Module 2D - Vascular System Flashcards
What is peripheral arterial disease usually due to?
PAD = disease process resulting from stenosis of large peripheral arteries, exclusive of coronary and intracranial cerebrovascular system, most commonly due to atherosclerosis
(note: random vasospams can also occur)
4 main risk factors for PAD
- Smoking
- Diabetes
- Hypertension
- Dyslipidaemias —> LDH up, HDL down
Clinical presentation of PAD –> Fontaine classification
- short distance is < 200m walking distance
Site of pain in vascular disease –> artery affected:
- Buttock and hip –>
- Thigh –>
- Upper 2/3 of calf –>
- Lower 1/3 of calf –>
- Foot claudication –>
- Buttock and hip - aorta/iliac disease
- Thigh - aortoiliac or common femoral artery
- Upper two-thirds of the calf - superficial femoral artery
- Lower one-third of the calf - popliteal artery
- Foot claudication - tibial or peroneal artery
Leriche syndrome triad
- claudication
- absent femoral pulses
- erectile dysfunction (impotence)
exacerbating + relieving factors
Intermittent claudication is the most common symptom of PAD –> what is it
- Exercised-induced muscle pain - oxygen demand of muscles cannot be met
- Most commonly in the calf, thighs, buttocks
- Worse walking uphill or hurrying - muscles require more oxygen as working harder
- Relieved by rest < 10 minutes - oxygen requirements decrease which relieves pain
appearance of each –> borders?
dry gangrene vs wet gangrene –> which is more serious?
- wet gangrene is more serious and treatment must be done promptly
- dry gangrene tends to be well-demarcated, whereas wet gangrene tends to be more diffuse
Buerger’s test
Buerger’s Test - used to assess the adequacy of arterial supply to the leg
- Patient supine and elevate both legs to 45 degrees and hold for one or two minutes - observe colour of feet (pallor indicates ischaemia)
- Patient sat up with legs hanging over side of the bed at 90 degrees - the skin at first becomes blue (as blood is deoxygenated in its passage through the ischaemic tissue), and then red. This is due to reactive hyperaemia from post-hypoxic vasodilation
- Ischaemia occurs when the peripheral arterial pressure is inadequate to overcome the effects of gravity - the poorer the arterial supply, the less the angle to which the legs have to be raised for them to become pale
Vascular investigations if you suspect patient has PAD
- First line is ABPI –> < 0.9 indicates PAD
- Second line is duplex ultrasound
- Invasive –> CT angiography
Management of asymptomatic PAD or mild claudication
- Lifestyle modification - smoking cessation, exercise (supervised exercise classes), diet control
- Risk factor modification –> control BP, diabetes, statin (atorvastatin 80mg)
- Antiplatelet therapy –> clopidogrel 75mg OD
include surgical options
Management of short-distance claudication PAD
- Lifestyle modification - smoking cessation, exercise (supervised exercise classes), diet control
- Risk factor modification: control BP, diabetes, statin (atorvastatin 80mg)
- Antiplatelet therapy –> clopidogrel 75mg OD
- Intermittent claudication drugs (used if other initial management not worked) –> Naftidrofuryl, Cilostazol
(used if pt refuses to undergo surgery and has tried the other management options) - Endovascular procedures - angioplasty +/- stent placement
- Surgical procedures - endarterectomy, peripheral bypass graft (autologous vein, prosthetic)
When would surgical bypass be used in PAD
Surgical bypass is used when lesions are diffuse (not focal) and angioplasty is not appropriate
Complications of surgery in PAD
- Bleeding and Infection (main risks)
- Distal embolism
- Limb loss - if graft blocks and causes complete ischaemia
- Heart/lung/kidney - MI, chest infections, renal failure
- DVT - patients have reduced mobility post-procedure - all patients have thromboprophylaxis (eg. DOAC)
- Death - if patient has multiple of these complications then increased risk of death
ABPI ?
Symptoms of critical limb ischaemia
- Ischaemic rest pain for greater than 2 weeks –> severe pain at rest due to inadequate oxygen perfusion
- Ischaemic ulcers or gangrene –> typically form at sites of increased focal pressure (malleoli, tips of toes, metatarsal heads, heels - usually dry and punctuate)
- ABPI < 0.5
Management of critical limb ischaemia
- Lifestyle modification
- Pharmacological therapy –> including analgesia
- Wound care in patients with tissue loss or gangrene - important to manage conservatively
- Revascularisation –> angioplasty (with or without stenting) or bypass –> to relieve rest pain or for the management of tissue loss/gangrene in order to avoid amputation
- Amputation –> PAD is leading cause of amputation in the Western world –> amputations considered for pts who are unsuitable for revascularisation with ischaemia causing incurable symptoms or gangrene leading to sepsis
Amputation complications
- Failure of wound to heal (most important complication)
- Wound infection
- Post-amputation pain - 70% of patients report phantom limb pain (important to start neuropathic pain medication - eg. gabapentin)
- Psychological problems
Amputation rehab
- Rehab should start ASAP post-operatively - prevents flexion contractures + start practicing transferring, sitting up in bed
- Once stump healed - elasticated compression stump socks fitted to shrink stump to an acceptable size for fitting for prosthesis
6 Ps of acute limb ischaemia
- Pain
- Pulselessness
- Pallor
- Paraesthesia
- Paralysis
- Poikilothermic (Perishingly cold)
Aetiology of acute limb ischaemia
due to a thrombus (clot) or emboli blocking the arterial supply of a distal limb –> 90% are due to emboli
Rutherford classification of acute limb ischaemia
Once a diagnosis of acute arterial occlusion has been made –> what should the next steps in management be?
