Arterial Disease Flashcards
Anatomy of lower limb arteries
Aorta
Iliacs – common, external, internal
Femorals – common, superficial, profunda
Popliteal
Tibials (calf vessels) – posterior, anterior, peroneal
Collaterals
Risk factors for arterial disease
Smoking - toxins in bloodstream, ROS, endothelial damage
Diabetes – dislipidaemia, cellular dysfunction + signalling impairment
Hyperlipidaemia – plaque deposition
Hypertension – flow turbulence/ shear forces lead to plaque formation
Sedentary lifestyle -
Age - inflammatory processes, reduced organ function etc
Heart disease – ‘arteriopath’
Family history – genetic factors
Indications For Study
Pain (claudication or rest pain)
Cold feet, hair loss, delayed CRT >5s
Tissue necrosis, gangrene or ulceration
Pre-op evaluation /post-op assessment
Suitability for compression therapy
Long term monitoring
Source of distal embolisation
Aneurysmal disease
What is intermittent claudication?
Cramping pain on walking
Hip, thigh, buttock or calf
Site of pain relates to the level of disease
Reproducible – patient can walk for a set distance before needing to rest. After resting patient can walk further again
Blood supply is sufficient at rest, but not
good enough for increased muscle demand
(10-20 x 0₂ demand)
What is rest pain?
Burning pain even without increased muscle demand
Ball of foot and toes
Worse at night
Critical limb ischaemia
Precursor to tissue loss
Exacerbated on limb elevation, relieved by sitting or standing
What is chronic limb ischaemia, ulcers and gangrene?
Treatment?
Poor perfusion of leg and foot leads to poor wound healing, development of ulcers and ultimately tissue loss.
Debridement, antibiotics, revascularisation, amputation.
Leg Pain:Differential Diagnoses
Sciatica / spinal stenosis
Venous disease
Arthritis / joint disease
Soft tissue injury
Infection
Acute Limb Ischaemia
Surgical emergency
6 hours to get limb revascularised before irreversible tissue loss
High associated morbidity (limb loss 40%) and mortality (20%)
High limb loss from local atherosclerotic thrombosis
High mortality from embolic cases
Causes of ALI
60% atherosclerotic-thrombo occlusion
Embolus (usually cardiac)
Aortic dissection
Thrombosed aneurysm (popliteal)
Trauma
Thrombosed bypass graft
Intra-arterial drug administration
Signs and Symptoms of ALI
6 Ps
Pain
Pale (initially)
Pulseless
Paraesthesia
Perishingly cold
Paralysis
Rationale for ALI scanning
Confirm clinical diagnosis
Identify site, nature and length of block
Assess proximal and distal vessels
Assess collaterals
Identify site / cause of embolus
Monitor effectiveness of treatment
Treatment for ALI
Thrombolysis
- Streptokinase via catheter
Thrombectomy
Anticoagulation
Bypass grafting
Amputation
What is atherosclerosis
Narrowing of vessel lumen due to build up of plaque
Invasion of white blood cells & proliferation of smooth muscle cells
Plaque forms diffuse disease or focal stenoses
Stenoses can develop into full occlusions
Precursor to heart attack, stroke and PVD.
What is thrombectomy?
A thrombectomy is a procedure to remove a blood clot, also known as a thrombus. It’s done by opening up the affected vein or artery and removing the clot.
Two general types of procedures can be used for a thrombectomy. These are:
Surgical (open) thrombectomy: A surgeon opens a blood vessel and extracts the clot with a vacuum or catheter.
Percutaneous (minimally invasive) thrombectomy: A surgeon uses image guidance (such as a continuous X-ray) to lead one of several types of devices to the clot. The device might suction the clot out of the blood vessels, or it could break the clot apart so the pieces can be vacuumed out.
