vascular Flashcards

(52 cards)

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
how common is varicose veins
* Extremely common. | * Incidence of 2.6% in women and 2% in men.
26
who does varicose veins affect
• More common with increasing age and post-pregnancy
27
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)
28
risk factors for varicose veins
* Pregnancy * Obesity * Prolonged standing * Family history * Oral contraceptive pill * Prior DVT
29
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 ```
30
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
31
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
32
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
33
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 ```
34
prognosis and complications of varicose veins
prognosis - a fairly high recurrence rate. 15-20% of surgeries are for recurrence. complications: • Haemorrhage • Thrombophlebitis • Venous ulcers
35
Arterial Embolism definition
• Long, tortuous, dilated veins of the superficial venous system which normally occur in the legs but can occur elsewhere.
36
how common is Arterial embolism
* 550,000 people die from these kind of complications | * More common with increasing age and post-pregnancy.
37
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
38
risk factors of arterial embolism
* Advanced age | * Cigarette smoking
39
symptoms /signs of arterial embolism
* 6Ps: pallor, paralysis, pulselessness, paraesthesia, pain, perishingly cold * Muscle spasm * Light-headedness
40
DDx of arterial embolism
* Thrombophlebitis * MI * AF
41
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
42
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
43
prognosis and complications of arterial embolism
prognosis - Good prognosis when treated complications - Necrosis, gangrene
44
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
45
how common is Chronic Venous Insufficiency
• CVI affects about 7% of the population
46
risk factors for Chronic Venous Insufficiency
* Increasing age * Fx * Smoking * DVT * Orthostatic occupation * Female * Obese * Ligamentous laxity
47
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
48
DDx for Chronic Venous Insufficiency
* Diabetic foot ulcer * Arterial ulcer * SCC * Kaposis sarcoma * Pyoderma gangrenosum * CHF * Renal disease
49
Investigations for Chronic Venous Insufficiency
* 1st LINE: | * DUPLEX USS: retrograde or reversed flow, valve closure time >0.5 seconds
50
Treatment of Chronic Venous Insufficiency
• 1ST LINE: | - GRADED COMPRESSION STOCKINGS
51
Prognosis and complications from Chronic Venous Insufficiency
Prognosis - Not limb threatening, dependent on compliance with stockings complications - • Haemorrhage, infection, lipodermatosclerosis
52
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