- IV heparin bolus followed by a continuous heparin infusion
- Then its either thrombolysis or surgery –> thrombolysis is preferred if appropriate
details of how thrombolysis works
What is thrombolysis and why is it not suitable for limb-threatening ischaemia
- Stimulates secondary fibrinolysis by plasmin –> through the infusion of analogues of tissue plasminogen activator (tPA), the protein that normally activates plasmin
- Usually takes 6-72hrs to achieve clot lysis, and so patients with limb-threatening ischaemia are not candidates for thrombolysis, and require emergent embolectomy
- Local thrombolytic therapy is therefore reserved for patients with non-life-threatening limb ischaemia
What is a limb-threatening condition that can occur after reperfusion of the ischaemic tissue?
Compartment syndrome;
- Post-op –> limb is perfused but, patient reports severe pain in the calf and inability to dorsiflex the foot
- Reperfusion of ischaemic muscle results in muscle oedema –> swelling due to failure of cellular membrane function and capillary leakage
- As muscles are enclosed in bony fascial compartments, an increase in volume leads to increased compartmental pressure - causes pressure on nerves, veins, arteries within compartments
- As compartment pressure rises, tissue perfusion decreases
- As muscle perfusion decreases you get further ischaemic injury, increasing muscle oedema
- This causes obstruction of veins, arteries, and capillaries, nerve dysfunction, and muscle infarction
NOTE: The anterior compartment is the most vulnerable
Types of aneurysms
- True aneursyms –> involves all 3 layers of arterial wall –> can be fusiform or saccular
- False (or ‘pseudo) aneurysms –> hole in arterial wall –> pulsatile haematoma contained by adventitia and surrounding tissues
- Dissection –> tear in the intima, blood enters the arterial wall itself
4 main risk factors for AAA
- Men
- Smokers
- Age > 50 yrs
- Atherosclerosis
Aortic dissection –> what is it
Arterial dissection = tear in arterial wall and blood enters the arterial wall itself, as a haematoma
Two types of aortic dissections
- Type A –> more common and more dangerous –> proximal lesions involving either both the ascending and descending aorta or just the ascending aorta
- Type B –> distal lesions usually begin distal to the subclavian artery –> only affects descending aorta
Symptoms of aortic dissection + differentials
- Sudden onset of excruciating pain –> beginning in anterior chest
- radiating to back between scapulae
- moves downwards as dissection progresses
- Dx —> AAA, MI
Buerger’s disease (aka thromboangitis obliterans) –> what is it + symptoms + management
What is it?:
- Non-atherosclerotic vasculitis characterized by the occlusion of small and medium-sized arteries
Symptoms:
- Chronic ulcerations of the toes, feet, or fingers may appear, which can be followed by frank gangrene
- Severe pain (even at rest) –> related to neural involvement in contrast to the insufficiency caused by atherosclerosis
- Cold sensitivity of hands (similar to Raynaud)
Management:
- Smoking cessation –> if done early then dramatic relief from further attacks
- Vasodilator medications –> Nifedipine (Ca channle blocker), Iloprost (prostacyclin vasodilator)
What are varicose veins? –> size? + aetiology
- distended superficial veins measuring more than 3mm in diameter
- basically increased blood pressure within your veins –> usually affects legs
- Can happen because of age, pregnancy, obesity, prolonged sitting or standing
+ which area is most commonly affected
2 main skin changes that are seen in chronic venous insufficiency/disease
- Chronic pooling of blood in the legs leads to skin changes
- Gaiter area –> most commonly affected area
. - Haemosiderin staining –> bown/yellow appearance
- Venous ulcers
Raynaud phenomenon
Surgical options for AAA
- Open repair or EVAR (endovascular repair)
. - Open repair –> better for younger, more fit patients
- For EVAR –> preferred for older, more sick pts –> as lower risk, but need set amount of aorta above and below aneursym to work with
An endoleak is blood flowing outside the stent graft but inside the aneurysm sac –> type 1 vs type 2 endoleak
- Type 1 endoleak (less common) –> more serious as higher pressure –> high risk of rupture
- Type 2 endoleak (more common) –> less serious as lower pressure –> low risk of rupture
which structure controls the diameter of the blood vessel?
Structure of an artery
- Tunica intima - layer of endothelium which rests on the basement membrane
- Tunica media - made up of vascular smooth muscle
- Tunica externa - elastic connective tissue
Note: The vascular smooth muscle (tunica media) controls the diameter of the blood vessel
Fontaine and Rutherford classifications
Well’s score for DVT
Type A vs Type B aortic dissection
- Type A –> 70%
- Type B –> 30%
Aorta anatomy
Diagram –> normal abdominal aorta vs AAA
Arteriogram showing occlusion
Ulcers –> venous vs arterial v neuropathic vs pressure
Arterial/venous ulcers occur due to poor perfusion –> tissue damage –> poor wound healing
Aortic arch anatomy
Abdominal aorta anatomy