PAD treatment
Lifestyle changes (exercise, stop smoking)
Medical management – statins (cholesterol), anti-hypertensives, anti-platelets
Control of diabetes
Surgery – angioplasty/stenting or bypass grafts or amputation
Bypass grafts
Reversed vein (LSV) or synthetic graft (i.e. Dacron)
Require surveillance – risk of stenosis/occlusion/infection
Aorto-bifemoral bypass
Femoral-popliteal bypass
Femoro-femoral crossover
Other Pathology causing PAD symptoms
Arteritis
Aneurysms/false aneurysms
Thrombus
Arterio-venous malformation
Popliteal entrapment
Cystic adventitial disease
Dissection
Buergers disease (thromboangitis obliterans)
Raynauds disease
Soft tissue mass
Lymphadenopathy
Haematoma / seroma
Arteritis
Inflammation of the vessel wall
Infectious or autoimmune
Large or medium vessels
Smooth thickening of wall causes narrowing of lumen
Can cause thrombosis
Takayasu’s arteritis/temporal arteritis
Fever, malaise, weight-loss, reduced pulses
Aneurysms
Vessel diameter >50% more than normal
All 3 layers of the vessel wall involved
Saccular or fusiform
Atherosclerotic / infective / traumatic in origin
Common sites are aorta and popliteals, but can be anywhere
UK screening programme – males at 65
Rupture carries very high mortality
Aneurysm treatment
Intervention at 5.5cm or if quickly growing
Open repair (higher risk, fewer ongoing complications)
EndoVascular Aneurysm Repair (EVAR) (lower risk, needs more surveillance, higher risk of complications/further intervention)
False Aneurysms
Arterial wall not intact – outer layer(s) involved
Eccentric in shape
Usually due to trauma, intervention, injury (intra-venous drug use)
May have a discernible neck
Characteristic in-out flow
Treatment:
Large ones (>2cm) usually surgically ligated
Thrombin injection under U/S guidance
Compression with U/S probe
Difficult and painful!!
Dissection
Separation of the intimal layer from the rest of the wall
Blood can enter space between layers causing stenosis or complete occlusion
Traumatic or spontaneous (high BP, connective tissue disorders)
Carotid stroke
Aortic severe chest pain
Microvascular disease
Arterioles, venules & capillaries
Blood pressure maintenance and nutrient delivery (macrovessels deliver blood to organs)
Adaptive response to alter permeability and flow
Diabetes thickening and loss of microvascular function
Hypertension, delayed wound healing, tissue hypoxia
Macrovascular: PVD, ischaemic heart disease, stroke
Microvascular: Nephropathy, neuropathy, retinopathy
Arterio-Venous Malformation
Communication between artery and vein, where blood passes quickly from artery to vein, bypassing the normal capillary network!
May be congenital, traumatic or surgically created (fistula for dialysis)
Arterial flow shows greatly increased diastolic flow
Venous flow shows arterialisation
Managed by embolisation
Arterio-Venous Fistulas
For dialysis
High flow rate
Take time to mature
Risk of steal/aneurysm
Popliteal Entrapment
Popliteal artery compressed by heads of gastrocnemius muscle
Occurs on exercise or knee extension
Usually young athletic patients
Caused by anomalous course of vessel / muscle head
If uncorrected may lead to occlusion / distal embolus
Cystic Adventitial Disease
A cyst-like structure within the adventitial layer of the artery wall
Usually occurs in the popliteal artery
Rare, usually males, fourth decade in life
Clinical appearance of calf pain
Treatment by surgical resection
Buergers Disease
Affects small and medium sized arteries of the limbs
Predominantly young males 20 – 40yrs
Usually heavy smokers – auto-immune response to tobacco
Long string-like arteries with inadequate collaterals
Thoracic outlet syndrome
Compression of the subclavian artery/vein and nerve
Positional
Cervical rib, trauma, muscular hypertrophy, repetitive injury
Can result in DVT/claudication/numbness/cold fingers
Resection of cervical rib/stenting
Mesenteric ischaemia
Acute/chronic
Ischaemia & gangrene of bowel wall
Extreme abdominal pain on eating +/- nausea & vomiting
Patients very thin – avoid eating
Thrombolysis/angioplasty/stenting/
bypass surgery
Technical Limitations
Obesity
Calcified vessels
Ulceration/gangrene
Recent surgery/intervention
Tortuous vessels / anatomical variants
Bowel gas (aorto-iliac segment)
Pain
Imaging Modalities
Arteriography
Duplex ultrasound
CT
MRI
Doppler spectral analysis
Arteriography
Gold Standard examination (?)
