vascular Flashcards
Peripheral Vascular/Artery Disease definition
• Obstruction or narrowing of arteries distal to the aorta and not within the coronary or brain circulation.
• Different classifications FONTAINE’S STAGES:
- I – asymptomatic
- II – intermitten claudication
- IIa – pain with walking more than 200m
- IIb – pain with walking less than 200m
- III – rest/nocturnal pain
- IV – necrosis, gangrene and/or ulceration
how common is Peripheral Vascular/Artery Disease
- Affects 4-12% of people aged 55-70 and 15-20% of people aged >70
- Acute limb ischaemia has an incidence of around 1 in 12,000 people per year
- Chronic limb ischaemia is much more common than this
who does Peripheral Vascular/Artery Disease affect
- 7% of middle-aged men and 4.5% of middle-aged women
* Strongly age-related
biological causes of Peripheral Vascular/Artery Disease
- PVD can result from atherosclerosis, inflammatory processes leading to stenosis, an embolism, or thrombus formation
- It causes either acute or chronic ischaemia.
symptoms of Peripheral Vascular/Artery Disease
ACUTE LIMB ISCHAEMIA:
- Onset of leg pain over minutes, hours or days
- Pulseless, pallor, painful, paraesthesia, paralysis and perishingly cold
CHRONIC LIMB ISCHAEMIA:
- Progressive development of cramp like pain in the calf, thigh or buttock after walking a given distance (claudication distance) – buttock pain suggests iliac disease, calf pain suggests femoral disease; buttock pain + male impotence suggests Leriche syndrome
BOTH:
- Pain resolves with rest
- Pain at night resolved by hanging leg out of bed
- Male impotence – suggests Leriche syndrome if with buttock pain
- Painful ulcer
signs for Peripheral Vascular/Artery Disease
6 Ps of Acute Limb Ischaemia (Acute Occlusion Causing Ischaemia):
• Pallor – redness returns on lowering leg
• Pulselessness – absent femoral, popliteal or foot pulses
• Pain
• Paralysis
• Parasthaesia
• Perishing with cold
General Signs: • Hair loss • Delayed capillary refill (>15s) • Small, painful, ‘punched-out’ ulcers over bony prominences • Thickened, brittle toenails • Smooth, shiny, dry skin • Hang legs over the bed • +ve Buerger’s test – angle to which the leg has to be raised for it to turn pale; normal = no pallor even at 90 degrees; <20 degrees is positive sign
DDx for Peripheral Vascular/Artery Disease
- Sciatica/spinal cord claudication - all pulses present; shooting pain
- DVT/venous claudication – hot, swollen leg; no hair loss; painless ulcer with ragged edges; haemosiderin
- Knee or hip osteoarthritis – joint pain and stiffness; worse in evening; pulses present; no pallor or hair loss
- Peripheral neuropathy – numbness or tingling; pulses present; weakness; gait abnormalities; not cold or pale
- Popliteal artery entrapment – young patients; congenital; myotomy of gastrocnemius; diminished pulses on forced plantar/dorsiflexion
- Buerger’s disease – young to middle aged presentation; affects mainly males; two or more limbs affected; Raynaud’s phenomenon
Investigations for Peripheral Vascular/Artery Disease
ABPI (ANKLE BRACHIAL PRESSURE INDEX):
• Measure 4 ankle and 2 arm pressures
• Right ABPI = highest of right ankle pressures/highest arm pressure
• Left ABPI = highest of left ankle pressures/highest arm pressure
• <1 = circulatory problems
• >0.9 = borderline – higher prognosis
• 0.5-0.9 = PAD
