vascular Flashcards

1
Q

Peripheral Vascular/Artery Disease definition

A

• 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

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2
Q

how common is Peripheral Vascular/Artery Disease

A
  • 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
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3
Q

who does Peripheral Vascular/Artery Disease affect

A
  • 7% of middle-aged men and 4.5% of middle-aged women

* Strongly age-related

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4
Q

biological causes of Peripheral Vascular/Artery Disease

A
  • PVD can result from atherosclerosis, inflammatory processes leading to stenosis, an embolism, or thrombus formation
  • It causes either acute or chronic ischaemia.
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5
Q

symptoms of Peripheral Vascular/Artery Disease

A

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
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6
Q

signs for Peripheral Vascular/Artery Disease

A

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
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7
Q

DDx for Peripheral Vascular/Artery Disease

A
  • 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
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8
Q

Investigations for Peripheral Vascular/Artery Disease

A

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

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9
Q

Management for Peripheral Vascular/Artery Disease

A
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

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10
Q

Prognosis for Peripheral Vascular/Artery Disease

A

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.

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11
Q

Abdominal Aortic Aneurysm (AAA) definition

A
  • 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)
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12
Q

how common is Abdominal Aortic Aneurysm (AAA)

A
  • Incidence increases with age.

* Present in 3% of population >50y.

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13
Q

who does Abdominal Aortic Aneurysm (AAA) affect

A
  • 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.
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14
Q

biological causes of Abdominal Aortic Aneurysm (AAA)

A

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
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15
Q

pathophysiology of Abdominal Aortic Aneurysm (AAA)

A
  • 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
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16
Q

risk factors of Abdominal Aortic Aneurysm (AAA)

A
  • 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
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17
Q

symptoms of Abdominal Aortic Aneurysm (AAA)

A
  • 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
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18
Q

signs of Abdominal Aortic Aneurysm (AAA)

A
  • 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
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19
Q

DDx of Abdominal Aortic Aneurysm (AAA)

A
  • Acute abdomen e.g. cholecystitis, appendicitis, bowel obstruction, pancreatitis, pyelonephritis
  • If TAA then other causes of chest pain e.g. MI, PE
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20
Q

Investigations of Abdominal Aortic Aneurysm (AAA)

A

• 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

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21
Q

Management of Abdominal Aortic Aneurysm (AAA)

A

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

22
Q

Prognosis Abdominal Aortic Aneurysm (AAA)

A

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

23
Q

complications of Abdominal Aortic Aneurysm (AAA)

A
  • 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
24
Q

varicose veins definition

A

• Long, tortuous, dilated veins of the superficial venous system which normally occur in the legs but can occur elsewhere.

25
Q

how common is varicose veins

A
  • Extremely common.

* Incidence of 2.6% in women and 2% in men.

26
Q

who does varicose veins affect

A

• More common with increasing age and post-pregnancy

27
Q

biological causes for varicose veins

A

• 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)

28
Q

risk factors for varicose veins

A
  • Pregnancy
  • Obesity
  • Prolonged standing
  • Family history
  • Oral contraceptive pill
  • Prior DVT
29
Q

symptoms of varicose veins

A
My Legs Are Ugly”
•	Pain
•	Cramps
•	Tingling
•	Heaviness
•	Restless legs
•	Itching
•	May be aggravated by prolonged standing, pregnancy, menstruation, sexual intercourse
30
Q

signs of varicose veins

A
  • 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
31
Q

DDx of varicose veins

A
  • 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
32
Q

Investigations of varicose veins

A

• 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

33
Q

Treatment - biological

A
•	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
34
Q

prognosis and complications of varicose veins

A

prognosis - a fairly high recurrence rate. 15-20% of surgeries are for recurrence.

complications:
• Haemorrhage
• Thrombophlebitis
• Venous ulcers

35
Q

Arterial Embolism definition

A

• Long, tortuous, dilated veins of the superficial venous system which normally occur in the legs but can occur elsewhere.

36
Q

how common is Arterial embolism

A
  • 550,000 people die from these kind of complications

* More common with increasing age and post-pregnancy.

37
Q

causes of arterial embolism

A
  • 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
38
Q

risk factors of arterial embolism

A
  • Advanced age

* Cigarette smoking

39
Q

symptoms /signs of arterial embolism

A
  • 6Ps: pallor, paralysis, pulselessness, paraesthesia, pain, perishingly cold
  • Muscle spasm
  • Light-headedness
40
Q

DDx of arterial embolism

A
  • Thrombophlebitis
  • MI
  • AF
41
Q

Investigations of arterial embolism

A
  • 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
42
Q

treatment of arterial embolism

A
  • 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
43
Q

prognosis and complications of arterial embolism

A

prognosis -
Good prognosis when treated

complications - Necrosis, gangrene

44
Q

chronic venous insufficiency

A
  • 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
45
Q

how common is Chronic Venous Insufficiency

A

• CVI affects about 7% of the population

46
Q

risk factors for Chronic Venous Insufficiency

A
  • Increasing age
  • Fx
  • Smoking
  • DVT
  • Orthostatic occupation
  • Female
  • Obese
  • Ligamentous laxity
47
Q

symptoms/signs for Chronic Venous Insufficiency

A
  • 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
48
Q

DDx for Chronic Venous Insufficiency

A
  • Diabetic foot ulcer
  • Arterial ulcer
  • SCC
  • Kaposis sarcoma
  • Pyoderma gangrenosum
  • CHF
  • Renal disease
49
Q

Investigations for Chronic Venous Insufficiency

A
  • 1st LINE:

* DUPLEX USS: retrograde or reversed flow, valve closure time >0.5 seconds

50
Q

Treatment of Chronic Venous Insufficiency

A

• 1ST LINE:

- GRADED COMPRESSION STOCKINGS

51
Q

Prognosis and complications from Chronic Venous Insufficiency

A

Prognosis - Not limb threatening, dependent on compliance with stockings

complications - • Haemorrhage, infection, lipodermatosclerosis

52
Q

causes for Chronic Venous Insufficiency

A
  • 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