Costly
Invasive
Time consuming
Has morbidity / mortality
Delivers radiation and contrast
Technical limitations
Requires aftercare
But can be combined with intervention
MRI / CT
Costly
Limited availability
Contrast delivered
Radiation exposure (CT)
Patient tolerance issues
Duplex Ultrasound Examination
Pulsed wave Doppler
Shows anatomy and functional information
Identifies specific lesions
Differentiates diffuse and focal disease
Identifies other pathology
Competes with arteriography
Takes longer and is more costly than continuous wave
Can be used for ‘specific’ purposes
Haemodynamics
High resistance flow pattern (muscle beds)
Plug flow in the Aorta, parabolic flow distally
Triphasic waveform
- Result of arterial compliance and propagation of pulse pressure wave
Age related changes
-Biphasic waveform
Various indices can be utilised
Vasodilation
affects the degree of diastolic flow
Proximal disease
Prolongs acceleration time (damping) and reduces velocity
Reduces resistance due to distal vasodilation
Distal disease
Increases resistance and affects deceleration
Waveform Indices
Velocity ratios
-Grade stenosis
Pulsatility index
- (S-D)/M
Resistance index
- (S-D)/S
Acceleration time
- Time from start of systole to peak velocity
Indices used to infer status of upstream and downstream vessels
Abnormal Flow patterns
Spectral broadening
Turbulence
Increased velocities
Decreased velocities
Damped flow
Resistance changes
Other waveform changes
Spectral analysis study
Patient supine and rested
Acquire spectral waveforms from the CFA, POPA, PTA & ATA
Compare each waveform with normal and with proximal waveform
Infer disease status in each arterial segment
Classify as normal, mild, moderate, severe, blocked
Perform ABPI
Duplex Scanning
Imaging & visualisation of disease
Use B-mode (greyscale), colour and spectral Doppler and possibly power Doppler
Identify low-grade and diffuse disease
Interrogate severe lesions to assess degree of stenosis
Identify site and length of occlusions
Duplex Scanning Technique
Patient rested and supine with access to the legs (+/- abdomen).
Scan the vessels fully in longitudinal section using all modes (heel-toe to optimise angles).
Use spectral Doppler to interrogate focal lesions.
Identify blocks
Assess collaterals
Patient Position
Aorto-iliac segment
Supine, occasionally lateral decubitus
Femoral
Supine, legs externally rotated
Popliteal
Lateral decubitus or supine
Tibials
Supine with knee bent / lateral decubitus
Disease classification
Low grade disease
Plaque evident. Velocities less than double proximal vessel
50% Stenosis
Velocities more than double proximal vessel
75% Stenosis
Ratios usually >4 fold increase for LL.
Disease classification
Occlusion
-No flow
Thrombus
-Usually non / low-grade echogenicity (same as blood)
Other
Ankle-brachial Pressure Index (ABPI)
Gives reproducible and quantitative measure of disease severity.
Results independent of systemic BP.
Can be done segmentally
Normally ankle pressure should be roughly the same as brachial pressure
Significant lower limb arterial disease causes a drop in distal pressure
ABPI formula
ankle systolic pressure/ brachial systolic pressure mmHg (units cancels out)
Patient preparation for ABPI
Explain test – will feel tight
History & consent
Patient should be rested supine (10 minutes)
Position is important – brachial and ankle vessels should be at level of heart
Use cling-film if necessary to cover ulcers
Infection control – clean cuff and probe between patients
Risk assessment – DVT, distal graft
ABPI Method
Put blood pressure cuffs around BOTH upper arms and both ankles.