• <0.5 = critical limb ischaemia – low prognosis
• If resting ABPI is normal then an exercise one can be done – measure before and after exercise, if there is a drop of 15-20% then this is diagnostic of PAD
• >1.4 = incompressible arteries – seen in DM or renal disease, falsely high results
COLOUR DUPLEX USS:
• If ABPI abnormal
• To assess extent of atherosclerosis
MR/CT ANGIOGRAPHY:
• If considering intervention
• Largely replaced digital subtraction angiography
Management for Peripheral Vascular/Artery Disease
RISK FACTOR MODIFICATION: • Quit smoking • Treat HTN and high cholesterol • Weight reduction if overweight • DM control • Exercise to point of maximal pain • Supervised exercise programmes – reduce symptoms by improving collateral blood flow
MEDICAL:
• Clopidogrel to reduce MI/stroke risk 1st line
• Vasoactive drugs e.g. naftidrofuryl oxidate offer modest benefit and recommended only in those who do not wish to undergo revascularisation and if exercise fails to improve symptoms
SURGICAL – if conservative measures fail; PAD severely affecting patient’s life-style or becoming limb threatening
PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY:
• For disease limited ot a single arterial segment
• Balloon inflated in narrowed segment
SURGICAL RECONSTRUCTION:
• If atheramotous disease is extensive but distal run-off is good
• Arterial reconstruction with bypass graft
• Femoral-popliteal bypass, femoral-femoral crossover, aorto-bifemoral bypass grafts
• Autolgous vein grafts are superior to prosthetic grafts
AMPUTATION:
• In sever ischaemia with unreconstructable arterial disease
• <3% patients with intermittent claudication require major amputation within 5 years
• Knee should be preserved wherever possible as it improves mobility and rehabilitation potential
Prognosis for Peripheral Vascular/Artery Disease
Outcome for patients presenting with intermittent claudication over five years:
• 50% will improve, 25% will stabilise and 25% will worsen. Of those who worsen, 20% (5% of total) will need intervention and 8% (2% of total) will need a major limb amputation.
• 5-10% will have a non-fatal cardiovascular event.
• 30% will die: cardiac 16%, cerebral 4%, other vascular 3%, non-vascular 7%.
• 55-60% will survive with no cardiovascular event.
Abdominal Aortic Aneurysm (AAA) definition
- A permament and irreversible localised dilatation of the abdominal aorta by more than 50% of its normal diameter
- The abdominal aorta is normally 2cm so an AAA is classed as >3cm
- Majority of aortic aneurysms are abdominal but some can be thoracic and can also extend to affect the iliac, femoral and popliteal arteries
- 90% of AAAs oocur infrarenally, below the level of the renal arteries.
- TRUE ANEURYSM - involves all layers of the arterial wall. False aneurysms (pseudoaneurysms) involve a collection of blood in the outer layer only (adventitia) which communicates with the lumen
- Aneurysms can be fusiform (most AAAs) or sac-like (e.g. Berry Aneurysms)
how common is Abdominal Aortic Aneurysm (AAA)
- Incidence increases with age.
* Present in 3% of population >50y.
who does Abdominal Aortic Aneurysm (AAA) affect
- M 3x>F and in ¼ of male children of an affected individual.
- 8:1 in smokers.
- Rarely affects African/Hispanic, low prevalence in Asians, mainly affects Caucasians.
- Less common in diabetics.
