Vascular Flashcards
(36 cards)
Acute limb ischaemia is …
Sudden decreased in limb perfusion causing a potential threat to viability. Usually due to the occlusion of an artery or prosthesis.
Presentation less than 2 weeks duration
mortality up to 20% and morbidity up to 30%
What is the Rutherford Classification of Acute Limb Ischaemia
I - viable
II A - threatened - salvageable if promptly treated
II B - threatened - salvageable if immediately treated
III - irreversible
Ischaemic Effect on cells?
Reduced cellular oxygen => Loss of oxidative phosphorylation => depletion of ATP => failure of sodium pump => Influx of calcium, sodium and water =>cell swelling - reversible injury
Ca also activates lysosomal enzymes => break down to cytoskeleton => increased damage to cell membrane from shearing due to cell swelling
Increased anaerobic glycolysis => lactic acid accumulation, reduced intracellular H and decreased cellular enzyme activity
Reduced protein synthesis from detachment of ribosomes from RER
Impaired cellular function => neuromuscular compromise
If ischaemia persists → irreversible injury to mitochondrial and lysosomal membranes => cell necrosis (apoptosis by mitochondrial pathway is also thought to contribute)
Ischaemic limb morphology
- Pallor phase die to vasoconsriction
- After 6-12 hours: smooth muscle hypoxia causes vasodilation and fill-in with stagnant deoxygenated blood => mottled skin which blanched with pressure
- Eventually - arteries thrombus, capillaries rupture => fixed blue staining (irreversible)
Ischaemia- Reperfusion injury
Restoration of blood flow to ischaemic tissues but viable tissues results, paradoxically, in increased cell injury
Reoxygenation generation of reactive oxygen species by damaged mitochondria and inflammatory cells + impaired cellular antioxidant mechanisms from ischaemia =>
accumulation of free radicals
-
Exacerbated by inflammation due to influx of leukocytes and plasma proteins
Activation of the complement system may also contribute => bind to injured tissue or deposited antibodies => injury and inflammation
Result is further tissue damage + Reperfusion of a large mass of ischaemic tissue will lead to systemic inflammatory reaction +/- multiple organ dysfunction
What are the 6 ps
Pain
pallor
pulselessness
perishingly cold
paralysis
paraesthesia
– not predictive of extent of ischaemia
Fontaine Severity classification
- for Peripheral vascular disease?
I - asymptomatic
II - intermittent claudication
III - rest pain
IV - tissue loss (ulcers/ gangrene)
Features of critical limb ischaemia?
Rest pain for > 2 weeks OR ulceration/gangrene
AND
Ankle pressure < 50mmHg or toe pressure < 30mmHg
Where ischaemic rest pain, ulcers or gangrene are attributable to proven arterial occlusive disease.
Pathophysiology of Atherosclerosis?
- FATTY STREAK Endothelial cell injury => increased permeability, leukocyte + platelet adhesion and thrombosis => accumulation of lipoproteins within vessel wall (esp LDL which is taken up by macrophages to form foam cells)
- ATHEROMA => smooth muscle proliferation driven by release from activated platelets, macrophages and endothelial cells
- Intra and extra cellular lipid accumulation
- Synthesis of extracellular matrix => FIBROUS CAP + central core of lipid laden cells and fatty debris => can become calcified
What is Leriche syndrome?
Erectile dysfunction, buttock claudication and absent femoral pulses.