Cuff width > limb diameter
Record systolic BP in BOTH brachial arteries
Identify signal with HHD and note waveform
Inflate cuff until signal disappears (taking care to remain over artery)
Inflate the cuff 20-30mmHg further
Slowly reduced the pressure until the signal returns – that is the systolic pressure
Record systolic BP in the PT and DP/ATA arteries in both ankles
ABPI – identifying the signal
Continuous-wave Doppler (Hand-held Doppler) – 8MHz
Assess the strength and waveform of the posterior tibial artery (PTA) and the anterior tibial artery (ATA) on each ankle.
Place the probe directly above the vessel at a 45-60 degree angle (towards the heart) to the skin surface.
Use slow movements to identify the area where the signal is loudest then make adjustments to the angle to achieve the optimum Doppler signal.
Divide each ankle reading by the HIGHEST brachial reading.
Normally the ankle pressure should be approx equal to or slightly higher than the brachial pressure.
The lower the ABPI the more severe the disease.
Higher values than expected suggest calcified vessels. DIABETICS!!
Resting ABPI vs Severity of Disease
> 1.2 Calcification may be present
1.0 Probably no arterial disease
1.00-0.81 No significant arterial disease or mild/insig disease
0.80-0.5 Mode disease
<0.5 Severe disease
<0.3 Critical ischaemia
ABPI Pitfalls
Probe movement
Room temperature
Arterial / venous signal confusion
Ulceration / gangrene / oedema / obesity
R/L brachial asymmetry
Calcification
Cardiac arrhythmia
Cuff size (too small falsely high, too large falsely low)
Toe Pressures
Useful in cases of vessel calcification (diabetics) or venous ulcers / gangrene
Digital vessels generally spared from disease
Feet must be warm to avoid vasoconstriction
Photoplethysmography usually used
Normal index >0.65
Absolute pressure of <33mmHg
suggestive of CLI
Exercise Study and techniques
Useful if a good history of claudication but normal resting CW study.
Exercise the patient for a set time or until pain occurs.
Immediately repeat ABPI measurements.
A significant reduction (≥20mmHg) in ABPI indicates haemodynamically significant disease
Treadmill
Reproducible program
Corridor walk
Steps / stairs
Tip-toes / foot-flex
Ergometer (bike/rower)
Reactive Hyperaemia
What is Diabetic PAD?
Diabetic PAD is an occlusive arterial disease, affecting distal vessels below the knee. Diabetes augments the process of atherosclerosis through a variety of ways (hypoglycaemia and insulin resistance contribute to endothelial dysfunction by decreasing NO bioavailability and altering the fn of various cell mediators. Oxidative stress therefore promotes the formation of foam cells and fatty streaks. Additionally vascular smooth muscle cells migrate to newly formed lesions, further augmenting plaque development. In advanced atherosclerosis pts with diabetes have less smooth muscle cells in lesions and are more susceptible to plaque rupture than in earlier stages of atherosclerosis. Furthermore, increased platelet aggregation and impaired firbinolaysis also increases risk of thrombosis, therefore pt is high risk for complications. Diabetic patients at higher risk for PAD, with symptoms such as claudication, CLI, and lower extremity amputation
Surgical approaches for PAD
if causing symptoms ro progressing to dangerous level and need more than medial control; standard is bypass - taking tube (vein from leg or synthetic) to connect above and below area of blockage, getting blood downstream to where it is needed in the leg or foot.
Endovascular techniques (avoid surgery) - transposing and sending wire through clogged up material, balloon inflated in area of obstruction to squeeze plaque aside and opens vessel. Stent is put in to restore potency of vessel. Can use suction to suck out plaque via catheter. If plaque is so solid, can use laser to bore a hole in it, to then go to angioplasty. Cryoangioplasty uses liquid nitrogen to freeze plaque and cool down cell types within plaque, prevents restenosis.