biological causes of Abdominal Aortic Aneurysm (AAA)
Most will have no clear identifiable cause in these cases there may be:
- Atherosclerosis - new evidence suggests this is not the only factor and that there is also a distinct arterial pathology
- Trauma
- Infection e.g. mycotic aneurysm in endocarditis, tertiary syphilis
- Connective tissue disorders (e.g. Marfan’s, Ehlers-Danlos)
- Inflammatory e.g. Takayasu’s aortitis
pathophysiology of Abdominal Aortic Aneurysm (AAA)
- AAA results from a failure of the major structural proteins of the aorta – elastin and collagen
- The mechanism is not fully understood but it is to do with proteolysis or degradation of the proteins
- The elimination of elastin from the tunica media means the aortic wall is more susceptible to the influence of blood pressure
- The diameter of the aorta gradually decreases distally and infrarenally it contains less elastin which means the mechanical tension is higher
- This is why abdominal aneurysms are more common than thoracic
risk factors of Abdominal Aortic Aneurysm (AAA)
- Smoking – 8x more likely
- Male
- Fx– 15% of first degree releatives will also develop an AAA; probably strong genetic links
- Age
- HTN
- Hyperlipidaemia
- COPD
- DM seems to decrease the risk
symptoms of Abdominal Aortic Aneurysm (AAA)
- Most are asymptomatic and found on routine abdo exam
- As it expands it may cause:
- Epigastric pain radiating to back
- Pulsating sensations in abdomen
- Pain in chest, lower back or scrotum – due to pressure on nearby structures; back pain may be due to erosion of vertebral bodies
signs of Abdominal Aortic Aneurysm (AAA)
- Pulsatile abdominal swelling
- Aortic bruits
RUPTURED AAA MAY PRESENT WITH: • Pain in abdomen, back or loin – may be sudden and severe • Hypotension • Pulsatile and expansile abdominal mass • Syncope, shock or collapse • Sudden death
DDx of Abdominal Aortic Aneurysm (AAA)
- Acute abdomen e.g. cholecystitis, appendicitis, bowel obstruction, pancreatitis, pyelonephritis
- If TAA then other causes of chest pain e.g. MI, PE
Investigations of Abdominal Aortic Aneurysm (AAA)
• If suspected rupture, then investigations need to be swift and pertinent.
INVESTIGATIONS:
• BLOODS – FBC, clotting, renal function, liver function, cross-match if surgery planned, ESR/CRP if inflammatory cause suspected
• ECG
• IMAGING – do not waste time on if rupture, CT can be useful in more stable patient with uncertain diagnosis
• USS – used for intial assessment and follow-up, can assess to accuracy of 3mm
• MRI Angiography – put in two cannulas, call a vascular surgeon and anaesthetist, treat with ORh –ve, keep systolic bP <100mmHg, take blood for amylase, Hb, cross match
Management of Abdominal Aortic Aneurysm (AAA)
CONSERVATIVE MANAGEMENT:
• For asymptomatic AAAs where risk of repair is higher than risk of not treating
• Modify and treat risk factors
• Treat underlying causes e.g. infection
• Regular monitoring
• DVLA must be notified of aneurysms >6cm. >6.5cm disqualifies person from driving.
MEDICAL MANAGEMENT:
• To treat risk factors and underlying causes
• Some evidence that some drugs may reduce diameter of small aneurysms e.g. doxycycline, roxithromycin, ACE-I, losartan, statins, low-dose aspirin
SURGICAL MANAGEMENT:
• Indicated for all aneurysms >5.5cm, rupture, rapid expansion or onset of sinister symptoms
• Open repair
EVAR (ENDOVASCULAR ANEURYSM REPAIR):
• Stent-graft system through femoral arteries
• Less invasive but failure of graft can occur
Prognosis Abdominal Aortic Aneurysm (AAA)
prognosis -
• Overall mortality for elective surgery repair is 2.4%.
• Increasing size = increasing risk of rupture.
• 1 in 3 patients with rupture reach hospital alive and 20% of those that do don’t reach theatre
complications of Abdominal Aortic Aneurysm (AAA)
- Aortic dissection
- Rupture
- Ureterohydronephrosis – due to compression of the ureters
- Distal embolization leading to limb ischaemia – mirco-embolic lower limb infarcts with palpable pedal pulses suggest popliteal or abdominal aneurysm
- Retroperitoneal fibrosis or inflammation
varicose veins definition
• Long, tortuous, dilated veins of the superficial venous system which normally occur in the legs but can occur elsewhere.
how common is varicose veins
- Extremely common.
* Incidence of 2.6% in women and 2% in men.
who does varicose veins affect
• More common with increasing age and post-pregnancy
biological causes for varicose veins
• Blood from superficial veins drain into the deep veins via perforator veins (perforate deep fascia) and at the sapeno-femoral and sapheno-popliteal junctions.
• Valves prevent blood from flowing from the deep to superficial veins
• If these valves become incompetent, then there is venous hypertension and dilatation of the superficial veins occurs.