(aorto-iliac claudication)
What is Buerger’s test
Buerger’s test=> sunset foot
- Pallor and venous guttering when leg is elevated
- Dependent rubor (impaired autoregulation capillary vasodilation)
- Ischaemic angle angle at which pallor occurs (or Doppler signal lost)
ABPI = ankle brachial pressure index
Technique
- Handheld doppler over peripheral pulse - brachial and ankle
- Inflate BP cuff after finding doppler
- record when pulse reappears
- highest pressure of either pulse at the ankle/ highest brachial pressure
Normal 1-1.2
<0.9 suggests arterial disease
< 0.5 suggest critical ischaemia
>1.2 suggest calcification - diabetes/CKD
Benefits of Exercise therapy program on Claudication
Exercise therapy program (RCT and MA evidence) e.g. supervised 30-45mins at least 3 x per week for min 12w -> re-evaluation (during each session exercise is sufficiently intense to elicit claudication)
- Improves walking distance
- Muscle adaptation
o Improved mitochondrial muscle function and muscle metabolism
o Improved muscle architecture -> Transformation of muscle fibre type
o Improved strength and endurance - Vascular adaptation
o Increased muscle capillary blood flow
o Improved endothelial function
o Vascular angiogenesis
o Reduction in red cell aggregation, blood viscosity and fibrinogen - Reduces cardiovascular mortality
Endovascular/ surgical Rx TASC II working group
A = usually PTA, B = PTA preferred, C = surgery preferred but if high risk surgical candidate -> PTA, D = usually surgery
Iliac
- Type A: stenosis <3cm
- Type B: stenosis 3-10cm, unilateral CIA or EIA occlusion
- Type C: Bilateral CIA occlusion, unilateral CIA + EIA occlusion
- Type D: Bilateral EIA occlusion, disease extending into aorta or CFAs
Femoral
- Type A: SFA stenosis <10cm, occlusion <5cm
- Type B: SFA stenosis or occlusion <15cm, multiple lesions <5cm
- Type C: Multiple lesions totalling >15cm, recurrent disease
- Type D: Chronic total occlusion of CFA or SFA >20cm or involving popliteal
artery
Popliteal
- Type B: Single stenosis
- Type D: Chronic total occlusion of popliteal artery or proximal bifurcation
vessels-
Crural
Type C: Stenoses <4cm, occlusions <2cm ->PTA has modest results and indicated when surgery is contraindicated for patient or technical reasons
Type D: Diffuse disease or occlusions >2cm ->PTA is not advised unless symptoms are limb threatening and surgery is not possible
What is an aneurysm?
An aneurysm is a pathological full-thickness dilation of a blood vessel to >50% of its normal diameter
Pathophysiology of aneurysm
In general results from degeneration of the media leading to abnormal dilatation, usually due to the structure of function of connective tissue being compromised.
Atherosclerosis - Thickening of the intimacy → ischaemia of the inner layers of media → loss of smooth muscle cells weaker muscle walls + Local inflammatory infiltration + production of matrix metalloproteinases → elastin and collagen (connective tissue) degradation
Hypertension - Narrowing of outer arterioles (vasa vasorum) → ischaemia of the outer layers of media (cystic medial degeneration) + loss of smooth muscle weakens muscular wall
Abnormal connective tissue synthesis - Marfans (defect in the scaffolding protein fibrillin) → poor quality of vascular wall + Type IV ehlers danlos (defect in type 3 collagen synthesis)
Vasculitis - antibody mediated damage and necrosis
Infections - Syphilis → spirochetes cause an obliterative endarteritis within vast vasorum causing ischaemic injury and (thoracic) aortic dilatation. Mycotic Aneurysyms - more often saccular eccentric or multilobulated.
Types of Endoleak?
IA: failure to seal proximally
IB: failure to seal distally
II: continued filling of aneurysm sac by lumbar branches or IMA → If sac is expanding, requires intervention → Trans-arterial embolization via femoral vesselsTrans-lumbar direct aortic sac puncture and embolisation
III: failure of an individual component or a seal between
components
IV: seepage through porous graft material (usually self-limiting, uncommon with modern grafts)
V: endotension (sac pressurized but cannot detect leak, may be positional ie. not seen when patient is supine)
What is Chronic Venous Insufficiency?
Syndrome resulting from sustained venous hypertension in the lower legs leading to oedema, progressive skin changes and ulceration.
CEAP Classification -
Clinical Aetiological anatomy Pathophysiology?
Clinical → no signs to active venous ulcer (C0-6)
E → congenital, primary, secondary, no cause
Anatomical - superficial, perforating, deep veins or no venous location identified
Pathophysiology - reflux and or obstruction, no pathology identified
Starling Forces
Fluid movement across the wall of a capillary depends on hydrostatic pressure within the capillary vs interstitium and oncotic pressure in the capillary vs interstitium
Venous Perforators
May - Cockett - Boyd - Dodd - Hungarian
Long Saphenous Vein course
Dorsal venous arch → anterior to medial malleolus → posterior border of femoral epicondyle → 3-4cm inferolateral to pubic tubercle
Short Saphenous Vein Course …
Dorsal venous arch → posteroinferior to lateral malleolus → posterior calf with sural nerve → passes between heads of gastrocs → popliteal vein
Giacomini communicates between LSV and SSV
What is phlegmasia Alba dolens
White leg syndrome due to iliofemoral thrombus
Hypogastric and collateral veins are patent causing white limbs that are swollen and painful without ischaemia
