What are the treatment options for deep venous insufficiency?
* Conservative:
* Rx underlying cause and complications
* avoid long periods of standing, leg elevation, compression stockings
*
40
What are varicose veins?
Tortuous dilated viens
most often affecting long (greater) & short (lesser) saphenous veins of lower limbs
41
What are the causes of varicose veins?
* 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
What investigations would you consider for varicose veins?
* History and examination
* Venous duplex scan:
* site of incompetence
* assess deep venous system
43
What is the management of varicose veins?
* 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
What is gangrene?
abnormal irreversible tissue necrosis due to decreased vascular nutrient supply
45
How would you classify gangrene?
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
What are the treatment options for gangrene?
* Conservative: treatment strategies - preventatic/Rx underlying cause
* Medical: Infection -\> ABx
* Surgical: debridement/amputation