• CAUSES:
- Idiopathic
- Congenital valve disease – very rare; primary cause
- Obstruction due to DVT, foetus, ovarian tumour
- Valve desctruction due to DVT
- Arteriovenous malformation – causes increased pressure
- Constipation – causes increased pressure
- Overactive muscle pumps (e.g. cyclists)
risk factors for varicose veins
- Pregnancy
- Obesity
- Prolonged standing
- Family history
- Oral contraceptive pill
- Prior DVT
symptoms of varicose veins
My Legs Are Ugly” • Pain • Cramps • Tingling • Heaviness • Restless legs • Itching • May be aggravated by prolonged standing, pregnancy, menstruation, sexual intercourse
signs of varicose veins
- Oedema
- Dilated tortuous veins
- Venous eczema – due to waste products building up in the leg
- Ulcers
- Haemosiderin
- Haemorrhage
- Phlebitis
- Atrophie blanche – white scarring at the site of a previous healed ulcer
- Lipodermatosclerosis - skin hardness from subcutaneous fibrosis caused by inflammation and fat necrosis
DDx of varicose veins
- Cellulitis – red, hot, swollen legs; systemic symptoms
- Superficial phlebitis – can occur secondary to varicose veins; redness and tenderness along the vein with swelling
- DVT – hot, swollen, red legs; varicose veins can form secondarily
Investigations of varicose veins
• TRENDELENBURG’S TEST – not to be confused with Trendelenberg’s sign for adductor weakness in the hip:
- This can sometimes distinguish patients with superficial venous reflux from those with incompetent deep venous valves.
- The patient should lie flat with the leg elevated, allowing the veins to empty. A tourniquet is applied to the thigh at the saphenous opening.
- If the valve is competent, the vein should fill from below.
- If the valve is incompetent, the vein will fill from above on removal of the tourniquet.
- This can be repeated at various levels, until the location of an incompetent vale is located.
• PERTHES’ MANOEUVRE:
- This manoeuvre is used to distinguish antegrade flow from retrograde flow in superficial varicosities.
- Antegrade flow is an indicator of collateral flow around a deep venous obstruction.
- A tourniquet is applied to a varicose leg in such a way that the superficial veins are compressed without pressure being applied to the deep vessels.
- The patient is then asked to stand repeatedly on tiptoe, activating the calf muscles.
- Normally this would empty the varicosities but, in the presence of deep vein obstruction, they would paradoxically become congested.
• COUGH IMPULSE - at saphenofemoral junction
• PERCUSSION TEST - tap VVs ditally and palpated for transmitted impulse at the SFJ (interrupted by competent valves)
• DOPPLER USS - listen for flow in incompetent valves when calf is squeezed, this has superseded all the above tests but doctors are asked to understand the principles behind those tests
Treatment - biological
• TREAT ANY UNDERLYING CAUSE • EDUCATION: - Avoid prolonged standing - Support stockings - Lose weight - Regular walks (aid venous return) • ENDOVASCULAR TREATMENT: - RADIOFREQUENCY ABLATION o Catheter inserted into vein and heated to 120 degrees destroying the endothelium and closing the vein - ENDOVENOUS LASER ABLATION o Same as above but with laser - INJECTION SCLEROTHERAPY o Liquid or foam sclerosealant is injected into the vein o Liquid requires vein compression for a few weeks o Foam spreads rapidly • SURGERY: • Saphenofemoral ligations (Trendelenburg procedure) • Multiple avulsions • Stripping from groin to upper calf • Very effective long-term
prognosis and complications of varicose veins
prognosis - a fairly high recurrence rate. 15-20% of surgeries are for recurrence.
complications:
• Haemorrhage
• Thrombophlebitis
• Venous ulcers
Arterial Embolism definition
• Long, tortuous, dilated veins of the superficial venous system which normally occur in the legs but can occur elsewhere.
how common is Arterial embolism
- 550,000 people die from these kind of complications
* More common with increasing age and post-pregnancy.
causes of arterial embolism
- Solid mass in the circulation from the constituents of the blood during life
- Emboli may break off and block vessels further down
- Arterial thrombosis is usually the result of atheroma, which forms particularly in areas of turbulent blood flow such as the bifurcation of arteries
- Platelelts adhere to the damaged vascular endothelium and aggregate in response to ADP and thromboxane A2
- This may stimulate blood coagulation, leading to complete occlusion of the vessel, or embolism resulting in distal obstruction
- Arterial emboli may also form in the LF after MI, in the LA in mitral valve disease or on the surface of prosthetic valves
risk factors of arterial embolism
- Advanced age
* Cigarette smoking
symptoms /signs of arterial embolism
- 6Ps: pallor, paralysis, pulselessness, paraesthesia, pain, perishingly cold
- Muscle spasm
- Light-headedness
DDx of arterial embolism
- Thrombophlebitis
- MI
- AF
Investigations of arterial embolism
- 1ST LINE:
- DOPPLER ULTRASOUND: checks bloodflow, examine arteries to the brain
- ECHOCARDIOGRAPHY: diagnoses MI
- ARTERIOGRAPHY: check the affected extremity or organ, can do a digital subtraction angiography where administration of radiopaque contrast material must be kept to a minimum
- BLOOD TESTS: measures elevated enzymes in the blood e.g. specific troponin T/I, myoglobins and CK isoenzymes which indicate embolization to the heart that has caused MI
treatment of arterial embolism
- 1st LINE:
- ANTICOAGULANTS: warfarin
- ANTIPLATELETS: aspirin – prevents new clots
- PAINKILLERS: give IV e.g. morphine
- VASODILATORS: relax and dilate blood vessels e.g. adenosine
- SURGERY: arterial bypass, embolectomy – thromboaspiration, angioplasty
prognosis and complications of arterial embolism
prognosis -
Good prognosis when treated
complications - Necrosis, gangrene
chronic venous insufficiency
- Functional changes that may occur in the lower extremity due to perisistent elevation of venous pressures
- Commonly results from venous reflux due to faulty valve function developing as a long-term sequela of DVT
how common is Chronic Venous Insufficiency
• CVI affects about 7% of the population
risk factors for Chronic Venous Insufficiency
- Increasing age
- Fx
- Smoking
- DVT
- Orthostatic occupation
- Female
- Obese
- Ligamentous laxity
symptoms/signs for Chronic Venous Insufficiency
- Corona phlebectatica (mallelolar flare or ankle flare)
- Ankle swelling
- Hyperpigmentation (brawny oedema)
- Lipodermatosclerosis
- Atrophie blanchie
- Leg ulcers
- Leg fatigue
- Heavy legs
- Leg cramps
- Telangiectasias
- Retiuclar veins
- Dilated tortuous veins
- Dry and scaly skin
DDx for Chronic Venous Insufficiency
- Diabetic foot ulcer
- Arterial ulcer
- SCC
- Kaposis sarcoma
- Pyoderma gangrenosum
- CHF
- Renal disease
Investigations for Chronic Venous Insufficiency
- 1st LINE:
* DUPLEX USS: retrograde or reversed flow, valve closure time >0.5 seconds
Treatment of Chronic Venous Insufficiency
• 1ST LINE:
- GRADED COMPRESSION STOCKINGS
Prognosis and complications from Chronic Venous Insufficiency
Prognosis - Not limb threatening, dependent on compliance with stockings
complications - • Haemorrhage, infection, lipodermatosclerosis
causes for Chronic Venous Insufficiency
- CVI is caused by functional abnormalities in lower extremity veins
- This abnormality is usually reflux, but it can also be chronic obstruction or a combination of the two
- It occurs in as many as 50% of people within 5 to 10 years of an episode of DVT
- Cogenital absence of the venous valves is a less common cause and isolated primary varicose veins (pure superficial incompetence) uncommonly causes severe CVI
